: Most patients are asymptomatic and MVP is an incidental auscultatory finding. Beta-blockers may markedly attenuate or abolish the symptoms, a fact that is important to remember while evaluating a patient who is receiving these agents. Findings are more marked when patients are examined in the outpatient department rather than in the inpatient setting, reflecting the contributory role of adrenergic state.
Chest pain occurs in 10% of patients diagnosed with MVP and may be caused by any of the following factors:
Excessive stretching of the chordae tendineae, leading to traction on papillary muscles
Coronary microembolism from platelet aggregates and fibrin deposits in the angle between the left atrium and the posterior mitral leaflet
Inappropriate tachycardia and excessive postural changes and physical and emotional stresses
Hyperadrenergic state, which increases myocardial oxygen demand
Coronary artery spasm
Palpitations are present in 7.4% of patients.
Occurrence may be related to cardiac arrhythmia, although this is not proved conclusively.
Fatigability and dyspnea
These often develop on exertion.
The cause may be alterations in centrally modulated breathing cycle control.
Panic attacks may occur.
Nervousness, presyncope, and syncope occur in 0.9% of patients.
Thromboembolism, arrhythmia, or vasodepressor-vasovagal problems may be involved.
Findings usually are normal.
Pulse occasionally is irregular in the presence of premature contractions.
Exaggerated tachycardia (high-volume in severe MR) following exertion is not unusual
Skeletal abnormalities are observed in two thirds of patients. These do not fit into any of the recognized connective tissue disorders, although an occasional patient may have Marfan or other related syndromes. Common findings are as follows:
Height-to-weight ratio greater than normal
Arm span greater than height (dolichostenomelia)
Narrow anteroposterior chest diameter (straight back)
Pectus excavatum or pectus carinatum
Crowding of teeth
Apical midsystolic nonejection click and late systolic murmur are the hallmarks, but either may occur alone.
Heart sounds usually are normal, but the first heart sound (S1) may be accentuated when prolapse occurs early in systole, due to the summation of S1 and mitral click.
Multiple clicks occur when prolapse of different leaflets occurs at different times during the systole and may resemble pericardial friction rub.
In patients with redundant floppy mitral valves and significant MR, the murmur may be holosystolic and the click absent.
Where the posterior mitral valve leaflet is prolapsing, the murmur may radiate along the left sternal border to the aortic area, thus mimicking left ventricular outflow tract
murmur. If the anterior leaflet prolapses, the murmur radiates to the axilla and the spine.
In the sitting or standing position in late systole, the click may appear earlier and the murmur may be more prominent. The systolic click moves towards S1 on standing, often merging with S1 if marked postural tachycardia occurs, and new clicks may appear. If an exaggerated heart rate response occurs, the murmur becomes longer and often louder to holosystolic. Occasionally the murmur is present only in the upright posture.
When squatting from standing position, the click and murmur may move back to late systole. Continuous auscultation, while the patient is standing from squatting position, reveals the click and murmur moving back to early systole on a beat-to-beat basis as the heart rate accelerates.
Occasionally, a systolic precordial honk or whooping sound may be heard with the murmur. Often these are heard only in the sitting or standing position and may be limited to a few beats immediately after standing.
Dynamic auscultatory changes reflect alterations in the timing of the MVP, the timing and extent of the MR, the expected changes in left ventricular volume, myocardial contractility, and heart rate. In the upright posture, venous return decreases and so does the left ventricular volume. The reflex tachycardia that occurs in the upright position will further reduce left ventricular volume. Timing and degree of the prolapse are determined by the position of the mitral leaflets at end diastole, which in turn is dependent on the distance from the mitral valve annulus to the attachment of the chordae to papillary muscles. Low left ventricular end-diastolic volume shortens the mitral annular papillary muscle distance, allowing the leaflets to prolapse earlier in systole.
Prompt squatting from standing position increases venous return and left ventricular volume; thus, the systolic click and murmur may become late systolic. Squatting, however, may also be associated with an increase in peripheral vascular resistance, which in turn increases the tension on the mitral valve apparatus, directing blood flow preferentially into the left atrium, rather than to the peripheral circulation. The late systolic click and murmur then become accentuated in the squatting position.
Other maneuvers are possible as follows, but none is as practical and helpful as a systematically performed postural dynamic auscultation.
Isometric hand grip exercise
Application of tourniquets to the extremities
Lower body negative pressure or amyl nitrate inhalation
Heritable disorders of connective tissue
types I, II, IV
Polycystic kidney disease, adult type
Fragile X syndrome
Straight back syndrome
Atrial septal defect
(ostium secundum), including atrial septal aneurysm, tricuspid valve prolapse
, aortic valve prolapse, and Ebstein anomaly of tricuspid valve
Accessory atrioventricular pathways
Coronary artery anomalies
Sickle cell disease
Von Willebrand disease
Several reports suggest magnesium deficiency
underlies the disease in some patients.
Most patients with MR (mitral regurg. have dizzy spells).