eMedicine Specialties > Emergency Medicine > Cardiovascular

Mitral Regurgitation

Author: Daniel DiSandro, MD, Clinical Assistant Professor, Department of Emergency Medicine, Drexel University
Contributor Information and Disclosures

Updated: Jun 8, 2009

Introduction

Background

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 or papillary muscle 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 mitral valve prolapse 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.

Clinical

History

• 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.

Physical

• 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.

Causes

• 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:
  • Ehlers-Danlos syndrome
  • Marfan syndrome
  • Osteogenesis imperfecta
  • Systemic lupus erythematosus (SLE)

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