Aortic Valve Disease

Aortic valve disease means two distinct diseases. Aortic stenosis (AS) is a fixed, mechanical outflow obstruction — the valve area becomes too small to eject blood without a large pressure gradient, producing concentric LV hypertrophy. Aortic regurgitation (AR) is a leaking valve that lets blood flow backward into the left ventricle during diastole, producing chronic volume overload and eccentric LV dilation. Calcific (degenerative) AS in an aging population is now the most common clinically significant valve disease encountered in practice, followed by bicuspid-valve disease in younger adults; AR is less common overall but follows an entirely different, and in its acute form immediately life-threatening, management logic.^[1]

The single most important teaching point for both conditions: no drug therapy changes the natural history of the diseased valve itself — nothing slows AS progression, and nothing reverses AR. Pharmacotherapy in this chapter treats concomitant hypertension, bridges a patient to a procedure, or manages left ventricular dysfunction once it develops; it is never a substitute for correctly timed aortic valve replacement or repair. Acute severe AR is a surgical emergency, managed on an entirely different and much faster timeline than the chronic valve diseases covered elsewhere in this chapter.

Risk factors for aortic stenosis

• Age — calcific/degenerative AS is primarily a disease of aging.
• Bicuspid aortic valve — the leading cause of AS presenting before age 65.
• Chronic kidney disease and hemodialysis — accelerated valvular calcification.
• The same cardiovascular risk factors associated with atherosclerosis — hypertension, dyslipidemia, smoking, diabetes, obesity — even though, unlike atherosclerosis, treating these risk factors has not been shown to slow AS progression itself (see Choose Initial Treatment).
• Prior chest/mediastinal radiation therapy.
• Rheumatic heart disease — now an uncommon cause of isolated AS in Canada, but still relevant in patients who immigrated from regions where rheumatic fever remains common.
• A family history of bicuspid aortic valve or early valve disease.

Risk factors for aortic regurgitation

• Bicuspid aortic valve.
• Infective endocarditis, native or prosthetic valve — can cause acute, severe AR through leaflet destruction or perforation.
• Aortic root or ascending aortic disease — Marfan syndrome and other connective tissue disorders, bicuspid-valve-associated aortopathy, chronic hypertension, annuloaortic ectasia, and age-related aortic dilation.
• Acute aortic dissection involving the aortic root — can cause acute, severe AR.
• Chest trauma.
• Rheumatic heart disease.
• A prior aortic valve intervention (surgical or transcatheter) with a paravalvular leak, or structural bioprosthetic valve deterioration over time.
• Certain drugs associated with valvulopathy (e.g., ergot-derived dopamine agonists, some historical anorectic agents) — uncommon but worth a medication review in unexplained AR.

History

• Exertional symptoms specifically — dyspnea, angina, syncope/presyncope — and how they have changed over time; a patient may unconsciously self-limit activity to avoid triggering symptoms, masking true functional status.
• Known cardiac history — a childhood murmur, rheumatic fever, prior cardiac surgery or valve intervention, or a family history of bicuspid aortic valve or early valve disease.
• Risk factors for endocarditis or aortic dissection when an acute presentation is possible.

Physical examination

Murmur timing, location, and radiation (see Recognize the Condition), carotid upstroke, pulse pressure and peripheral pulse character, and signs of heart failure or hemodynamic instability.

Echocardiography — the primary diagnostic tool

Transthoracic echocardiography (TTE) is the first-line test for any suspected valve disease — it grades severity, measures LV size and function, and screens for other structural abnormalities (e.g., aortic root dilation, bicuspid morphology). Transesophageal echocardiography (TEE) is used when TTE windows are inadequate, when a prosthetic valve needs closer evaluation, or when endocarditis is suspected.^[1]

Aortic stenosis severity grading

Discordant results — a small valve area with only a moderate gradient — usually reflect a low-flow, low-gradient state rather than genuinely mild-to-moderate disease, and need further workup rather than being taken at face value.^[1]

Low-flow, low-gradient aortic stenosis

• Classical (reduced-EF) low-flow, low-gradient AS — LVEF under 50% with a low stroke volume index. Dobutamine stress echocardiography distinguishes true-severe AS (valve area stays 1.0 cm² or less and the gradient rises to 40 mmHg or more as flow is augmented) from pseudo-severe AS (the valve area increases above 1.0 cm² with augmented flow, meaning the stenosis was overestimated at baseline low flow). Absent contractile/flow reserve on this test is itself a poor prognostic sign.
• Paradoxical low-flow, low-gradient AS — a preserved EF (50% or more) but a small, hypertrophied, restrictive LV with a low stroke volume index despite the normal ejection fraction — typically an older patient, often a woman, with longstanding hypertension. Aortic valve calcium scoring on CT helps confirm true severe AS when echo findings are discordant: a score of 2000 Agatston units or more in men, or 1200 or more in women, makes severe AS likely.^[1]

