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Eduovisual

Cardiovascular

Aortic stenosis: severity grading and TAVR vs SAVR referral

Clinical Overview and When to Suspect Aortic Stenosis

Calcific (degenerative) AS — patients >70, share risk factors with atherosclerosis (HTN, hyperlipidemia, smoking, CKD, DM)

Bicuspid aortic valve (BAV) — accelerated calcification, symptomatic in 50s–60s; associated with aortopathy and coarctation

Rheumatic AS — almost always with mitral involvement; immigrant populations, history of rheumatic fever

— Older adult with exertional dyspnea, angina, or syncope (the classic triad — "ASD")

— Heart failure with preserved EF and a systolic murmur

— Unexplained syncope during exertion in an elderly patient

— Incidental systolic ejection murmur at a preop visit before non-cardiac surgery

— GI bleeding from angiodysplasia (Heyde syndrome — acquired vWF deficiency from shear stress)

Board pearl: Symptomatic severe AS is a Class I indication for valve replacement regardless of LV function — symptoms, not EF, drive the trigger.

Step 3 management: Any new murmur in an older patient with exertional symptoms → TTE before next visit, do not defer to "routine follow-up."

Aortic stenosis (AS) is the most common valvular lesion requiring intervention in adults; prevalence rises sharply after age 65 and approaches 10% by age 80.
Three dominant etiologies:
Pathophysiology: progressive leaflet calcification → fixed outflow obstruction → concentric LV hypertrophy → diastolic dysfunction → eventually systolic dysfunction, pulmonary HTN, and low-output state.
When to suspect on Step 3:
Once symptoms develop in severe AS, untreated 2-year mortality approaches 50%. The latency between subclinical severe AS and symptom onset is the key window for surveillance.
Ambulatory framing: AS is a longitudinal problem — most patients are identified in clinic, monitored with serial echos, then transitioned to a Heart Team when criteria are met.
Solid White Background
Presentation Patterns and Key History

Dyspnea/HF: median survival ~2 years untreated

Syncope (usually exertional, from inability to augment CO): ~3 years

Angina (even without CAD, from supply-demand mismatch in hypertrophied LV): ~5 years

Decreased exercise tolerance — older patients often self-limit and call themselves "asymptomatic"; ask about hill walking, stairs, grocery carrying

Fatigue disproportionate to comorbidities

— Near-syncope or lightheadedness with exertion

GI bleeding from cecal angiodysplasia (Heyde)

— Prior rheumatic fever, strep history, or recent immigration from endemic regions

Bicuspid valve family history or known aortopathy

Mediastinal radiation (Hodgkin survivors) → premature valvular calcification

CKD/dialysis and hyperparathyroidism → accelerated calcification

— NYHA class, METs, and 6-minute walk distance are documented to track decline

— A previously "asymptomatic" patient who restricts activity is functionally symptomatic

Key distinction: Asymptomatic severe AS vs symptomatic severe AS is the single most important historical determination — it changes management from surveillance to referral for AVR. When in doubt, order an exercise stress test (safe in asymptomatic severe AS under supervision) to unmask occult symptoms or blunted BP response.

Board pearl: A drop in systolic BP ≥10 mmHg on exercise testing in "asymptomatic" severe AS is itself a Class IIa indication for AVR — treat them as symptomatic.

Classic symptomatic triad ("SAD"): Syncope, Angina, Dyspnea — each has prognostic weight.
Subtler ambulatory complaints to probe:
High-yield historical clues:
Functional staging matters for Step 3:
Don't miss the preoperative scenario: an elderly patient before hip surgery with a crescendo-decrescendo murmur needs an echo before clearance — severe AS markedly raises perioperative MACE.
Solid White Background
Physical Exam Findings and Hemodynamic Assessment

Harsh, late-peaking, crescendo-decrescendo systolic ejection murmur at right upper sternal border, radiating to carotids

— Later peak = more severe stenosis

Soft or absent S2 (immobile calcified leaflets) — severe disease

Paradoxical splitting of S2 — delayed aortic closure

S4 gallop from stiff hypertrophied LV

Gallavardin phenomenon: high-frequency component radiates to apex, mimicking MR

Pulsus parvus et tardus — slow-rising, low-amplitude carotid upstroke (most specific bedside sign of severe AS)

— Narrow pulse pressure

— Sustained, non-displaced PMI from concentric LVH

Passive leg raise, squatting (↑ preload/afterload — ↑ flow across valve)

— Murmur decreases with Valsalva and standing (↓ preload)

— Elevated JVP, S3 (LV failure), bibasilar crackles, peripheral edema, hepatic congestion

— Cool extremities, hypotension → low-output state, urgent referral

— Mean gradient on echo correlates with severity but is flow-dependent — low gradients in low-flow states can hide severe disease (see chunk 5)

Board pearl: Pulsus parvus et tardus + soft single S2 + late-peaking murmur = severe AS until proven otherwise; this combination has higher specificity than any single sign.

Step 3 management: A new diminished/absent S2 in a patient with known moderate AS → expedite repeat echo; this is often the bedside marker of progression to severe disease.

