Interventional Cardiology

Every procedure, device, access technique, hemodynamic assessment, classification, complication, medication, and management algorithm across the full scope of interventional cardiology in one place.

01 Coronary Anatomy & Variants

Coronary Arterial System

The coronary circulation arises from two ostia in the sinuses of Valsalva of the aortic root. The left main coronary artery (LMCA) arises from the left coronary sinus and typically courses 1-2 cm before bifurcating into the left anterior descending artery (LAD) and the left circumflex artery (LCx). In approximately 15-20% of patients, a ramus intermedius arises as a trifurcation branch between the LAD and LCx.

Left Anterior Descending (LAD): Courses in the anterior interventricular groove toward the apex. Gives off septal perforators (supply anterior two-thirds of the interventricular septum) and diagonal branches (D1, D2 — supply the anterolateral wall). The LAD supplies approximately 45-55% of the LV myocardium and is the most commonly diseased coronary artery. The first septal perforator is a landmark separating the left main from the proximal LAD.

Left Circumflex (LCx): Courses in the left atrioventricular groove, giving off obtuse marginal branches (OM1, OM2) that supply the lateral and posterolateral LV wall. In approximately 15% of patients the LCx is dominant (gives rise to the PDA). The LCx also gives off the left atrial circumflex branch and, in some patients, the SA nodal artery.

Right Coronary Artery (RCA): Arises from the right coronary sinus and courses in the right atrioventricular groove. Proximal branches include the conus branch (supplies the RV outflow tract), SA nodal artery (in ~55% of patients), and acute marginal branches (supply the RV free wall). The distal RCA gives rise to the posterior descending artery (PDA) in right-dominant circulation (~85% of the population) and the posterolateral branches.

Coronary Dominance

DominancePrevalenceDefinitionPDA Origin
Right dominant~85%PDA arises from RCADistal RCA at the crux
Left dominant~8%PDA arises from LCxDistal LCx
Co-dominant~7%PDA from both RCA and LCxShared supply
In left-dominant circulation, the left main coronary artery supplies essentially 100% of the LV myocardium. Left main disease in left-dominant patients is a surgical emergency — even brief occlusion can cause cardiogenic shock and death.

Coronary Segments (Modified AHA 15-Segment Model)

The coronary tree is divided into 15 segments for standardized reporting: RCA — proximal (1), mid (2), distal (3), PDA (4); Left Main (5); LAD — proximal (6), mid (7), distal (8), D1 (9), D2 (10); LCx — proximal (11), distal (12), OM1 (12a), OM2 (12b); Ramus intermedius (16 — if present). This segmental model is the basis of the SYNTAX score calculation.

Coronary Collaterals

Collateral circulation develops in response to chronic ischemia and high-grade stenoses. The Rentrop classification grades collateral filling: Grade 0 — no visible filling; Grade 1 — filling of side branches only; Grade 2 — partial filling of the epicardial artery; Grade 3 — complete filling of the epicardial artery. Well-developed collaterals (Rentrop 2-3) reduce infarct size and improve outcomes in CTO PCI.

Coronary Anomalies

Congenital coronary anomalies occur in ~1% of the general population. Anomalous origin from the opposite sinus (ACAOS) is the most clinically significant. An anomalous left main or LAD arising from the right coronary sinus with an interarterial course (between the aorta and pulmonary artery) carries risk of sudden cardiac death due to compression during exercise. An anomalous RCA from the left sinus is more common but less often clinically significant. Other anomalies include myocardial bridging (most commonly mid-LAD, prevalence 5-25% at angiography), coronary fistulae, and anomalous origin from the pulmonary artery (ALCAPA/ARCAPA).

AnomalyPrevalenceClinical SignificanceManagement
Anomalous LCA from right sinus (interarterial)0.02-0.05%Highest risk — SCD during exertionSurgical reimplantation or unroofing; restrict competitive sports
Anomalous RCA from left sinus (interarterial)0.1-0.3%Lower risk; rarely causes SCDObservation vs surgery based on symptoms/ischemia testing
Myocardial bridging5-25% (angiographic)Systolic compression of mid-LAD; rarely causes ischemiaBeta-blockers first-line; avoid nitrates (worsen compression); myotomy if refractory
Coronary AV fistula0.1-0.2%Left-to-right shunt; steal phenomenon; endocarditis riskTranscatheter coil/plug embolization if symptomatic or Qp/Qs >1.5
ALCAPA (Bland-White-Garland)1 in 300,000LCA from PA; myocardial ischemia in infancySurgical reimplantation of LCA to aorta

Coronary Artery Territory & ECG Correlation

Coronary ArteryMyocardial TerritoryECG LeadsComplications if Occluded
Proximal LADAnterior wall, septum, apexV1-V4 (anterior); I, aVL if diagonalLarge anterior MI, LV dysfunction, CHB (septal necrosis)
LAD (mid/distal)Apical anterior wallV3-V6Apical aneurysm, mural thrombus
LCxLateral, posterolateral wallI, aVL, V5-V6; reciprocal V1-V3 depressionLateral MI; papillary muscle rupture (posteromedial)
RCA (proximal)Inferior wall, RV, conduction systemII, III, aVF; V1, V4R (RV infarct)Inferior MI, RV infarct, bradycardia (AV block)
PDAInferior septum, inferior wallII, III, aVFInferior MI; AV nodal dysfunction
Always obtain a right-sided ECG (V4R) in inferior STEMI to assess for RV involvement. RV infarction occurs in 30-50% of inferior STEMIs (when the RCA is occluded proximally) and requires volume resuscitation rather than diuretics or nitrates, which can precipitate profound hypotension.
Diagram of the coronary arteries showing the left main, LAD, circumflex, and right coronary artery distributions
Figure 1 — Coronary Artery Anatomy. The left main coronary artery bifurcates into the LAD and LCx. The RCA courses in the right AV groove. In right-dominant circulation (~85%), the PDA arises from the RCA. Source: Wikimedia Commons. Public domain.

02 The Cardiac Catheterization Lab

Radiation Safety

The cath lab uses fluoroscopy and cineangiography (digital acquisition) to visualize coronary arteries and cardiac structures. Radiation exposure is measured in air kerma (Gy) — cumulative dose at the interventional reference point — and dose-area product (DAP, Gy·cm²). Key principles include: maintaining maximum distance from the source (inverse square law), using collimation to limit field size, minimizing fluoroscopy time, reducing frame rate (7.5-15 fps vs 30 fps), avoiding steep angulations (which increase tissue penetration depth), and using lead shielding. The sentinel event threshold for skin dose is 5 Gy (risk of deterministic skin injury). Operators should monitor cumulative air kerma in real time during complex cases (CTO, structural procedures).

Operator dose limits: The annual effective dose limit for radiation workers is 50 mSv/year (ALARA principle — As Low As Reasonably Achievable). Cumulative lifetime limit: 10 mSv × age in years. Occupational hazards include cataract formation (lens dose threshold ~500 mGy), thyroid cancer (wear thyroid shield), and left-sided brain tumors (reported in interventional cardiologists — wear lead cap). Recommended protective equipment: lead apron (0.5 mm Pb equivalent), thyroid shield, lead glasses (0.75 mm Pb), ceiling-mounted lead glass shield, under-table lead drape, and radiation dosimeter badges (collar and waist levels).

The LAO cranial view generates the highest radiation dose to the operator because the X-ray tube is positioned close to the operator's left side. Steep angulations increase patient skin dose by up to 3-fold compared to straight PA projections.

Vascular Access — Radial vs Femoral

FeatureTransradial Access (TRA)Transfemoral Access (TFA)
Preferred forACS, diagnostic cath, standard PCIComplex PCI (some), structural, MCS
Sheath size5-7 Fr (slender sheathless 7.5 Fr)5-8 Fr (up to 14-24 Fr for structural)
Bleeding riskLower (MATRIX, RIVAL trials)Higher — retroperitoneal bleed risk
Mortality benefitYes in STEMI (MATRIX)
Crossover rate2-7%<1%
ComplicationsRadial artery occlusion (1-5%), spasmPseudoaneurysm, AV fistula, RP bleed
Allen testRecommended (dual palmar arch patency)Not applicable

Distal radial (snuffbox) access: Emerging technique with access at the anatomical snuffbox. Advantages include preserved antegrade radial flow, lower radial artery occlusion rates, and patient comfort (no wrist immobilization).

Catheters & Guidewires

Diagnostic catheters: Judkins Left (JL) — most common for LCA (JL 3.5 standard, JL 4.0 for dilated aortic root); Judkins Right (JR) — for RCA (JR 4.0 standard); Amplatz Left (AL) — alternative for LCA or anomalous RCA; Amplatz Right (AR) — for anomalous vessels; Multipurpose — for bypasses and anomalous coronaries. From radial access, Tiger, Jacky, or Ikari catheters can engage both left and right coronary arteries.

Guide catheters: 6 Fr is standard for PCI. EBU (Extra Backup) and XB (Xtra Backup) provide strong support for left coronary interventions. AL1/AL2 provide backup for RCA and anomalous vessels. Guide catheter selection is critical for adequate support in complex PCI — passive support (catheter shape), active support (deep seating), and guide extension catheters (GuideLiner, Trapliner) augment deliverability.

Coronary guidewires: 0.014-inch diameter is standard. Classified by tip stiffness — workhorse (Runthrough, BMW — 1 g tip load), intermediate (Pilot 50 — moderate steerability), stiff/CTO (Confianza Pro 9/12, Gaia 2nd/3rd — 9-12 g tip), and polymer-jacketed (Fielder XT, Gladius — for microchannel tracking). Wire tip shape, torque response, and prolapse resistance determine performance in different lesion types.

Vascular Closure Devices

Used after femoral access to achieve hemostasis and allow early ambulation. Types include: Collagen plug (Angio-Seal — deploys anchor and collagen sandwich), suture-mediated (Perclose ProGlide — pre-close technique for large-bore access up to 24 Fr), clip-based (StarClose), and extravascular sealant (Mynx). The pre-close technique with two Perclose devices deployed at 10 and 2 o'clock positions before sheath upsizing is standard for large-bore femoral access in TAVR and MCS.

Modern cardiac catheterization laboratory with fluoroscopy equipment
Figure 2 — Cardiac Catheterization Laboratory. Modern cath lab with C-arm fluoroscopy, hemodynamic monitoring, and intravascular imaging consoles. Source: Wikimedia Commons. CC BY-SA 3.0.

03 Hemodynamic Assessment & Right Heart Catheterization

Right Heart Catheterization (Swan-Ganz)

A balloon-tipped pulmonary artery catheter (PAC) is advanced from venous access (internal jugular or femoral vein) through the RA → RV → PA and into the wedge position. Continuous monitoring provides: RA pressure, RV pressure, PA pressure, PCWP (pulmonary capillary wedge pressure), cardiac output, and mixed venous oxygen saturation (SvO2).

Normal Hemodynamic Values

ParameterNormal RangeUnits
RA pressure (mean)0-8mmHg
RV pressure (systolic/diastolic)15-30 / 0-8mmHg
PA pressure (systolic/diastolic/mean)15-30 / 4-12 / 9-18mmHg
PCWP (mean)4-12mmHg
Cardiac output (CO)4.0-8.0L/min
Cardiac index (CI)2.5-4.0L/min/m²
Systemic vascular resistance (SVR)800-1200dynes·s/cm&sup5;
Pulmonary vascular resistance (PVR)20-120 (<3 Wood units)dynes·s/cm&sup5;
Mixed venous O2 saturation (SvO2)60-80%

Cardiac Output Measurement

Fick method: CO = VO2 / (CaO2 - CvO2), where VO2 is oxygen consumption (ideally measured, often assumed 125 mL/min/m² × BSA), CaO2 is arterial oxygen content, and CvO2 is mixed venous oxygen content. Most accurate when VO2 is directly measured. Thermodilution: Cold saline bolus injected via proximal port; temperature change detected at the PA thermistor generates a curve — CO is inversely proportional to the area under the curve. Less accurate in severe TR, low-output states, and intracardiac shunts.

Shunt Calculations

An intracardiac shunt is detected by an oxygen saturation step-up at the level of the shunt. A step-up of ≥7% at the atrial level (ASD), ≥5% at the ventricular level (VSD), or ≥5% at the PA level (PDA) is considered significant. Qp/Qs ratio = (SaO2 - SvO2) / (SpvO2 - SpaO2). A Qp/Qs ≥ 1.5 generally indicates a hemodynamically significant shunt warranting closure.

Valve Gradient Assessment

Aortic stenosis: Simultaneous measurement of LV and aortic pressures yields the peak-to-peak gradient (catheter gradient) and mean gradient. The Gorlin formula calculates valve area: AVA = CO / (44.3 × SEP × HR × √mean gradient). A Gorlin AVA ≤ 1.0 cm² with mean gradient ≥ 40 mmHg confirms severe AS. In low-flow, low-gradient AS, dobutamine stress hemodynamics help distinguish true-severe from pseudo-severe AS.

Mitral stenosis: The PCWP-to-LV diastolic gradient defines mitral valve gradient. MVA is calculated using the Gorlin formula or estimated by the pressure half-time method on echo. MVA ≤ 1.5 cm² is moderate; ≤ 1.0 cm² is severe.

Pulmonary Hypertension Assessment

Right heart catheterization is the gold standard for diagnosing pulmonary hypertension. Pre-capillary PH: mPAP >20 mmHg, PCWP ≤15 mmHg, PVR ≥3 Wood units. Post-capillary PH (group 2): mPAP >20 mmHg, PCWP >15 mmHg. Combined pre- and post-capillary PH: mPAP >20 mmHg, PCWP >15 mmHg, PVR ≥3 Wood units. Vasoreactivity testing with inhaled nitric oxide (10-20 ppm), IV epoprostenol, or IV adenosine is performed in idiopathic PAH — a positive response (≥10 mmHg decrease in mPAP to ≤40 mmHg with maintained or increased CO) identifies candidates for calcium channel blocker therapy.

PVR calculation: PVR = (mPAP - PCWP) / CO. Normal PVR is <3 Wood units (240 dynes·s/cm&sup5;). Conversion: 1 Wood unit = 80 dynes·s/cm&sup5;. In pre-TAVR assessment, PVR >5 Wood units raises concern for prohibitive surgical risk and may warrant vasodilator challenge to assess reversibility.

Intracardiac Shunt Detection — Oximetry Run

A complete oximetry run involves sampling oxygen saturations from the SVC, IVC, RA, RV, PA, LA (if accessible), LV, and aorta. Significant step-ups indicate left-to-right shunting at the corresponding level:

Shunt LevelSignificant Step-UpDiagnosis
SVC → RA≥7% O2 sat increaseASD, partial anomalous pulmonary venous return (PAPVR)
RA → RV≥5% O2 sat increaseVSD
RV → PA≥5% O2 sat increasePDA, aortopulmonary window
In constrictive pericarditis, the hallmark hemodynamic finding is equalization and elevation of diastolic pressures (RA = RVEDP = PCWP = LVEDP, typically within 5 mmHg of each other) with a "dip and plateau" (square root sign) pattern in ventricular pressure tracings and discordant RV/LV systolic pressure variation with respiration.
Swan-Ganz pulmonary artery catheter with multiple lumens and balloon tip
Figure 3 — Pulmonary Artery (Swan-Ganz) Catheter. The balloon-tipped catheter is advanced from venous access through the right heart chambers to the pulmonary artery. Ports measure RA and PA pressures; the thermistor measures cardiac output by thermodilution. Source: Wikimedia Commons. Public domain.

