Mitral Regurgitation

Mitral regurgitation, in the acute and chronic decompensated states, is commonly encountered in the emergency department. An understanding of the underlying etiologies and pathophysiology of the condition is critical to direct appropriate treatment.
Pathophysiology
Mitral regurgitation can be divided into the following 3 stages: acute, chronic compensated, and chronic decompensated.
In the acute stage, which usually occurs with a spontaneous chordae tendineae rupture secondary to myocardial infarction, a sudden volume overload occurs on an unprepared left ventricle and left atrium. The volume overload on the left ventricle increases left ventricular stroke work. Increased left ventricular filling pressures, combined with the transfer of blood from the left ventricle to the left atrium during systole, results in elevated left atrial pressures. This increased pressure is transmitted to the lungs resulting in acute pulmonary edema and dyspnea.
If the patient tolerates the acute phase, the chronic compensated phase begins. The chronic compensated phase results in eccentric left ventricular hypertrophy. The combination of increased preload and hypertrophy produces increased end-diastolic volumes, which, over time, result in left ventricular muscle dysfunction. This muscle dysfunction impairs the emptying of the ventricle during systole. Therefore, regurgitant volume and left atrial pressures increase, leading to pulmonary congestion.

Frequency
United States
Previously, chronic rheumatic heart disease was the most common cause of acquired mitral valve disease in the Western world. More recently, however, mitral valve prolapse (MVP) has become the most common cause, being responsible for 45% of cases of mitral regurgitation. MVP has been estimated to be present in 4% of the population; however, significant regurgitation in this population only occurs in those with abnormalities of the valve.
International
In areas other than the Western world, rheumatic heart disease remains the leading cause of mitral regurgitation.
Mortality/Morbidity
The prognosis of patients with mitral regurgitation depends on the underlying etiologies and the state of the left ventricular function.
Acute pulmonary edema and cardiogenic shock often complicate the course of acute regurgitation. The operative mortality in these cases approaches 80%. A patient with ruptured chordae tendineae and minimal symptoms has a much better prognosis.
With chronic regurgitation, volume overload is tolerated very well for years before symptoms of failure develop. Left atrial enlargement predisposes patients to the onset of atrial fibrillation with the subsequent complication of embolization. In addition, these patients are susceptible to endocarditis. A study of the survival of patients with chronic regurgitation was performed using randomly selected patients. The study revealed that 80% of the patients were alive 5 years later, and 60% were alive after 10 years.
Most patients with MVP are asymptomatic. Prolapse in those older than 60 years is frequently associated with chest pain, arrhythmias, and heart failure. The prognosis of these patients is good; however, sudden death, endocarditis, and progressive regurgitation occur rarely.
When ischemic heart disease is the mechanism for regurgitation, the extent of anatomic disease and left ventricular performance are prognostic determinants. Complicating events include sudden death and myocardial infarction.

Sex
In those younger than 20 years, males are affected more often than females.
In those older than 20 years, no sexual predilection exists.
Males older than 50 years are affected more severely.

Age
Of those cases caused by prior rheumatic disease, the mean age is 36, plus or minus 6 years.
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