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Mitral valve prolapse frequently resembles coronary heart disease. Retrospective clinical, ECG and angiographic analysis of 100 consecutive patients with mitral prolapse and normal coronary arteries, but complaining of anginal pain, shows how difficult it is to establish the correct diagnosis. When resting, 44% of patients have nonspecific ECG disorders of repolarization phase. During periods of chest pain 3 patients experienced transient ST segment changes very similar to acute myocardial ischemia. The exercise test was positive in 39% of cases, and in 2 patients during exercise a sudden drop in blood pressure suggested coronary perfusion failure. In all patients the coronary arteries were normal, but left ventriculography showed mitral valve prolapse predominantly on the posterior leaflet. At rest, 35% of patients had diastolic compliance failure, 32% had left ventricular hyperkinesia and only in 3% was slight hypokinesia present. Finally, early systolic relaxation of the anteroapical wall was observed in 75% of patients.
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BACKGROUND: The conventional strategy for primary angioplasty during acute myocardial infarction is angioplasty of the infarct-related vessel, even in patients with multi-vessel disease. Patients, however, often have significant lesions in multiple coronary arteries and a strategy for multi-vessel angioplasty during acute myocardial infarction has not been explored. The purpose of this study was to examine whether multi-vessel angioplasty is as safe as infarct-related vessel angioplasty in patients with multi-vessel coronary artery disease during acute myocardial infarction. METHODS: Using the 2000-2001 New York State Angioplasty Registry database, we compared the in-hospital clinical outcomes of patients with multi-vessel disease (>70% stenosis in at least two major coronary arteries), who underwent either multi-vessel angioplasty (n=632) or infarct-related vessel angioplasty (n=1350) within 24 h of acute myocardial infarction. Patients with previous myocardial infarction, angioplasty, bypass surgery, or cardiogenic shock were excluded. RESULTS: Patients in the multi-vessel angioplasty group were less likely to be female, to have peripheral vascular disease or diabetes. They had more complex lesions and were more likely to receive stents. In-hospital mortality was three-fold lower (0.8 versus 2.3%, P=0.018) in the multi-vessel angioplasty group. No differences were observed in other ischemic complications, renal failure, or length of stay. After multivariate analysis, multi-vessel angioplasty remained a significant predictor of lower in-hospital death (odds ratio=0.27, 95% confidence interval=0.08-0.90, P=0.03). CONCLUSIONS: Despite the added complexity of multi-vessel angioplasty, patients in this group had significantly lower in-hospital mortality. Therefore, a strategy of multi-vessel angioplasty during acute myocardial infarction may be safe compared with infarct-related angioplasty in selected patients.
The shortterm results (mean follow-up 0.9 years) in 61 patients with single vessel disease (1-VD) who had undergone percutaneous transluminal coronary angioplasty (PTCA) were compared with those in 33 patients with 1-VD treated medically and in 36 patients with 1-VD treated by bypass surgery. All medically and surgically treated patients had coronary artery stenoses which were classified in a retrospective analysis as suitable for PTCA. Initially there were no significant differences between the three groups with respect to functional impairment (NYHA class), incidence of prior myocardial infarction, left ventricular ejection fraction and localization of the coronary stenoses. Comparison of follow-up results at the end of the first year showed (1) that the NYHA class was reduced to a similar extent both in patients treated surgically and in those treated by PTCA, (2) that the NYHA class in the medically treated group was significantly greater than in the other two groups, and (3), that there was no difference among the three groups with respect to infarct and mortality rate.
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The relationships between cardiac performance, coronary flow, minimal coronary vascular resistance and myocardial oxygen consumption (MVO2) were explored in isolated hearts from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) and in hearts from SHR given a combination of metoprolol and felodipine (selective calcium antagonist) for 35 weeks. Antihypertensive therapy markedly reduced arterial pressure and caused a substantial regression of left ventricular hypertrophy. An antegrade working-heart perfusion system was used, allowing measurements of stroke volume, coronary flow and MVO2 at varying pre- and afterloads. In untreated SHR cardiac function was reduced at low and enhanced at high perfusion pressure compared with WKY. Minimal coronary vascular resistance, which was greatly increased in SHR, was significantly reduced by treatment, allowing higher coronary flow for any given perfusion pressure and consequently a lower degree of oxygen extraction. In addition, at a given workload, MVO2 was reduced in both untreated and treated SHR. These results stress the importance of having adequate coronary perfusion within a hypertensive structurally redesigned coronary vascular bed in order to maintain cardiac performance. With antihypertensive therapy in SHR, an improved coronary flow capacity was created due to regression of the hypertensive vascular changes.
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