The hypothesis that brief ischemia (preconditioning) protects the isolated heart from prolonged global ischemia was tested. Isovolumic rat hearts were preconditioned with either 5 min of ischemia followed by 5 min of perfusion (P1) or two 5-min episodes of ischemia separated by 5 min of perfusion (P2). Control hearts received no preconditioning. All hearts received 40 min of sustained ischemia and 30 min of reperfusion. Preconditioning (P1 or P2) significantly (P less than 0.0005) improved recovery of the rate-pressure product; percentage recoveries were 17.8 +/- 3.2 (n = 14), 59.9 +/- 5.5 (n = 6), and 46.4 +/- 4.7 (n = 8) for control, P1, and P2, respectively. Improved functional recovery of preconditioned hearts was associated with reduced end-diastolic pressure and improved myocardial perfusion. During the 40-min ischemic period, myocardial pH decreased from approximately 7.4 to 6.3 +/- 0.1 (n = 7) in the control hearts and to 6.7 +/- 0.1 (n = 7) in the preconditioned hearts (P less than 0.01). Also during the 40-min ischemic period, myocardial lactate (expressed as nmol/mg protein) increased to 146 +/- 11 (n = 7) and 101 +/- 12 (n = 8) in control and preconditioned hearts, respectively (P less than 0.02). The results demonstrate that a brief episode of ischemia can protect the isolated rat heart from a prolonged period of ischemia. This protection is associated with decreased tissue acidosis and anaerobic glycolysis during the sustained ischemic period.

Mitral valve regurgitation (MR) is a frequent Doppler echocardiographic finding in patients after acute myocardial infarction (AMI) and an independent predictor of long-term cardiovascular mortality. Reported risk factors include advanced age, prior myocardial infarction, infarct extension, and recurrent ischemia. During the early phase of AMI, transient ischemic MR is common and rarely causes hemodynamic compromise. However, when several chordae tendineae or a papillary muscle ruptures, acute left atrial and ventricular volume overload ensues, leading to abrupt hemodynamic deterioration with cardiogenic shock. Auscultation may be unrevealing due to decreased turbulence. Hence, the importance of a high index of suspicion for acute MR in any patient with acute pulmonary edema in the setting of AMI, especially if left ventricular systolic function is well preserved. Later, ventricular remodeling may lead to MR through annular dilatation or papillary muscle migration with malcoaptation of the leaflets. The widespread availability, ease of use and non-invasive nature of Doppler echocardiography have made it the standard diagnostic tool for detecting MR. Mechanical reperfusion of the infarct-related artery seems to be superior to fibrinolysis in decreasing its incidence acutely and in the long run. Nevertheless, when acute severe MR occurs, unless rapidly diagnosed and treated, this dreaded complication is associated with high morbidity and mortality. Prompt surgical intervention after hemodynamic stabilization is essential to ensure a good short-term and long-term prognosis. This review discusses the incidence, long-term prognosis, associated risk factors, complex pathophysiology, time of occurrence, clinical manifestations, diagnosis, and management of patients with MR after AMI.

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