04 Diagnostic Coronary Angiography

Standard Angiographic Views

ViewAngulationBest Visualizes
RAO caudalRAO 20-30°, caudal 20-30°Left main bifurcation, proximal LAD/LCx
RAO cranialRAO 20-30°, cranial 20-30°Mid/distal LAD, diagonal branches
LAO cranial (spider view)LAO 40-60°, cranial 20-30°Left main, LAD/LCx bifurcation, proximal LAD
LAO caudalLAO 40-50°, caudal 20-30°LCx, obtuse marginals, ramus
AP cranialAP, cranial 30-40°Mid LAD, diagonal branches, LAD/septal perforators
AP caudalAP, caudal 20-30°Left main, proximal LCx, ramus
LAO straightLAO 30-45°RCA (mid), crux, PDA
RAO straightRAO 30°RCA (proximal/mid), PDA bifurcation
The "spider view" (LAO cranial) is the single best view for evaluating left main disease and the LAD/LCx bifurcation. However, it generates the highest scatter radiation to the operator. Always obtain at least two orthogonal views of any significant stenosis before making revascularization decisions.

Stenosis Grading & Quantitative Coronary Angiography (QCA)

Visual estimation of diameter stenosis remains standard but has significant interobserver variability. QCA provides objective measurements: reference vessel diameter (RVD), minimum lumen diameter (MLD), percent diameter stenosis (%DS), and lesion length. The threshold for "significant" stenosis is generally ≥70% diameter stenosis for epicardial coronary arteries and ≥50% for the left main.

TIMI Flow Grade

GradeDefinition
TIMI 0No perfusion — no antegrade flow beyond the point of occlusion
TIMI 1Penetration without perfusion — contrast passes beyond obstruction but fails to opacify the distal bed
TIMI 2Partial perfusion — contrast opacifies the distal bed but with delayed filling or clearance
TIMI 3Complete perfusion — antegrade flow fills the distal bed completely with normal clearance

TIMI Myocardial Perfusion Grade (TMPG)

Assesses microvascular perfusion independent of epicardial flow: TMPG 0 — no myocardial blush; TMPG 1 — slow entry, staining persists on next injection; TMPG 2 — slow entry and exit; TMPG 3 — normal entry and exit. TMPG 3 after primary PCI is associated with the lowest mortality.

SYNTAX Score

The SYNTAX (Synergy Between PCI with Taxus and Cardiac Surgery) score is an angiographic tool that quantifies the complexity of coronary artery disease based on lesion location, severity, bifurcation involvement, calcification, tortuosity, thrombus, and vessel characteristics across all segments. Low SYNTAX (≤22): PCI and CABG equivalent; Intermediate (23-32): discuss with Heart Team; High (≥33): CABG preferred. The SYNTAX II score incorporates clinical variables (age, LVEF, CrCl, COPD, PVD) to improve prognostic accuracy.

Diagram showing the path of a cardiac catheter from femoral artery to the heart for coronary angiography
Figure 4 — Cardiac Catheterization Approach. A catheter is advanced retrograde from the femoral or radial artery through the aorta to selectively engage the coronary ostia for contrast injection and angiographic imaging. Source: Wikimedia Commons. Public domain.

05 Percutaneous Coronary Intervention (PCI)

Evolution of Coronary Stents

GenerationExamplesDrug / PolymerKey Features
POBAPlain old balloon angioplastyNone30-40% restenosis rate; acute vessel closure risk
BMSPalmaz-Schatz, LibertéNone / bare metalReduced acute closure vs POBA; 20-30% ISR
1st gen DESCypher (sirolimus), Taxus (paclitaxel)Sirolimus/paclitaxel; durable polymerReduced ISR to ~5-8%; concerns for VLST
2nd gen DESXience (everolimus), Resolute (zotarolimus)Everolimus/zotarolimus; thinner polymerCurrent standard; thinner struts (81 μm); lower VLST
3rd gen DESOrsiro (sirolimus, biodegradable polymer), Synergy (everolimus, abluminal)Ultrathin struts; bioabsorbable polymer60 μm struts; rapid endothelialization
BVSAbsorb (everolimus, PLLA scaffold)Everolimus; bioresorbable scaffoldWithdrawn — increased scaffold thrombosis (ABSORB III)

PCI Technique — Step-by-Step

1. Guide catheter engagement — Coaxial alignment with the coronary ostium; adequate backup support. 2. Wiring the lesion — Advance a 0.014" guidewire across the stenosis into the distal vessel. 3. Predilation — Compliant balloon (sized 1:1 to reference vessel or slightly undersized) inflated across the lesion to create a channel for stent delivery. 4. Stent deployment — Select stent diameter to match reference vessel (by QCA or intravascular imaging); stent length should cover the lesion with 2-3 mm margin on each side. Inflate at nominal pressure (8-12 atm) for deployment. 5. Post-dilation — Non-compliant balloon (NC) inflated at high pressure (14-20 atm) to ensure full stent expansion and apposition; sized 1:1 to the reference vessel. 6. Final angiography — Confirm TIMI 3 flow, no dissection, no residual stenosis, good distal runoff.

Stent Sizing Principles

Stent diameter should match the distal reference vessel diameter by angiography (or the media-to-media diameter by IVUS/OCT). Stent undersizing leads to malapposition (risk of stent thrombosis); oversizing leads to edge dissection and vessel injury. IVUS-guided PCI targets minimum stent area (MSA) ≥ 5.5 mm² in non-left-main vessels and ≥ 8.0 mm² in the left main. OCT criteria include: stent expansion ≥80% of reference lumen area, no edge dissection >200 μm, and complete stent apposition.

Kissing Balloon Inflation

Simultaneous inflation of two balloons in the main vessel and side branch at bifurcation stenting. Purpose: correct carina shift, maintain side branch patency, optimize stent apposition at the bifurcation. POT-side-POT (proximal optimization technique) is an alternative strategy: short NC balloon inflated in the proximal main vessel to flare the stent, followed by wire rewiring and kissing balloon or POT.

Specialty Balloons

Balloon TypePropertiesUse
CompliantGrows with increasing pressure; conforms to vessel shapePredilation; lesion assessment
Semi-compliantModerate growth with pressure; used on stent delivery systemsStent deployment (nominal pressure)
Non-compliant (NC)Minimal growth beyond rated burst pressure; predictable diameterPost-dilation; high-pressure expansion of underexpanded stents
Scoring/cutting balloonAtherotome blades or wires on surface; concentrate force on plaqueFibrotic/resistant lesions; ISR; prevent balloon slippage
Drug-coated balloon (DCB/DEB)Paclitaxel or sirolimus coating; local drug delivery without permanent implantISR (AGENT IDE); small vessels; de novo lesions (BASKET-SMALL 2)
Intravascular lithotripsy (IVL)Sonic pressure waves fracture calcium via Shockwave emittersSeverely calcified lesions; superficial and deep calcium

Guide Extension Catheters

GuideLiner (Teleflex) and Guidezilla (Boston Scientific) are rapid-exchange coaxial guide extension catheters that telescope within the guide catheter and extend ~25 cm into the coronary artery. They provide enhanced backup support for device delivery in tortuous anatomy, calcified lesions, and distal lesions. The "trapping" technique (inflating a balloon in the guide to trap a wire) allows wire exchange through the extension catheter without losing position. Guide extensions also serve as conduits for delivering thrombus aspiration catheters, coils, and covered stents to distal locations.

Intravascular imaging (IVUS or OCT) during PCI reduces the rates of stent thrombosis, restenosis, target vessel revascularization, and cardiovascular death compared to angiography-guided PCI alone (ILUMIEN IV, ULTIMATE trials). Its use is especially important in left main PCI, CTO PCI, and long lesions.
Diagram showing coronary stent deployment during percutaneous coronary intervention
Figure 5 — Coronary Stent Deployment. A balloon-expandable stent is positioned across the coronary stenosis and deployed by balloon inflation, restoring luminal patency. Source: Wikimedia Commons. Public domain (NIH).

06 STEMI Intervention & Cardiogenic Shock

Primary PCI for STEMI

Primary PCI is the preferred reperfusion strategy for STEMI when it can be performed within 120 minutes of first medical contact (door-to-balloon time target <90 minutes at PCI-capable hospitals; <120 minutes with transfer). Emergency Primary PCI achieves TIMI 3 flow in >90% of cases, compared to ~50-60% with fibrinolysis. Radial access is preferred (MATRIX trial — reduced bleeding and mortality in STEMI).

Culprit Lesion PCI vs Complete Revascularization

In STEMI with multivessel disease, culprit-lesion-only PCI is the standard acute approach. The COMPLETE trial demonstrated that staged complete revascularization of non-culprit lesions (during index hospitalization or within 45 days) reduced the composite of cardiovascular death and MI compared to culprit-only PCI. FFR-guided non-culprit PCI is supported by the DANAMI-3-PRIMULTI and Compare-Acute trials. Non-culprit PCI should generally not be performed at the time of primary PCI unless there is hemodynamic instability, ongoing ischemia, or cardiogenic shock.

Thrombus Management

Large thrombus burden is common in STEMI. Routine aspiration thrombectomy is no longer recommended (TOTAL, TASTE trials — no mortality benefit, increased stroke risk). Aspiration may be considered as a bailout strategy for massive thrombus burden with TIMI 0-1 flow despite wire crossing. GP IIb/IIIa inhibitors (abciximab, eptifibatide) may be used as bailout for large thrombus burden or no-reflow.

Cardiogenic Shock — STEMI

Emergency Cardiogenic shock complicates 5-10% of STEMI cases and carries 40-50% in-hospital mortality. The SHOCK trial established early revascularization (PCI or CABG within 6 hours) as the standard of care — 6-month mortality reduction from 63% to 50%. Key management principles:

Hemodynamic support: Vasopressors (norepinephrine preferred over dopamine — SOAP II trial), inotropes (dobutamine, milrinone), and mechanical circulatory support (MCS) — see Section 16. The SCAI shock classification (stages A-E) guides escalation of support. Stage C (classic shock: hypotension, CI <2.2, PCWP >15, lactate rising) should prompt MCS consideration. Stage D (deteriorating) and Stage E (extremis — refractory cardiac arrest) require emergent MCS or ECMO.

Mechanical Complications of STEMI

Mechanical complications typically occur 2-7 days post-MI (earlier with reperfusion). All are surgical emergencies:

ComplicationTimingPresentationDiagnosisManagement
Free wall ruptureDays 3-7Sudden PEA, tamponadeEcho: pericardial effusion, tamponadeEmergency Pericardiocentesis → emergent surgery
Ventricular septal rupture (VSR)Days 3-5New harsh holosystolic murmur, acute HFEcho with color Doppler; PA sat step-upMCS (IABP/Impella) → surgical repair (delayed if possible)
Papillary muscle ruptureDays 2-7Acute severe MR, pulmonary edema, shockEcho: flail mitral leaflet, severe MREmergency MCS → emergent MVR/repair

Papillary muscle rupture most commonly involves the posteromedial papillary muscle (single blood supply from PDA — affected in inferior MI) rather than the anterolateral papillary muscle (dual supply from LAD and LCx). Complete rupture is rapidly fatal without surgical intervention. Partial rupture may present subacutely.

Door-to-balloon time <90 minutes is the quality benchmark for primary PCI in STEMI. Every 30-minute delay in reperfusion increases 1-year mortality by approximately 7.5%. The most important modifiable delay is in activation of the cath lab — prehospital ECG and direct cath lab activation bypass ED delays.
12-lead ECG showing ST-segment elevation in anterior leads consistent with STEMI
Figure 6 — ST-Elevation Myocardial Infarction (STEMI) ECG. 12-lead ECG demonstrating ST-segment elevation, the hallmark finding that triggers emergent primary PCI. Source: Wikimedia Commons. Public domain.

07 Complex PCI — CTO, Bifurcation & Left Main

Chronic Total Occlusion (CTO) PCI

A CTO is defined as a coronary occlusion with TIMI 0 flow for ≥3 months. CTO PCI is among the most technically demanding coronary interventions. The hybrid algorithm guides strategy selection based on four angiographic features: (1) ambiguity of the proximal cap, (2) lesion length (>20 mm), (3) presence of an interventional collateral for retrograde access, and (4) quality of the distal vessel target.

Antegrade wire escalation (AWE): First-line strategy for short CTOs (<20 mm) with a clear proximal cap. Escalation from soft-tipped wires through intermediate to stiff, tapered CTO wires (Confianza Pro 12, Gaia 3rd). Antegrade dissection re-entry (ADR): For long CTOs (>20 mm). A knuckled polymer wire is advanced into the subintimal space, and a re-entry device (Stingray balloon) redirects back into the true lumen distally. Retrograde approach: A wire is passed through a collateral channel (septal or epicardial) to the distal cap of the CTO. Techniques include reverse CART (Controlled Antegrade and Retrograde subintimal Tracking) — the most common retrograde strategy.

CTO PCI success rates at experienced centers exceed 85-90%. The J-CTO score predicts procedural difficulty: 0 = easy, 1 = intermediate, 2 = difficult, ≥3 = very difficult. Variables scored: blunt proximal cap, calcification, bending >45°, occlusion length >20 mm, and prior failed attempt.

CTO Crossing Strategies — Detailed

StrategyWhen to UseKey StepsSuccess Rate
Antegrade Wire Escalation (AWE)Short CTO (<20 mm), clear proximal cap, no suitable collateralsEscalate wire tip stiffness: workhorse → polymer-jacketed → tapered stiff (Gaia 2nd, Confianza Pro 12)60-70% as primary strategy
Antegrade Dissection Re-entry (ADR)Long CTO (>20 mm), clear proximal cap, no collateralsKnuckle wire into subintima → Stingray balloon for re-entry → confirm true lumen with IVUS70-80%
Retrograde via septal collateralAmbiguous proximal cap; good septal collateral; prior failed antegradeCorsair/Caravel microcatheter through septal channel → reverse CART → externalize wire75-85%
Retrograde via epicardial collateralNo septal collaterals availableHigher risk of donor vessel injury; Sion wire preferred for tortuosityLower; higher complication rate

Reverse CART (Controlled Antegrade and Retrograde subintimal Tracking): The most common retrograde crossing technique. An antegrade knuckle wire creates a subintimal space; the retrograde wire punctures into this space, connecting the retrograde and antegrade paths. A balloon is inflated over the antegrade wire to enlarge the connection point, allowing the retrograde wire to cross into the antegrade guide catheter. The retrograde wire is then externalized (pulled through the antegrade guide) and used as a rail for stent delivery.

