Heart Valve Disease — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Heart valve disease encompasses a range of conditions affecting the four heart valves — aortic, mitral, tricuspid, and pulmonary — causing either stenosis (narrowing restricting forward flow) or regurgitation (incompetence allowing backward flow). Valvular heart disease affects approximately 2.5% of the general population, rising to 13% of adults over 75. In developed countries, degenerative (calcific) aortic stenosis is the most prevalent lesion, while in developing countries, rheumatic heart disease affecting the mitral valve remains a major burden. Severe valve disease, if untreated after symptom development, carries a prognosis worse than many cancers — untreated severe symptomatic aortic stenosis has 50% mortality within 2 years. Advances in transcatheter interventions (TAVR, MitraClip) have expanded treatment access to previously inoperable patients. Valve disease severity is graded as mild, moderate, or severe based on echocardiographic parameters — the 'severe' threshold triggers decisions about intervention timing. The principle 'operate before symptoms but not too early' guides the watchful waiting period for chronic regurgitant lesions.

Aortic stenosis: degenerative calcification of the valve (most common in the elderly — accelerated by age, male sex, hypertension, hyperlipidaemia, smoking, and bicuspid aortic valve — a congenital variant in 1–2% of the population causing stenosis at 40–60 years); rheumatic fever (historic in developed countries). Aortic regurgitation: aortic root dilatation (Marfan syndrome, hypertension, aortic dissection); degenerative, bicuspid valve, infective endocarditis, rheumatic disease. Mitral stenosis: predominantly rheumatic heart disease (streptococcal infection causing immune-mediated valve destruction — remains common in low-income countries; 25 million affected globally). Mitral regurgitation: degenerative mitral valve prolapse (Barlow disease — most common in developed countries), ischaemic (papillary muscle dysfunction, LV remodelling), infective endocarditis, rheumatic. Tricuspid regurgitation: most commonly functional (right ventricular dilatation from pulmonary hypertension or left heart disease), rarely primary (rheumatic, carcinoid syndrome, endocarditis in IV drug users). Pulmonary stenosis: primarily congenital.

Aortic stenosis classic triad: angina (exertional chest pain from increased myocardial oxygen demand), syncope (exertional — from inability to increase cardiac output), and dyspnoea (heart failure symptoms — the most ominous). Aortic stenosis murmur: harsh ejection systolic murmur radiating to the carotids; slow-rising, low-volume carotid pulse (pulsus parvus et tardus); reduced pulse pressure; displaced apex beat (left ventricular hypertrophy). Mitral regurgitation: exertional dyspnoea, palpitations from atrial fibrillation (complication), holosystolic murmur at the apex radiating to the axilla. Mitral stenosis: progressive dyspnoea, atrial fibrillation, haemoptysis; opening snap with mid-diastolic rumbling murmur. Aortic regurgitation: wide pulse pressure (collapsing 'water-hammer' pulse), early diastolic murmur at the left sternal edge; chronic MR can remain asymptomatic for decades before heart failure develops. Right heart failure signs: peripheral oedema, raised JVP, ascites, hepatomegaly (from tricuspid regurgitation or pulmonary stenosis with right heart failure).

Echocardiography (transthoracic echo — TTE) is the cornerstone of diagnosis and severity grading: measures valve area (aortic valve area <1.0 cm² = severe AS), gradient across the valve (mean gradient >40 mmHg = severe AS), and assessment of ventricular function. Transoesophageal echo (TOE) provides superior valve morphology detail — essential before mitral valve repair. Cardiac catheterisation: coronary angiography before planned valve surgery (to identify co-existing CAD requiring concomitant bypass); haemodynamic assessment when echo and symptoms are discordant. CT cardiac: calcium scoring of aortic valve (high calcium predicts worse outcome), aortic root anatomy for TAVR planning (annulus dimensions, coronary heights). Stress echocardiography: identifies 'pseudo-severe' aortic stenosis (low-gradient, low-flow AS with preserved or reduced EF) and reveals symptoms in apparently asymptomatic severe valve disease. ECG: left ventricular hypertrophy (concentric in AS), AF (in mitral disease). Blood tests: BNP/NT-proBNP (elevated in decompensated heart failure, prognostic).

