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Cardiology›Condition·Updated Jul 11, 2026·v1

Aortic Stenosis

Aortic stenosis is a progressive valvular disease characterized by left ventricular outflow obstruction, leading to heart failure and death if untreated. Diagnosis relies on echocardiography with severity grading by velocity, gradient, and valve area. Valve replacement (TAVR or SAVR) is the definitive therapy, with a paradigm shift toward earlier intervention in asymptomatic severe AS. Post-procedural medical therapy, particularly SGLT2 inhibitors, reduces heart failure events. Concomitant conditions (cardiac amyloidosis, frailty, extravalvular cardiac damage) significantly impact prognosis and should be systematically assessed.

High Evidence375 references·6,862 words·28 min read·v1
aortic stenosisvalvular heart diseaseTAVRSAVRheart failurecardiac amyloidosisSGLT2 inhibitordapagliflozinechocardiographycardiac imaging

Quick Reference

RxDrug of choiceDapagliflozin 10 mg PO daily after TAVR (DAPA-TAVI trial) for HF risk reduction; SGLT2i class recommended by ESC HFA/EAPCI post-TAVR in HF patients.
AltAlternativesEmpagliflozin 10 mg PO daily; renin-angiotensin system inhibitors (ACE-I/ARB/ARNI) for GDMT; tafamidis for ATTR-CA.
⊘AvoidNon-dihydropyridine CCBs (verapamil, diltiazem) in severe AS due to risk of hypotension; statins not indicated for AS modification alone; vitamin K2 and DPP-4 inhibitors have no proven benefit.
DxTest of choiceTransthoracic echocardiography with Doppler for diagnosis and severity grading; CT calcium scoring for discordant low-gradient AS; exercise stress echo for asymptomatic severe AS.
ScKey scoreStaging classification of cardiac damage (Stage 0-4) predicts 1-year mortality (4.4% to 24.5%); Essential Frailty Toolset (EFT) score ≥3 is strongest predictor of 1-year mortality after TAVR (OR 3.72).
→When to referSymptomatic severe AS; asymptomatic severe AS with LVEF <50%, abnormal exercise test, rapid progression, cardiac damage stage ≥2, or elevated biomarkers; patient preference after shared decision-making.
Aortic stenosis is a highly lethal disease once symptomatic; valve replacement (TAVR or SAVR) is the only definitive therapy, with early intervention in asymptomatic patients now supported by trial data. Post-procedural SGLT2i and GDMT reduce HF events.
Aortic stenosis (AS) is a progressive valvular heart disease affecting 1-2% of adults >65 years and 12% of those >75 years, with a 1-year mortality exceeding 50% once symptoms develop. The cornerstone of management is valve replacement (surgical or transcatheter), which restores near-normal life expectancy. Early recognition and accurate severity grading are critical, as timely intervention, now supported for asymptomatic severe AS in selected patients, reduces mortality and heart failure hospitalizations. This page provides an integrated overview of diagnosis, risk stratification, and treatment.

Overview and Recommendations

Background

  • •Aortic stenosis (AS) is a progressive valvular heart disease characterized by narrowing of the aortic valve orifice during systole, leading to left ventricular outflow obstruction, pressure overload, and eventually heart failure and death if untreated. The most common cause in developed countries is calcific (degenerative) AS, affecting 1-2% of adults >65 years and approximately 12% of those >75 years; other causes include congenital bicuspid aortic valve (presenting at age 40-65 years) and rheumatic heart disease (rare in developed countries).
  • •The pathophysiology of AS extends beyond passive calcium deposition: it is a lipoprotein-driven process involving endothelial injury, lipid infiltration (particularly lipoprotein(a)), inflammation, and ectopic osteogenesis in valve leaflets. This triggers left ventricular concentric hypertrophy as an adaptive response to pressure overload, but maladaptive remodeling, including myocardial fibrosis, microvascular rarefaction, and diastolic dysfunction, ultimately leads to decompensation.
  • •Once symptoms (exertional dyspnea, angina, syncope) develop in severe AS, 1-year mortality exceeds 50% without intervention. The classic triad of angina, syncope, and heart failure signals advanced disease, with median survival of 2-3 years after symptom onset. Valve replacement (surgical or transcatheter) restores near-normal life expectancy.
  • •Severity is graded by Doppler echocardiography: severe AS is defined by aortic velocity ≥4.0 m/s, mean gradient ≥40 mm Hg, or aortic valve area ≤1.0 cm². Discordant low-gradient patterns (small valve area but lower gradient) occur in up to 30% of patients and require additional testing (dobutamine stress echo or CT calcium scoring) to differentiate true-severe from pseudo-severe AS.
  • •Concomitant conditions modulate risk: transthyretin cardiac amyloidosis (ATTR-CA) is present in 8-18% of severe AS patients, especially older men with low-flow/low-gradient physiology; cardiovascular-kidney-metabolic syndrome is present in 90% of TAVI patients and incrementally raises 1-year mortality.