Dual injection (simultaneous opacification of both the donor and recipient coronary arteries) is essential before starting CTO PCI. It defines the occlusion length, distal vessel quality, collateral anatomy, and the relationship between proximal and distal caps. Without dual injection, accurate strategy selection is not possible.

Bifurcation PCI

Bifurcation lesions account for 15-20% of PCI. The Medina classification describes involvement of the proximal main vessel, distal main vessel, and side branch (1 = ≥50% stenosis, 0 = <50%): e.g., Medina 1,1,1 = all three segments diseased; Medina 1,1,0 = main vessel only.

Provisional stenting is the default strategy: stent the main vessel, then assess the side branch. If the side branch has ≥75% stenosis, TIMI <3 flow, or threatened territory >10% of myocardium, perform side branch intervention (wire, balloon, or T-stent). Two-stent strategies are reserved for true bifurcations with large side branches:

TechniqueDescriptionBest For
Crush (DK-crush)Side branch stent crushed by main vessel stent; sequential kissing and POTTrue bifurcations; best evidence (DKCRUSH-V)
CulotteBoth stents protrude into the main vessel; full coverage of the carinaY-shaped bifurcations with similar vessel sizes
TAP (T and Protrusion)Side branch stent with minimal protrusion into main vesselWide-angle bifurcations
V-stenting / Simultaneous kissing stentsTwo stents deployed simultaneously in a V configurationDistal left main bifurcation

Left Main PCI

Left main PCI is an alternative to CABG in selected patients. The EXCEL trial (5-year follow-up) showed no significant difference in the composite of death, MI, or stroke between PCI and CABG for left main disease with low-intermediate SYNTAX scores (≤32), though CABG had lower rates of repeat revascularization. The NOBLE trial favored CABG at 5 years, driven by higher non-procedural MI and repeat revascularization with PCI. Current guidelines recommend Heart Team discussion for all left main decisions.

Technical considerations: Distal left main bifurcation (most common location) is treated based on LCx ostial involvement — provisional stenting if LCx not significantly diseased, DK-crush or culotte if both LAD and LCx require stenting. Intravascular imaging is strongly recommended (class IIa). IVUS MSA targets: ≥8 mm² in the left main body, ≥7 mm² at the polygon of confluence, ≥6 mm² in the LAD ostium, ≥5 mm² in the LCx ostium.

Calcified Lesion Modification

Severe calcification impairs stent delivery and expansion. Calcium modification techniques:

TechniqueMechanismKey Considerations
Rotational atherectomy (RA)Diamond-coated burr (1.25-2.5 mm) ablates calcium at 135,000-180,000 rpmBurr:artery ratio ≤0.7; avoid decelerations >5,000 rpm; risk of slow-flow/no-reflow
Orbital atherectomy (OA)Diamond-coated crown sands calcium at 80,000-120,000 rpm via centrifugal forceSingle crown size treats varying lumens; bidirectional; reduced no-reflow risk
Intravascular lithotripsy (IVL)Shockwave balloon emits pulsatile sonic waves that fracture calciumBalloon sized 1:1 to vessel; treats deep (medial) calcium; easiest to use; DISRUPT CAD III data
Laser atherectomyExcimer laser ablates tissue via photochemical, photothermal, and photomechanical effectsUsed for ISR with underexpanded stents; also for lead extraction
In CTO PCI, the most common cause of procedural failure is inability to cross the proximal cap with a guidewire. The hybrid algorithm emphasizes dual injection (simultaneous injection of both donor and recipient arteries) to delineate the CTO length, distal vessel quality, and collateral anatomy before selecting a crossing strategy.

08 Intravascular Imaging & Coronary Physiology

Intravascular Ultrasound (IVUS)

IVUS uses a miniaturized ultrasound transducer (20-60 MHz) on a catheter to produce cross-sectional images of the vessel wall. Resolution: axial ~100 μm, lateral ~200 μm. IVUS penetrates through calcium (unlike OCT) and visualizes the full vessel wall thickness. Grayscale IVUS identifies plaque burden, lumen area, external elastic membrane (EEM) area, and stent expansion. Virtual histology (VH-IVUS) uses radiofrequency backscatter analysis to characterize plaque composition (fibrous, fibrofatty, necrotic core, dense calcium).

IVUS-guided PCI targets: MSA ≥5.5 mm² (non-left main), MSA ≥8.0 mm² (left main body), no edge dissection involving the media, stent expansion ≥80% of reference lumen, and absence of geographic miss (lesion extending beyond stent edges). The ULTIMATE trial and ADAPT-DES study confirmed IVUS guidance reduces MACE compared to angiography alone.

Optical Coherence Tomography (OCT)

OCT uses near-infrared light (1,300 nm wavelength) to produce ultra-high-resolution images of the vessel wall. Resolution: axial ~10-15 μm (10x better than IVUS), lateral ~20-40 μm. Limitation: poor tissue penetration (~1-2 mm) — cannot see through calcium or deep plaque; requires blood clearance (contrast flush). OCT excels at identifying: thin-cap fibroatheroma (TCFA) — cap thickness <65 μm overlying a lipid-rich core (vulnerable plaque); stent malapposition (strut-to-intima distance >strut thickness + polymer); stent underexpansion; edge dissection (flap >200 μm or involving the media); thrombus (red vs white); and neoatherosclerosis (lipid-laden intima within stents).

The ILUMIEN IV trial demonstrated that OCT-guided PCI achieved larger MSA and lower rates of stent underexpansion compared to angiography-guided PCI, though the primary clinical endpoint was not significantly different at 2 years.

Fractional Flow Reserve (FFR)

FFR is the ratio of distal coronary pressure (Pd) to aortic pressure (Pa) at maximal hyperemia (adenosine 140 μg/kg/min IV or IC bolus). FFR = Pd/Pa. An FFR ≤0.80 indicates a hemodynamically significant stenosis warranting revascularization. Landmark trials:

FAME — FFR-guided PCI vs angiography-guided PCI in multivessel disease: FFR guidance reduced death, MI, and repeat revascularization at 1 year. FAME 2 — FFR-guided PCI + OMT vs OMT alone for FFR ≤0.80: PCI reduced urgent revascularization (trial stopped early); no mortality difference at 5 years. DEFER — Deferring PCI when FFR >0.75 was safe at 15-year follow-up.

Non-Hyperemic Pressure Ratios (NHPR)

iFR (instantaneous wave-free ratio) and RFR (resting full-cycle ratio) measure the Pd/Pa ratio during a specific diastolic window (iFR) or the lowest Pd/Pa during the entire cardiac cycle (RFR), without requiring hyperemia. An iFR/RFR ≤0.89 indicates hemodynamic significance. The DEFINE-FLAIR and iFR-SWEDEHEART trials demonstrated non-inferiority of iFR-guided revascularization compared to FFR-guided revascularization at 1 year.

Coronary Flow Reserve (CFR) & Index of Microcirculatory Resistance (IMR)

CFR is the ratio of hyperemic to resting coronary flow velocity (measured by Doppler wire) or transit time (thermodilution). CFR <2.0 indicates impaired flow reserve, which may reflect epicardial stenosis, microvascular disease, or both. IMR = Pd × transit time at hyperemia; IMR ≥25 indicates microvascular dysfunction. In STEMI, elevated IMR post-PCI predicts larger infarct size and worse LV recovery. Combined assessment of FFR + CFR + IMR allows differentiation between epicardial disease, microvascular disease, and normal hemodynamics — the endotype classification guides targeted therapy.

Angioscopy & Near-Infrared Spectroscopy (NIRS)

NIRS (TVC Imaging System, Infraredx/Lipid-Rich Plaque) identifies lipid-core plaques within the vessel wall by measuring the absorption of near-infrared light. A lipid core burden index (LCBI) at the maximal 4 mm segment (maxLCBI4mm) ≥400 is associated with increased risk of periprocedural MI during PCI and future MACE (LRP study). NIRS is often combined with IVUS on a single catheter platform (Makoto, TVC) for simultaneous structural and compositional assessment.

Intravascular ultrasound (IVUS) image showing cross-section of a coronary artery with plaque
Figure 7 — Intravascular Ultrasound (IVUS). Cross-sectional IVUS image of a coronary artery demonstrating plaque burden, lumen area, and external elastic membrane. IVUS guidance improves PCI outcomes by optimizing stent expansion and apposition. Source: Wikimedia Commons. Public domain.

09 Acute Coronary Syndromes — Antithrombotic Management

NSTEMI — Timing of Catheterization

Risk stratification guides timing: Immediate (<2 hours) — hemodynamic instability, ongoing chest pain despite medical therapy, life-threatening arrhythmias, mechanical complications. Early (<24 hours) — GRACE score >140, dynamic ST/T changes, rise/fall in troponin (TIMACS trial — early invasive strategy reduced the composite of death, MI, stroke in high-risk patients). Delayed invasive (24-72 hours) — lower-risk patients without high-risk features. Selective invasive (ischemia-guided) — low-risk patients with no recurrent symptoms and negative stress test.

Antiplatelet Therapy

AgentMechanismLoading / MaintenanceKey Trial Data
AspirinIrreversible COX-1 inhibition325 mg load / 81 mg dailyCornerstone of antiplatelet therapy; lifelong after ACS
ClopidogrelIrreversible P2Y12 inhibition (prodrug)600 mg load / 75 mg dailyCURE, CURRENT-OASIS 7; 3-15% poor metabolizers (CYP2C19)
PrasugrelIrreversible P2Y12 inhibition (prodrug)60 mg load / 10 mg dailyTRITON-TIMI 38; contraindicated if prior stroke/TIA; avoid if ≥75 years or <60 kg
TicagrelorReversible P2Y12 inhibition (direct-acting)180 mg load / 90 mg BIDPLATO; side effects: dyspnea, bradycardia; avoid with strong CYP3A4 inhibitors
CangrelorIV reversible P2Y12 inhibition30 μg/kg bolus + 4 μg/kg/min infusionCHAMPION PHOENIX; onset 2 min, offset 60 min; bridging agent

DAPT Duration

Standard: 12 months of DAPT (aspirin + P2Y12 inhibitor) after ACS regardless of stent type. Extended (>12 months): Consider in high ischemic risk / low bleeding risk (PEGASUS-TIMI 54 — ticagrelor 60 mg BID beyond 12 months reduced CV events). Shortened (3-6 months): Consider in high bleeding risk (TWILIGHT — ticagrelor monotherapy after 3 months of DAPT reduced bleeding without increasing ischemic events; STOPDAPT-2 — 1 month DAPT followed by clopidogrel monotherapy). The DAPT score (≥2 favors prolonged DAPT; <2 favors shortened) incorporates: age, diabetes, smoking, prior MI/PCI, stent diameter <3 mm, CHF/LVEF <30%, paclitaxel-eluting stent, and vein graft PCI.

Anticoagulation in ACS

Unfractionated heparin (UFH): Standard during PCI — 70-100 U/kg bolus (50-70 U/kg if GP IIb/IIIa used); target ACT 250-350 s (200-250 s with GP IIb/IIIa). Bivalirudin: Direct thrombin inhibitor — 0.75 mg/kg bolus + 1.75 mg/kg/h infusion; alternative to UFH, especially in high bleeding risk patients (HORIZONS-AMI, EUROMAX). No need for ACT monitoring. Enoxaparin: LMWH — 0.5-1 mg/kg SC or IV; if used pre-cath, additional 0.3 mg/kg IV bolus if last dose >8 hours ago. Fondaparinux: Factor Xa inhibitor — 2.5 mg SC daily; if used pre-cath, must supplement with UFH during PCI (OASIS-5 — catheter thrombosis risk without supplemental UFH).

GP IIb/IIIa Inhibitors

Routine upstream use is no longer recommended. Bailout use is appropriate for: large thrombus burden, no-reflow, threatened vessel closure, or slow flow. Agents: Abciximab (0.25 mg/kg bolus + 0.125 μg/kg/min × 12 h), eptifibatide (180 μg/kg double bolus + 2 μg/kg/min × 18-24 h), tirofiban (25 μg/kg bolus + 0.15 μg/kg/min × 18-24 h). Eptifibatide and tirofiban require dose adjustment in renal impairment.

10 Stent Complications & No-Reflow

In-Stent Restenosis (ISR)

ISR is defined as ≥50% diameter stenosis within the stent or within 5 mm of the stent edges. It is caused by neointimal hyperplasia (smooth muscle cell proliferation and extracellular matrix deposition) and, in late ISR, neoatherosclerosis. ISR rates: BMS 20-30% at 1 year; first-gen DES 5-10%; second/third-gen DES 3-5%. The Mehran classification describes ISR patterns: Type I (focal, ≤10 mm), Type II (intra-stent, >10 mm), Type III (proliferative, extending beyond stent edges), Type IV (total occlusion).

Treatment algorithm for ISR: Step 1 — Perform IVUS or OCT to identify mechanical causes (stent underexpansion is the most common correctable cause). Step 2 — If underexpanded, high-pressure NC balloon inflation (≥20 atm) or IVL to crack calcified plaque restricting expansion. Step 3 — If adequately expanded, treat the neointimal tissue: Drug-eluting balloon (DEB) — preferred for focal ISR (AGENT IDE trial — sirolimus DEB showed 76% freedom from TLR at 12 months); DES (different drug) — preferred for diffuse ISR (RIBS IV — everolimus DES superior to DEB for diffuse ISR); Laser atherectomy or rotational atherectomy — for severely underexpanded stents with circumferential calcium that cannot be dilated with balloons.

Stent fracture is an underrecognized cause of ISR and stent thrombosis. Risk factors: long stents, hinge points (RCA), overlapping stents, and right coronary artery location. Diagnosis: fluoroscopic "gap" in stent struts, confirmed by IVUS/OCT showing strut discontinuity. Treatment: additional DES deployment across the fracture site.

Stent Thrombosis

Stent thrombosis is a catastrophic event presenting as acute MI with high mortality (20-45%). The Academic Research Consortium (ARC) classification defines certainty (definite, probable, possible) and timing:

TimingIntervalPrimary Mechanism
Acute0-24 hoursProcedural factors (dissection, malapposition, underexpansion)
Subacute1-30 daysDAPT non-compliance, platelet reactivity
Late30 days - 1 yearDelayed endothelialization, polymer hypersensitivity
Very late (VLST)>1 yearNeoatherosclerosis, late malapposition, polymer degradation

Risk factors: premature DAPT discontinuation (most important modifiable factor), stent underexpansion, edge dissection, residual stenosis, bifurcation stenting, long stents, small vessel diameter, diabetes, renal failure, and low LVEF. Treatment: emergent PCI with IVUS/OCT to identify and correct the mechanical cause.

