Mitral regurgitation natural history
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The natural history of mitral regurgitation (MR) may follow one of two patterns, acute or chronic. Chronic MR can be either compensated or decompensated. The natural history and prognosis of MR depend on the underlying etiology and the degree of severity of the valvular abnormality. Mild MR is associated with few if any complications. However, when severe, MR may lead to development of pulmonary edema, pulmonary hypertension, and right heart failure.
The natural history of MR may follow one of two patterns, acute or chronic. In acute MR, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature leading to sudden onset of dyspnea, PND, orthopnea and rales. Chronic MR can be either compensated or decompensated. During the chronic compensated phase of MR, compensatory changes in the left ventricle and left atrium maintain the forward cardiac output of the left ventricle, and minimize the signs and symptoms of pulmonary congestion that occur in the acute phase of the disease. Individuals in the chronic compensated phase may be asymptomatic and have normal exercise tolerance. An individual may remain in the compensated phase of mitral regurgitation for years, but will eventually develop left ventricular dysfunction, the hallmark for the chronic decompensated phase of mitral regurgitation. Once the patient transitions into the decompensated phase, there may not be recovery of left ventricular funtion following operative repair or replacement of the mitral valve. The decompensated stage is defined on the basis of a decompensated ventricular function. At this stage, the patients are at risk for a poor results of valve replacement.
Mild MR is associated with few if any complications. However, when severe, MR may lead to development of (in alphabetical order):
- Atrial fibrillation
- Cardiogenic Shock
- Pulmonary edema
- Pulmonary hypertension
- Right heart failure
Patients with asymptomatic chronic severe MR have a high likelihood of developing symptoms or left ventricular dysfunction over the course of 6 to 10 years. The incidence of sudden death in asymptomatic patients with normal left ventricular function varies widely among studies.
The prognosis is poor in patients with severe symptomatic MR with an estimated eight year survival rate of only 33% in the absence of surgical intervention. Heart failure and sudden death due to ventricular arrhythmia are common causes of death.
Among subjects with severe MR due to a ﬂail posterior mitral leaﬂet, 90% of patients are either dead or require mitral valve surgery by 10 years with a mortality rate of 6% to 7% per year. However, the risk of death is higher in those patients with a left ventricular ejection fraction <60% or with NYHA functional class III–IV symptoms.
Severe symptoms are associated with a poor outcome after mitral valve repair or replacement. Postoperative survival rates in patients with NYHA functional class III–IV symptoms at 5 and 10 years are 73 ± 3% and 48 ± 4% respectively, compared to 5 and 10 years survival rates of 90 ± 2% and 76 ± 5% respectively among patients with NYHA functional class I/II symptoms before surgery.
In a long-term retrospective study, 198 patients with an effective oriﬁce area >40 mm² had a risk of cardiac death of 4% per year during a mean follow-up period of 2.7 years.
Acute MR with cardiogenic shock is associated with an operative mortality of 80%.
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