Auscultation:
Pulse and pressure findings:
Maneuvers that increase AS murmur intensity:
Key distinction: AS murmur softens with Valsalva (most murmurs do); HOCM murmur intensifies with Valsalva and standing — this is the classic Step 3 differential at the bedside.
Signs of decompensation to recognize at clinic visits:
Hemodynamic correlations:
Solid White Background
Diagnostic Workup — Initial Labs, ECG, Imaging

— Quantifies aortic valve area (AVA), peak velocity (Vmax), mean gradient, LV size/EF, LV mass, diastolic function, concomitant valve disease, and pulmonary pressures.

Mild: Vmax 2.0–2.9 m/s, mean gradient <20 mmHg, AVA >1.5 cm²

Moderate: Vmax 3.0–3.9 m/s, mean gradient 20–39 mmHg, AVA 1.0–1.5 cm²

Severe: Vmax ≥4.0 m/s, mean gradient ≥40 mmHg, AVA ≤1.0 cm²

Very severe (D1 critical): Vmax ≥5.0 m/s or mean gradient ≥60 mmHg

— Stage A — at risk (BAV, sclerosis)

— Stage B — progressive (mild–moderate)

— Stage C — asymptomatic severe (C1 normal EF, C2 EF <50%)

— Stage D — symptomatic severe (D1 high-gradient, D2 low-flow/low-gradient with reduced EF, D3 paradoxical low-flow with preserved EF)

— BNP/NT-proBNP — rising BNP in asymptomatic severe AS predicts faster symptom onset (Class IIa AVR indication if markedly elevated)

— CBC, BMP, lipids, HbA1c (modify risk factors)

— TSH, iron studies if HF features

— Type and screen, coags if planning intervention

Board pearl: AVA <1.0 cm² alone does not define severe AS if gradients are low — always integrate with flow state.

Transthoracic echocardiogram (TTE) is the diagnostic test of choice — first study ordered whenever AS is clinically suspected.
AHA/ACC severity grading (peak velocity, mean gradient, AVA):
ACC/AHA stages (used for management trigger):
ECG: LVH with strain, LAE, sometimes LBBB or conduction disease (calcium extending into septum).
CXR: often normal early; later — boot-shaped heart, calcified aortic knob, pulmonary congestion.
Labs to order in ambulatory workup:
CCS pearl: Order TTE, ECG, CXR, CBC, BMP, BNP, lipid panel at the first visit when AS is suspected — these are your foundational orders before deciding on referral pathway.
Solid White Background
Diagnostic Workup — Advanced and Confirmatory Studies

Classic LFLG (D2): EF <50%, low stroke volume index (<35 mL/m²) → dobutamine stress echo (DSE)

True severe AS: AVA stays ≤1.0 cm² and gradient rises ≥40 mmHg with augmented flow

Pseudo-severe AS: AVA increases, gradient stays low — primary myocardial disease, not valve

No contractile reserve (failure to ↑SV by 20%) — poor prognosis but still benefits from AVR (esp. TAVR)

Paradoxical LFLG (D3): preserved EF, low SVi, often elderly women with small hypertrophied LV

Men ≥2000 AU, Women ≥1200 AU = very likely severe AS

— Used to adjudicate LFLG cases

— Annular sizing, aortic root and ascending aorta dimensions

— Iliofemoral access vessel size, tortuosity, calcification

— Distance from annulus to coronary ostia (risk of coronary occlusion)

— Age ≥40, angina, or CAD risk factors — to plan concomitant CABG or PCI

Key distinction: DSE in classic LFLG (D2) distinguishes true vs pseudo-severe; AV calcium score is the tool for paradoxical LFLG (D3) with preserved EF.

Step 3 management: A patient with AVA 0.9 cm², mean gradient 28 mmHg, EF 35% → next step is dobutamine stress echo, not direct referral, to confirm true severe AS before AVR.

Low-flow, low-gradient AS (LFLG) — the trickiest scenario; AVA suggests severe but gradient is <40 mmHg.
Aortic valve calcium scoring by non-contrast CT — sex-specific cutoffs:
CT angiography before TAVR:
Coronary angiography before any AVR in patients with:
TEE — when TTE is suboptimal, evaluating endocarditis, or guiding TAVR.
Cardiac MRI — myocardial fibrosis (late gadolinium enhancement) predicts post-AVR outcomes; useful when other imaging is equivocal.
Exercise stress testing — for asymptomatic severe AS to confirm true asymptomatic status; contraindicated in symptomatic severe AS.
Solid White Background
Risk Stratification and Indications for Intervention

Stage D: symptomatic severe AS (any subtype — high-gradient, LFLG with confirmed severity, paradoxical LFLG)

Stage C2: asymptomatic severe AS with LVEF <50%

Severe AS undergoing other cardiac surgery (CABG, mitral, aortic surgery)

— Asymptomatic severe AS with abnormal exercise test (symptoms, hypotension)

— Asymptomatic very severe AS (Vmax ≥5.0 m/s) at low surgical risk

— Asymptomatic severe AS with rapid progression (ΔVmax ≥0.3 m/s/yr)

— Asymptomatic severe AS with markedly elevated BNP (>3× normal)

— Cardiologist, interventional cardiologist, cardiothoracic surgeon, imaging, anesthesia, geriatrics where relevant

— Determines surgical risk (STS-PROM, frailty, comorbidities), anatomic suitability, patient values

Low risk: <4%

Intermediate: 4–8%

High: >8%

Prohibitive: predicted mortality/major morbidity >50% at 1 year

Age <65 or life expectancy >20 yrSAVR preferred

Age 65–80shared decision (TAVR or SAVR — anatomy and patient preference)

Age >80 or life expectancy <10 yrTAVR preferred (transfemoral)

Prohibitive surgical risk → TAVR

Bicuspid valve, concomitant CABG/other valve disease, unfavorable TAVR anatomy → favor SAVR

Step 3 management: Refer to Heart Team within 2 weeks of confirmed severe symptomatic AS — do not wait for "next available cardiology slot."