Saphenous Vein Graft (SVG) Intervention

SVG PCI carries higher risk of distal embolization and no-reflow due to the friable, degenerated plaque within vein grafts. The SAFER trial demonstrated that a distal embolic protection device (EPD) — FilterWire or SpiderFX — reduces 30-day MACE by 42% during SVG PCI. Key principles: Always use embolic protection (class I recommendation); avoid direct stenting without predilation (risk of distal embolization from bulky plaque); use DES over BMS (lower restenosis rates); keep stent margins away from the aortic anastomosis; and avoid GP IIb/IIIa inhibitors as first-line (no proven benefit in SVG PCI; increase bleeding). For severely degenerated SVGs with diffuse disease, consider native vessel PCI (including CTO PCI of the native vessel) as an alternative to SVG intervention.

Coronary artery bypass graft showing saphenous vein graft connected to coronary artery
Figure 20 — Saphenous Vein Graft. Bypass grafts are susceptible to atherosclerotic degeneration over time, with 50% of SVGs occluded or significantly stenosed at 10 years. Intervention on degenerated SVGs requires embolic protection. Source: Wikimedia Commons. Public domain.

Coronary Perforation

The Ellis classification grades perforation severity:

TypeDescriptionManagement
Type IExtraluminal crater without extravasationObservation; usually self-limited
Type IIMyocardial or pericardial blush without contrast jetProlonged balloon inflation; reversal of anticoagulation; observation
Type IIIContrast streaming through a frank perforation (≥1 mm)Emergency Covered stent (PK Papyrus, Graftmaster); pericardiocentesis if tamponade; surgical backup
Cavity spillingPerforation into a cardiac chamberCovered stent or coil embolization; surgical repair if refractory
Type III coronary perforation can rapidly progress to cardiac tamponade. Immediate steps: inflate a balloon proximal to the perforation to seal the defect, reverse anticoagulation with protamine (1 mg per 100 U heparin), prepare a covered stent for deployment, and have a pericardiocentesis kit at the bedside. Do NOT remove the guidewire.

No-Reflow Phenomenon

No-reflow is defined as TIMI ≤2 flow in the absence of epicardial obstruction (dissection, thrombus, spasm, or residual stenosis). It is caused by distal embolization of thrombus/plaque debris, microvascular spasm, and reperfusion injury. Occurs in 2-5% of PCI and up to 10-30% of primary PCI for STEMI. Treatment: Intracoronary adenosine (100-200 μg boluses), nitroprusside (100-200 μg IC), verapamil (100-200 μg IC), nicardipine (200 μg IC), and epinephrine (50-200 μg IC for refractory cases). GP IIb/IIIa inhibitors may be used if thrombus burden is suspected. Distal protection devices (FilterWire, SpiderFX) are recommended for SVG interventions (SAFER trial) but not for native coronary PCI.

Illustration of coronary artery occlusion causing myocardial infarction
Figure 8 — Coronary Artery Thrombosis. Acute thrombus formation at a ruptured plaque or within a stent leads to coronary occlusion and myocardial infarction. Stent thrombosis is a catastrophic complication requiring emergent PCI. Source: Wikimedia Commons. CC BY 3.0.

11 Transcatheter Aortic Valve Replacement (TAVR)

Indications & Evidence

TAVR is approved for symptomatic severe aortic stenosis across the surgical risk spectrum. Landmark trials by risk category:

Risk CategoryKey TrialsFindings
Inoperable / extreme riskPARTNER 1B (Edwards SAPIEN)TAVR reduced mortality by 20% at 1 year vs medical therapy
High riskPARTNER 1A (SAPIEN), CoreValve US PivotalTAVR non-inferior (PARTNER 1A) or superior (CoreValve) to SAVR at 1 year
Intermediate riskPARTNER 2A (SAPIEN 3), SURTAVI (Evolut R)TAVR non-inferior to SAVR; lower stroke/bleeding with TAVR
Low riskPARTNER 3 (SAPIEN 3), Evolut Low RiskTAVR non-inferior to SAVR at 1 year; PARTNER 3 showed superiority of TAVR at 1 year (composite of death, stroke, rehospitalization)

Device Platforms

Edwards SAPIEN 3 / SAPIEN 3 Ultra: Balloon-expandable bovine pericardial valve; cobalt-chromium frame; sizes 20, 23, 26, 29 mm; outer skirt to reduce paravalvular leak; 14-16 Fr eSheath (expandable). Medtronic CoreValve Evolut R / Evolut PRO / Evolut FX: Self-expanding porcine pericardial valve; nitinol frame; sizes 23, 26, 29, 34 mm; supra-annular leaflet position; recapturable and repositionable; 14 Fr InLine sheath.

CT Planning for TAVR

Multidetector CT is the gold standard for pre-procedural planning: Annular sizing — perimeter-derived diameter (most accurate), area-derived diameter, and mean diameter determine valve size; Coronary heights — distance from annulus to left and right coronary ostia (risk of coronary obstruction if <12 mm with SAPIEN or <10 mm with self-expanding); Sinus of Valsalva dimensions — small sinuses increase coronary obstruction risk; Calcium scoring — valve and LVOT calcium distribution predict paravalvular leak, conduction disturbance, and annular rupture risk; Iliofemoral access — minimum diameter ≥5.5 mm for current-generation devices; tortuosity and calcification assessment.

TAVR Access Routes

Transfemoral (TF): Preferred approach (>95% of cases); lowest morbidity. Alternative routes (when TF not feasible): transaxillary/subclavian (surgical cutdown or percutaneous), transaortic (mini-sternotomy), transapical (left thoracotomy — largely abandoned due to higher mortality), transcaval (IVC-to-aorta puncture — emerging), transcarotid.

TAVR Procedural Steps

1. Access and sheath placement: Percutaneous femoral access with pre-close (2 Perclose ProGlide devices); eSheath (Edwards) or InLine sheath (Medtronic) advanced to the descending aorta. 2. Crossing the aortic valve: A straight-tipped wire crosses the stenotic aortic valve; exchanged for an extra-stiff guidewire (Safari, Lunderquist, Confida) positioned in the LV apex. 3. Balloon aortic valvuloplasty (BAV): Optional predilation with a 20-25 mm balloon under rapid ventricular pacing (180-220 bpm) to create a passage for the TAVR device. Increasingly, BAV is deferred ("direct implantation"). 4. Valve deployment: Balloon-expandable (SAPIEN) — positioned at the annular level under fluoroscopy and rapid pacing, then inflated with precise volume to deploy the valve. Self-expanding (Evolut) — unsheathed gradually; repositionable; no rapid pacing required. 5. Assessment: Aortography and TEE/TTE to assess paravalvular leak, valve position, coronary patency, and hemodynamics. Post-dilation with a larger balloon if significant PVL. 6. Closure: Tighten Perclose sutures; angiography to confirm hemostasis.

Valve-in-Valve TAVR

TAVR within a previously implanted surgical bioprosthetic valve that has degenerated (stenosis or regurgitation). Sizing is based on the true internal diameter (ID) of the surgical valve (available in manufacturer charts). Key considerations: risk of patient-prosthesis mismatch (PPM) — small surgical valves (≤21 mm) may result in high residual gradients after VIV; coronary obstruction risk is higher with VIV (especially with externally mounted leaflets that can cover the coronary ostia upon TAVR deployment); BASILICA technique (Bioprosthetic or native Aortic Scallop Intentional Laceration to prevent Iatrogenic Coronary Artery obstruction) — intentional electrosurgical laceration of a bioprosthetic leaflet before TAVR to maintain coronary flow.

TAVR Complications

ComplicationIncidenceManagement
Paravalvular leak (PVL)Mild 20-30%; moderate-severe 3-5%Post-dilation; valve-in-valve; surgical conversion for severe
Conduction disturbance / new LBBBLBBB 15-30%; PPM 10-20%Higher with self-expanding; monitor 24-48 h; PPM if high-degree AVB
Coronary obstruction<1%Emergency PCI of obstructed ostium; BASILICA technique (laceration of leaflet to prevent obstruction)
Stroke2-4%Cerebral embolic protection devices (Sentinel); anticoagulation
Vascular complications5-15%Covered stent for iliac rupture; surgical repair
Annular rupture<1%Emergency Contained — observation; uncontained — emergent surgery; almost always fatal if free rupture
The most feared acute TAVR complication is annular rupture, which presents as sudden hemodynamic collapse during or immediately after valve deployment. Risk factors include aggressive oversizing (>20% area oversizing), severe LVOT calcification, and small aortic annulus. Prevention: careful CT-based sizing and avoidance of excessive oversizing, especially in heavily calcified annuli.
Illustration of aortic valve stenosis with calcified leaflets restricting valve opening
Figure 9 — Aortic Valve Stenosis. Calcified aortic valve with restricted leaflet mobility — the primary indication for TAVR. Severe AS is defined by AVA ≤1.0 cm², mean gradient ≥40 mmHg, and peak velocity ≥4.0 m/s. Source: Wikimedia Commons. CC BY 3.0.

12 Mitral & Tricuspid Interventions

Transcatheter Edge-to-Edge Repair (TEER) — MitraClip / PASCAL

TEER creates a tissue bridge between the anterior and posterior mitral leaflets, mimicking the surgical Alfieri edge-to-edge repair. The MitraClip (Abbott) is delivered via transseptal puncture from the femoral vein, guided by TEE and fluoroscopy.

COAPT trial: In patients with heart failure (LVEF 20-50%) and severe secondary (functional) mitral regurgitation on maximally tolerated GDMT, TEER reduced heart failure hospitalizations by 47% and all-cause mortality by 29% at 2 years compared to GDMT alone. Key enrollment criterion: effective regurgitant orifice area (EROA) ≥30 mm² and LVEDV ≤200 mL (disproportionate MR concept). MITRA-FR trial: Did not show benefit of TEER in secondary MR — different patient population (proportionate MR, larger ventricles, lower EROA threshold).

Primary (degenerative) MR: TEER is indicated for patients with symptomatic severe primary MR who are at prohibitive or high surgical risk. The EVEREST II trial showed MitraClip was less effective than surgery for reducing MR but had superior safety.

PASCAL device: The PASCAL system (Edwards Lifesciences) is a newer TEER platform with a central spacer that fills the regurgitant orifice and broad paddles for leaflet grasping, plus independent clasping of each leaflet. It may be advantageous for wide flail gaps and complex anatomy where MitraClip grasping is difficult. The CLASP IID/IIF trials evaluated PASCAL in both degenerative and functional MR.

Mitral Annuloplasty Devices

Cardioband (Edwards): Percutaneous direct annuloplasty — anchors deployed along the posterior mitral annulus via transseptal approach under TEE guidance; a contraction wire reduces annular dimensions, similar to surgical annuloplasty. Approved for functional MR in Europe. Carillon (Cardiac Dimensions): Indirect annuloplasty via the coronary sinus — a nitinol device placed in the coronary sinus compresses the posterior mitral annulus to reduce annular dimensions and MR. Limitation: may impinge on the LCx artery.

Transcatheter Mitral Valve Replacement (TMVR)

Multiple devices in development or early clinical use (Tendyne, Intrepid/APOLLO, Evoque) for patients not amenable to TEER. Challenges include: large device profile, LVOT obstruction risk, leaflet interaction, paravalvular leak, and need for transseptal or transapical access. Valve-in-valve TMVR for failed surgical bioprostheses (using SAPIEN 3) is established with good outcomes.

Percutaneous Balloon Mitral Valvuloplasty (PBMV)

Indicated for symptomatic moderate-severe rheumatic mitral stenosis with favorable valve morphology. The Wilkins score (0-16) assesses leaflet mobility, thickening, calcification, and subvalvular disease — a score ≤8 predicts good results. Contraindications: moderate-severe MR, left atrial thrombus, severe calcification. Performed via transseptal puncture using an Inoue balloon. Success defined as MVA >1.5 cm² and ≤1+ MR increase.

Tricuspid Interventions

Severe tricuspid regurgitation (TR) is increasingly recognized as an important contributor to morbidity and mortality. Transcatheter options are expanding:

TriClip (TEER for tricuspid): The TRILUMINATE Pivotal trial demonstrated TEER reduced TR severity at 1 year compared to medical therapy, though the primary endpoint of composite of death, tricuspid surgery, heart failure hospitalization, or improvement in quality of life narrowly missed superiority. PASCAL tricuspid TEER: Similar edge-to-edge concept with a broader clasping mechanism. Transcatheter tricuspid valve replacement (TTVR): Devices in trial include EVOQUE (heterotopic — placed in the IVC/SVC to reduce TR regurgitant volume) and orthotopic replacement systems. The TRISCEND II trial (EVOQUE) showed significant TR reduction. Cardioband: Percutaneous annuloplasty device delivering anchors along the tricuspid annulus; provides annular reduction similar to surgical ring annuloplasty.

Illustration of mitral valve prolapse with regurgitation
Figure 10 — Mitral Valve Regurgitation. Incompetent mitral valve with regurgitant flow into the left atrium — the target of transcatheter edge-to-edge repair (TEER/MitraClip). Source: Wikimedia Commons. CC BY 3.0.

13 Left Atrial Appendage Closure

Rationale

The left atrial appendage (LAA) is the source of >90% of thrombi in non-valvular atrial fibrillation. LAA closure (LAAC) provides an alternative to long-term oral anticoagulation (OAC) for stroke prevention in patients with AF who have contraindications to OAC or high bleeding risk.

WATCHMAN Device

The WATCHMAN (Boston Scientific) is a nitinol frame with a permeable polyester fabric cap that is delivered via transseptal puncture and deployed in the LAA ostium. The PROTECT-AF trial demonstrated non-inferiority of WATCHMAN to warfarin for the composite of stroke, systemic embolism, and cardiovascular death at 5-year follow-up, with a significant reduction in hemorrhagic stroke and all-cause mortality. The PREVAIL trial confirmed non-inferiority for ischemic stroke at 5 years. The WATCHMAN FLX (next generation) has improved sealing, lower device-related thrombus, and higher procedural success (>98%).

Amulet Device

The Amulet (Abbott) is a dual-seal device with a lobe and disc that provides two levels of LAA sealing. The Amulet IDE trial demonstrated non-inferiority to WATCHMAN for safety and efficacy at 18 months, with numerically lower rates of peri-device leak.

Lariat Device (Epicardial LAA Ligation)

The Lariat system uses a combined epicardial and endocardial approach to deliver a suture loop around the LAA. A magnet-tipped wire is placed in the LAA via transseptal puncture, and a corresponding epicardial wire is advanced through a subxiphoid pericardial puncture. The Lariat snare is then delivered over the epicardial wire to lasso and ligate the LAA base. Advantages: no implanted device; complete LAA exclusion. Limitations: requires pericardial access (not feasible with prior cardiac surgery or pericardial adhesions), risk of pericarditis, pericardial effusion, and incomplete closure. The device has fallen out of favor relative to endocardial devices (WATCHMAN, Amulet).

Post-Implant Management

Standard protocol: DAPT (aspirin + clopidogrel) or short-term anticoagulation (45 days to 6 months) post-implant until device endothelialization, confirmed by TEE showing complete LAA seal and absence of device-related thrombus. Then transition to aspirin monotherapy or discontinuation of all antithrombotic therapy based on individual risk.

