Heart Valve Disease

Valvular heart disease reduces, mechanically, to the same two problems repeated across four valves: stenosis — a fixed obstruction to forward flow through a narrowed, poorly mobile valve — and regurgitation (insufficiency) — a leak that lets blood flow backward once the valve should be sealed. The Aortic Valve Disease chapter covers aortic stenosis and aortic regurgitation in depth; this chapter covers the same two mechanical problems as they affect the mitral, tricuspid, and pulmonic valves, plus the anticoagulation and infective endocarditis prophylaxis principles that apply across every valve type, aortic included.

Valvular heart disease overall affects roughly 2.5% of the general population, rising sharply with age — from 0.7% in adults under 45 to 13.3% at age 75 and older.^[1] Among the non-aortic lesions, three are clinically dominant. Mitral stenosis (MS) is now an uncommon diagnosis in Canadian-born patients, but remains genuinely relevant in patients who grew up in regions where rheumatic fever remains common, and carries a notable, clinically important association with atrial fibrillation from chronic left atrial dilation and pressure overload. Mitral regurgitation (MR) — the most common valve lesion overall — most often arises from myxomatous degeneration/mitral valve prolapse in Canada and other developed countries, from ischemic papillary muscle dysfunction or left ventricular remodeling after myocardial infarction, or from infective endocarditis.^[2] Tricuspid regurgitation (TR) is most often functional/secondary — right ventricular and tricuspid annular dilation from pulmonary hypertension, left-sided heart disease, or right heart strain (including from chronic atrial fibrillation itself) — rather than a primary disease of the tricuspid leaflets.^[2] Isolated pulmonic valve disease in an adult is uncommon and is discussed only briefly here (see Special Populations).

Two threads run through this chapter as the pharmacotherapy pharmacists are genuinely asked about day to day: anticoagulant selection matched precisely to valve type and rhythm — where the mechanical-valve/moderate-to-severe-mitral-stenosis-plus-AF distinction is a real, high-stakes prescribing-safety point — and infective endocarditis antibiotic prophylaxis, now reserved for a much narrower group of high-risk patients than older practice suggested.

Mitral stenosis

• Rheumatic heart disease — the dominant cause worldwide and, historically, in Canada; now uncommon in Canadian-born patients but still relevant in patients who immigrated from, or spent their childhood in, regions where rheumatic fever remains common (South Asia, sub-Saharan Africa, parts of the Pacific and Latin America) — ask specifically about a history of rheumatic fever or unexplained childhood joint pains with fever.
• Mitral annular calcification — an uncommon cause of functional MS in older adults, mechanistically distinct from rheumatic disease.
• Congenital mitral stenosis — rare, identified in childhood.
• Prior mitral valve repair with a restrictive annuloplasty ring.

Mitral regurgitation

• Myxomatous degeneration / mitral valve prolapse — the most common cause of primary (degenerative) MR in Canada and other developed countries.
• Ischemic MR — papillary muscle dysfunction or rupture, or left ventricular remodeling/dilation, after myocardial infarction; this is often functional (secondary) rather than a primary leaflet problem.
• Infective endocarditis, native or prosthetic valve — leaflet destruction or perforation.
• Rheumatic heart disease — commonly produces mixed MS/MR rather than pure MR.
• Functional (secondary) MR from any cardiomyopathy or left ventricular dilation that displaces the papillary muscles and prevents normal leaflet coaptation, without a primary leaflet abnormality.
• Connective tissue disease (Marfan syndrome, Ehlers-Danlos syndrome) predisposing to myxomatous change.
• Certain drugs associated with valvulopathy (ergot-derived dopamine agonists, some historical anorectic agents) — as with aortic regurgitation, worth a medication review in unexplained MR.

Tricuspid regurgitation

• Functional (secondary) TR — by far the most common mechanism: right ventricular and tricuspid annular dilation from pulmonary hypertension of any cause, left-sided heart disease (including MS and MR themselves), or chronic atrial fibrillation causing isolated right atrial and annular dilation independent of RV dysfunction ("atrial functional TR").
• A right ventricular pacemaker or ICD lead interfering with leaflet coaptation.
• Infective endocarditis, particularly in people who inject drugs — classically right-sided and tricuspid-valve-specific.
• Carcinoid heart disease.
• Rheumatic heart disease — usually accompanies rheumatic MS/MR rather than occurring in isolation.
• Ebstein anomaly and other congenital causes.

Pulmonic valve disease

Almost always congenital in origin — isolated acquired pulmonic valve disease in an adult without a congenital or iatrogenic (post-surgical) explanation is rare and should prompt consideration of carcinoid heart disease or endocarditis.

