Cause of acute myocardial infarction late after successful coronary artery bypass grafting.
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Biomedical subjects
Publications and source records attributed to M A Kutcher.
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We have reported the case of a 38-year-old white woman with substernal chest pain, hypotension, and ECG changes suggesting acute anterior myocardial infarction. Cardiac catheterization revealed no coronary artery pathology, but severe global hypokinesia was noted on left ventriculogram and endomyocardial biopsy revealed myocytic degeneration and mononuclear cell infiltration consistent with acute viral myocarditis. Viral serologies confirmed a recent Epstein-Barr virus infection.
Rapid and accurate assessment of coronary artery stenotic severity is important in therapy and understanding of coronary artery disease. Since automated systems minimize prejudice and variations in analysis, we developed an automated, quantitative coronary analysis system utilizing an IBM PC-XT computer. Film images (35 mm) were cine-to-video converted and subsequently digitized by an IBM PC-XT computer. Given an approximate center line, the computer automatically detected edges, corrected for X-ray magnification, and calculated arterial dimensions. On objects of known dimensional sizes, the correlation coefficient between actual and calculated dimensions was 0.996 (p less than 0.01) with a standard error of estimate of 0.07 mm and +/- 3.0% reproducibility. For objects less than 1 mm in diameter, the standard error of estimate was 0.05 mm with +/- 4.1% reproducibility. However, with minimal contrast material (25%), the standard error of estimate increased to 0.20 mm with +/- 7.2% reproducibility. The results indicate that automated, quantitative coronary angiography can be achieved using an inexpensive IBM PC-XT based system, provided that the vessels are adequately opacified.
To help determine if coronary angiography can predict the site of a future coronary occlusion that will produce a myocardial infarction, the coronary angiograms of 42 consecutive patients who had undergone coronary angiography both before and up to a month after suffering an acute myocardial infarction were evaluated. Twenty-nine patients had a newly occluded coronary artery. Twenty-five of these 29 patients had at least one artery with a greater than 50% stenosis on the initial angiogram. However, in 19 of 29 (66%) patients, the artery that subsequently occluded had less than a 50% stenosis on the first angiogram, and in 28 of 29 (97%), the stenosis was less than 70%. In every patient, at least some irregularity of the coronary wall was present on the first angiogram at the site of the subsequent coronary obstruction. In only 10 of the 29 (34%) did the infarction occur due to occlusion of the artery that previously contained the most severe stenosis. Furthermore, no correlation existed between the severity of the initial coronary stenosis and the time from the first catheterization until the infarction (r2 = 0.0005, p = NS). These data suggest that assessment of the angiographic severity of coronary stenosis may be inadequate to accurately predict the time or location of a subsequent coronary occlusion that will produce a myocardial infarction.
Because of the close anatomic association, the volume or pressure in one ventricle can directly influence the volume and pressure in the other ventricle. Disease states that reduce pericardial compliance should accentuate this coupling between the ventricles. We examined this hypothesis in six dogs. Constrictive pericarditis was induced by injecting an irritant mixture into the pericardial cavity. Three to 4 weeks after this injection, the hearts were removed and placed in cool cardioplegic solution. Balloons were inserted into each ventricle and the pressure and volume changes caused by increasing the contralateral ventricular volume were measured. Compared with that in a control group of four dogs, the coupling between the ventricles was significantly augmented in the group with constrictive pericarditis. All the measured changes in ventricular pressure or volume caused by increasing contralateral ventricular pressure or volume were significantly greater (p less than .05) in the group with constrictive pericarditis. The results of these experiments show increased coupling between the ventricles with constrictive pericarditis, which helps to explain some of the signs and symptoms of constrictive pericarditis.