Patient Selection for LAAC

LAAC is most appropriate for AF patients with: CHA2DS2-VASc ≥2 (stroke risk warrants OAC), HAS-BLED ≥3 (high bleeding risk), and specific contraindications to long-term OAC (prior life-threatening bleed, intracranial hemorrhage, end-stage renal disease on dialysis, recurrent falls, or labile INR). Current guidelines give LAAC a class IIb recommendation for patients with AF unsuitable for long-term anticoagulation.

Device-related thrombus (DRT) on the LAAC device occurs in 2-4% of patients and is associated with a 2-4 fold increased stroke risk. TEE surveillance at 45 days post-implant is critical. DRT is treated with anticoagulation (usually DOACs or LMWH) for 6 weeks with repeat imaging to confirm resolution.

14 ASD/PFO Closure & Septal Ablation

Patent Foramen Ovale (PFO) Closure

PFO is present in ~25% of the general population. The association between PFO and cryptogenic stroke led to pivotal closure trials:

TrialDeviceKey Finding
RESPECT (extended follow-up)Amplatzer PFO Occluder45% relative risk reduction in recurrent stroke vs medical therapy
CLOSEVarious devices97% relative risk reduction in recurrent stroke; NNT = 20 at 5 years
REDUCEGORE Helex / Cardioform77% relative risk reduction in recurrent ischemic stroke
DEFENSE-PFOAmplatzer PFO OccluderSignificant reduction in composite of stroke, vascular death, TIMI major bleeding

Current indications for PFO closure: age 18-60, cryptogenic stroke (thorough workup excluding other causes), PFO with moderate-large shunt or atrial septal aneurysm (ASA), and high RoPE score (Risk of Paradoxical Embolism — higher score indicates greater probability that PFO is causal). Post-closure: DAPT for 1-6 months, then aspirin alone for 5 years.

Atrial Septal Defect (ASD) Closure

Transcatheter closure is standard for secundum ASD with adequate rims (≥5 mm on all borders except the aortic rim). Devices: Amplatzer Septal Occluder (most widely used), GORE Cardioform. Indications: Qp/Qs ≥1.5, right heart enlargement, or paradoxical embolism. Primum, sinus venosus, and coronary sinus ASDs require surgical closure. Sizing is guided by TEE and/or intracardiac echocardiography (ICE). Complications: device embolization (1-2%), erosion (<0.1%), residual shunt, AF, air embolism.

Alcohol Septal Ablation (ASA)

Percutaneous treatment for hypertrophic obstructive cardiomyopathy (HOCM) with symptomatic LVOT obstruction (gradient ≥50 mmHg at rest or with provocation) refractory to medical therapy. Technique: identify the first or second septal perforator branch supplying the basal septum; confirm territory with myocardial contrast echocardiography; inject 1-3 mL of absolute (96-100%) ethanol to create a controlled septal infarction. Result: septal thinning and regression of LVOT gradient over 3-6 months. Success rate: 85-95% gradient reduction.

Complications: complete heart block requiring PPM (10-20%), LAD dissection, coronary spasm, VSD (rare), and RV perforation. ASA is an alternative to surgical septal myectomy (gold standard), particularly in patients at high surgical risk, elderly patients, or those with comorbidities. The long-term scar from ASA may serve as a substrate for ventricular arrhythmias, though large registries have not shown excess sudden death.

ASA vs Septal Myectomy — Comparison

FeatureAlcohol Septal AblationSurgical Septal Myectomy
ApproachPercutaneous (cath lab)Open heart surgery (sternotomy)
Gradient reduction75-85% reduction90-95% reduction
Mortality1-2%0.5-1% (experienced centers)
Pacemaker rate10-20%2-5%
Concomitant MV repairNot possibleCan address SAM and MR simultaneously
Preferred forElderly, high surgical risk, comorbiditiesYoung patients, very thick septum (>30 mm), concomitant MV disease
Recovery1-3 days5-7 days; full recovery 6-8 weeks

Paravalvular Leak (PVL) Closure

Paravalvular leaks occur around surgically implanted prosthetic valves, causing hemolysis (mechanical shear stress), heart failure (volume overload), or both. Transcatheter closure uses Amplatzer Vascular Plug (AVP II, AVP IV) or other occluder devices delivered via retrograde aortic (for aortic PVL) or transseptal (for mitral PVL) approach. Success rates: 75-90%. Complications include device embolization, valve impingement, and residual leak.

Diagram of atrial septal defect showing shunt flow from left to right atrium
Figure 11 — Atrial Septal Defect. A defect in the interatrial septum allows left-to-right shunting. Secundum ASDs with adequate rims are amenable to percutaneous device closure. Source: Wikimedia Commons. Public domain.

15 Peripheral Vascular Interventions

Carotid Artery Stenting (CAS) & TCAR

CAS is an alternative to carotid endarterectomy (CEA) for significant carotid stenosis. Indications: symptomatic carotid stenosis ≥50% or asymptomatic stenosis ≥70% with high surgical risk. Embolic protection devices (EPDs) — distal filter (FilterWire, SpiderFX) or proximal occlusion (Mo.Ma) — are mandatory during CAS to reduce stroke risk. TCAR (transcarotid artery revascularization) uses direct carotid access with flow reversal via an arteriovenous circuit, providing superior neuroprotection. The ROADSTER trials demonstrated 30-day stroke/death rates <2% with TCAR.

Renal Artery Interventions

Renal artery stenting for atherosclerotic renal artery stenosis was not shown to improve outcomes over medical therapy in the CORAL and ASTRAL trials. However, intervention may be considered for: flash pulmonary edema (Pickering syndrome), refractory hypertension on ≥3 medications, progressive renal deterioration with bilateral disease, and fibromuscular dysplasia (balloon angioplasty without stenting — good results). For FMD, the "string of beads" appearance on angiography is characteristic of the medial fibroplasia subtype.

Renal denervation (RDN): Catheter-based ablation of the renal sympathetic nerves for resistant hypertension. Radiofrequency (Symplicity Spyral) or ultrasound-based (Paradise) energy is delivered to the renal artery adventitia. The SPYRAL HTN-ON MED and RADIANCE-HTN SOLO trials showed modest but significant BP reductions (5-10 mmHg systolic) vs sham. RDN is approved in Europe and under FDA review. Patient selection is critical — best candidates are those with true resistant hypertension after confirming medication adherence.

Lower Extremity Peripheral Arterial Disease (PAD)

Endovascular revascularization is indicated for lifestyle-limiting claudication refractory to exercise therapy and pharmacotherapy, and for chronic limb-threatening ischemia (CLTI) with rest pain, ulceration, or gangrene. The Global Vascular Guidelines (GVG) use the WIfI classification (Wound, Ischemia, foot Infection) to stage CLTI severity and guide management.

AnatomyPreferred ApproachTechniques
Aorto-iliac (TASC A/B)EndovascularBalloon-expandable stent (kissing stents for aortic bifurcation); covered stents for long lesions
Femoropopliteal (SFA)Endovascular (short/intermediate) or surgical bypass (long occlusions)DCB (drug-coated balloon), self-expanding stent (Supera interwoven), atherectomy + DCB
Infrapopliteal (tibial)Endovascular for CLTIPOBA, DCB, atherectomy; angiosome-directed revascularization

Aortic Interventions

Thoracic Endovascular Aortic Repair (TEVAR): Endograft placement for descending thoracic aortic aneurysms (≥5.5 cm or rapid growth >0.5 cm/year) and complicated type B aortic dissections (malperfusion, rupture, refractory pain/hypertension). Landing zone classification (Ishimaru zones 0-4) determines feasibility and need for supra-aortic debranching. Zone 2 (distal to left common carotid) is the minimum proximal landing zone without left subclavian revascularization (though LSA coverage should be revascularized if possible — CSRA, left carotid-subclavian bypass).

Endovascular Aneurysm Repair (EVAR): For infrarenal abdominal aortic aneurysms (≥5.5 cm in men, ≥5.0 cm in women, or growth >0.5 cm/6 months). Anatomic requirements: infrarenal neck ≥10-15 mm, neck angle <60°, iliac diameter ≥7 mm for device delivery. Complications: endoleak (Type I — proximal/distal seal failure; Type II — branch vessel back-bleeding [most common]; Type III — graft fabric/junction failure; Type IV — graft porosity; Type V — endotension), limb occlusion, and post-implantation syndrome.

Pulmonary Embolism Interventions

Catheter-directed therapy (CDT) for massive and submassive PE includes: catheter-directed thrombolysis (CDT) — ultrasound-facilitated low-dose tPA delivery (EKOS/EkoSonic — ULTIMA, SEATTLE-II trials), aspiration thrombectomy (FlowTriever — FLARE trial; Indigo — EXTRACT-PE trial), and rheolytic thrombectomy. The FlowTriever device uses large-bore aspiration and self-expanding nitinol discs to mechanically remove thrombus without fibrinolytic agents, reducing bleeding risk. CDT for submassive PE (RV dysfunction without hemodynamic instability) remains an area of active investigation (HI-PEITHO trial).

In chronic limb-threatening ischemia (CLTI), the angiosome concept guides revascularization to the specific tibial artery feeding the territory of tissue loss: anterior tibial → dorsum of foot; posterior tibial → heel and sole; peroneal → lateral ankle. Direct angiosome revascularization improves wound healing rates compared to indirect revascularization.
Normal artery compared to atherosclerotic artery with plaque narrowing the lumen
Figure 12 — Atherosclerotic Peripheral Artery. Normal artery (left) compared to an atherosclerotic artery with plaque burden reducing luminal patency (right). Peripheral arterial interventions aim to restore adequate blood flow to the affected territory. Source: Wikimedia Commons. CC BY 3.0.

16 Mechanical Circulatory Support

Intra-Aortic Balloon Pump (IABP)

The IABP is a counterpulsation device inserted via the femoral artery and positioned in the descending aorta just distal to the left subclavian artery. Inflation during diastole augments coronary perfusion pressure and diastolic blood pressure. Deflation during systole reduces afterload, LV wall stress, and myocardial oxygen demand. Timing: inflation at the dicrotic notch; deflation just before systole. The IABP-SHOCK II trial showed no mortality benefit of IABP in cardiogenic shock complicating MI, leading to a downgrade in guidelines. IABP remains useful as an adjunct for mechanical complications (acute MR, VSD) and as a bridge in selected patients.

Impella Devices

DeviceFlow (L/min)AccessMechanismIndications
Impella CPUp to 4.314 Fr femoral arteryAxial flow pump across aortic valve (LV → aorta)High-risk PCI, cardiogenic shock (SCAI C-D)
Impella 5.0Up to 5.021 Fr axillary artery (surgical cutdown)Same axial flowSevere cardiogenic shock, bridge to recovery/transplant/LVAD
Impella 5.5Up to 5.521 Fr axillary arterySame, with purge-free motorExtended MCS support; ambulatory support possible
Impella RPUp to 4.422 Fr femoral veinAxial flow (RA → PA)RV failure after LVAD implant, cardiac surgery, or MI

The PROTECT III trial demonstrated that Impella-supported high-risk PCI reduced major adverse events at 90 days compared to IABP support. Complications of Impella include: hemolysis (monitor plasma-free hemoglobin), limb ischemia, aortic valve injury, device migration, and ventricular perforation.

Venoarterial ECMO (VA-ECMO)

VA-ECMO provides full cardiopulmonary support by draining deoxygenated blood from the venous system (femoral vein or RA), passing it through an oxygenator and heat exchanger, and returning oxygenated blood to the arterial system (femoral artery or aorta). VA-ECMO can provide flows of 3-7 L/min independent of cardiac function. Emergency Indications include: refractory cardiogenic shock (SCAI D-E), cardiac arrest (ECPR — extracorporeal CPR), post-cardiotomy shock, massive pulmonary embolism, and bridge to transplant/LVAD decision.

Key consideration: VA-ECMO increases LV afterload (retrograde arterial flow) and may worsen LV distension, pulmonary edema, and LV thrombus formation. LV venting strategies — Impella, IABP, atrial septostomy, or direct LA/LV vent — are often required to unload the LV during VA-ECMO support.

TandemHeart

The TandemHeart is a percutaneous left atrial-to-femoral artery bypass system. A 21 Fr transseptal inflow cannula is placed in the LA; oxygenated blood is withdrawn and pumped to the femoral artery via an extracorporeal centrifugal pump, providing up to 5 L/min of flow. Advantages: effective LV unloading (bypasses the LV entirely). Disadvantages: requires transseptal puncture, large-bore venous and arterial access, residual ASD after decannulation, and risk of limb ischemia. Largely supplanted by Impella in current practice.

Device Selection by Shock Severity

SCAI StageFirst-Line MCSEscalationNotes
B (Beginning)Vasopressors aloneIABP or Impella CP if deterioratingMonitor lactate trend, urine output
C (Classic)Impella CPImpella 5.0/5.5 or VA-ECMOPA catheter placement; goal CI >2.2, CPO >0.6
D (Deteriorating)VA-ECMO ± Impella (ECPELLA)Surgical MCS (LVAD)Bridge to decision; multidisciplinary shock team
E (Extremis)VA-ECMO (ECPR)Consider futility; neurologic assessment after ROSC
Cardiac power output (CPO) is the strongest independent hemodynamic predictor of mortality in cardiogenic shock. CPO = (MAP × CO) / 451. Normal CPO is ~1 watt; CPO <0.6 watts identifies patients at highest risk of death who should be considered for aggressive MCS escalation.

SCAI Shock Classification

StageDescriptionHemodynamicsClinical
A — At riskNot in shock; at riskNormal BP, HRNo signs of hypoperfusion; large MI, severe HF
B — BeginningHypotension or tachycardia without hypoperfusionSBP <90 or MAP <60; HR >100Warm extremities, normal mentation, normal lactate
C — ClassicHypoperfusion requiring interventionCI <2.2, PCWP >15Cool extremities, altered mentation, rising lactate, oliguria
D — DeterioratingFailing to stabilize despite initial interventionsWorsening CI despite vasopressors/MCSEscalating lactate, multiorgan dysfunction
E — ExtremisCardiac arrest or refractory hemodynamic collapseNear-pulseless; PEA/VF/asystoleCPR, refractory VT/VF; pH <7.2; consider ECPR
In cardiogenic shock, early MCS escalation before the onset of multiorgan failure (SCAI stage C, before progression to D) is associated with improved survival. The concept of "door-to-support" time parallels "door-to-balloon" time — delays in MCS initiation worsen outcomes. PA catheter-guided hemodynamic management is essential to select the appropriate device and titrate support.
Intra-aortic balloon pump device in the descending aorta
Figure 13 — Intra-Aortic Balloon Pump (IABP). The balloon inflates during diastole (augmenting coronary perfusion) and deflates during systole (reducing afterload). Despite the IABP-SHOCK II trial, it remains a widely available first-line MCS device. Source: Wikimedia Commons. CC BY-SA 3.0.

