Acute Mitral Regurgitation Clinical Presentation
- Author: Daniel DiSandro, MD; Chief Editor: Barry E Brenner, MD, PhD, FACEP more...
Note the following:
Mitral regurgitation can be tolerated for many years.
The initial symptoms of dyspnea and fatigue can rapidly progress to orthopnea and paroxysmal nocturnal dyspnea.
Patients with anginal-type pain may have underlying ischemia.
Atypical chest pain can be associated with MVP syndrome.
In patients with mitral valve prolapse (MVP), palpitations and atypical chest pain are the most frequent complaints. Two thirds of these patients are female, often with an underlying panic disorder.
With underlying coronary artery disease (CAD), regurgitation usually is associated with symptoms of angina pectoris.
Regurgitation also can develop acutely with myocardial infarction, secondary to papillary muscle rupture.
Coronary artery disease often is accompanied by dyspnea, fatigue, orthopnea, and fluid retention. Chest pain is usually minimal in these patients.
When mitral regurgitation is due to left ventricular dilatation and altered valve function, patients often have chronic left-sided heart failure.
In acute mitral regurgitation from sudden disruption of the mitral valve, the symptoms are due to acute pulmonary edema.
The classic murmur of mitral regurgitation is a high-pitched holosystolic murmur beginning with the first heart sound and extending to the second heart sound. The intensity usually is constant throughout systolic ejection, often radiating to the axilla. The harshness of the murmur does not correlate with the magnitude of the valvular defect. Patients with severe disease often have a third heart sound, a consequence of the increased ventricular filling volume that is ejected into the left ventricle under higher than normal pressure. Patients with mitral valve prolapse often have a mid-to-late systolic click and a late systolic murmur. These patients are usually female and often have orthostatic hypotension.
Patients with coronary artery disease can have the above mentioned murmur any time during systole, accompanied by an atrial gallop.
In acute mitral regurgitation, the examination usually is consistent with acute pulmonary edema and left ventricular failure. The heart size usually is normal, but an audible systolic thrill is often present. The murmur often is harsh. It may be heard over the back of the neck, vertebra, and/or sacrum and may radiate to the axilla, back, and left sternal border.
Acute rheumatic heart disease remains a significant consideration in those with mitral regurgitation who are younger than 40 years.
Mitral valve prolapse (MVP) (ie, myxomatous degeneration) accounts for approximately 45% of the cases of mitral regurgitation in the Western world. The causative agent is unknown in this condition. Myxomatous degeneration is usually a slow process, with a major complication being the rupture of the chordae tendineae. (Acute regurgitation, as mentioned earlier, can be caused by chordae tendineae rupture or papillary muscle dysfunction.) The literature now seems to suggest that MVP has become the most common cause of mitral regurgitation in the adult population.
In addition, MVP and coronary artery disease (CAD) have become major mechanisms for incompetence of the mitral valve. Ischemia is responsible for 3-25% of mitral regurgitation. The severity of regurgitation is directly proportional to the degree of left ventricular hypokinesis.
Mitral annular calcification can contribute to regurgitation. Impaired constriction of the annulus results in poor valve closure.
Left ventricular dilatation and heart failure can produce annular dilatation and poor valve closure resulting in mitral regurgitation.
Tendineae rupture can be due to endocarditis, myocardial infarction, or trauma.
Papillary muscle dysfunction usually is caused by myocardial ischemia or infarction.
Other causes include the following:
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