[Cardiac amyloidosis: a case diagnosed by endomyocardial biopsy].
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Biomedical subjects
Publications and source records attributed to E Marchant.
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Dipyridamole has been proposed as an ideal agent to evaluate coronary vascular reserve because it produces selective coronary vasodilation without systemic hemodynamic effect. The actions of intracoronary (IC) and intravenous (IV) dipyridamole on coronary blood flow and systemic hemodynamics were compared in 15 patients with chest pain syndrome and normal coronary arteries. They received IC dipyridamole, followed 10 minutes later by 0.5 mg/kg of IV dipyridamole. IC dipyridamole produced a 73% increase in coronary sinus flow without hemodynamic changes, except for a slight increase in pulmonary systolic and diastolic pressures. IV dipyridamole administration produced an additional 88% increase in coronary sinus flow, reaching 172% over baseline; it was also associated with a significant (p less than 0.01) increase in heart rate (78 +/- 14 vs 102 +/- 19 beats/min), cardiac index (4 +/- 0.7 vs 6.3 +/- 1.7 liters/min/m2), and pulmonary artery systolic (27 +/- 5 vs 34 +/- 7 mm Hg) and diastolic pressures (12 +/- 4 vs 19 +/- 7 mm Hg). These data suggest that the coronary vasodilatory effect seen after IV dipyridamole administration is related to mechanisms other than direct coronary vasodilation.
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The effects of i.v. dipyridamole were studied in 9 patients with isolated total left anterior descending coronary artery (LAD) obstruction, in 6 patients with isolated 90 to 99% diameter reduction of the LAD and in 10 patients with normal coronary arteries and normal left ventricular function. Coronary sinus and great cardiac vein flows were determined by continuous thermodilution. Flows were measured at rest and 1, 3, 5 and 10 minutes after i.v. dipyridamole. Great cardiac vein flow represents the venous outflow from the LAD territory. In the presence of coronary steal from the LAD territory, great cardiac vein flow is expected to decrease while coronary sinus flow increases. Intravenous dipyridamole induced a similar flow increase in the coronary sinus and the great cardiac vein in all 3 groups (p less than 0.001 between rest and dipyridamole, difference not significant among groups), suggesting that no coronary steal was induced. The maximal increase in great cardiac vein flow was 118 +/- 74% in the control group, 86 +/- 74% in the group with 90 to 99% LAD obstruction and 102 +/- 29% in the group with total LAD obstruction (difference not significant). These data show that i.v. dipyridamole produces a similar increase in coronary flow in ischemic and nonischemic areas and suggests that an increase in collateral flow is the underlying mechanism for increased flow to the ischemic area.
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This study analyzes the prevalence of coronary artery disease (CAD) among patients with rheumatic valvular heart disease (VHD) in Chile. Coronary angiography was performed in all patients referred to cardiac catheterization with VHD who were over age 50 years and who had angina or ECG signs of ischemia. A total of 100 patients entered the study. Significant CAD (greater than 50% obstruction) was found in 14% of the cases: 7% in patients with mitral valve disease (MVD), 18% in aortic valve disease (AVD), and 21% in combined mitral and aortic valve disease (MAVD). Angina was present in 14% of the patients with MVD, 63% with AVD, and 53% with MAVD. Only 57% of patients with CAD had angina pectoris; 20% with angina had CAD. Hemodynamic parameters and left ventricular ejection fraction were not correlated with the presence or absence of CAD. We conclude that in patients with valvular heart disease, the incidence of CAD is lower in Chile than previously reported in the English literature. We confirmed the fact that angina is often not associated with CAD, and that CAD is often present in the absence of angina.
We have previously demonstrated that a large V wave in the pulmonary capillary wedge tracing may occur in the absence of mitral regurgitation. This study evaluates the role of left atrial and pulmonary vein compliance on such a finding. We studied 11 patients with coronary disease, without clinical or angiographic mitral regurgitation. Heart rate, pulmonary capillary wedge mean, A and V waves, V-wave slope, left ventricular and aortic pressures, cardiac output, and left atrial echo and apical phonocardiogram were recorded simultaneously. Preload was modified acutely by volume overload and by the administration of i.v. nitroglycerine. Volume administration induced a marked increase in V-wave pressure (13.0 +/- 9.6 vs. 27.0 +/- 9.6 mmHg, p less than 0.05), without producing mitral regurgitation, and without appreciable change in left atrial dimension by echo (33.0 +/- 4.9 vs. 35.5 +/- 5.2 mm, NS), or stroke volume (101.7 +/- 26.2 vs. 97.8 +/- 34.3 ml, NS). An increase was also seen in the A wave (13.6 +/- 8.9 vs. 23.3 +/- 8.5 mmHg, p less than 0.05), pulmonary capillary wedge mean pressure (9.8 +/- 7.2 vs. 20.6 +/- 7.8 mmHg, p less than 0.05), and left ventricular diastolic pressure (7.4 +/- 5.5 vs. 14.6 +/- 6.3 mmHg, p less than 0.05). All values returned to baseline after nitroglycerine. The compliance of the left atrium/pulmonary veins decreased with increasing pulmonary capillary wedge pressures. With large filling volumes, a small stroke volume brings on a large pressure change, thus explaining the finding of large V waves in patients with elevated pulmonary capillary wedge pressure and without mitral regurgitation.
Two cases with acute myocardial infarction are presented. Both had thrombotic occlusion of the infarct-related artery. Following successful thrombolysis with streptokinase, coronary angiography was normal. These cases prove that "myocardial infarction with normal coronaries" can be associated with coronary thrombosis in the acute stage.
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