Mid-systolic click ± late systolic murmur from billowing mitral leaflet — usually benign, occasionally progresses to severe MR.
Also known as: MVP, Barlow disease, click-murmur syndrome, floppy mitral valve
Overview
Systolic displacement of one or both mitral leaflets ≥2 mm above the mitral annular plane into the left atrium, with or without leaflet thickening, as seen on the parasternal long-axis echo view.
Epidemiology
Affects roughly 2-3% of the general population with equal sex distribution when defined by strict echocardiographic criteria. Most patients are asymptomatic. Severe MR develops in a small minority, often after decades.
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Question 1CardiovascularMedium
A 45-year-old woman is evaluated for atypical chest discomfort. On auscultation she has a midsystolic click followed by a late systolic murmur best heard at the cardiac apex. Which of the following maneuvers is most likely to cause the click to occur earlier in systole?
ASustained handgrip
BStanding or Valsalva
CPassive leg elevation
DRapid deep squatting
Reveal answer & full explanation
Correct answer: B — Standing or Valsalva
ASustained handgrip
BStanding or Valsalva✓
CPassive leg elevation
DRapid deep squatting
Why Standing or Valsalva is correct
The midsystolic click with a late systolic murmur at the apex is the hallmark of mitral valve prolapse.
Maneuvers that decrease left ventricular preload (standing, the Valsalva strain phase) reduce ventricular volume, so the redundant leaflets prolapse earlier in systole and the click moves toward S1.
This preload dependence is the key auscultatory principle of mitral valve prolapse dynamics.
Why the others are wrong
Sustained handgrip — raises afterload, increasing ventricular volume and delaying prolapse, so the click moves later (direction-reversal trap for students who know preload matters but reverse the direction).
Passive leg elevation — augments venous return and preload, enlarging the ventricle and delaying the click (direction-reversal trap).
Rapid deep squatting — increases both preload and afterload, expanding ventricular volume and moving the click later in systole (direction-reversal trap).
Question 2CardiovascularMedium
A 24-year-old woman presents with intermittent palpitations and brief, sharp, non-exertional chest pain. She is tall and thin with a pectus excavatum and a long-standing history of scoliosis. Vital signs are normal. On cardiac auscultation, a mid-to-late systolic click followed by a soft late systolic murmur is best heard at the apex. When she stands from a squatting position, the click moves closer to S1 and the murmur lengthens. Lungs are clear and there is no peripheral edema. Which of the following is the most likely diagnosis?
AMitral valve prolapse
BAortic stenosis
CHypertrophic cardiomyopathy
DTricuspid valve prolapse
Reveal answer & full explanation
Correct answer: A — Mitral valve prolapse
AMitral valve prolapse✓
BAortic stenosis
CHypertrophic cardiomyopathy
DTricuspid valve prolapse
Why Mitral valve prolapse is correct
A mid-to-late systolic click best heard at the apex, with or without a late systolic murmur, is the auscultatory hallmark of MVP; the click marks sudden chordal tension as a myxomatous leaflet bows into the left atrium.
Maneuvers that decrease LV size (standing from a squat, Valsalva strain phase) move the click earlier (closer to S1) and lengthen the murmur, the opposite behavior of most other left-sided murmurs and a classic dynamic-auscultation clue.
The thin, tall habitus with pectus excavatum and scoliosis points to connective-tissue-associated MVP, the most common cause of chronic non-ischemic MR in developed countries.
Why the others are wrong
Hypertrophic cardiomyopathy produces a crescendo-decrescendo systolic murmur at the left lower sternal border that also increases with standing and Valsalva, but there is no mid-systolic click; the murmur arises from dynamic LV outflow obstruction with systolic anterior motion, not a prolapsing apical leaflet.
Aortic stenosis gives a crescendo-decrescendo systolic ejection murmur at the right upper sternal border radiating to the carotids with no click, and is uncommon at this age with an otherwise normal apex.
Tricuspid valve prolapse can also produce a click and murmur, but they are right-sided (left lower sternal border) and increase with inspiration rather than localizing to the apex; it is far rarer than MVP.
For isolated asymptomatic MVP, ACC/AHA valvular guidelines call for reassurance and serial echo; routine endocarditis prophylaxis is no longer recommended.
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Family history (autosomal dominant in some kindreds)
Female sex (symptomatic but not anatomic predominance)
Skeletal anomalies: pectus excavatum, scoliosis, straight back syndrome
Polycystic kidney disease
Pathophysiology
Myxomatous degeneration of the mitral leaflets and chordae (excess proteoglycan deposition) produces redundant, floppy tissue. During systole, leaflets bow into the LA; chordal stretch or rupture can produce mitral regurgitation. The classic click marks sudden chordal tension; the murmur follows as MR develops.
Clinical presentation
Symptoms
Most patients asymptomatic — incidental auscultatory or echo finding
Transesophageal echo for preoperative planning or unclear anatomy
Cardiac MRI for severity quantification in selected patients
ECG: usually normal; may show inferior T-wave inversion or ventricular ectopy; rarely prolonged QT
Diagnostic algorithm
Maneuver
LV preload/size
Effect on MVP click and murmur
Valsalva (strain)
Decreased
Click EARLIER, murmur LONGER
Standing from squat
Decreased
Click EARLIER, murmur LONGER
Squatting / passive leg raise
Increased
Click LATER, murmur SHORTER
Sustained handgrip (↑afterload)
Increased
Click LATER, murmur LOUDER if MR present
Amyl nitrite (↓afterload)
Decreased
Click EARLIER, murmur LONGER but softer
How bedside maneuvers shift the MVP click-murmur complex.
Treatment
First-line
Reassurance and lifestyle counseling for asymptomatic isolated MVP without significant MR
Avoid stimulants (caffeine, nicotine, decongestants) if palpitations symptomatic
Beta-blocker (metoprolol, atenolol, propranolol) for symptomatic palpitations or atypical chest pain
Routine endocarditis prophylaxis NOT recommended for isolated MVP (per current ACC/AHA guidelines)
Serial echo every 3-5 years if mild MR; every 6-12 months if moderate-severe MR
Second-line / adjunct
Mitral valve repair (preferred over replacement) — Class I for severe symptomatic MR, or asymptomatic severe MR with LVEF 30-60% or LV end-systolic diameter ≥40 mm
Mitral valve replacement when repair not feasible
Anticoagulation only if atrial fibrillation, prior embolic event, or LV thrombus — not for MVP alone
Complications
Progressive mitral regurgitation requiring surgery
Chordae tendineae rupture → acute severe MR and pulmonary edema
Infective endocarditis (low absolute risk but elevated vs general population)
Atrial fibrillation
Ventricular arrhythmia and rare sudden cardiac death (especially bileaflet MVP with mitral annular disjunction)
PANCE pearls
Mnemonic: Valsalva (decreased preload) brings the MVP click CLOSER to S1 — opposite of most other murmurs.
Routine antibiotic endocarditis prophylaxis is NOT indicated for MVP per modern guidelines.
Bileaflet MVP plus mitral annular disjunction (MAD) carries an elevated risk of ventricular arrhythmia.
Repair is favored over replacement for degenerative MVP — better survival and ventricular function.
MVP is the most common cause of chronic non-ischemic MR in developed countries.
References
ACC/AHA 2020 VHD — 2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease (Otto et al., Circulation 2021)
AHA 2007 IE Prophylaxis — Prevention of Infective Endocarditis (Wilson et al., Circulation 2007)
Framingham — Prevalence and Clinical Outcome of Mitral Valve Prolapse (Freed et al., NEJM 1999)
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