History and examination

Characterize exertional symptoms and how they have changed over time, ask specifically about a history of rheumatic fever or childhood immigration from a region where it remains common, and screen for palpitations suggesting atrial fibrillation — a common first presentation of significant mitral valve disease. Murmur timing, location, and radiation (see Recognize the Condition), along with signs of right or left heart failure, guide the initial impression, but echocardiography is required to confirm and grade any suspected lesion.

Echocardiography — the primary diagnostic and severity-grading tool

Transthoracic echocardiography (TTE) is first-line for any suspected valve disease — grading severity, assessing left and right ventricular size and function, and identifying the underlying mechanism (primary leaflet disease vs. functional/secondary disease). Transesophageal echocardiography (TEE) is used for inadequate TTE windows, suspected endocarditis, or detailed pre-procedural planning, such as before mitral valve repair or transcatheter edge-to-edge repair.^[2]

Mitral stenosis severity

Mean transmitral gradient and estimated pulmonary artery pressure support the diagnosis, but valve area by planimetry is the primary anatomic measure used for staging in current guidance.^[2]

Mitral regurgitation severity — applies to primary and secondary MR alike

Distinguish primary MR (a structural leaflet/chordal abnormality — prolapse, rheumatic disease, endocarditis) from secondary/functional MR (structurally normal leaflets tethered by a dilated, dysfunctional left ventricle) — the mechanism directly determines whether surgery, optimized heart failure therapy, or a transcatheter edge-to-edge repair is the right next step (see Choose Initial Treatment).^[2]

Tricuspid regurgitation severity

Assess right ventricular size and function, right atrial size, inferior vena cava diameter/collapsibility, and hepatic vein systolic flow reversal alongside these thresholds — a multiparametric assessment, not a single cutoff, as with every valve lesion.^[2]

Differential diagnosis

Dyspnea and peripheral edema in a patient with a murmur are not automatically valve disease — consider primary pulmonary disease, anemia, thyroid dysfunction, and other causes of heart failure (ischemic or nonischemic cardiomyopathy, hypertensive heart disease) before attributing symptoms entirely to an incidentally found murmur. Conversely, a soft or absent murmur does not exclude significant, even acute severe, regurgitant disease (see Recognize the Condition).

Additional investigations

• ECG — look specifically for atrial fibrillation, left atrial enlargement (P mitrale) in MS, or right ventricular strain/hypertrophy in significant TR or pulmonary hypertension.
• Chest X-ray — left atrial enlargement, pulmonary vascular congestion, valve calcification.
• BNP/NT-proBNP as an objective adjunct when symptom status is genuinely unclear, particularly in a minimally symptomatic patient being considered for early intervention.
• Exercise testing to unmask symptoms or an abnormal hemodynamic response in a patient who reports being asymptomatic but has reduced or uncertain functional capacity.
• Cardiac catheterization when echocardiographic findings are discordant with the clinical picture, or when concomitant coronary disease needs to be excluded before surgery.

• Relieve symptoms and correct the hemodynamic consequences of significant valve disease — pulmonary congestion in MS/MR, right heart congestion in TR.
• Prevent and manage the complications valve disease predisposes to — atrial fibrillation, thromboembolism, heart failure, infective endocarditis, and pulmonary hypertension.
• Match anticoagulant choice precisely to valve type/position and rhythm — this is the single highest-stakes prescribing decision in this chapter.
• Provide antibiotic prophylaxis only to the specific, narrow group of patients now considered genuinely high-risk for infective endocarditis, and only before a qualifying procedure.
• Recognize when symptoms, ventricular size/function, or pulmonary pressures cross a threshold that should prompt referral for valve repair or replacement, rather than escalating medical therapy indefinitely.
• Once significant valve disease produces volume overload or reduced LV/RV function, apply standard heart failure pharmacotherapy — see the Heart Failure chapter for the complete approach.