AVR is indicated (Class I) when:
Class IIa indications (consider AVR):
Heart Team evaluation — required for every AVR decision:
Surgical risk tiers (STS predicted mortality):
TAVR vs SAVR — 2020 ACC/AHA-guided choice (refined in 2023 focused update):
Board pearl: Bicuspid AS in a young patient = SAVR (often with concurrent aortopathy repair if root ≥4.5–5.0 cm). TAVR data in BAV are evolving but not first-line for the young.
Solid White Background
Medical Therapy and Pharmacologic Principles

Hypertension — present in ~50% of AS patients; treat to standard targets

— Use ACE inhibitors/ARBs cautiously — start low, titrate slowly; safe and beneficial when tolerated

— Avoid abrupt vasodilation; never use nitrates aggressively in severe AS — preload reduction → syncope

Atrial fibrillation — rate control with beta-blocker; anticoagulate per CHA₂DS₂-VASc

CAD — statins, aspirin if indicated for ASCVD (not for AS itself)

HF symptoms — careful diuresis for congestion; the LV is preload-dependent

— High-dose nitrates, hydralazine in heavy doses — precipitous afterload drop

— Negative inotropes (non-dihydropyridine CCBs) if reduced EF

— Phosphodiesterase-5 inhibitors — vasodilation in fixed-output state

Mechanical valve → lifelong warfarin (INR 2.5 for AVR), plus low-dose ASA

Bioprosthetic SAVR → warfarin (INR 2.0–3.0) or DOAC for 3–6 months, then ASA 81 mg

TAVR → ASA 81 mg lifelong if no other indication; add OAC only for AF or other thromboembolic indication; DOACs are not recommended empirically post-TAVR without AF

Board pearl: Starting sildenafil or high-dose nitrates in a patient with severe AS for "atypical chest pain" can cause syncope or cardiac arrest — this is a tested Step 3 safety scenario.

No medical therapy halts AS progression — statins do not slow calcific AS (SEAS, ASTRONOMER, SALTIRE trials negative). This is a frequent Step 3 distractor.
Pharmacologic care is about comorbidity control and bridging to AVR, not "treating" the valve:
Drugs to avoid or use with caution in severe AS:
Endocarditis prophylaxisnot routinely indicated for native AS; only for prosthetic valves, prior IE, certain CHD, and cardiac transplant valvulopathy.
Statins and ASA — based on ASCVD risk, not AS itself.
Anticoagulation after valve replacement:
Solid White Background
TAVR vs SAVR — Procedural Details and Decision Logic

— Median sternotomy or mini-thoracotomy, cardiopulmonary bypass

— Mechanical valve (durable, requires lifelong warfarin) or bioprosthetic (durable 10–20 yr, no long-term OAC)

— Permits concomitant CABG, root/ascending aortic repair, other valve surgery

— Preferred in: young patients (<65), BAV with aortopathy, complex anatomy, endocarditis, low surgical risk with long life expectancy

— Transfemoral (preferred), transapical, transcarotid, transaxillary access

— Balloon-expandable (SAPIEN) or self-expanding (Evolut) bioprosthesis

— Faster recovery (1–3 day LOS), no sternotomy

— Now approved across all risk strata (PARTNER 3, Evolut Low Risk trials)

— Preferred in: age >80, high/prohibitive surgical risk, hostile chest (prior CABG, radiation), frailty

— Small annulus or severe LVOT calcification (annular rupture risk)

— Low coronary ostia (<10–12 mm) — occlusion risk

— Severe peripheral vascular disease without alternative access

— Bulky asymmetric BAV calcification (relative)

Paravalvular leak — even mild ≥ moderate worsens survival

Permanent pacemaker post-TAVR ~10–15% (higher with self-expanding); from injury to AV node/LBB

Stroke ~2–3% within 30 days

Vascular access complications (femoral hematoma, dissection)

Coronary obstruction (rare but lethal)

Key distinction: TAVR → pacemaker risk; SAVR → AF and sternal infection risk. Match procedure to anatomy + life expectancy + patient values.

CCS pearl: Post-TAVR orders day 0–1: telemetry (watch for AVB), TTE before discharge, ASA 81 mg, ambulate POD1, dual-antiplatelet only if recent stent — otherwise ASA monotherapy.

