Obstruction to LV inflow at the mitral valve — almost always rheumatic; opening snap with diastolic rumble.
Also known as: MS, mitral stenosis, rheumatic mitral disease
Overview
Narrowing of the mitral valve orifice that obstructs diastolic flow from left atrium to left ventricle. Worldwide, almost exclusively rheumatic; degenerative calcific MS is increasingly recognized in older Western patients.
Epidemiology
Most common cause of valvular disease in regions with endemic rheumatic fever. Female predominance ~3:1. Symptoms typically develop 10-30 years after the inciting streptococcal infection.
Try two board-style Mitral Stenosis questions
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Question 1CardiovascularMedium
A 65-year-old woman with a history of rheumatic fever in childhood reports several months of exertional dyspnea and palpitations. On auscultation there is a low-pitched diastolic rumbling murmur best heard at the apex, preceded by an opening snap and loudest in the left lateral decubitus position. A chest radiograph shows left atrial enlargement with straightening of the left heart border. Which of the following is the most likely diagnosis?
AMitral stenosis
BAortic stenosis
CMitral regurgitation
DAortic regurgitation
Reveal answer & full explanation
Correct answer: A — Mitral stenosis
AMitral stenosis✓
BAortic stenosis
CMitral regurgitation
DAortic regurgitation
Why Mitral stenosis is correct
A low-pitched diastolic rumble at the apex with an opening snap, accentuated in the left lateral decubitus position, is the classic auscultatory signature of mitral stenosis.
The opening snap reflects the abrupt halt of doming, thickened (rheumatic) mitral leaflets; a shorter snap-to-S2 interval correlates with more severe disease.
Obstruction at the mitral valve raises left atrial pressure, producing the left atrial enlargement on chest radiograph and explaining the dyspnea and palpitations (atrial fibrillation risk). Rheumatic heart disease is the leading cause, fitting her childhood history.
Why the others are wrong
Aortic stenosis — a systolic ejection murmur at the right upper sternal border radiating to the carotids, not a diastolic apical rumble. Trap: buzzword-matching 'stenosis' without timing the murmur.
Mitral regurgitation — a holosystolic murmur at the apex radiating to the axilla; it occurs in systole and has no opening snap. Trap: right valve, wrong part of the cardiac cycle.
Aortic regurgitation — an early diastolic decrescendo murmur at the left sternal border with a wide pulse pressure, not an apical rumble with an opening snap. Trap: pairing 'diastolic murmur' with the wrong valve.
Question 2CardiovascularMedium
A 70-year-old woman with known mitral stenosis presents with acute dyspnea. She is found to be in new atrial fibrillation at a ventricular rate of 145 beats per minute, with bibasilar crackles, an oxygen saturation of 88%, and frothy sputum consistent with acute pulmonary edema. Her blood pressure is 118/76 mm Hg. Which of the following is the most appropriate initial intervention to relieve her pulmonary edema?
AIntravenous metoprolol
BIntravenous furosemide
CPercutaneous mitral balloon commissurotomy
DSurgical mitral valve replacement
Reveal answer & full explanation
Correct answer: A — Intravenous metoprolol
AIntravenous metoprolol✓
BIntravenous furosemide
CPercutaneous mitral balloon commissurotomy
DSurgical mitral valve replacement
Why intravenous metoprolol is correct
In mitral stenosis, left atrial emptying depends on adequate diastolic filling time; tachycardia shortens diastole, raises left atrial pressure, and rapidly drives pulmonary edema.
The most urgent priority is rate control: intravenous metoprolol (or a non-dihydropyridine calcium channel blocker such as diltiazem) slows the ventricular rate, lengthens diastolic filling time, and lowers left atrial pressure.
She is normotensive (BP 118/76 mm Hg), so a rate-controlling agent is safe.
Why the others are wrong
B) Intravenous furosemide — Reduces preload and is a useful adjunct, but used alone it does not correct the rate-driven mechanism causing the edema, so it is not the single most effective first move.
C) Percutaneous mitral balloon commissurotomy — This is the definitive treatment for symptomatic severe mitral stenosis with suitable valve anatomy, but it is an elective or semi-elective procedure that does not address this acute decompensation in real time.
D) Surgical mitral valve replacement — Reserved for severe disease unsuitable for balloon valvuloplasty or with significant mitral regurgitation; not an emergency intervention for acute rate-driven pulmonary edema.
Additional high-yield points
Rate control combined with diuresis stabilizes the patient before valvular intervention is considered.
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Prior rheumatic fever after untreated group A strep pharyngitis
Living in or migrating from areas with endemic rheumatic disease
Mitral annular calcification (degenerative MS in elderly)
Radiation therapy to the chest
Carcinoid heart disease, SLE (Libman-Sacks), congenital MS
Pathophysiology
Rheumatic inflammation causes commissural fusion, leaflet thickening, and chordal shortening — producing a fish-mouth or funnel-shaped orifice. Obstruction raises left atrial pressure, leading to LA enlargement, pulmonary venous congestion, and eventually pulmonary arterial hypertension and right heart failure. The LV itself is typically protected.