• Definitive treatment of significant mitral or tricuspid valve disease is procedural — surgical repair (preferred over replacement for degenerative MR whenever anatomically feasible, given better long-term LV function and survival), surgical replacement when repair is not feasible, or transcatheter edge-to-edge repair for prohibitive-surgical-risk primary MR or persistent severe secondary MR despite optimized heart failure therapy.^[2][6]
• Balloon mitral valvotomy is the preferred procedure for symptomatic severe MS with favourable leaflet morphology and no significant concomitant MR, avoiding open surgery in appropriately selected patients.^[2]
• Transcatheter tricuspid edge-to-edge repair is an emerging option for severe, symptomatic TR in patients at high surgical risk — a rapidly evolving, specialist-directed area rather than an established first-line option.
• Rhythm and rate strategy for atrial fibrillation complicating valve disease follows the same principles as the Atrial Fibrillation chapter, with the important anticoagulation exception covered in Choose Initial Treatment.
• Sodium restriction and fluid management education for symptomatic volume overload, mirroring standard heart failure counselling.
• Reinforce dental hygiene and regular dental care for every patient with valve disease — genuinely protective against endocarditis independent of antibiotic prophylaxis, and the correct advice even for the many patients who do not meet the narrow criteria for prophylaxis itself.
• Individualize exercise recommendations to the specific lesion and its severity; avoid high-intensity or competitive exercise in severe, symptomatic stenotic or regurgitant disease pending specialist clearance.
• Recommend routine influenza and pneumococcal vaccination as part of general cardiac preventive care.

Pregnancy

Significant valve disease can be poorly tolerated in pregnancy, and mitral stenosis specifically deserves early attention — the physiologic rise in heart rate and plasma volume during pregnancy both worsen the transmitral gradient, and decompensation can occur at any point in gestation, labour, or the immediate postpartum period. Arrange pre-conception counselling and, where possible, correct severe symptomatic MS before conception rather than during pregnancy. Anticoagulant choice in a pregnant patient with a mechanical valve is especially complex and high-stakes: warfarin crosses the placenta and carries teratogenic risk (particularly in the first trimester) but is generally the most effective anticoagulant for preventing valve thrombosis, while heparin-based alternatives avoid fetal warfarin exposure at the cost of a materially higher valve-thrombosis risk if not dosed and monitored meticulously. This is an individualized, multidisciplinary decision made with cardio-obstetric and anticoagulation specialists, never a default switch made unilaterally — 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 heart failure pharmacotherapy is genuinely needed. DOAC data in lactation remain limited — this does not create any new exception to the DOAC restriction in valvular AF.

Older adults

Advanced age is a risk factor for mitral annular calcification (a cause of functional MS) and for the degenerative changes underlying MR, and older patients are more likely to have multiple comorbidities that complicate the surgery-versus-transcatheter-repair decision. Age or frailty alone is not a reason to withhold intervention in symptomatic severe disease — it is instead a factor that shifts the heart team's choice toward a transcatheter approach when one is available for the specific lesion.

Renal impairment / chronic kidney disease

Adjust ACE inhibitor/ARB and diuretic dosing and monitoring for renal function as for any other indication. Pre-procedural imaging for a transcatheter mitral or tricuspid intervention may involve iodinated contrast — plan renal-protective measures and coordinate timing with the interventional team in a patient with reduced eGFR.

Hepatic impairment

Hepatic congestion from significant TR or right heart failure can itself impair hepatic synthetic function and elevate baseline INR — interpret warfarin dosing and INR trends cautiously in this setting, and monitor more closely as congestion is treated and INR requirements shift.

Pediatrics and congenital heart disease

Congenital mitral, tricuspid, and pulmonic valve disease — including Ebstein anomaly and post-tetralogy-of-Fallot pulmonic regurgitation — is managed by pediatric or adult congenital heart disease specialists using dedicated protocols and does not follow the adult severity thresholds or intervention criteria in this chapter.

• Echocardiographic surveillance by severity: mild — every 3-5 years; moderate — every 1-2 years; asymptomatic severe MS or MR — every 6-12 months; very severe or rapidly progressive disease — every 3-6 months. Reassess promptly, out of cycle, for any new symptom rather than waiting for the next scheduled echo.
• For warfarin in a mechanical valve or valvular AF: INR every 4-12 weeks once stable, more often if labile; point-of-care/self-testing is a reasonable option where available.
• 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.^[7]
• Counsel every patient on dental antibiotic prophylaxis to make sure their dentist and other care providers know their specific cardiac condition and whether it does or does not qualify for prophylaxis — this avoids both missed prophylaxis in a genuinely high-risk patient and unnecessary antibiotic use in one who does not qualify.
• Counsel patients on infective endocarditis symptom awareness (unexplained fever, new fatigue, or symptoms alongside a known high-risk condition) and when to seek prompt assessment.
• Reassess ventricular rate control in AF-associated mitral stenosis specifically at follow-up, given how directly heart rate affects symptoms in this lesion.
• Once heart failure pharmacotherapy is started for LV dysfunction from valve disease, follow the monitoring schedule in the Heart Failure chapter.
• Reinforce adherence to anticoagulant therapy — missed doses in a mechanical-valve or valvular-AF patient carry a genuinely higher stroke/thrombosis stake than in most other anticoagulation indications.