SAVR (surgical AVR):
TAVR (transcatheter AVR):
Anatomic disqualifiers for TAVR:
TAVR-specific complications to know:
SAVR-specific complications: sternal wound infection, AKI, AF, longer ICU/hospital stay, perioperative MI, bleeding.
Bridging therapyballoon aortic valvuloplasty (BAV) is palliative or a bridge to definitive AVR in cardiogenic shock; durability is poor, restenosis within 6–12 months.
Solid White Background
Special Populations — Elderly and Renal/Hepatic Impairment

— TAVR is the preferred strategy — lower 30-day mortality, faster recovery, preserved quality of life

Frailty assessment is mandatory — Fried criteria, gait speed (5-meter walk >6 s = frail), Katz ADLs, grip strength, albumin

— Severe frailty + cognitive impairment + dependency may shift decision toward palliative care rather than intervention — futility is a legitimate Heart Team conclusion

— Polypharmacy review — deprescribe nitrates, alpha-blockers, sildenafil before TAVR

— Pre-procedural geriatric/cognitive screening, fall risk, social support for discharge planning

— AS and CKD share calcification biology; prevalence high in dialysis

— Contrast load for TAVR planning CT and angiography — minimize, use isotonic saline, hold ACEi/ARB and diuretics periprocedure

AKI is a major TAVR complication (5–10%) and independent mortality predictor

— Dialysis patients: TAVR is feasible but carries higher mortality; SAVR also higher risk — shared decision

— Coagulopathy and thrombocytopenia increase bleeding risk

— Cirrhosis (Child-Pugh B/C) → significantly elevated SAVR mortality; TAVR may be safer

— Synthetic dysfunction complicates warfarin dosing post-mechanical valve — favor bioprosthetic

— Assess decision-making capacity; involve surrogate

— Delirium risk after SAVR is substantial — TAVR may better preserve cognition

— Iron deficiency from GI angiodysplasia bleeding due to acquired vWF deficiency (loss of high-molecular-weight multimers across stenotic valve)

— Often resolves after AVR — definitive treatment of recurrent GI bleed in severe AS is valve replacement

Board pearl: Recurrent iron-deficiency anemia + negative endoscopy + new AS murmur → Heyde syndrome; do not just keep transfusing — refer for AVR.

Step 3 management: Before TAVR in an 85-year-old, document frailty score, MoCA, and goals-of-care discussion — these are expected components of pre-procedure care.

Elderly (>80) considerations:
Chronic kidney disease (CKD):
Hepatic impairment:
Cognitive impairment / dementia:
Anemia and Heyde syndrome:
Solid White Background
Special Populations — Pregnancy, Young Adults, Bicuspid Disease

— Severe AS is WHO maternal cardiovascular risk class III–IV; ideally valve assessed and treated pre-conception

— Hemodynamics of pregnancy (↑CO ~50%, ↓SVR) poorly tolerated with fixed obstruction

— Severe symptomatic AS during pregnancy: percutaneous balloon valvuloplasty is the bridging option (avoids CPB risk to fetus)

— Mode of delivery: vaginal delivery with assisted second stage generally preferred; epidural with careful preload management; C-section for obstetric indications

— Preconception counseling for known BAV: TTE, aortic root imaging (root >4.5 cm = repair before pregnancy)

— Etiology typically BAV or rheumatic

SAVR preferred; choice of mechanical vs bioprosthetic is a key shared-decision moment:

Mechanical: durability >20 yr, requires lifelong warfarin (INR 2.5), pregnancy-incompatible without bridging

Bioprosthetic: 10–15 yr durability, no long-term OAC, but reoperation or valve-in-valve TAVR later

Ross procedure (pulmonary autograft) — option in select young patients at experienced centers; avoids anticoagulation

— Screen first-degree relatives with TTE (10% prevalence in families)

— Associated aortopathy — image the entire thoracic aorta; repair ascending aorta when ≥5.5 cm (≥5.0 cm with risk features, ≥4.5 cm if undergoing AVR)

— Associated with coarctation — check BP in both arms and a leg

— Severe congenital AS → balloon valvuloplasty; AVR (Ross or mechanical) when older

Key distinction: Warfarin is teratogenic (especially weeks 6–12); a woman of childbearing age with a mechanical valve requires preconception counseling on LMWH bridging during the first trimester.

Board pearl: New severe AS in pregnancy with HF symptoms → balloon valvuloplasty, not SAVR, during gestation.

Pregnancy and AS:
Young adults (<65) with severe AS:
Bicuspid aortic valve specifics:
Pediatric/congenital AS:
Solid White Background
Complications and Adverse Outcomes

Sudden cardiac death — risk ~1%/yr in truly asymptomatic, rises sharply with symptoms

Heart failure — initially HFpEF from concentric LVH, later HFrEF

Atrial fibrillation — from LA enlargement; loss of atrial kick is catastrophic in stiff LV → acute decompensation

Pulmonary hypertension and right HF in advanced disease

Heyde syndrome — GI bleeding from angiodysplasia

Syncope, falls, hip fracture cascade in elderly

Infective endocarditis on diseased valve

— Bleeding, transfusion, AKI, stroke (~2%), perioperative MI

Postoperative AF (~30%) — anticoagulate per CHA₂DS₂-VASc

— Sternal wound infection, mediastinitis (esp. in DM, obesity)

— Prosthesis-patient mismatch — small valve in large patient → residual high gradient

Conduction disease / permanent pacemaker (10–15%, higher with self-expanding valves and preexisting RBBB)