Aortic regurgitation severity grading

Multiple semiquantitative and quantitative echo parameters are combined rather than relying on any single number — jet width relative to the LV outflow tract, vena contracta width, regurgitant volume and fraction, pressure half-time, and holodiastolic flow reversal in the descending aorta all support a severe-AR classification when concordant.^[2]

Once severe AR is confirmed, LV size and function become the key parameters to track over time — LV end-systolic and end-diastolic dimensions (and their body-surface-area-indexed values) and LVEF directly determine surgical timing (see Choose Initial Treatment).^[1]

Bicuspid aortic valve

Refer first-degree relatives of a patient with a bicuspid aortic valve for an echocardiogram, given its heritable component, and arrange periodic aortic root/ascending aorta imaging in the patient themselves — bicuspid-valve-associated aortopathy carries its own aneurysm and dissection risk independent of the valve lesion.

• For AS: recognize the transition to severe, symptomatic disease promptly and refer for timely valve replacement — there is no pharmacologic target to reach, since no drug alters the valve's natural history.^[3]
• For AR: control blood pressure/afterload where it genuinely helps (see Choose Initial Treatment), track LV size and function over time, and refer for surgery before irreversible LV dysfunction develops.
• Recognize and manage acute severe AR as a surgical emergency, not a medical-therapy problem.
• Select and maintain the correct antithrombotic regimen for any prosthetic valve or valve repair, matched specifically to valve type (mechanical vs. bioprosthetic) and position.
• Prevent infective endocarditis in patients who meet the specific high-risk criteria — see the Infective Endocarditis chapter for the full prophylaxis regimen and eligibility list, which applies unchanged to a prosthetic aortic valve and to valve repair material.
• Once LV systolic dysfunction (reduced LVEF) develops from either AS or AR, apply standard heart failure pharmacotherapy — see the Heart Failure chapter for the complete 4-pillar GDMT approach.

• Definitive treatment of clinically significant AS or AR is procedural, not pharmacologic — surgical or transcatheter valve replacement (or, for AR, valve-sparing repair when feasible) decided by a multidisciplinary heart team.^[4]
• Discuss TAVI versus SAVR based on age, surgical risk, frailty, valve and vascular anatomy, and patient preference — a lower age and longer life expectancy generally favours SAVR, while advanced age (over 80) or a high/prohibitive surgical risk generally favours transfemoral TAVI; patients in between are managed through shared decision-making incorporating both options.^[4]
• Refer first-degree relatives of a bicuspid aortic valve patient for echocardiographic screening, and arrange periodic surveillance imaging of the aortic root/ascending aorta in the patient.
• Reinforce good dental hygiene and regular dental care, especially before elective valve intervention — see the Infective Endocarditis chapter for the specific high-risk conditions (which include a prosthetic aortic valve) that warrant antibiotic prophylaxis before a qualifying dental procedure.
• Manage cardiovascular risk factors — smoking cessation, blood pressure, lipids, glucose, weight — for their own cardiovascular benefit, not with any expectation of slowing AS progression.
• Individualize exercise recommendations: low-to-moderate intensity activity is generally appropriate in asymptomatic mild-to-moderate valve disease; avoid high-intensity or competitive static/isometric exercise in severe AS given the syncope and sudden-death risk, and reassess exercise tolerance objectively (formal exercise testing) rather than relying on self-reported activity level, which is often unconsciously self-limited.
• Recommend routine influenza and pneumococcal vaccination as part of general cardiac preventive care.

Pregnancy

Severe AS is poorly tolerated in pregnancy — the fixed valvular obstruction limits the ability to increase cardiac output to meet the demands of pregnancy, and hemodynamic decompensation can occur at any point in gestation or delivery. Arrange pre-conception counselling and, where possible, correct severe symptomatic (or even severe asymptomatic, per specialist assessment) AS before conception rather than during pregnancy. Chronic AR is generally better tolerated in pregnancy, since the physiologic fall in systemic vascular resistance reduces the regurgitant volume, but still requires monitoring through pregnancy and the postpartum period by a combined cardio-obstetric team. If a vasodilator is needed for AR-associated hypertension in pregnancy, avoid ACE inhibitors and ARBs (teratogenic) — a dihydropyridine calcium channel blocker or methyldopa/labetalol (see the Hypertension chapter) are the appropriate alternatives. For a patient with a mechanical prosthetic valve, warfarin's teratogenicity (particularly in the first trimester) must be weighed against the materially higher valve-thrombosis risk of alternative regimens in pregnancy — this is a multidisciplinary, individualized decision, not a default switch to heparin; see the Atrial Fibrillation chapter for the general principles of anticoagulant selection in pregnancy.