17 Advanced Hemodynamic Profiles & Waveforms

Hemodynamic Profiles in Shock

ConditionRAPCWPCO/CISVRDistinguishing Feature
LV cardiogenic shock↑↑↓↓↑↑PCWP > 18; CI < 1.8; RA < PCWP
RV failure / RV infarct↑↑Normal/↓RA ≥ PCWP; RA/PCWP ratio >0.8; Kussmaul sign
Cardiac tamponade↑↑↑↑↑↑Equalization of diastolic pressures; blunted Y descent in RA
Constrictive pericarditis↑↑↑↑↓/NormalDip-plateau; prominent Y descent; discordance of RV/LV systolic pressures with respiration
Massive PE↑↑Normal/↓↓↓↑↑PA systolic ↑ (usually <60 mmHg in acute PE); RA > PCWP
Septic shock↓/Normal↓/Normal↑ (early)↓↓High CO, low SVR (warm shock); low CO in late/refractory

RA Waveform Analysis

The RA waveform consists of: a wave (atrial contraction), c wave (tricuspid closure/bulging), x descent (atrial relaxation/tricuspid annular descent), v wave (passive atrial filling against a closed tricuspid valve), and y descent (tricuspid opening and passive ventricular filling). Key abnormalities: Giant a waves — tricuspid stenosis, pulmonary hypertension, RV hypertrophy; Cannon a waves — AV dissociation, complete heart block, V-pacing without AV synchrony; Large v waves — severe TR; Absent a waves — atrial fibrillation; Prominent x descent — tamponade (exaggerated); Blunted y descent — tamponade; Steep y descent — constriction, severe TR.

PCWP Waveform

The PCWP tracing mirrors the LA pressure waveform with a phase delay of 50-100 ms. Key findings: Large v waves in the PCWP suggest severe mitral regurgitation (v wave amplitude ≥2x mean PCWP is highly suggestive). However, large v waves can also occur with increased LA compliance (chronic MR) or with VSD (left-to-right shunt increasing pulmonary venous return). The a wave in PCWP corresponds to LA contraction — absent in AF; giant a waves in mitral stenosis.

Provocative Maneuvers

Rapid volume loading (500-1000 mL saline): Used to unmask constrictive physiology — RVEDP and LVEDP will rise and equalize with characteristic dip-plateau pattern. Dynamic respiratory assessment: In constriction, RV and LV systolic pressures show discordance with respiration (RV pressure rises while LV pressure falls during inspiration) — this is the most sensitive and specific hemodynamic finding for constriction. In tamponade, RV and LV systolic pressures show concordance (both fall during inspiration). Exercise hemodynamics: Supine bicycle exercise in the cath lab unmasks heart failure with preserved ejection fraction (HFpEF) — a PCWP ≥25 mmHg with exercise is diagnostic.

PA Pulsatility Index (PAPi)

PAPi = (PA systolic - PA diastolic) / RA mean pressure. PAPi is a marker of RV function. A PAPi <0.9 predicts RV failure requiring RVAD support after LVAD implantation. In the setting of acute inferior MI, a PAPi <1.0 predicts hemodynamically significant RV infarction and the need for RV mechanical support. PAPi is increasingly used to assess RV reserve before MCS implantation and to guide the need for biventricular support (BiVAD or TAH) versus isolated LVAD.

Hemodynamic Assessment During Intervention

LVEDP measurement: Obtained by pigtail catheter in the LV; elevated LVEDP (>18 mmHg) correlates with HF and increased periprocedural risk. Used in the POSEIDON protocol for CIN prevention (hydration rate adjusted to LVEDP). Aortic regurgitation assessment: Aortography graded by Sellers classification (0-4+) based on density and washout of contrast from the LV. Simultaneous pressure measurement across the aortic valve (dual-lumen catheter or femoral artery + LV) provides peak-to-peak gradient and mean gradient for AS severity assessment.

The key hemodynamic distinction between constrictive pericarditis and restrictive cardiomyopathy is interventricular dependence: in constriction, RV and LV systolic pressures are discordant with respiration; in restriction, they are concordant. The RVEDP/RVSP ratio >1/3 favors restriction, while the presence of a prominent y descent and dip-plateau pattern favors constriction.

18 Access Site Complications

Femoral Access Complications

Retroperitoneal hemorrhage: Emergency Occurs with high femoral arterial puncture (above the inguinal ligament) or through-and-through puncture. Presents with hemodynamic instability, back/flank pain, ipsilateral abdominal distension, and unexplained Hgb drop. Diagnosis: CT abdomen/pelvis with contrast. Management: volume resuscitation, reversal of anticoagulation, blood transfusion, and covered stent or surgical repair for active extravasation. Maintain a low threshold for diagnosis — mortality is 4-12%.

Pseudoaneurysm: Pulsatile mass at the access site with a "to-and-fro" signal on duplex ultrasound. Small (<2 cm) pseudoaneurysms may thrombose spontaneously. Treatment: ultrasound-guided thrombin injection (first-line — 95% success rate), ultrasound-guided compression, or surgical repair for large or failed cases.

Arteriovenous (AV) fistula: Communication between the femoral artery and vein, detected by continuous bruit/thrill and confirmed by duplex showing arterialized venous flow. Most small fistulae (<5 mm) close spontaneously. Large or symptomatic fistulae require covered stent placement or surgical repair.

Femoral artery dissection / occlusion: Can result from catheter manipulation, closure device deployment, or guide wire trauma. Presents with limb ischemia (acute pain, pallor, pulselessness). Management: angiography with stenting or surgical repair.

Radial Access Complications

Radial artery occlusion (RAO): Occurs in 1-10% of cases; usually asymptomatic due to dual palmar arch supply. Prevention: use smallest effective sheath, patent hemostasis (maintain antegrade flow during compression with pulse oximetry/plethysmography), and adequate anticoagulation (UFH ≥50 U/kg). Radial artery spasm: Prevented with intra-arterial verapamil/nitroglycerin cocktail and hydrophilic-coated sheaths. Managed with additional vasodilators and gentle catheter manipulation — never force catheter withdrawal against spasm (risk of avulsion).

Compartment syndrome: Rare but devastating complication from perforation of a small radial branch. Presents with forearm swelling, pain, and neurovascular compromise. Emergency Treatment: emergent fasciotomy.

Large-Bore Access Complications

TAVR, MCS, and ECMO require large-bore femoral access (14-24 Fr). Specific complications include:

Iliac rupture / dissection: Occurs during sheath insertion in calcified, tortuous, or small iliofemoral arteries. Presents with sudden hypotension and contrast extravasation on iliac angiography. Management: balloon tamponade followed by covered stent deployment (iCAST, Viabahn). Surgical repair if endovascular approach fails.

Acute limb ischemia: Large sheaths can obstruct distal flow, especially if sheath diameter exceeds the vessel lumen. Prevention: place a distal perfusion catheter (DPC) for VA-ECMO and prolonged large-bore access. Treatment: thrombectomy, fasciotomy if compartment syndrome develops.

Lymphocele / lymphatic injury: Disruption of inguinal lymphatics during access, presenting as a fluctuant non-pulsatile groin mass days to weeks after the procedure. Most resolve spontaneously; aspiration or sclerotherapy for large or symptomatic collections.

BARC Bleeding Classification

TypeDefinition
Type 0No bleeding
Type 1Bleeding not actionable; does not cause unscheduled evaluation or treatment
Type 2Any overt, actionable bleeding not meeting criteria for Type 3-5
Type 3aOvert bleeding + Hgb drop 3-5 g/dL (or HCT drop 9-15%); any transfusion
Type 3bOvert bleeding + Hgb drop ≥5 g/dL; cardiac tamponade; requiring surgical or percutaneous intervention; vasoactive agents
Type 3cIntracranial hemorrhage (confirmed by imaging)
Type 4CABG-related bleeding (perioperative intracranial bleeding, reoperation for bleeding, transfusion ≥5 units, chest tube output ≥2 L/24 h)
Type 5aProbable fatal bleeding
Type 5bDefinite fatal bleeding
Anatomy of the femoral artery and vein showing access site for cardiac catheterization
Figure 14 — Femoral Vascular Anatomy. The common femoral artery and vein, with the inguinal ligament and femoral head landmarks. Optimal arterial puncture is over the lower third of the femoral head to minimize access site complications. Source: Wikimedia Commons. Public domain.

19 Procedural Complications

Contrast-Induced Nephropathy (CIN)

CIN is defined as a rise in serum creatinine of ≥0.5 mg/dL or ≥25% from baseline within 48-72 hours of contrast exposure. Risk factors: pre-existing CKD (eGFR <60), diabetes, volume depletion, contrast volume, hemodynamic instability, and nephrotoxic agents. Prevention: adequate hydration (IV NS 1 mL/kg/h for 3-12 h pre- and 6-12 h post-procedure — POSEIDON protocol targets LVEDP-guided hydration), minimize contrast volume (target contrast/eGFR ratio <3.7), use iso-osmolar or low-osmolar contrast, avoid nephrotoxic agents (NSAIDs, aminoglycosides), and hold metformin for 48 hours post-contrast. N-acetylcysteine has not shown consistent benefit (PRESERVE trial — no benefit of NAC or IV sodium bicarbonate over IV saline).

Coronary Perforation

See Section 10 for Ellis classification and management. Additional considerations: Wire perforation (most common cause) — typically Type I-II; managed by balloon inflation proximal to the perforation, reversal of anticoagulation with protamine, and observation. Balloon/stent perforation — oversized balloon or stent in a diseased vessel; managed with covered stent (PK Papyrus). Atherectomy perforation — rotational or orbital atherectomy in a tortuous or thin-walled segment; high risk of Type III perforation.

Stroke During Cardiac Catheterization

Periprocedural stroke occurs in 0.1-0.4% of diagnostic catheterizations and 0.2-0.6% of PCI. Risk factors: aortic arch atheroma, prolonged procedure, catheter manipulation in the aortic root, atrial fibrillation, and left heart catheterization via femoral approach. Management: immediate neurology consultation, CT head to exclude hemorrhagic stroke, catheter-directed thrombectomy or IV tPA if within the appropriate time window, and supportive care.

Air Embolism

Coronary air embolism presents with acute ST elevation, hemodynamic collapse, and chest pain. Emergency Management: vigorous aspiration through the guide catheter, forceful injection of saline and blood (to fragment air bubbles), 100% oxygen (accelerates nitrogen reabsorption), and intracoronary vasodilators for associated spasm. Prevention: meticulous catheter aspiration and flushing, avoiding back-bleeding of guide catheters, and careful attention to manifold connections. Large-volume air embolism (manifold disconnection or sheath flushing error) can cause immediate cardiovascular collapse requiring CPR and potentially emergent percutaneous aspiration from the coronary arteries or aortic root.

Coronary Spasm (Iatrogenic)

Catheter-induced spasm occurs at the site of guide catheter engagement or wire manipulation. More common with radial access (spasm of the radial artery itself is distinct from coronary spasm). Treatment: intracoronary nitroglycerin (100-200 μg bolus, may repeat), intracoronary verapamil (100-200 μg if NTG ineffective), or intracoronary nicardipine (100-200 μg). Refractory spasm may mimic acute occlusion — always consider spasm before escalating to emergent intervention. Patients with known variant (Prinzmetal) angina may have heightened vasoreactivity; pretreat with IC NTG before diagnostic injection.

Radiation Skin Injury

Prolonged fluoroscopy during complex PCI (CTO, chronic total occlusions) can cause radiation dermatitis. Effects are dose-dependent: 2-5 Gy — transient erythema; 5-10 Gy — prolonged erythema, dry desquamation; 10-15 Gy — moist desquamation, pain; >15 Gy — dermal necrosis, ulceration. The patient's back is the most commonly affected site (entrance skin dose). Monitoring: real-time air kerma display; alert at 5 Gy (sentinel event). Management: dermatology referral for skin injuries >5 Gy; wound care for ulceration. Prevention: limit fluoroscopy time, use low-dose protocols, change angulation to distribute dose across skin surface.

Catheter-Induced Coronary Dissection

Occurs during guide catheter engagement or aggressive manipulation, particularly with Amplatz-type catheters in the RCA. The NHLBI dissection classification grades severity:

TypeDescriptionManagement
AMinor radiolucency within the lumen; minimal or no persistenceConservative; observation
BParallel tracts or double lumen; may persist after contrast clearanceConservative if flow maintained; stent if flow-limiting
CExtraluminal cap with contrast persistence (dissection pocket)Stent to seal flap
DSpiral dissection; contrast staining of vessel wallStent; may require multiple stents
ENew persistent filling defect (intimal flap)Stent if flow-limiting
FDissection leading to total occlusion (TIMI 0)Emergency Immediate stenting; wire past dissection flap

Left main dissection is a catastrophic complication requiring immediate stenting to restore flow. If left main dissection extends to the aortic root, emergent surgical consultation is required.

The single most important step in preventing catheter-induced coronary dissection is maintaining coaxial alignment of the guide catheter with the coronary ostium. Never inject contrast with a dampened or ventricularized pressure waveform — this indicates catheter obstruction of the coronary ostium and injection will propagate a dissection.

Cholesterol Embolization Syndrome

Shower of cholesterol crystals from disrupted aortic atherosclerotic plaques during catheter manipulation. Presents days to weeks after the procedure with: blue/purple toes (livedo reticularis) with palpable pedal pulses, renal failure (progressive, may require dialysis), eosinophilia, elevated ESR, low complement, and Hollenhorst plaques on fundoscopy. Diagnosis is clinical; skin or renal biopsy shows biconvex "cleft" spaces (cholesterol crystals dissolved during processing). There is no specific treatment — supportive care, statin therapy, and avoidance of further catheterization if possible. Mortality rate is 70-90% when systemic involvement is severe.

Illustration of kidney showing contrast-induced nephropathy affecting renal tubules
Figure 18 — Contrast-Induced Nephropathy. CIN results from direct tubular toxicity, medullary vasoconstriction, and oxidative stress from iodinated contrast media. Prevention with adequate hydration and minimizing contrast volume is critical for high-risk patients. Source: Wikimedia Commons. CC BY 3.0.

20 Antithrombotic Protocols & Bleeding Management

DAPT Protocols by Indication

IndicationStandard DAPT DurationPreferred P2Y12Notes
ACS + DES12 monthsTicagrelor or prasugrelConsider extended (>12 mo) if high ischemic risk, low bleed risk
Stable CAD + DES6 months (may shorten to 3 mo)ClopidogrelTWILIGHT/STOPDAPT support shortened DAPT
Left main PCI12 monthsTicagrelor or clopidogrelImaging-guided optimization recommended
CTO PCI12 monthsTicagrelor or clopidogrelLong stented segments; consider extended
TAVR3-6 months DAPT or anticoagulationClopidogrelSingle antiplatelet (aspirin) may suffice per POPular TAVI
LAAC45 days DAPT → ASA monotherapyClopidogrelSome centers use short-term anticoagulation

Triple Therapy — AF + PCI

Patients with AF requiring OAC who undergo PCI face competing risks of thromboembolism (stent thrombosis, stroke) and bleeding (triple therapy). Current evidence favors minimizing triple therapy duration:

WOEST — Dual therapy (OAC + clopidogrel, no aspirin) reduced bleeding without increasing ischemic events. RE-DUAL PCI — Dabigatran + P2Y12 inhibitor vs triple therapy: non-inferior for ischemic events, lower bleeding. AUGUSTUS — Apixaban + P2Y12 inhibitor (without aspirin) was the safest strategy; aspirin should be dropped by 1-4 weeks. ENTRUST-AF PCI — Edoxaban + P2Y12 inhibitor was non-inferior to triple therapy.