Evaluation

  • •Suspect aortic stenosis in any patient aged ≥65 years with a systolic ejection murmur at the right upper sternal border radiating to the carotids, especially if accompanied by exertional dyspnea, angina, syncope, or reduced exercise tolerance. Many patients unconsciously limit activity, so a careful exercise history is essential.
  • •Ask about the classic symptom triad: dyspnea on exertion, angina (due to increased oxygen demand from LV hypertrophy and reduced supply), and exertional syncope (from vasodilation outstripping fixed cardiac output). Also ask about orthopnea, paroxysmal nocturnal dyspnea, and symptoms of heart failure.
  • •Examine for a late-peaking crescendo-decrescendo systolic murmur (louder with squatting, softer with Valsalva), diminished and delayed carotid upstroke (pulsus parvus et tardus), an S4 gallop, narrow pulse pressure (late sign), and signs of pulmonary congestion (crackles) or elevated jugular venous pressure.
  • •Order transthoracic echocardiography with Doppler as the first-line gold-standard test. Document peak aortic velocity, mean gradient, and aortic valve area (by continuity equation). Severe AS: Vmax ≥4 m/s, mean gradient ≥40 mm Hg, AVA ≤1.0 cm² (indexed ≤0.6 cm²/m²).
  • •If the three measures are concordant, severity classification is straightforward. If discordant (AVA ≤1.0 cm² but mean gradient <40 mm Hg), measure stroke volume index (SVi). If SVi ≤35 mL/m² and LVEF <50% → low-dose dobutamine stress echo to differentiate true-severe vs pseudo-severe. If SVi ≤35 mL/m² and LVEF ≥50% → CT calcium scoring (thresholds: ≥1274 AU in women, ≥2065 AU in men). If SVi >35 mL/m² → CT calcium scoring.
  • •In asymptomatic patients with severe AS, consider exercise stress echocardiography to unmask symptoms or abnormal blood pressure response. An abnormal response identifies higher-risk patients who may benefit from earlier intervention.
  • •Assess for concomitant cardiac amyloidosis in older patients (≥75 years) with low ECG voltage relative to LV hypertrophy, discordant low-flow low-gradient AS, or unexplained right ventricular dysfunction. Order DPD scintigraphy and serum free light chains if suspicion is high.
  • •Order baseline laboratory studies: NT-proBNP and high-sensitivity cardiac troponin T (both strong independent predictors of outcomes), renal function (eGFR), and electrolytes before initiating GDMT.
  • •Consider imaging for coronary artery disease before valve intervention: CT coronary angiography or invasive angiography based on age and risk factors. In patients with significant CAD, PCI before TAVR reduces MACE (NOTION-3 trial).
  • •Evaluate frailty using the Essential Frailty Toolset (EFT), a score ≥3 is the strongest predictor of 1-year mortality after TAVR (OR 3.72).
  • •Assess for extravalvular cardiac damage using the staging classification (Stage 0-4, based on LV, left atrial, pulmonary, and right ventricular involvement), which independently predicts mortality after TAVR (HR 1.46 per stage increment).
  • •Consider cardiac MRI if myocardial fibrosis is suspected (late gadolinium enhancement), it is associated with a 23% increase in hazard of death or AS-related hospitalization per 1% rise in extracellular volume. However, the EVOLVED trial showed early intervention did not reduce the primary composite endpoint in fibrosis-positive patients.
  • •Differential diagnoses include hypertrophic cardiomyopathy (dynamic LVOT obstruction on Doppler), hypertensive heart disease (LV hypertrophy without transvalvular gradient), aortic sclerosis (thickening without obstruction, Vmax <2 m/s), and mitral regurgitation (blowing systolic murmur at apex).