Paravalvular leak — predictor of mortality

Stroke (~2–3%) — cerebral embolic protection devices considered

Vascular access complications — femoral pseudoaneurysm, retroperitoneal bleed

Annular rupture (rare, catastrophic)

Coronary obstruction (low ostia, bulky leaflet calcium)

Acute kidney injury from contrast

Structural valve deterioration — bioprosthetic, typically beyond 10 years

Prosthetic valve thrombosis — clinical or subclinical leaflet thrombosis (HALT on CT); manage with OAC

Prosthetic valve endocarditis — early (<1 yr) usually staphylococcal/nosocomial; late more typical IE microbiology

Hemolysis — paravalvular leak; check LDH, haptoglobin, schistocytes

Board pearl: New conduction block (especially new LBBB or AV block) post-TAVR within 48 hours → keep monitored; persistent block beyond 48 hours is the strongest predictor of need for permanent pacemaker.

Step 3 management: Post-AVR patient returns with fever, new murmur, embolic phenomena → blood cultures ×3, TTE then TEE, empiric IE coverage — treat as prosthetic valve endocarditis until disproven.

Natural history complications of untreated severe AS:
Periprocedural complications — SAVR:
Periprocedural complications — TAVR:
Late prosthesis complications:
Solid White Background
When to Escalate Care — ICU, Consult, Inpatient Triage

— Symptomatic severe AS with new or worsening HF, syncope, or angina at rest

— Hemodynamic instability — SBP <90, hypoperfusion, lactic acidosis

— Acute pulmonary edema in known severe AS

— New atrial fibrillation with rapid response in severe AS

— Suspected infective endocarditis

— Acute coronary syndrome with concomitant severe AS

— Cardiogenic shock from critical AS — initiate inotropes cautiously (dobutamine), avoid vasodilators; vasopressors (norepinephrine) preserve coronary perfusion of the hypertrophied LV

— Refractory pulmonary edema needing NIV/intubation

— Sustained ventricular arrhythmia or complete heart block

— Post-TAVR with persistent high-grade AV block or hemodynamic instability

Emergent balloon aortic valvuloplasty (BAV) to stabilize for definitive TAVR/SAVR

Mechanical circulatory support — IABP is contraindicated/ineffective in severe AS conventionally; Impella or VA-ECMO may be used as bridge in select centers

Cardiology — any new diagnosis of moderate or severe AS, before AVR planning

Interventional cardiology + CT surgery (Heart Team) — all AVR candidates

Anesthesia preop — high-risk patients before non-cardiac surgery

Palliative care — symptomatic severe AS deemed not a candidate for AVR; ongoing symptom management with diuretics, oxygen, opioids

— Severe symptomatic AS → address valve first if surgery elective

— Severe asymptomatic AS undergoing intermediate/high-risk non-cardiac surgery → cardiology consult; many proceed with careful intraoperative monitoring (arterial line, avoid hypotension, careful preload)

— Emergent non-cardiac surgery: proceed with hemodynamic optimization

CCS pearl: Patient with critical AS arrives in shock — orders: arterial line, central line, norepinephrine, cautious dobutamine, avoid nitrates, urgent cardiology and CT surgery consults, TTE, BAV as bridge to definitive AVR.

Triggers for ED/inpatient admission:
Triggers for ICU/CCU admission:
Bridging in cardiogenic shock from critical AS:
Consult triggers:
Perioperative AS for non-cardiac surgery:
Solid White Background
Key Differentials — Other Valvular and Structural Causes of a Systolic Murmur

— Dynamic LVOT obstruction; murmur increases with Valsalva and standing (↓ preload), decreases with squat/handgrip

— Bisferiens carotid pulse, S4, family history of sudden death

— Echo: asymmetric septal hypertrophy, SAM of mitral valve, dynamic gradient

— Thickened valve without significant gradient (Vmax <2.0 m/s)

— Marker of atherosclerotic risk; manage CV risk factors

— Murmur shorter, peaks early, S2 preserved, normal pulses

— Holosystolic murmur at apex, radiates to axilla

— Increases with handgrip (↑ afterload), unlike AS which decreases

— S3, displaced PMI

— Gallavardin phenomenon of AS can mimic MR at apex — but Gallavardin still has the harsh carotid component

— Holosystolic at left lower sternal border; Carvallo sign — increases with inspiration

— Elevated JVP with prominent v wave, pulsatile liver

— Holosystolic, harsh, at left lower sternal border; thrill

— Increases with handgrip

— Systolic ejection at left upper sternal border; murmur decreases with inspiration if dynamic (rare in adults — usually congenital)

— Soft, early-peaking, no radiation, normal S2 and pulses

— Resolve when underlying state corrected

— Williams syndrome (elfin facies, hypercalcemia, intellectual disability); murmur radiates more to right carotid; BP higher in right arm

Key distinction: Maneuvers are the bedside crux:

— AS: ↓ Valsalva/standing, ↑ squat/leg raise

— HOCM: ↑ Valsalva/standing, ↓ squat

— MR/VSD: ↑ handgrip; AS ↓ handgrip

Board pearl: A young athlete with exertional syncope + systolic murmur that gets louder on standingHOCM, not AS — order echo and avoid exertion.

