Cardiology · Cardiology

Valvular Heart Disease

A board-focused tour of the five tested valvular lesions — aortic stenosis/regurgitation, mitral stenosis/regurgitation, and mitral valve prolapse — linking each murmur and buzzword to its pathophysiology, echo findings, and next-best-step intervention. Includes maneuver tables, the acute-regurgitation surgical emergencies, and the crucial acute-vs-chronic AR distinction.

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Framework: timing first, then localize

Valvular disease is a plumbing problem. Every lesion is either pressure overload (obstruction → concentric hypertrophy) or volume overload (regurgitation → eccentric dilation). On the boards, nail the timing before you localize:

Systolic murmurs: aortic/pulmonic stenosis (ejection, crescendo-decrescendo) and mitral/tricuspid regurgitation (holosystolic).
Diastolic murmurs: aortic/pulmonic regurgitation (early decrescendo) and mitral/tricuspid stenosis (mid-diastolic rumble). Diastolic and continuous murmurs are never innocent.

Two bedside rules unlock most vignettes: left-sided murmurs are loudest in expiration, and right-sided murmurs get louder with inspiration (Carvallo sign). When two lesions sound alike (AS vs HCM vs MVP), maneuvers that shift preload/afterload break the tie.

Must-know buzzwords

Aortic stenosis (AS): harsh crescendo-decrescendo systolic murmur, RUSB → carotids; pulsus parvus et tardus, soft/absent S2, S4. Symptom triad = SAD (Syncope, Angina, Dyspnea).
Bicuspid aortic valve → AS presenting in the 50s-60s; calcific/senile → 70s+. Heyde syndrome = AS + GI angiodysplasia bleeding + acquired von Willebrand (type 2A) deficiency.
Aortic regurgitation (AR): early diastolic decrescendo at LSB, leaning forward; wide pulse pressure, water-hammer pulse, head-bobbing — these hyperdynamic signs mark chronic AR. Austin Flint rumble at apex.
Mitral stenosis (MS): rheumatic until proven otherwise; opening snap + apical diastolic rumble, loud S1; presents with AFib, hemoptysis, dysphagia/hoarseness from LA enlargement.
Mitral regurgitation (MR): holosystolic at apex → axilla; S3. Louder with handgrip.
MVP: mid-systolic click + late systolic murmur; young women, myxomatous degeneration (Marfan/Ehlers-Danlos).

Labeled cross-section of the human heart showing the four chambers and the aortic, mitral, tricuspid, and pulmonary valves. — Valve anatomy orientation: aortic and pulmonic valves are semilunar (systolic ejection when stenotic), mitral and tricuspid are atrioventricular (holosystolic when regurgitant). · Wikimedia Commons — Wapcaplet — CC BY-SA 3.0, via Wikimedia Commons

The five lesions at a glance

Lesion	Murmur & exam	Classic cause	Management
Aortic stenosis	Crescendo-decrescendo systolic → carotids; parvus et tardus, S4	Calcific (>70), bicuspid (younger), rheumatic	AVR / TAVR when symptomatic or LVEF <50%
Aortic regurgitation	Early diastolic decrescendo, LSB; wide pulse pressure (chronic)	Root dilation (Marfan), bicuspid; acute: dissection, endocarditis	Surgery (AVR) for symptoms or LV dysfunction; vasodilators only if hypertensive; acute = emergency
Mitral stenosis	Opening snap + diastolic rumble, loud S1	Rheumatic heart disease	Balloon valvuloplasty; warfarin (not DOAC) for AFib
Mitral regurgitation	Holosystolic → axilla; S3	MVP, ischemic (papillary rupture), endocarditis	Repair > replace; operate for symptoms/LV dysfunction
MVP	Mid-systolic click + late murmur	Myxomatous degeneration	Reassure; surgery only if severe MR

Vignette — exertional syncope in an older adult

Stem: A 74-year-old man reports two episodes of exertional syncope and chest tightness. Exam: a harsh crescendo-decrescendo systolic murmur at the right upper sternal border radiating to the carotids, a weak, delayed carotid upstroke (parvus et tardus), and a single soft S2.