Low-pitched mid-diastolic rumble with presystolic accentuation, best heard at apex in left lateral decubitus with bell
Shorter A2-OS interval indicates more severe stenosis
Right heart failure signs: elevated JVP, peripheral edema, hepatomegaly
Mitral facies — pinkish-purple cheek discoloration in advanced disease
Loud P2 with pulmonary hypertension
Differential diagnosis
Left atrial myxoma — Positional dyspnea, tumor plop instead of opening snap, embolic events; echo shows mobile LA mass
Cor triatriatum — Congenital fibromuscular membrane dividing LA; presents in childhood with MS-like physiology
Severe mitral annular calcification — Degenerative cause in elderly; echo shows annular Ca²⁺ without commissural fusion
Mitral regurgitation — Holosystolic, not diastolic; volume-overload LV instead of pressure-loaded LA only
Pulmonary hypertension of other cause — Right-sided signs without diastolic rumble or opening snap
Austin Flint murmur of AR — Diastolic rumble at apex but with decrescendo diastolic AR murmur and wide pulse pressure; no opening snap
Diagnostic workup
Diagnostic criteria
Severe MS: mitral valve area ≤1.5 cm² (very severe ≤1.0), mean transmitral gradient >5-10 mmHg at heart rate 60-80, pulmonary artery systolic pressure >50 mmHg with exercise.
Labs
CBC, BMP, TSH (Afib workup)
BNP, troponin if dyspnea acute
Anti-streptolysin O if history unclear
Imaging
Transthoracic echo — diagnostic; planimetry of mitral valve area, mean gradient, pulmonary artery pressure, Wilkins score for valvuloplasty candidacy
Transesophageal echo to exclude LA appendage thrombus before percutaneous mitral balloon valvuloplasty (PMBV) or cardioversion
ECG: P mitrale (broad notched P in lead II), atrial fibrillation, right axis deviation, RVH
CXR: straightened left heart border (LA enlargement), Kerley B lines, double density at right heart border, elevated left mainstem bronchus
Diagnostic algorithm
flowchart TD
A[Symptomatic MS<br/>MVA ≤1.5 cm²] --> B[Transesophageal echo<br/>Wilkins score, LA thrombus?]
B --> C{Favorable anatomy<br/>Wilkins ≤8?<br/>No thrombus, no MR?}
C -->|Yes| D[Percutaneous mitral<br/>balloon valvuloplasty]
C -->|No| E[Surgical mitral<br/>valve replacement]
D --> F[Lifelong rheumatic<br/>prophylaxis if indicated]
E --> F
A --> G[Concurrent: diuretic,<br/>rate control,<br/>WARFARIN if Afib]
Decision pathway for severe symptomatic mitral stenosis.
Treatment
First-line
Diuretics (furosemide, torsemide) for pulmonary and systemic congestion
Rate control for Afib: beta-blocker (metoprolol, bisoprolol) or non-dihydropyridine CCB (diltiazem, verapamil) to lengthen diastolic filling time
Anticoagulation with WARFARIN (target INR 2-3) for Afib, prior embolism, or LA thrombus — DOACs are CONTRAINDICATED in rheumatic MS
Secondary rheumatic fever prophylaxis with IM benzathine penicillin G every 3-4 weeks for at-risk patients
Second-line / adjunct
Percutaneous mitral balloon valvuloplasty (PMBV) — preferred when symptomatic severe MS with favorable valve morphology (low Wilkins score ≤8, no significant MR, no LA thrombus)
Surgical mitral valve repair or replacement (mechanical or bioprosthetic) — for unfavorable anatomy, concomitant valve disease, or failed PMBV
Bioprosthetic valve preferred in older patients; mechanical in younger patients willing to take lifelong warfarin
Complications
Atrial fibrillation and systemic embolism (especially stroke)
Pulmonary hypertension and right heart failure
Infective endocarditis
Hemoptysis
Recurrent rheumatic activity
PANCE pearls
DOACs (apixaban, rivaroxaban, dabigatran) are NOT used in rheumatic MS — use warfarin only.
Pregnancy unmasks MS: increased blood volume and HR shorten diastole, raising LA pressure dramatically.
A shorter A2-OS interval suggests more severe stenosis (higher LA pressure opens the valve sooner).
Ortner syndrome — hoarseness from giant LA compressing the recurrent laryngeal nerve.
PMBV requires absence of LA thrombus on TEE and low Wilkins score; otherwise pursue surgery.
References
ACC/AHA 2020 VHD — 2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease (Otto et al., Circulation 2021)
ESC/EACTS 2021 — 2021 ESC/EACTS Guidelines for the Management of Valvular Heart Disease (Vahanian et al., Eur Heart J 2022)
INVICTUS Trial — Rivaroxaban vs Vitamin K Antagonist in Rheumatic Atrial Fibrillation (Connolly et al., NEJM 2022)
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