Current approach: Triple therapy (OAC + DAPT) for 1 week to 1 month maximum → dual therapy (DOAC + P2Y12 inhibitor, drop aspirin) for up to 12 months → OAC monotherapy lifelong. Use a DOAC (not warfarin) and clopidogrel (not prasugrel or ticagrelor) to minimize bleeding.

Special Considerations — Mechanical Heart Valves

Patients with mechanical prosthetic valves requiring PCI present a unique challenge — warfarin (not DOACs) is mandatory for valve thrombosis prevention. The INR target is 2.5-3.5 for mechanical mitral valves and 2.0-3.0 for mechanical aortic valves. After PCI: triple therapy (warfarin + ASA + clopidogrel) for 1 month → warfarin + single antiplatelet for 12 months → warfarin alone. Radial access and BMS (to shorten DAPT) or second-gen DES with shortened DAPT should be considered. DOACs are contraindicated with mechanical valves (RE-ALIGN trial — dabigatran caused thromboembolic and bleeding complications).

CKD & Dialysis Patients

Patients with CKD (eGFR <30) and dialysis patients have higher rates of bleeding, stent thrombosis, and mortality after PCI. Key considerations: minimize contrast volume (consider IVUS-guided "zero-contrast" PCI for severe CKD); iso-osmolar contrast (iodixanol) may reduce CIN risk; BMS vs DES decision is individualized (DES preferred if life expectancy >1 year); prasugrel and ticagrelor lack strong safety data in dialysis — clopidogrel is generally preferred; bivalirudin may be preferred over UFH (predictable pharmacokinetics); fondaparinux is contraindicated if CrCl <30. Dialysis timing: schedule dialysis 24-48 hours post-procedure if contrast was used.

Perioperative Bridging of DAPT

Elective non-cardiac surgery should ideally be deferred for 6 months after DES implantation (minimum 3 months with newer-gen DES) and 1 month after BMS. If surgery cannot be delayed, aspirin should be continued perioperatively in most cases. P2Y12 inhibitors should be held for 5 days (clopidogrel, ticagrelor) or 7 days (prasugrel) before surgery. Bridging with cangrelor or GP IIb/IIIa inhibitors is reserved for very high-risk patients (recent stent <30 days) who require urgent surgery. There is no evidence supporting routine bridging with IV heparin for DAPT cessation.

Timing of Surgery After Stent Implantation

Stent TypeElective Surgery TimingSemi-Urgent SurgeryMinimum DAPT Before Surgery
Balloon angioplasty≥14 daysProceed with aspirin14 days
BMS≥30 daysProceed after 14 days with aspirin1 month
DES (older generation)≥6 monthsProceed after 3 months with aspirin6 months
DES (newer generation)≥3-6 monthsProceed after 1-3 months with aspirin3 months
Complex PCI (LM, CTO, bifurcation)≥12 monthsProceed after 6 months with aspirin12 months
The decision to interrupt DAPT for surgery requires balancing the risk of stent thrombosis (which peaks in the first 30 days and declines over time) against the risk of surgical bleeding. The highest-risk period is the first month after stent implantation — performing surgery during this window carries a 5-20% risk of stent thrombosis. A multidisciplinary discussion involving the interventional cardiologist, surgeon, and anesthesiologist is essential.

Bleeding Management & Reversal Agents

AgentReversalNotes
Unfractionated heparinProtamine sulfate (1 mg per 100 U UFH)Maximum dose 50 mg; risk of anaphylaxis (fish allergy, prior protamine exposure)
EnoxaparinProtamine (1 mg per 1 mg enoxaparin, within 8 h)~60% reversal of anti-Xa activity
BivalirudinNo specific reversal; short half-life (25 min)Stop infusion; supportive care; consider hemodialysis if renal failure
Aspirin / P2Y12Platelet transfusionTransfuse only for life-threatening bleeding; ticagrelor inhibits transfused platelets (reversible)
DabigatranIdarucizumab (Praxbind, 5 g IV)Complete reversal within minutes
Rivaroxaban / Apixaban / EdoxabanAndexanet alfa (Andexxa)Factor Xa decoy; high dose for rivaroxaban, low dose for apixaban
Warfarin4-factor PCC (KCentra), vitamin KPCC for immediate reversal; vitamin K (10 mg IV) for sustained effect
In the setting of active life-threatening bleeding during PCI, the first step is to achieve hemostasis at the source (balloon inflation for perforation, compression for access bleeding). Then reverse anticoagulation with protamine (for heparin) and withhold further GP IIb/IIIa inhibitors. Platelet transfusion should be reserved for refractory bleeding — ticagrelor's reversible mechanism means it will inhibit transfused platelets, unlike clopidogrel or prasugrel.

21 Classification Systems

SYNTAX Score

Angiographic scoring system for coronary disease complexity. Low (≤22): PCI equivalent to CABG; Intermediate (23-32): Heart Team discussion; High (≥33): CABG preferred. Variables: number of lesions, segments involved, total occlusions, trifurcation/bifurcation, aorto-ostial lesions, severe tortuosity, calcification, thrombus, vessel length >20 mm, small vessels, and diffuse disease.

TIMI Risk Score — STEMI

Predicts 30-day mortality in STEMI (0-14 points): Age (65-74 = 2, ≥75 = 3), diabetes/HTN/angina (1), SBP <100 (3), HR >100 (2), Killip II-IV (2), weight <67 kg (1), anterior STEMI or LBBB (1), time to treatment >4 h (1).

TIMI Risk Score — UA/NSTEMI

Predicts 14-day risk of death, MI, or urgent revascularization (0-7 points, 1 each): Age ≥65, ≥3 CAD risk factors, known CAD (≥50% stenosis), ASA use in past 7 days, ≥2 anginal events in 24 h, ST deviation ≥0.5 mm, elevated cardiac biomarkers.

GRACE Score

Most validated risk score for in-hospital and 6-month mortality in ACS. Variables: age, heart rate, SBP, creatinine, Killip class, cardiac arrest, ST deviation, elevated biomarkers. Low risk (<109): <1% mortality; Intermediate (109-140): 1-3%; High (>140): >3% — early invasive strategy recommended.

CRUSADE Bleeding Score

Predicts in-hospital major bleeding risk in NSTEMI patients. Variables (0-100 points): baseline hematocrit, creatinine clearance, heart rate, SBP, sex, diabetes, prior vascular disease, and signs of CHF. Very low (≤20): 3% bleed risk; Low (21-30): 6%; Moderate (31-40): 9%; High (41-50): 12%; Very high (>50): 19%. Helps guide selection of antithrombotic intensity and vascular access strategy.

HEART Score

Used for chest pain risk stratification in the emergency department (0-10 points): History (0-2), ECG (0-2), Age (0-2), Risk factors (0-2), Troponin (0-2). Score 0-3: low risk (safe for discharge); 4-6: moderate risk (observation, further testing); 7-10: high risk (early invasive strategy). Validated in the HEART Pathway trial for safe early discharge of low-risk chest pain patients.

CCS Angina Classification

ClassDescription
IAngina with strenuous or prolonged exertion; ordinary activity does not cause angina
IISlight limitation of ordinary activity — angina with walking >2 blocks on level ground or climbing >1 flight of stairs
IIIMarked limitation — angina with walking 1-2 blocks or climbing 1 flight of stairs
IVInability to perform any physical activity without angina; may be present at rest

Killip Classification — Acute MI

ClassClinical FindingsMortality
INo heart failure signs~6%
IIRales, S3, JVD~17%
IIIPulmonary edema~38%
IVCardiogenic shock~80% (without revascularization)

NYHA Functional Classification

ClassDescription
INo limitation of physical activity; ordinary activity does not cause symptoms
IISlight limitation; comfortable at rest; ordinary activity causes fatigue, dyspnea, palpitations, or angina
IIIMarked limitation; comfortable at rest; less than ordinary activity causes symptoms
IVUnable to carry out any physical activity without discomfort; symptoms at rest

ARC Stent Thrombosis Classification

Definite: Angiographic or pathological confirmation of thrombus within the stent. Probable: Unexplained death within 30 days of stent implantation, or any MI in the stented territory without angiographic confirmation. Possible: Unexplained death >30 days after stent implantation. Timing: Acute (0-24 h), subacute (1-30 d), late (30 d-1 y), very late (>1 y).

Ellis Coronary Perforation Classification

See Section 10 for full details. Type I: extraluminal crater; Type II: myocardial/pericardial blush; Type III: frank perforation with streaming; Cavity spilling: into cardiac chamber.

Mehran In-Stent Restenosis Classification

Type I: focal (≤10 mm); Type II: diffuse intra-stent (>10 mm); Type III: proliferative (extending beyond stent margins); Type IV: total occlusion.

Medina Bifurcation Classification

Three-digit code describing involvement (1 = ≥50% stenosis, 0 = <50%) of the proximal main branch, distal main branch, and side branch: 1,1,1 = all three segments; 1,1,0 = main vessel only; 0,0,1 = side branch only; 1,0,1 = proximal main and side branch (Medina classification is essential for bifurcation PCI planning).

Rentrop Collateral Classification

Grade 0: No filling of collateral channels. Grade 1: Filling of side branches of the occluded vessel via collateral channels, without visualization of the epicardial segment. Grade 2: Partial filling of the epicardial artery via collateral channels. Grade 3: Complete filling of the epicardial artery by collateral channels.

Wilkins Score (Mitral Balloon Valvuloplasty)

Each parameter scored 1-4 (total 4-16): Leaflet mobility (1 = mobile, 4 = immobile); Leaflet thickening (1 = near-normal, 4 = severe); Subvalvular thickening (1 = minimal, 4 = extensive); Calcification (1 = none, 4 = extensive). Score ≤8: favorable for PBMV; >8: consider surgical MVR.

RoPE Score (PFO-Associated Stroke)

Risk of Paradoxical Embolism score (0-10 points): age (0-5 points based on age 18-≥70), no hypertension (1), no diabetes (1), no stroke/TIA (1), nonsmoker (1), cortical infarct on imaging (1). Higher score = greater probability that PFO is causally related to the stroke (and greater benefit from closure). RoPE ≥7: ~84% probability PFO is pathogenic.

J-CTO Score (CTO Difficulty)

Predicts guidewire crossing within 30 minutes (0-5 points, 1 each): Blunt proximal cap, Calcification, Bending >45°, Occlusion length >20 mm, Prior failed attempt. Score 0: easy (success ~90%); 1: intermediate (~75%); 2: difficult (~55%); ≥3: very difficult (<40% wire crossing in 30 min).

PROGRESS-CTO Score

Predicts technical success of CTO PCI using the hybrid algorithm (0-6 points): proximal cap ambiguity (1), absence of interventional collateral (1), moderate-severe tortuosity (1), circumferential calcification (1), CTO length ≥20 mm (1), prior failed attempt (1). Score 0-1: >90% success; 2: ~85%; 3: ~75%; ≥4: <65% success. Unlike the J-CTO score, PROGRESS-CTO accounts for collateral quality, which is essential for retrograde strategy selection.

Sellers Classification (Aortic Regurgitation on Aortography)

GradeDescription
1+Contrast enters the LV but clears with each systole; no opacification of the entire LV
2+Faint, incomplete opacification of the entire LV cavity
3+Complete opacification of the LV; equal density to the aorta
4+Complete opacification of the LV on the first beat; LV density greater than aorta; LV dilated

WIfI Classification (Chronic Limb-Threatening Ischemia)

The Wound, Ischemia, and foot Infection (WIfI) classification stages CLTI severity on a 0-3 scale for each domain: Wound (0 = no ulcer, 3 = extensive gangrene); Ischemia (0 = ABI ≥0.80, 3 = ABI ≤0.39 or absolute toe pressure <30 mmHg); foot Infection (0 = none, 3 = SIRS/sepsis). Combined staging predicts amputation risk and benefit from revascularization. WIfI stages 3-4 (high ischemia, high wound burden) benefit most from revascularization.

DAPT Score

Predicts benefit vs risk of prolonged DAPT after PCI (range -2 to 10): Positive score (≥2) — benefit from extended DAPT (ischemic risk reduction outweighs bleeding risk). Negative score (<2) — bleeding risk outweighs ischemic benefit; favor shorter DAPT. Variables: age (≥75 = -2, 65-74 = -1), smoking (+1), diabetes (+1), MI at presentation (+1), prior PCI or MI (+1), paclitaxel stent (+1), stent diameter <3 mm (+1), CHF/LVEF <30% (+2), vein graft PCI (+2).

22 Medications Master Table

Antiplatelet Agents

DrugMechanismDoseKey Considerations
AspirinIrreversible COX-1 inhibitorLoad 325 mg; maintenance 81 mg dailyLifelong after ACS/PCI; GI protection with PPI
ClopidogrelIrreversible P2Y12 (prodrug, CYP2C19)Load 600 mg; maintenance 75 mg daily3-15% poor metabolizers; consider PFT or CYP2C19 genotyping
PrasugrelIrreversible P2Y12 (prodrug)Load 60 mg; maintenance 10 mg dailyContraindicated: prior stroke/TIA; caution: age ≥75, wt <60 kg (5 mg dose)
TicagrelorReversible P2Y12 (direct-acting)Load 180 mg; maintenance 90 mg BIDDyspnea (14%), bradycardia; avoid with strong CYP3A4 inhibitors; 60 mg BID for extended DAPT
CangrelorIV reversible P2Y1230 μg/kg bolus + 4 μg/kg/minOnset 2 min; offset 60 min; bridging for surgery

Anticoagulants

DrugMechanismDose (PCI)Monitoring / Reversal
Unfractionated heparinAntithrombin III potentiator (anti-IIa, anti-Xa)70-100 U/kg bolus; target ACT 250-350 sACT; reverse with protamine
BivalirudinDirect thrombin inhibitor0.75 mg/kg bolus + 1.75 mg/kg/h infusionACT; no specific reversal (t½ 25 min)
EnoxaparinLMWH (primarily anti-Xa)0.5 mg/kg IV bolus during PCIAnti-Xa level; partial reversal with protamine
FondaparinuxSelective factor Xa inhibitor2.5 mg SC daily (pre-PCI); add UFH for PCIAnti-Xa level; no effective reversal

GP IIb/IIIa Inhibitors

DrugDoseDurationRenal Adjustment
Abciximab0.25 mg/kg bolus + 0.125 μg/kg/min12 h post-PCINone; cleared by RES (not renal)
Eptifibatide180 μg/kg ×2 bolus (10 min apart) + 2 μg/kg/min18-24 h1 μg/kg/min if CrCl <50; contraindicated if dialysis
Tirofiban25 μg/kg bolus + 0.15 μg/kg/min18-24 h50% dose reduction if CrCl <30

Vasodilators & Vasopressors

DrugUse in Cath LabDose
NitroglycerinIC for spasm assessment; IC for no-reflow100-200 μg IC bolus
AdenosineFFR hyperemia; IC for no-reflowIV: 140 μg/kg/min; IC: 100-200 μg (RCA), 200-300 μg (LCA)
NitroprussideIC for no-reflow / spasm100-200 μg IC
VerapamilIC for no-reflow / radial spasm100-200 μg IC (caution if LV dysfunction)
NorepinephrineVasopressor of choice in cardiogenic shock0.05-0.4 μg/kg/min IV
PhenylephrinePure alpha — vasodilation with adequate CO100-200 μg IV bolus; 0.5-5 μg/kg/min
DopamineInotrope/vasopressor (dose-dependent)2-20 μg/kg/min IV
DobutamineInotrope for low CO states2-20 μg/kg/min IV
MilrinoneInodilator (PDE3 inhibitor)0.375-0.75 μg/kg/min IV (no bolus in shock)
AtropineSymptomatic bradycardia; RCA injection vagal response0.5-1 mg IV; may repeat
Illustration of clopidogrel mechanism as an antiplatelet agent blocking the P2Y12 receptor
Figure 15 — Antiplatelet Mechanism (P2Y12 Inhibition). Clopidogrel, prasugrel, and ticagrelor block the P2Y12 receptor on platelets, inhibiting ADP-mediated platelet activation and aggregation. This forms the basis of dual antiplatelet therapy after coronary stenting. Source: Wikimedia Commons. CC BY 3.0.

