What Is the Pathophysiology of Mitral Valve Prolapse?

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Pathophysiology is a convergence of pathology with physiology. Pathology is the medical discipline that describes conditions typically observed during a disease state, whereas physiology is the biological discipline that describes processes or mechanisms. Mitral valve prolapse pathophysiology is a branch of pathology related to mitral valve prolapse. As such, pathophysiology is a central focus of active research as it relates to mitral valve prolapse. By which scientists study the etiology and pathogenesis of the mitral valve prolapse, as well as the changes in the body function and metabolism of mitral valve prolapse, so as to explore the general rules of the occurrence, development and outcome of mitral valve prolapse, to provide a theoretical basis for the clinical diagnosis and prevention of the mitral valve prolapse. The pathophysiology of mitral valve prolapse can be broken into three phases of the disease process: the acute phase, the chronic compensated phase, and the chronic decompensated phase.
  • Acute phase Acute mitral valve prolapse (as may occur due to the sudden rupture of a chorda tendinae or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle. The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke volume) but also the blood that regurgitates into the left atrium (the regurgitant volume). The combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle. In the acute setting, the stroke volume of the left ventricle is increased (increased ejection fraction); this happens because of more complete emptying of the heart. However, as it progresses the LV volume increases and the contractile function deteriorates, thus leading to dysfunctional LV and a decrease in ejection fraction.[10] The increase in stroke volume is explained by the Frank–Starling mechanism, in which increased ventricular pre-load stretches the myocardium such that contractions are more forceful. The regurgitant volume causes a volume overload and a pressure overload of the left atrium and the left ventricle. The increased pressures in the left side of the heart may inhibit drainage of blood from the lungs via the pulmonary veins and lead to pulmonary congestion.
  • Chronic compensated phase If the mitral valve prolapse develops slowly over months to years or if the acute phase cannot be managed with medical therapy, the individual will enter the chronic compensated phase of the disease. In this phase, the left ventricle develops eccentric hypertrophy in order to better manage the larger than normal stroke volume. The eccentric hypertrophy and the increased diastolic volume combine to increase the stroke volume (to levels well above normal) so that the forward stroke volume (forward cardiac output) approaches the normal levels. In the left atrium, the volume overload causes enlargement of the left atrium, allowing the filling pressure in the left atrium to decrease. This improves the drainage from the pulmonary veins, and signs and symptoms of pulmonary congestion will decrease. These changes in the left ventricle and left atrium improve the low forward cardiac output state and the pulmonary congestion that occur in the acute phase of the disease. Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerances.
  • Chronic decompensated phase An individual may be in the compensated phase of mitral valve prolapse for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral insufficiency. It is currently unclear what causes an individual to enter the decompensated phase of this disease. However, the decompensated phase is characterized by calcium overload within the cardiac myocytes. In this phase, the ventricular myocardium is no longer able to contract adequately to compensate for the volume overload of mitral regurgitation, and the stroke volume of the left ventricle will decrease. The decreased stroke volume causes a decreased forward cardiac output and an increase in the end-systolic volume. The increased end-systolic volume translates to increased filling pressures of the left ventricle and increased pulmonary venous congestion. The individual may again have symptoms of congestive heart failure. The left ventricle begins to dilate during this phase. This causes a dilatation of the mitral valve annulus, which may worsen the degree of MI. The dilated left ventricle causes an increase in the wall stress of the cardiac chamber as well. While the ejection fraction is less in the chronic decompensated phase than in the acute phase or the chronic compensated phase, it may still be in the normal range (i.e.: > 50 percent), and may not decrease until late in the disease course. A decreased ejection fraction in an individual with mitral insufficiency and no other cardiac abnormality should alert the physician that the disease may be in its decompensated phase.
  Keywords: mitral valve prolapse pathophysiology.
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