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1 Division of Cardiology, Department of Medicine, Mount Sinai Hospital, Miami Beach, Florida, and the Department of Medicine, the University of Miami School of Medicine, Coral Gables, Florida
The study of the immediate hemodynamic effects of acute mitral valvar insufficiency (MI) has previously been limited to the experimental animal. The presence of a mitral valvar prosthesis, however, enables one to produce MI through passage of a transseptal catheter into the prosthesis to temporarily prevent proper seating of the ball or disc. In acute MI, so produced, there resulted a significant increase in heart rate, left ventricular end-diastolic pressure, pulmonary artery "wedge" pressure, and pulmonary artery pressure. Cardiac output and effective forward stroke volume decreased. The development of dyspnea and restlessness in three of six patients necessitated relief of the MI after seven to ten minutes. Withdrawal of the catheter, out of the prosthetic valve, returned the hemodynamic values to control levels within five minutes. Evidence is presented which indicates a protecting role for the pulmonary veins during the development of acute MI. No complications were noted in these six patients; however, only previously well-anticoagulated patients should be studied in this manner and then with great care.
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