23 Imaging & Diagnostics Reference

Coronary Angiography Views — Quick Reference

Vessel / SegmentOptimal Views
Left mainAP caudal, LAO cranial (spider), RAO caudal
Proximal/mid LADRAO cranial, AP cranial, LAO cranial
Distal LADRAO cranial, lateral
Diagonal branchesRAO cranial, AP cranial, LAO cranial
LCx / OMRAO caudal, LAO caudal, AP caudal
Proximal/mid RCALAO straight, RAO straight
Distal RCA / PDALAO cranial, RAO cranial

IVUS vs OCT Comparison

FeatureIVUSOCT
Energy sourceUltrasound (20-60 MHz)Near-infrared light (1,300 nm)
Axial resolution~100 μm~10-15 μm
Penetration depth4-8 mm (full vessel wall)1-2 mm
Blood clearanceNot requiredRequired (contrast flush)
Calcium assessmentIdentifies but cannot measure thicknessMeasures calcium thickness and arc
Stent appositionGoodSuperior (resolution advantage)
Thrombus detectionLimitedExcellent (red vs white thrombus)
Vulnerable plaqueLimited (VH-IVUS)Superior — identifies TCFA (cap <65 μm)
Aorto-ostial lesionsPreferred (no flush needed)Difficult (flush inadequacy)

FFR / iFR Decision Matrix

ValueFFRiFR / RFRDecision
Not significant>0.80>0.89Defer PCI; optimal medical therapy
Significant≤0.80≤0.89Revascularization recommended
Grey zone (FFR)0.75-0.80Consider clinical context; IVUS/OCT may help

Coronary CTA (CCTA)

Coronary CT angiography is a non-invasive alternative to invasive angiography for evaluating coronary anatomy and stenosis. Key metrics: CT-FFR (FFRCT) — computational fluid dynamics applied to CCTA images to estimate FFR non-invasively (PLATFORM, ADVANCE trials); Stenosis severity — <50% (non-obstructive), 50-69% (moderate), ≥70% (severe), ≥50% left main; High-risk plaque features — positive remodeling, low-attenuation plaque (<30 HU), napkin-ring sign, spotty calcification. CCTA is endorsed as a first-line test for chest pain evaluation in low-intermediate risk patients (NICE guidelines, PROMISE, SCOT-HEART trials).

CT Coronary Calcium Scoring (Agatston Score)

ScoreInterpretationRisk
0No identifiable calciumVery low risk; CAD unlikely
1-99Mild calcificationLow risk
100-399Moderate calcificationModerate risk; indicates established CAD
≥400Severe calcificationHigh risk; advanced CAD

Echocardiography for Structural Procedures

TEE for TAVR: Confirms annular sizing, guides valve positioning, assesses paravalvular leak, detects pericardial effusion, and evaluates LV function. TEE for TEER: Guides transseptal puncture, visualizes leaflet grasping, assesses residual MR, and monitors for complications (pericardial effusion, single-leaflet device attachment). ICE (intracardiac echo): Increasingly used for ASD/PFO closure, LAA closure, and transseptal puncture guidance — eliminates need for general anesthesia required with TEE.

Transseptal Puncture — Technical Considerations

Transseptal access is the gateway to all left-sided structural interventions (TEER, LAAC, TMVR, PBMV, PFO/ASD closure). The ideal puncture site varies by procedure: TEER — posterior and superior (4-4.5 cm above the mitral annulus); LAAC — posterior and inferior (directed toward the LAA ostium); PBMV — posterior and inferior. Equipment: Brockenbrough needle (BRK or BRK-1), Mullins sheath or deflectable sheath (Agilis). Puncture site is confirmed by tenting of the fossa ovalis on TEE or ICE. Complications: cardiac perforation/tamponade (0.5-1%), aortic root puncture, air embolism, and residual ASD (usually closes spontaneously; rarely hemodynamically significant).

Cross-sectional diagram of the heart showing all four chambers, valves, and great vessels
Figure 19 — Cardiac Anatomy (Cross-Section). Cross-sectional view showing the four cardiac chambers, valves, and great vessels. The interatrial septum (fossa ovalis) is the target for transseptal puncture in structural heart interventions. Source: Wikimedia Commons. Public domain.
Echocardiogram showing four-chamber view of the heart
Figure 16 — Transthoracic Echocardiogram (Four-Chamber View). Echocardiography is essential for pre- and post-procedural assessment in structural heart interventions. TEE provides superior imaging for intraprocedural guidance. Source: Wikimedia Commons. Public domain.

24 Abbreviations Master List

AbbreviationFull Term
ACTActivated clotting time
ADRAntegrade dissection re-entry
ARCAcademic Research Consortium
ASDAtrial septal defect
ASAAlcohol septal ablation (or atrial septal aneurysm, per context)
AVAAortic valve area
AWEAntegrade wire escalation
BARCBleeding Academic Research Consortium
BMSBare metal stent
BVSBioresorbable vascular scaffold
CABGCoronary artery bypass grafting
CASCarotid artery stenting
CICardiac index
CINContrast-induced nephropathy
CLTIChronic limb-threatening ischemia
COCardiac output
CTOChronic total occlusion
DAPTDual antiplatelet therapy
DCBDrug-coated balloon
DEBDrug-eluting balloon
DESDrug-eluting stent
DOACDirect oral anticoagulant
EBUExtra backup (guide catheter)
ECMOExtracorporeal membrane oxygenation
ECPRExtracorporeal cardiopulmonary resuscitation
EROAEffective regurgitant orifice area
FFRFractional flow reserve
GDMTGuideline-directed medical therapy
HOCMHypertrophic obstructive cardiomyopathy
IABPIntra-aortic balloon pump
ICEIntracardiac echocardiography
iFRInstantaneous wave-free ratio
ISRIn-stent restenosis
IVLIntravascular lithotripsy
IVUSIntravascular ultrasound
LAALeft atrial appendage
LAACLeft atrial appendage closure
LADLeft anterior descending artery
LCxLeft circumflex artery
LMCALeft main coronary artery
LVEFLeft ventricular ejection fraction
LVOTLeft ventricular outflow tract
MACEMajor adverse cardiovascular events
MCSMechanical circulatory support
MLDMinimum lumen diameter
MRMitral regurgitation
MSAMinimum stent area
MVAMitral valve area
NCNon-compliant (balloon)
NHPRNon-hyperemic pressure ratio
NSTEMINon-ST-elevation myocardial infarction
OAOrbital atherectomy
OCTOptical coherence tomography
OMTOptimal medical therapy
PAPulmonary artery
PACPulmonary artery catheter
PADPeripheral arterial disease
PBMVPercutaneous balloon mitral valvuloplasty
PCIPercutaneous coronary intervention
PCWPPulmonary capillary wedge pressure
PDAPosterior descending artery
PFOPatent foramen ovale
POBAPlain old balloon angioplasty
POTProximal optimization technique
PPMPermanent pacemaker
PVLParavalvular leak
PVRPulmonary vascular resistance
QCAQuantitative coronary angiography
RARotational atherectomy (or right atrium, per context)
RAORight anterior oblique
RCARight coronary artery
RFRResting full-cycle ratio
RVDReference vessel diameter
SAVRSurgical aortic valve replacement
SCAISociety for Cardiovascular Angiography & Interventions
STEMIST-elevation myocardial infarction
SVGSaphenous vein graft
SVRSystemic vascular resistance
TAVRTranscatheter aortic valve replacement
TCARTranscarotid artery revascularization
TCFAThin-cap fibroatheroma
TEERTranscatheter edge-to-edge repair
TEETransesophageal echocardiography
TFTransfemoral
TIMIThrombolysis in Myocardial Infarction
TMPGTIMI myocardial perfusion grade
TMVRTranscatheter mitral valve replacement
TRTricuspid regurgitation
TRATransradial access
TTVRTranscatheter tricuspid valve replacement
UFHUnfractionated heparin
VA-ECMOVenoarterial extracorporeal membrane oxygenation
VH-IVUSVirtual histology intravascular ultrasound
VLSTVery late stent thrombosis
VSDVentricular septal defect

25 Landmark Trials

Coronary Revascularization Strategy

TrialYearKey FindingReference
COURAGE2007PCI + OMT did not reduce death or MI vs OMT alone in stable CADPMID 17387127
ISCHEMIA2020Invasive strategy did not reduce death or MI vs conservative strategy in stable CAD with moderate-severe ischemiaPMID 32227755
SYNTAX2009CABG superior to PCI in 3-vessel/left main disease; SYNTAX score predicts PCI outcomesPMID 19228612
EXCEL2019PCI non-inferior to CABG for left main (low-intermediate SYNTAX) at 5 years; higher repeat revascularization with PCIPMID 31562134
NOBLE2020CABG superior to PCI for left main at 5 years (non-procedural MI, repeat revascularization)PMID 31813566

Coronary Physiology & Imaging

TrialYearKey FindingReference
FAME2009FFR-guided PCI reduced MACE vs angiography-guided PCI in multivessel diseasePMID 19144937
FAME 22012FFR-guided PCI + OMT reduced urgent revascularization vs OMT alone when FFR ≤0.80PMID 22998338
DEFINE-FLAIR2017iFR-guided revascularization non-inferior to FFR-guided at 1 yearPMID 28317438
iFR-SWEDEHEART2017iFR-guided revascularization non-inferior to FFR-guided at 1 yearPMID 28317439
ULTIMATE2021IVUS-guided PCI reduced MACE vs angiography-guided PCI at 3 yearsPMID 33454528

STEMI & ACS

TrialYearKey FindingReference
SHOCK1999Early revascularization reduced 6-month mortality in cardiogenic shock complicating MIPMID 10471456
COMPLETE2019Staged complete revascularization after primary PCI reduced CV death and MI vs culprit-onlyPMID 31475799
MATRIX2015Radial access reduced net adverse clinical events (including bleeding and mortality) vs femoral in ACSPMID 26466021
TOTAL2015Routine aspiration thrombectomy did not reduce CV death, MI, cardiogenic shock, or NYHA IV HF in STEMIPMID 25638659
TIMACS2009Early invasive strategy (<24 h) reduced composite endpoint vs delayed (>36 h) in high-risk NSTEMIPMID 19458363

Antiplatelet Therapy

TrialYearKey FindingReference
PLATO2009Ticagrelor reduced CV death, MI, stroke vs clopidogrel in ACSPMID 19717846
TRITON-TIMI 382007Prasugrel reduced ischemic events vs clopidogrel in ACS-PCI; more bleedingPMID 17982182
TWILIGHT2019Ticagrelor monotherapy after 3 months DAPT reduced BARC 2-5 bleeding without increasing ischemic eventsPMID 31556372
AUGUSTUS2019Apixaban + P2Y12 (without ASA) safest antithrombotic strategy in AF + PCI patientsPMID 30883055

Structural Heart

TrialYearKey FindingReference
PARTNER 1A/1B2010-11TAVR superior to medical Rx (inoperable) and non-inferior to SAVR (high risk)PMID 20961243
PARTNER 32019TAVR superior to SAVR in low-risk patients at 1 year (composite of death, stroke, rehospitalization)PMID 30883058
COAPT2018TEER (MitraClip) reduced HF hospitalization and death in HFrEF with severe secondary MR on GDMTPMID 30280640
MITRA-FR2018TEER did not reduce death or HF hospitalization in secondary MR (different patient selection vs COAPT)PMID 30280674
PROTECT-AF2014WATCHMAN non-inferior to warfarin for stroke prevention in AF; reduced hemorrhagic stroke and mortality at 3.8 yrPMID 25065991
RESPECT2017PFO closure reduced recurrent stroke vs medical therapy in cryptogenic stroke patientsPMID 28902580

Mechanical Circulatory Support

TrialYearKey FindingReference
IABP-SHOCK II2012IABP did not reduce 30-day mortality in cardiogenic shock complicating MIPMID 23013624
PROTECT III2024Impella-supported high-risk PCI reduced 90-day major adverse events vs IABPPMID 38587237

Bifurcation & CTO Trials

TrialYearKey FindingReference
DKCRUSH-V2017DK-crush technique superior to provisional stenting for distal left main bifurcation (true bifurcations)PMID 28622955
EBC MAIN2023Systematic two-stent strategy non-inferior to provisional stenting for left main bifurcation with complex anatomyPMID 37634136
EURO-CTO2018CTO PCI improved angina, quality of life, and functional status vs medical therapyPMID 30366740
DISRUPT CAD III2021IVL safe and effective for calcium modification before stenting; 92.4% procedural successPMID 33465776

Triple Therapy Trials

TrialYearKey FindingReference
WOEST2013OAC + clopidogrel (no aspirin) reduced bleeding vs triple therapy in AF + PCIPMID 23415013
RE-DUAL PCI2017Dabigatran dual therapy reduced bleeding vs triple therapy in AF + PCIPMID 28844200
ENTRUST-AF PCI2019Edoxaban + P2Y12 non-inferior to VKA-based triple therapy for bleeding/ischemic eventsPMID 31556371
Anterior view of the heart showing coronary arteries and cardiac chambers
Figure 17 — Cardiac Anatomy (Anterior View). The anterior surface of the heart showing the distribution of the coronary arteries. The LAD courses in the anterior interventricular groove; the RCA courses in the right atrioventricular groove. Source: Wikimedia Commons. CC BY 3.0.