Hypertrophic obstructive cardiomyopathy (HOCM):
Aortic sclerosis (Stage A AS):
Mitral regurgitation:
Tricuspid regurgitation:
Ventricular septal defect:
Pulmonic stenosis:
Flow murmurs (anemia, hyperthyroidism, fever, pregnancy):
Supravalvular AS:
Solid White Background
Key Differentials — Non-Valvular Causes of AS-Like Presentation

— Exertional chest pain — but no ejection murmur, normal pulses, normal S2

— Older adults can have both CAD and AS; angina in severe AS doesn't always mean obstructive CAD, but coronary angiography is part of preop workup

— Dyspnea, edema, elevated BNP — same demographics

— Distinguish by TTE — HFpEF without significant valve disease

— Concentric LVH from chronic HTN can mimic AS hemodynamics

— Exertional dyspnea — but cough, smoking history, hyperinflation on CXR

— PFTs and echo distinguish

— Exertional dyspnea, flow murmur, fatigue; CBC quickly screens

— Syncope without exertional trigger; positional

— In AS, syncope is exertional and often without prodrome

— Focal neuro signs, dizziness with head turning

— Acute dyspnea, pleuritic chest pain, tachycardia, hypoxia, risk factors — distinct presentation

— Congenital; echo shows membrane below valve; common in young adults

— Williams syndrome, Shone complex; CT/MRI delineates

— Can produce mitral inflow obstruction mimicking diastolic murmur; sometimes confused on TTE for valvular pathology

Key distinction: Exertional syncope = AS, HOCM, or arrhythmia until proven otherwise. Reflex/vasovagal syncope is rest-onset with prodrome; AS syncope is on exertion from failure to augment CO.

Board pearl: Elderly woman with HFpEF features and a systolic murmur — always confirm or exclude paradoxical low-flow low-gradient AS (D3) with calcium score before labeling as "just HFpEF."

Coronary artery disease / stable angina:
Heart failure with preserved EF (HFpEF):
Pulmonary disease (COPD, pulmonary HTN):
Anemia:
Neurocardiogenic / orthostatic syncope:
Vertebrobasilar insufficiency / cerebrovascular syncope:
Pulmonary embolism:
Subaortic membrane (discrete subvalvular AS):
Supravalvular AS:
Severe MAC (mitral annular calcification with caseation):
Solid White Background
Secondary Prevention, Discharge Medications, Long-Term Plan

Mechanical valve (AVR position): warfarin INR target 2.5 (range 2.0–3.0) lifelong + ASA 81 mg lifelong

— Higher INR (2.5–3.5) if mitral mechanical, AF, prior thromboembolism, hypercoagulable state

DOACs are NOT approved for mechanical valves (failed in RE-ALIGN)

Bioprosthetic SAVR: warfarin INR 2.0–3.0 for 3–6 months post-op (Class IIa), then ASA 81 mg lifelong; DOAC acceptable alternative for the early period

TAVR: ASA 81 mg monotherapy lifelong if no other indication; DAPT not routine (POPular TAVI showed more bleeding without benefit); add OAC only if AF or other indication

Endocarditis prophylaxisYES for prosthetic valves before dental procedures involving gingival manipulation (amoxicillin 2 g PO 30–60 min pre-procedure; clindamycin no longer first-line for penicillin allergy — use cephalexin, azithromycin, or doxycycline)

— BP control (goal <130/80 in most)

— LDL per ASCVD risk — typically statin given comorbid CAD risk

— DM control, smoking cessation

— Weight, diet, activity counseling

— Beta-blocker if CAD, AF, or HFrEF

— ACEi/ARB for HTN or HFrEF — now safe post-AVR

— Diuretics for residual congestion

Board pearl: A fib + mechanical AVR → warfarin (not DOAC), INR 2.5; do not combine DOAC with mechanical valve.

Step 3 management: Discharge bundle after AVR — antithrombotic per valve type, ASA, statin if indicated, BP regimen, cardiac rehab referral, dental visit plan with prophylaxis, follow-up TTE in 30 days.

Post-AVR discharge medication framework:
Cardiovascular risk factor optimization:
Concomitant medications:
Vaccinations: annual influenza, pneumococcal, COVID, RSV per age — especially post-prosthetic valve
Activity: sternotomy precautions for 6–8 weeks post-SAVR (no lifting >10 lb, no driving until cleared); TAVR patients ambulate POD1 and resume normal activity within 1–2 weeks
Cardiac rehabilitation — Class I recommendation post-SAVR and post-TAVR; improves functional capacity and quality of life
Solid White Background
Follow-Up, Monitoring, and Counseling

Mild (Stage B, Vmax 2.0–2.9): every 3–5 years

Moderate (Vmax 3.0–3.9): every 1–2 years

Severe asymptomatic (Stage C): every 6–12 months

— Any change in symptoms → repeat TTE promptly regardless of schedule

Symptom diary — dyspnea on exertion, chest pain, lightheadedness, syncope, palpitations

— Encourage reporting any new exercise limitation immediately

— Avoid strenuous competitive sports in severe AS; moderate aerobic activity often okay in mild–moderate

— Hydration, avoiding sudden volume shifts

— Medication review — flag nitrates, alpha-blockers, sildenafil

30-day post-op visit with TTE — establishes baseline prosthesis function (gradients, regurgitation, EF)

