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Biomedical subjects

F Pileggi

Publications and source records attributed to F Pileggi.

At least 271 records · Page 15Linked to original sources
PubMed1988

Lack of correlation between anatomic infarct size and ventriculographic variables following coronary occlusion in closed-chest dogs.

1. Although the effects of therapeutic interventions upon infarct size are frequently assessed on the basis of left ventricular ejection fraction and segmental contraction, the correlation of these variables with infarct size has not been thoroughly evaluated. To explore such relationships, we occluded the left anterior descending coronary artery of 22 closed-chest dogs and performed contrast ventriculography one week later. Regional myocardial function was evaluated by a computer system in 60 radial segments. 2. Infarct size, measured by triphenyl-tetrazolium chloride staining, ranged from 1.4 to 43.6% of the left ventricle. Infarcted dogs were arbitrarily divided into 3 groups by percentage of necrotic area: Group 1 (less than or equal to 15%, N = 5), Group 2 (15 to 30%, N = 10) and Group 3 (greater than or equal to 30%, N = 7). 3. Although the ejection fraction was significantly reduced in infarcted animals as compared to preselected normal controls (38.9 +/- 11.6 [SD] vs 74.1 +/- 7.5%, P less than 0.001), it was similar within each infarct subgroup. 4. There was a linear inverse correlation between ejection fraction and percentage of abnormally contracting segments (R = -0.63, P = 0.0017). However, neither ejection fraction nor abnormally contracting segments were correlated with infarct size (R = -0.17 and R = 0.11, respectively). 5. A more detailed analysis revealed that infarcted or infarct-adjacent segments were less depressed in Group 1 than in Group 2 or 3 and extent of depression was similar between Groups 2 and 3. Conversely, the extent of shortening of non-infarcted inferior wall segments increased from Group 1 to Group 3. 6. Thus, regional myocardial contraction is significantly affected by non-necrotic infarct-adjacent segments and the ejection fraction is significantly influenced by non-ischemic myocardium. For infarcted areas up to 40% of the left ventricle, a single post-infarction determination of ejection fraction or the percentual of abnormally contracting segments seems unreliable, on a population basis, to judge the effects of infarct-sparing interventions.

Animals↗
PubMed1988

Effects of calcium blockers on ventricular fibrillation during acute myocardial infarction.

1. The effects of the calcium blockers bepridil and verapamil on latency time to ventricular fibrillation (VF) and VF incidence were assessed in 109 anesthetized dogs, submitted to coronary occlusion and reperfusion. 2. In 19 dogs (Group I) submitted to global left ventricular ischemia, both bepridil and verapamil significantly (P less than 0.05) prolonged latency time as compared to 14 untreated controls. However, VF was not prevented by any of these drugs. Both drugs were given 15 min before coronary ligation. 3. In 76 dogs (Group II) submitted to regional myocardial ischemia (left anterior descending coronary artery (LAD) occlusion for 2 hours followed by 30 min reperfusion), VF incidence during occlusion was significantly reduced by verapamil as compared to controls (0/21 vs 10/25; P less than 0.05) but not by bepridil (10/25 vs 12/30; P = ns). During reperfusion, however, neither drug affected fibrillation incidence or latency time. 4. No correlation was observed between anti-arrhythmic drug effects and infarct size as measured by triphenyl tetrazolium chloride. 5. We conclude that both bepridil and verapamil significantly delayed the occurrence of fibrillation in acute ischemia due to coronary ligation. However, only verapamil prevented fibrillation and this effect was restricted to the occlusion phase. In contrast, during reperfusion, neither drug prevented fibrillation. Thus, VF during occlusion and reperfusion is likely to be mediated by different mechanisms.

Animals↗
PubMed1987

Perioperative acute myocardial infarction after valve replacement.

The incidence of fatal acute myocardial infarction (AMI) after valve replacement has decreased with use of cold potassium-induced cardioplegia. Despite this method of myocardial preservation, 12 of 662 consecutive patients submitted to valve replacement had this complication. This study retrospectively analyzes, in those 12 patients, the etiologic profile of fatal perioperative AMI, together with its morphologic aspects. The clinical picture in 11 patients was a refractory low cardiac output state. In only 3 cases was AMI diagnosis confirmed during life. Six patients either had a technical complication or a coronary embolus; in these patients AMI was localized in the vascular bed of a single occluded coronary artery, and its morphologic picture resembled that of usual AMI. The 6 other patients did not have a defined cause for AMI and coronary occlusion was not present. In 4 such patients, there was massive circumferential necrosis, mainly in the subendocardium; comparatively, there was a greater prevalence of hemorrhage, contraction bands and necrosis of the layer of subendocardial cells adjacent to the left ventricular cavity. The findings for this group suggest myocardial necrosis due to cell damage during cardiopulmonary bypass; no predisposing factor for perioperative AMI was identified.

Adolescent↗
PubMed1987

The role of active myocarditis in the development of heart failure in chronic Chagas' disease: a study based on endomyocardial biopsies.

The authors analyze the presence of active myocarditis in endomyocardial biopsies from 38 patients with chronic Chagas' disease diagnosed serologically. The patients were divided into three clinical groups of increasing severity. Group I: 13 patients with normal electrocardiograms, normal chest x-rays, and no symptoms; Group II: 13 patients with abnormal electrocardiograms and no cardiomegaly; and Group III: 12 patients with abnormal electrocardiograms, cardiomegaly and heart failure. In order to diagnose myocarditis activity, two sets of criteria were used: one mainly observing histopathologic aspects of inflammatory cells aggressing cardiac fibers; and the other counting the mean number of lymphocytes per high power microscopic field. The results of both methods showed a higher incidence of active myocarditis in the clinical group with heart failure. The present report clearly shows the important role played by activity of myocarditis in the development of heart failure in chronic Chagas' disease. Therefore, the possibility of using drugs to control early stages of the activity of the inflammatory process is suggested. On the other hand, endomyocardial biopsy (EMB) seems to be an adequate method to evaluate the intensity of the cardiac inflammatory process in Chagas' heart disease.

Adolescent↗