Diagnosis: severe aortic stenosis.
Confirm: transthoracic echocardiography — severe = valve area <1.0 cm², mean gradient ≥40 mmHg, jet velocity ≥4 m/s.
Next best step / definitive therapy: aortic valve replacement (SAVR or TAVR). Symptomatic severe AS mandates AVR regardless of ejection fraction.
Trap: avoid nitrates, other vasodilators, and aggressive diuresis — a fixed obstruction makes cardiac output preload-dependent, so dropping preload precipitates hypotension and syncope.

Phonocardiogram tracings comparing normal heart sounds with aortic stenosis, mitral regurgitation, aortic regurgitation, mitral stenosis, and patent ductus arteriosus. — Murmur timing side by side: systolic AS and MR versus diastolic AR and MS, plus the continuous machinery murmur of PDA. · Wikimedia Commons — Madhero88 — CC BY-SA 3.0, via Wikimedia Commons

Vignette — new murmur and flash edema after MI

Stem: Three to five days after an inferior STEMI, a patient develops abrupt flash pulmonary edema, hypotension, and a new holosystolic murmur. Echo shows a flail mitral leaflet.

Diagnosis: acute mitral regurgitation from papillary muscle rupture — classically the posteromedial papillary muscle, which has a single blood supply (from the PDA/RCA territory).
Pearl: the murmur may be soft or absent because LA and LV pressures equalize rapidly, so there is little gradient — do not be reassured by a quiet exam.
Next best step: stabilize with afterload reduction (IV nitroprusside) ± intra-aortic balloon pump, then emergent surgical repair/replacement.
Contrast — acute AR (aortic dissection or endocarditis): a short, soft early-diastolic murmur with tachycardia, a soft S1 (premature mitral-valve closure), and pulmonary edema/cardiogenic shock. Crucially, the wide pulse pressure and bounding peripheral signs of _chronic_ AR are ABSENT — the stiff, non-dilated LV equalizes with aortic diastolic pressure too fast. Still a surgical emergency.

Classics worth memorizing

AS symptoms = SAD: Syncope, Angina, Dyspnea. Once symptomatic, survival drops sharply and valve replacement is indicated — but the letters are not a prognostic ranking: classic post-symptom survival runs angina (~5 yr) > syncope (~3 yr) > heart failure/dyspnea (~2 yr), so dyspnea/CHF carries the worst prognosis.
Maneuver rule: almost every murmur softens when you stand / Valsalva (↓ preload) — the two exceptions, HCM and MVP, get louder (MVP click moves earlier). Squatting and handgrip reverse this.
Handgrip (↑ afterload) increases the backward-flow murmurs — MR, AR, VSD — and decreases AS and HCM.
Right-sided rises with Respiration (inspiration) = Carvallo sign for tricuspid regurgitation.
Austin Flint = the AR jet striking the anterior mitral leaflet, mimicking an MS rumble at the apex.

Bedside maneuvers decoded

Maneuver	Hemodynamic effect	Louder ↑	Softer ↓
Stand / Valsalva strain	↓ preload	HCM, MVP	AS, MR, AR, most others
Squat / passive leg raise	↑ preload (+afterload)	AS, MR, most	HCM, MVP
Handgrip	↑ afterload	MR, AR, VSD	AS, HCM
Inspiration	↑ venous return (right heart)	TR, PS, PR (right-sided)	Left-sided
Amyl nitrite	↓ afterload	AS, HCM	MR, AR, VSD

Next-best-step: when to intervene

Boards test the trigger for intervention, not the pills — most valvular disease has no mortality-improving drug, so the definitive fix is mechanical.

Severe AS: replace (SAVR or TAVR) once symptomatic, or if asymptomatic with LVEF <50%, or when undergoing other cardiac surgery. Otherwise, serial surveillance.
Chronic severe AR / MR: operate for symptoms or early LV dysfunction (falling EF or progressive LV dilation) — don't wait for an end-stage ventricle. For primary MR, repair beats replacement.
Severe MS: percutaneous balloon valvuloplasty if anatomy is favorable and there is no left-atrial thrombus or significant MR.
Rheumatic MS + AFib: anticoagulate with a VKA (warfarin) — DOACs are contraindicated here.
New murmur + fever or emboli: get blood cultures + echocardiography for endocarditis before labeling it chronic.
Acute severe regurgitation (dissection, papillary rupture, endocarditis) = surgical emergency.

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