— Annual TTE thereafter for bioprosthetic; mechanical valves at 5 years then as indicated, sooner if symptoms change

— INR monitoring if on warfarin — q4 weeks once stable

— Cardiac rehabilitation completion

— Maintain excellent oral hygiene

— Notify dentist of valve status; amoxicillin 2 g 30–60 min before procedures with mucosal manipulation

— Resume driving 4–6 weeks post-SAVR, 1–2 weeks post-TAVR if asymptomatic

— Travel safe; carry medication list and ID card noting prosthetic valve

— Fever >38°C for >48 h → blood cultures, evaluate for IE

— New dyspnea, syncope, embolic event → urgent eval

— Bleeding on warfarin → INR check, hold dose

Board pearl: A new mean gradient ≥20 mmHg on a previously normal bioprosthetic valve at 8–10 years suggests structural valve deterioration — refer for Heart Team evaluation for valve-in-valve TAVR.

Step 3 management: Asymptomatic severe AS, normal EF, stable echo — surveillance TTE q6–12 months and counsel to report any new symptom immediately; do not over-restrict activity.

Surveillance TTE intervals for native AS (pre-intervention):
Counseling points at each visit:
Post-AVR follow-up:
Dental care counseling:
Driving and lifestyle:
Red-flag symptom education:
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Ethical, Legal, and Patient Safety Considerations

— Discuss TAVR vs SAVR trade-offs: durability (longer with SAVR mechanical), recovery time (faster TAVR), pacemaker risk (higher TAVR), reoperation possibility, anticoagulation requirements, mortality risks specific to patient

— Document shared decision-making explicitly — required for valve type selection in 65–80 age band

— Capacity assessment in cognitively impaired patients — involve surrogate decision-maker; respect prior advance directives

— Severely frail patients with limited life expectancy (<1 year independent of AS), advanced dementia, or refractory comorbidities may not benefit from AVR

Palliative TAVR is not appropriate — Heart Team should decline intervention when futile and pivot to palliative care with symptom-directed therapy (diuretics, opioids for dyspnea)

— Document goals-of-care conversation; consider POLST/MOLST

— Post-AVR discharge: medication reconciliation — many patients arrive on nitrates, sildenafil, alpha-blockers that need stopping

Anticoagulation handoff — clear INR target, follow-up date, anticoagulation clinic referral; bridge plan if interruption for procedures

30-day readmission for AVR patients is a quality metric — ensure follow-up scheduled before discharge

— Mechanical AVR alone with no other risk factors → may not need heparin bridge for brief warfarin interruption (low thromboembolic risk)

— Mechanical mitral, prior thromboembolism, or multiple valves → bridge with heparin

— TAVR procedures are tracked in the STS/ACC TVT Registry — CMS coverage requires participation

— Adverse device events reported per MAUDE/FDA pathway

— Prescribing sildenafil for ED in patient with severe AS — preventable adverse event

— Failing to obtain echo before non-cardiac surgery in patient with new systolic murmur

— Anticoagulation overlap errors during warfarin initiation post-SAVR

Board pearl: Document shared decision-making with at least two valve options discussed for any patient 65–80 considering AVR — required by CMS and a frequent audit/board topic.

Informed consent for AVR:
Goals-of-care and futility:
Transitions of care — major Step 3 safety domain:
Bridging anticoagulation around procedures:
Reporting and registries:
Patient safety scenarios tested on Step 3:
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High-Yield Associations and Rapid-Fire Facts

Coarctation of aorta — check 4-extremity BP

Aortopathy — image entire thoracic aorta; repair root at ≥5.5 cm (≥5.0 with risk features, ≥4.5 if AVR concurrent)

Turner syndrome — 30% have BAV

— AS ↓ with Valsalva/standing/handgrip

— HOCM ↑ with Valsalva/standing

— MR ↑ with handgrip

— Severe AS: Vmax ≥4.0, mean grad ≥40, AVA ≤1.0

— Very severe: Vmax ≥5.0 or grad ≥60

— Vmax progression ≥0.3 m/s/yr = rapid

— Aortic valve calcium score: M ≥2000, W ≥1200 AU

— Symptomatic severe AS

— Asymptomatic severe AS + EF <50%

— Severe AS + other cardiac surgery

— <65 SAVR, 65–80 shared, >80 TAVR

— Mechanical: warfarin INR 2.5 + ASA 81

— Bioprosthetic SAVR: warfarin 3–6 mo, then ASA

— TAVR: ASA 81 lifelong

Board pearl: Memorize the triad SAD (Syncope, Angina, Dyspnea) and median survivals (3, 5, 2 yr) — these drive urgency on the test.