Breastfeeding

Warfarin is compatible with breastfeeding. An ACE inhibitor with strong breastfeeding safety data (e.g., enalapril, ramipril) can be used when a vasodilator is genuinely needed. DOAC data in lactation remain limited — this does not create any new exception to their contraindication in a mechanical valve.

Older adults

Advanced age or frailty is not, on its own, a reason to withhold aortic valve intervention in symptomatic severe AS — it is instead a factor that shifts the heart team's choice toward transfemoral TAVI over SAVR, since TAVI is generally preferred over SAVR in patients over 80 years of age or with a high or prohibitive surgical risk.^[4] Older adults are also more susceptible to hypotension from vasodilator or diuretic therapy in the setting of severe AS — titrate more cautiously and monitor more closely.

Renal impairment / chronic kidney disease

CKD and dialysis-dependent kidney disease accelerate valvular calcification and are independently associated with faster AS progression and worse outcomes. Pre-procedural CT angiography for TAVI planning involves iodinated contrast — plan renal-protective measures and coordinate timing with the interventional team in a patient with reduced eGFR. Adjust ACE inhibitor/ARB dosing and monitoring for renal function as for any other indication.

Bicuspid aortic valve and associated aortopathy

Refer first-degree relatives for echocardiographic screening given the heritable component, and arrange periodic imaging of the aortic root and ascending aorta in the patient — the aneurysm and dissection risk associated with bicuspid-valve aortopathy is managed on its own surveillance schedule, independent of the valve lesion itself.

Pediatrics

Congenital and pediatric aortic valve disease (including pediatric-onset bicuspid valve disease and congenital AS) is managed by pediatric cardiology using dedicated pediatric protocols and does not follow the adult severity thresholds or intervention criteria in this chapter.

• Echocardiographic surveillance by AS severity: mild — every 3-5 years; moderate — every 1-2 years; asymptomatic severe — every 6-12 months; very severe or rapidly progressive — every 3-6 months. Reassess promptly, out of cycle, for any new symptom rather than waiting for the next scheduled echo.
• Echocardiographic surveillance by AR severity: mild — every 3-5 years; moderate — every 1-2 years; severe with normal LV size/function — every 6-12 months, tracking LV end-systolic/end-diastolic dimensions and LVEF specifically, since these values (not symptoms alone) trigger surgical referral in asymptomatic severe AR.
• Reassess symptoms and functional status at every visit, regardless of the scheduled echo interval — new exertional dyspnea, angina, or syncope/presyncope warrants prompt reassessment, not deferral to the next routine appointment.
• After TAVI or SAVR: echocardiogram at discharge, 30 days, and 1 year, then annually — watch for paravalvular leak, prosthesis-patient mismatch, and (for a bioprosthetic valve) structural valve deterioration, which typically becomes clinically relevant after roughly 10-15 years.
• For warfarin in a mechanical valve: INR every 4-12 weeks once stable, more often if labile; point-of-care/self-testing is a reasonable option where available (see the Atrial Fibrillation chapter for the general principles of INR monitoring).
• Do not interrupt warfarin in a patient with a mechanical heart valve for a minor procedure — cataract surgery, routine dental procedures, and skin biopsy do not require holding anticoagulation.^[6]
• Monitor blood pressure at every visit in a patient on vasodilator therapy for AR, and reassess renal function/potassium if an ACE inhibitor or ARB is used.
• Once heart failure pharmacotherapy is started for LV dysfunction arising from AS or AR, follow the monitoring schedule in the Heart Failure chapter.