1. New or worsening symptoms in a patient with known valve disease are not a signal to add or increase medical therapy alone — they are a signal to re-image promptly and reassess referral timing; no drug regimen substitutes for correctly timed valve repair or replacement.
2. Confirm adherence to any prescribed anticoagulant, rate-control, or diuretic therapy before assuming a genuine treatment failure.
3. A thromboembolic event in a patient anticoagulated with warfarin for a mechanical valve or valvular AF 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.
4. Significant bleeding on warfarin for a mechanical valve or valvular AF should prompt review of correctable bleeding-risk factors and concurrent antiplatelet use; do not stop anticoagulation outright or substitute a DOAC.
5. Persistent symptoms despite adequate rate control in mitral stenosis should prompt reassessment of valve severity and surgical/interventional candidacy rather than further rate-control escalation alone.
6. Persistent severe secondary MR or TR despite optimized heart failure therapy should prompt reassessment for transcatheter edge-to-edge repair or surgery rather than continued medical therapy escalation alone.
7. 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.

• Prescribing a DOAC for "valvular AF" — a mechanical heart valve, or moderate-to-severe mitral stenosis with atrial fibrillation — this is contraindicated regardless of stroke-risk score.^[3][4]
• Assuming a bioprosthetic valve, valve repair, or mild mitral stenosis carries the same DOAC restriction as a mechanical valve or moderate-to-severe MS — it does not; a DOAC is appropriate once the early post-implantation window has passed.
• Giving dental antibiotic prophylaxis to a patient who does not have one of the current, narrower high-risk cardiac conditions — a common holdover from older, broader guidance, and a genuine risk with any degree of MR, TR, or mitral valve prolapse without a qualifying condition.^[5]
• Underestimating how much heart rate alone affects symptoms in mitral stenosis — even sinus tachycardia without atrial fibrillation can meaningfully worsen the transmitral gradient.
• Using vasodilator therapy in primary MR with an expectation that it will delay the need for surgery, the way it can in chronic aortic regurgitation — this has not been shown to work for MR.
• Interrupting warfarin for a mechanical heart valve or valvular AF for a minor procedure (cataract surgery, routine dental work, skin biopsy) — this is not recommended and increases thrombosis risk without a meaningful bleeding benefit.
• Treating secondary (functional) MR the same way as primary (degenerative) MR — optimizing heart failure therapy first is the correct initial approach for secondary MR, not prompt referral for the valve lesion itself.
• Delaying referral for symptomatic severe MS, MR, or TR to try additional medical therapy first — no medical therapy substitutes for timely, correctly timed intervention once a genuine indication is met.
• Missing an unexplained fever or new murmur as a possible sign of infective endocarditis in a patient with a prosthetic valve or other high-risk condition.

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

Rate control for atrial fibrillation — genuinely more urgent in mitral stenosis

Tachycardia shortens diastole, the only phase in which blood can cross a stenotic mitral valve, so heart-rate control matters even more here than in AF from most other causes. See the Atrial Fibrillation chapter for complete dosing by LV function.

Anticoagulation by valve type/lesion and rhythm

The central safety point of this chapter: "valvular AF" — a mechanical prosthetic valve in any position, or moderate-to-severe mitral stenosis, with atrial fibrillation — requires warfarin; DOACs were not studied and are not used.^[3][4] Regimens differ meaningfully for a bioprosthetic valve, valve repair, and lesser degrees of mitral stenosis. See the Aortic Valve Disease chapter's own table for the aortic-position-specific regimens (mechanical/bioprosthetic aortic valve, TAVI).^[7]

Anticoagulant and antiplatelet agents

Match the correct regimen to the specific valve type/lesion and rhythm using the table above. See the Atrial Fibrillation chapter for complete DOAC dosing/monitoring where a DOAC is genuinely appropriate.

Diuretic and heart failure pharmacotherapy for volume overload

Symptom/volume control only — does not treat the underlying valve lesion. See the Heart Failure chapter for the complete 4-pillar GDMT approach, which is first-line therapy for secondary (functional) MR from LV dysfunction.

Endocarditis prophylaxis — standard regimen

For the specific high-risk cardiac conditions and qualifying dental procedures defined in Choose Initial Treatment only — see the Infective Endocarditis chapter for the complete eligibility list. Give 30-60 minutes before the procedure (up to 2 hours after if inadvertently missed beforehand).^[5]

Endocarditis prophylaxis — allergic to penicillin/ampicillin, able to take oral medication

Clindamycin is no longer recommended for this indication given its association with Clostridioides difficile infection.

Endocarditis prophylaxis — unable to take oral medication

Avoid IM injection in an anticoagulated patient — use the IV route instead where anticoagulation is a factor.

Do not use