Bicuspid valve associations:
Heyde syndrome — severe AS + GI angiodysplasia bleeding + acquired von Willebrand syndrome (loss of high-MW vWF multimers); resolves after AVR
Williams syndrome — supravalvular AS, elfin facies, hypercalcemia, intellectual disability, friendly personality
Rheumatic AS — virtually always with mitral involvement; commissural fusion
Mediastinal radiation (Hodgkin survivor 10–20 years prior) — premature aortic valve calcification
CKD/dialysis — accelerated valve calcification; check parathyroid/calcium-phosphate
Pulsus parvus et tardus — most specific bedside sign of severe AS
Late-peaking murmur + soft/absent S2 — severe AS
Gallavardin phenomenon — AS murmur radiating to apex, mimicking MR
Maneuvers:
Critical numbers:
Class I AVR triggers:
TAVR age threshold rules:
Post-AVR antithrombotic:
DOACs contraindicated in mechanical valves
Endocarditis prophylaxis — prosthetic valves YES; native AS NO
PPM rate post-TAVR ~10–15%
Sudden cardiac death risk in truly asymptomatic severe AS ~1%/yr
Exercise testing safe and indicated in asymptomatic severe AS; contraindicated in symptomatic
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Board Question Stem Patterns

— 72M, exertional murmur, Vmax 4.2 m/s, EF 60%, asymptomatic. → Answer: Repeat TTE in 6–12 months and counsel symptom reporting; not immediate AVR.

— 70F with "asymptomatic" severe AS undergoes stress test, BP drops 20 mmHg with exertion. → Answer: Refer for AVR (Heart Team) — abnormal stress response = Class IIa.

— 84M, severe AS, syncope, frail. → Answer: Transfemoral TAVR, not SAVR.

— 52M, BAV, severe AS, ascending aorta 4.7 cm. → Answer: SAVR with concomitant aortic root replacement.

— 75F, AVA 0.9, mean grad 28, EF 30%. → Answer: Dobutamine stress echo to differentiate true vs pseudo-severe.

— 80F, AVA 0.85, grad 30, EF 65%, small LV. → Answer: Obtain aortic valve calcium score; if ≥1200 AU female, treat as severe and refer.

— Recurrent iron-deficiency anemia, AS murmur, negative endoscopy. → Answer: AVR is definitive treatment.

— Severe AS patient given sildenafil for ED → syncope. → Answer: Avoid PDE5 inhibitors / nitrates in severe AS.

— Day 2 post-TAVR, persistent complete AV block. → Answer: Permanent pacemaker.

— 55M, mechanical AVR + AF. → Answer: Warfarin INR 2.5–3.5, not DOAC.

— Bioprosthetic AVR, dental cleaning. → Answer: Amoxicillin 2 g PO 30–60 min pre-procedure.

— Severe asymptomatic AS, elective hip replacement. → Answer: Cardiology consult; many proceed with monitoring, but evaluate Heart Team for prior AVR if borderline.

— Refractory HF in pregnancy with severe AS. → Answer: Balloon valvuloplasty.

— Asked if statin slows AS. → Answer: No (negative trials); use only for ASCVD risk.

Board pearl: When the stem ends with a maneuver (Valsalva ↑ murmur), the answer pivots away from AS to HOCM — the maneuver question is a recurring test pattern.

Stem 1 — Asymptomatic severe AS surveillance:
Stem 2 — Symptom unmasking:
Stem 3 — Octogenarian symptomatic severe AS:
Stem 4 — Young bicuspid AS with aortopathy:
Stem 5 — LFLG dilemma:
Stem 6 — Paradoxical LFLG:
Stem 7 — Heyde syndrome:
Stem 8 — Dangerous prescribing:
Stem 9 — Post-TAVR bradycardia:
Stem 10 — Mechanical valve anticoagulation:
Stem 11 — Endocarditis prophylaxis:
Stem 12 — Preop non-cardiac surgery:
Stem 13 — Pregnancy with severe AS:
Stem 14 — Statin for AS progression:
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One-Line Recap

Aortic stenosis is a fixed outflow obstruction whose definitive treatment — AVR — is triggered by symptoms or LV dysfunction in severe disease, with the Heart Team selecting TAVR for older or higher-risk patients and SAVR for younger patients, bicuspid aortopathy, or complex concomitant cardiac surgery.

Board pearl: On exam day, anchor on the SAD triad + severity numbers + age-based valve choice — these three pillars solve nearly every aortic stenosis question.

Diagnosis: TTE first; severe = Vmax ≥4.0 m/s, mean gradient ≥40 mmHg, AVA ≤1.0 cm²; clarify low-flow/low-gradient with dobutamine stress echo (D2) or aortic valve calcium score (D3, cutoffs M ≥2000, W ≥1200 AU).
Indications for AVR (Class I): symptomatic severe AS at any EF, asymptomatic severe AS with EF <50%, severe AS undergoing other cardiac surgery; Class IIa for asymptomatic patients with abnormal stress test, very severe AS, rapid progression, or markedly elevated BNP.
TAVR vs SAVR by age: <65 → SAVR, 65–80 → shared decision, >80 → TAVR (transfemoral preferred); SAVR also favored for BAV with aortopathy, complex anatomy, or concomitant CABG/multivalve surgery.
Antithrombotic after AVR: mechanical → warfarin INR 2.5 + ASA lifelong (no DOACs); bioprosthetic SAVR → warfarin or DOAC 3–6 months then ASA; TAVR → ASA 81 mg lifelong unless other OAC indication.
Safety pearls: avoid nitrates, alpha-blockers, and sildenafil in severe AS; endocarditis prophylaxis for prosthetic valves but not native AS; serial echo every 6–12 months for asymptomatic severe AS; refer any new exertional syncope, angina, or dyspnea immediately.
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