1. New or worsening symptoms in a patient with known AS or AR are not a signal to add or increase medical therapy — they are a signal to re-image promptly and refer for intervention; no drug regimen substitutes for correctly timed valve replacement or repair.
2. Confirm adherence to any prescribed antihypertensive/vasodilator or antithrombotic therapy before assuming a genuine treatment failure.
3. If echocardiographic findings are discordant (e.g., a small aortic valve area with only a moderate gradient), pursue the specific low-flow, low-gradient workup (dobutamine stress echocardiography or aortic valve calcium scoring) rather than defaulting to "moderate" disease and continuing routine surveillance.
4. For a symptomatic patient judged not to be a candidate for AVR or repair (prohibitive surgical/procedural risk, or patient preference against intervention), shift the goals of care toward symptom palliation — cautious diuresis for congestion, continued avoidance of vasodilators/negative inotropes that worsen fixed-obstruction hypotension in AS — with specialist and, where appropriate, palliative care involvement.
5. New symptoms or a new murmur after a prior valve intervention should prompt evaluation for a paravalvular leak, structural valve deterioration, prosthetic valve thrombosis, or infective endocarditis — do not assume recurrence of native disease that has already been treated.
6. A thromboembolic event in a patient anticoagulated for a mechanical valve should prompt confirmation of therapeutic INR and adherence first; do not switch to a DOAC — escalation, when needed, is a specialist-directed change in INR target or added antiplatelet therapy, not a change in anticoagulant class.
7. Significant bleeding on warfarin for a mechanical valve should prompt review of correctable bleeding-risk factors and concurrent ASA use; do not stop anticoagulation outright or substitute a DOAC.

• Prescribing or continuing a statin specifically to slow AS progression — the SEAS trial found no effect on the course of aortic-valve stenosis.^[3]
• Using any DOAC (apixaban, dabigatran, edoxaban, or rivaroxaban) in a patient with a mechanical heart valve, including for an unrelated indication like atrial fibrillation — this is contraindicated regardless of AF status.^[5]
• Assuming a bioprosthetic valve carries the same DOAC restriction as a mechanical valve — it does not; a DOAC is appropriate for AF in a patient with a bioprosthetic valve once the early post-implantation window has passed.
• Giving a vasodilator, an aggressive diuretic, or a non-dihydropyridine calcium channel blocker to a patient with severe AS without recognizing the fixed-obstruction physiology — this can precipitate significant hypotension.
• Using a beta-blocker, or placing an intra-aortic balloon pump, in acute severe aortic regurgitation — both worsen the physiology rather than helping it.
• Ruling out acute severe AR because the diastolic murmur is soft or inaudible — rapid pressure equalization in the unprepared left ventricle often makes the murmur quiet.
• Delaying cardiology referral for symptomatic severe AS to try additional medical therapy first — no medical therapy substitutes for timely valve replacement once symptoms develop.
• Interrupting warfarin for a mechanical heart valve for a minor procedure (cataract surgery, routine dental work, skin biopsy) — this is not recommended and increases valve-thrombosis risk without a meaningful bleeding benefit.
• Missing family screening for a bicuspid aortic valve patient's first-degree relatives, and missing surveillance imaging of the aortic root/ascending aorta in the patient.
• Treating vasodilator therapy for chronic AR as a way to delay surgical referral once a genuine surgical indication (symptoms, LV dysfunction, or severe LV dilation) has been met.

How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment. Select any drug name to open its complete Pharmasist Drug Database page.

Vasodilator therapy — chronic aortic regurgitation

For a symptomatic severe-AR patient not currently a surgical candidate, or to treat concurrent hypertension (target systolic BP under 140 mmHg). Not shown to delay the need for surgery in an asymptomatic, normotensive patient with preserved LV function.

Emergency medical bridge — acute severe aortic regurgitation

A bridge to emergent surgery only, never a substitute for it. Do not use a beta-blocker or an intra-aortic balloon pump in this setting (see Choose Initial Treatment).

Antithrombotic therapy by prosthetic valve type

The central safety point for any mechanical valve, in any position, for any indication: warfarin is mandatory and DOACs are contraindicated.^[5] Regimens differ meaningfully for a bioprosthetic valve, a transcatheter valve, and after valve repair.^[6]

Anticoagulant and antiplatelet agents

Match the correct regimen to the specific valve type using the table above. See the Atrial Fibrillation chapter for complete DOAC dosing/monitoring where a DOAC is genuinely appropriate — a bioprosthetic valve or TAVI plus AF, beyond the early post-implantation window.

Endocarditis prophylaxis — prosthetic aortic valve, dental procedures

For the specific high-risk cardiac conditions and qualifying dental procedures defined in the Infective Endocarditis chapter only — a prosthetic aortic valve (including a transcatheter-implanted valve) is one of them. See that chapter for the complete regimen, timing, and penicillin-allergy alternatives.

Do not use