Management

  • •For symptomatic severe aortic stenosis, valve replacement is a class I recommendation. The choice between transcatheter (TAVR) and surgical (SAVR) AVR depends on age, surgical risk, anatomy, and patient preference. In low-risk patients, TAVR is noninferior to SAVR at 5 years; in intermediate-risk patients, 10-year mortality is similar.
  • •For asymptomatic severe AS, early intervention (TAVR or SAVR) reduces unplanned cardiovascular hospitalization (HR 0.40) and stroke (HR 0.62) compared with clinical surveillance (EARLY TAVR trial). The AVATAR trial showed a 58% relative reduction in the composite of death, MI, stroke, or HF hospitalization with early SAVR (HR 0.42).
  • •Initiate guideline-directed medical therapy (GDMT) for heart failure in all patients with AS and HF: renin-angiotensin system inhibitors (ACE-I/ARB/ARNI), beta-blockers, and mineralocorticoid receptor antagonists, as tolerated. In severe AS, vasodilators require cautious up-titration to avoid hypotension.
  • •Add an SGLT2 inhibitor after valve replacement: dapagliflozin 10 mg once daily reduced the composite of death or worsening HF by 28% (15.0% vs 20.1%; HR 0.72) in the DAPA-TAVI trial. Empagliflozin 10 mg daily is an alternative. Monitor volume status, eGFR, and for genital infections.
  • •Manage blood pressure per standard guidelines, but with close monitoring in severe AS. Statins do not slow AS progression (ASTRONOMER trial) but are indicated for coexisting atherosclerotic disease. Lipoprotein(a) should be measured at least once; Lp(a)-lowering therapies (antisense, siRNA) are under investigation but not yet guideline-recommended.
  • •Avoid therapies without proven benefit for AS modification: vitamin K2 (menaquinone-7), DPP-4 inhibitors (evogliptin), and statins (for AS alone). Do not prescribe these for the purpose of slowing AS progression.
  • •Periprocedural antithrombotic therapy: For patients without an indication for oral anticoagulation, single antiplatelet therapy (aspirin alone) is preferred over dual antiplatelet therapy after TAVR. For patients with atrial fibrillation or other indication, anticoagulation is indicated.
  • •Monitor for complications after valve replacement: stroke (2.1% at 30 days), major bleeding (9.3% with TAVR), paravalvular regurgitation (33.3% at 5 years), new permanent pacemaker (17.4% with TAVR in low-risk), acute kidney injury (0.9% stage 2/3), valve thrombosis (0.4-2.1%), and heart failure hospitalization (9.4% worsening HF).
  • •Post-procedural dapagliflozin reduces HF events; renin-angiotensin system inhibition promotes greater LV mass regression (adjusted mean difference -12.77 g/m²).
  • •Refer for valve replacement when: (1) symptomatic severe AS, (2) asymptomatic severe AS with LVEF <50%, (3) asymptomatic severe AS with abnormal exercise test or high-risk features (e.g., rapid progression, extremely severe stenosis, elevated biomarkers, cardiac damage stage ≥2), or (4) asymptomatic severe AS and patient preference after shared decision-making.
  • •Discharge criteria after valve intervention: stable hemodynamics, no high-grade AV block requiring pacing, adequate diuresis, no major bleeding, pain controlled, and follow-up plan for GDMT optimization and outpatient monitoring.
  • •In patients with concomitant cardiac amyloidosis, add tafamidis after valve replacement (if ATTR-CA confirmed), combined therapy confers additive survival benefit (weighted HR 0.40 for all-cause death).
  • •For patients with bicuspid aortic valve undergoing TAVR: be aware of higher stroke risk at 30 days (2.5% vs 1.6%) and need for careful pre-procedural CT sizing. Low-risk BAV patients have favorable outcomes with self-expanding valves.
  • •For patients with small aortic annulus (common in women): self-expanding valves reduce bioprosthetic valve dysfunction (8.4% vs 41.8%) and prosthesis-patient mismatch compared with balloon-expandable valves (SMART trial).
  • •For patients with concomitant coronary artery disease: PCI before TAVR reduces MACE (HR 0.71) but increases bleeding (HR 1.51). Percutaneous approach (FFR-guided PCI + TAVR) is superior to SAVR + CABG in patients with complex CAD (TCW trial).

Board Review — High Yield

  • •Classification of AS severity, Severe: Vmax ≥4 m/s, mean gradient ≥40 mm Hg, AVA ≤1.0 cm². Discordant low-gradient AS requires CT calcium scoring (≥1274 AU women, ≥2065 AU men) or dobutamine stress echo.
  • •Natural history, Once symptoms develop, 1-year mortality >50% without intervention. Median survival 2-3 years after symptom onset.
  • •TAVR vs SAVR, In low-risk patients, TAVR is noninferior at 5 years and reduces early mortality (HR 0.80). In intermediate-risk, 10-year mortality similar. Choice depends on age, anatomy, frailty.
  • •Asymptomatic severe AS, Early intervention (AVATAR, EARLY TAVR) reduces unplanned hospitalization and mortality (HR 0.42). Previously watchful waiting was standard; now guidelines shifting.
  • •DAPA-TAVI, Dapagliflozin 10 mg daily after TAVR reduces death or worsening HF by 28% (HR 0.72). NNT = 20 at 1 year.
  • •Cardiac amyloidosis, Screen in patients ≥75 with low voltage, disproportionate LVH, or low-flow low-gradient AS. Prevalence 8-18%. Tafamidis plus AVR improves survival.
  • •Extravalvular cardiac damage, Stage 0-4 classification predicts mortality after TAVR (HR 1.46 per stage). Stage ≥2 may lower threshold for early intervention.
  • •Essential Frailty Toolset, Score ≥3 is strongest predictor of 1-year mortality after TAVR (OR 3.72). Assess all candidates.
  • •Bicuspid aortic valve, More common in younger patients; TAVR feasible but with higher stroke risk (2.5% vs 1.6%). Self-expanding valves preferred for small annuli.
  • •Heyde syndrome, AS + GI angiodysplasia + acquired von Willebrand syndrome. Valve replacement resolves bleeding in 79-86% of cases.

Deep Dive — Evidence Details

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