Biomedical subjects
Publications and source records attributed to W F Duvernoy.
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Coronary spasm may occur with angiographically normal and diseased coronary arteries. General anesthesia has been described only rarely as a triggering event for coronary artery spasm, and only once before in the presence of angiographically normal coronary arteries. We have now seen three patients presenting with acute ST-segment elevation following induction of general anesthesia with enzyme evidence of myocardial necrosis in two patients. Cardiac catheterization was performed in all three patients with one of the procedures performed on an emergency basis owing to hemodynamic compromise. All three patients demonstrated angiographically normal coronary arteries. The electrocardiograms and coronary arteriograms are presented, and possible mechanisms for the injury pattern seen on the electrocardiogram are discussed. Coronary vasospasm causing an acute injury pattern on the electrocardiogram can be caused by general anesthesia and has to be recognized promptly and treated appropriately to prevent more serious complications.
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Anesthesia-induced coronary vasospasm has been reported only rarely. We report a case, without previous cardiac history, in which immediately after anesthesia induction a marked ST elevation was noted on the EKG monitor. Premature ventricular contractions as well as non-sustained ventricular tachycardia were noted. These changes resolved immediately after nitroglycerin infusion and 75 mg of lidocaine were given. A coronary angiogram revealed normal coronary arteries and left ventriculogram. Ergonovine stimulation was not performed. The patient was discharged home on calcium entry blockers and nitrates. Exercise stress test two weeks after discharge was negative for ischemia. Induction of anesthesia triggering coronary spasm has been reported rarely, and to our knowledge never in the presence of angiographically normal coronary anatomy. Coronary vasospasm with typical EKG changes--namely, ST elevation and ventricular arrhythmias--has to be included as a possible complication of general anesthesia. Recognition of this syndrome allows prompt treatment and prevention of future episodes.
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Four hundred and sixteen patients with documented arteriosclerotic heart disease (ASHD) underwent 424 diagnostic and therapeutic surgical procedures during the year 1970 at the Henry Ford Hospital. They were classified according to the specific clinical manifestation of their cardiac abnormality. Patients with a history of old, well-compensated myocardial infarction, and those with cardiac arrhythmia, bundle-branch block, congestive heart failure and A-V block (pacemaker-protected) but no evidence of previous myocardial infarction fared almost as well as subjects of the same age without cardiac disease, and were considered to run the lowest operative risk. Patients with angina, especially if there was a history of infarction, were an intermediate risk in terms of complications and mortality. Patients with a history of previous infarction complicated at the time of the surgical procedure by arrhythmia, A-V block, bundle-branch block, or congestive heart failure were in the "highest risk" category. A severe A-V block indicated the need for insertion of a "prophylactic" pacemaker before any attempt at a diagnostic or therapeutic procedure. No patient with clinical or electrocardiographic evidence of a recent infarction (less than three months' duration) should undergo any elective surgical procedure under any form of anesthesia unless the surgeon is prepared for a high mortality rate that may approach 90 percent. In contrast, the patient with old, well-compensated myocardial infarction and no evidence of dysrhythmia, block or congestive failure can tolerate even a major surgical operation under any form of anesthesia extremely well.
The clinical symptoms, laboratory findings, apexcardiograms, phonocardiograms and echocardiographic features are related to hemdoynamic and angiocardiographic measurements in 9 patients with atrial myxoma (6 left atrial and 3 right atrial tumors). Emphasis is placed on the clinical clues to the diagnosis. Echocardiography has become the most useful non-invasive method of investigation. However, angiocardiography remains the definitive diagnostic procedure.
Complications after prosthetic valve replacement may be multiple. In biologic valves, valve detachment and cusp perforation may occur. If this is of significant magnitude, reoperation may be required. This report describes recurrent mitral regurgitation after mitral valve replacement with a Hancock porcine xenograft. The regurgitation subsided spontaneously three months later. We felt that a paravalvular leak closed, with progressive fibrosis and tightening of the annulus. Functional results in this patient were excellent.
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