Medical therapy manages symptoms and co-existing conditions but does not reverse valve disease or delay surgical intervention. Diuretics for congestion; treat AF with rate/rhythm control; anticoagulation (warfarin, DOACs) for AF or mechanical valves. Infective endocarditis prophylaxis: oral amoxicillin 2 g 30–60 minutes before dental procedures for high-risk patients (mechanical valves, prior endocarditis, complex congenital heart disease). Aortic stenosis interventions: surgical aortic valve replacement (SAVR) — gold standard for low-to-intermediate-risk patients; mechanical valves (lifelong warfarin required) or bioprosthetic tissue valves (avoid anticoagulation but limited durability ~10–15 years). TAVR (transcatheter aortic valve replacement via femoral artery — the Heart Valve Revolution): now used in low-, intermediate-, and high-risk surgical patients and inoperable patients; valve-in-valve TAVR for failed bioprosthetic valves. Mitral valve: mitral valve repair is strongly preferred over replacement for degenerative MR (superior durability, no anticoagulation need, better LV function preservation); MitraClip (edge-to-edge repair device) for high-surgical-risk MR patients. Percutaneous mitral balloon valvuloplasty for pliable rheumatic mitral stenosis. Transcatheter tricuspid valve interventions (TriClip, TRILUMINATE trial) for severe functional TR in inoperable patients.

Heart failure is the most common complication of advanced valve disease — chronic pressure or volume overload causes progressive left ventricular dysfunction and dilatation, which may become irreversible even after valve intervention if correction is delayed. Infective endocarditis — bacterial or fungal infection of the valve leaflets — causes valve destruction, systemic septic emboli (stroke, splenic abscess, renal infarcts), and can be rapidly fatal without emergency surgery. Atrial fibrillation develops in 50–70% of patients with mitral valve disease from left atrial dilatation — increasing stroke risk 5-fold and requiring anticoagulation. Thromboembolic stroke occurs from left atrial or left ventricular mural thrombus in patients with AF or severely impaired LV function. Prosthetic valve complications include structural valve deterioration (bioprostheses — 10–15 year durability), prosthetic valve thrombosis (mechanical valves requiring warfarin), and prosthetic valve endocarditis — a particularly serious infection.

Rheumatic heart disease prevention (critical in developing countries): prompt diagnosis and treatment of streptococcal pharyngitis (Group A Streptococcus) with penicillin; secondary prophylaxis with monthly benzathine penicillin G injections for 5–10 years after rheumatic fever to prevent recurrence and cumulative valve damage. Degenerative valve disease risk reduction: control cardiovascular risk factors — hypertension management is critical as elevated blood pressure accelerates aortic valve calcification; statin therapy does not slow aortic stenosis progression despite early hope. Infective endocarditis prevention: dental hygiene, prompt treatment of dental infections, avoid IV drug use, use sterile technique for any invasive procedure; antibiotic prophylaxis before dentistry for high-risk patients (mechanical valves, prior endocarditis). Regular echocardiographic surveillance in patients with known mild-moderate valve disease per guideline-defined intervals allows optimal timing of intervention.

Go to the emergency department immediately for: acute severe breathlessness, chest pain, syncope, or sudden onset signs of heart failure in a patient with known valve disease — these may represent acute decompensation requiring urgent treatment. Call emergency services if there is sudden collapse with loss of consciousness in anyone with known aortic stenosis. See a cardiologist promptly if you develop the classic aortic stenosis symptoms of exertional chest pain, dizzy spells during exercise, or progressive breathlessness — symptom onset marks a critical turning point when mortality risk increases sharply without intervention. Any new heart murmur detected on examination should prompt echocardiography referral within weeks to grade severity. Do not miss regular surveillance echo appointments — intervention timing is critical for optimal outcomes.