RESUMEN

Administration of hGH during the acute phase of experimental myocardial infarctions in pigs showed several aspects which clearly distinguished the treated group from the control one. In the first case the necrotic segment appeared considerably smaller than in the control group but also exhibit a qualitative different necrotic pattern in the histologic aspect, i.e. the infarcted area is shown itself reduced to isolated cells; scarce clusters of them interspersed where found within larger areas of preserved tissue. Affected cells have been defined as "injured fibres" according to their particular aspect which notably differs to the classic expected picture of a 25th day infarction and exhibits itself as an "arrested necrosis". A remarkable preservation of capillary vessels has also been found in the treated cases by a contrasting disappearance of the capillary bed in the control group. Ventricular contractility was also explored with ECHO B which showed significant differences between both groups: wall thinning of the ventricular wall in the affected area did not appear in treated cases and normal contractility in the same area reappeared a few hours after the infarction. Contractility was never restored in the control group. hGH main action is directed towards the preservation of the myocardial collagen matrix, helping to maintain the structural integrity of ventricular wall. There are, however, other possible effects on immunological aspects of the macrophages partially noticed, and to be disclosed in the future.

Asunto(s)

Asunto(s)

Asunto(s)

RESUMEN

We administered human growth hormone to a group of rats with experimental myocardial infarctions, in order to observe its action on the connective tissue repair process and the consequent effect on postinfarction ventricular aneurysms. Myocardial connective tissue displays a complex layout around each myocyte and among neighboring ones. It has been shown to be highly vulnerable to acute coronary ischemia which affects its diverse components in accordance with a precise timetable. The ultimate consequence of ischemia on connective tissue is the disappearance of intermyocytic links and the collagen weave that surrounds each cell. Damage to this collagen framework of the heart is responsible for the final disarray of myocytes, with a parallel effect to the myocytolytic actions of ischemia within the very structure of each cell. Hence, the appearance of postinfarction ventricular aneurysms seems to be related to failure in normal repair processes resulting from maturation of new collagen tissue into the area of myocardial necrosis. It has been shown that, besides the well-known actions on chondrocytes, hypothalamic-hypophyseal human growth hormone and somatomedins activate the fibroblasts. Administration of human growth hormone resulted in a significant decrease in the incidence of ventricular aneurysms. Scanning electron microscopy showed a good preservation of connective tissue components of myocardium. A different histological pattern of necrosis resulted in the treated group.

Asunto(s)

Asunto(s)

Asunto(s)

RESUMEN

Human growth hormone (hGH) administered alone revealed itself as a useful drug to prevent ventricular aneurysm formation in experimental myocardial infarctions in rats and is also able to diminish and change the usually expected pattern of wall necrosis. A protective action on the collagen framework of myocytes has been confirmed as one of the main causes responsible for the above mentioned findings. There are other positive metabolic actions on the myocardial cell although not completely known yet. These actions are revealed by an atypical picture of infarction which appears regionally reduced and with a patchy intracellular distribution. In an opposite fashion, when hGH was administered together with beta blockers, a rapid and extensive deleterious action occurred at the ventricular wall, a very high incidence of ventricular aneurysms and an increased extension of myocardial infarcts were the most outstanding features. The histologic picture in this series resembles that of a rapidly evolving diabetic cardiomyopathy.

Asunto(s)

RESUMEN

A geometrical-dynamical model has been designed with the aim to reproduce the early phases of ventricular aneurysms formation. Possible deleterious forces within a solidary-dynamic structure start when a partial or localized loss of contractility arises. A following important aspect is related to the compressive effects of those altered cells over the normally contracting neighborhood. An abnormal packing of elements within a cyclic-dynamic structure has taken place and consequently new abnormal forces of compression between altered and normal cells will result in a longitudinal course of progression. When this circle crosses itself, a ventricular aneurysm will be completed. The process could be ascribed to an elastic phenomenon activated by a compressive stress. The chain of events included in this model has been matched with usual pathological findings of ventricular aneurysms, i.e. wavy and broken fibres neatness of aneurysmatic borders, and apical outstanding incidence of aneurysms etc. The proposed geometrical-dynamical model admits the possibility of an interruption in the 7 steps process of ventricular aneurysm formation by means of a "barrier effect". This effect has been related to the fibrous extracellular matrix with its differences in amount and quality of scar formation, which is possible to be observed in ischemic heart disease and chronic Chagas' cardiomyopathy and in some other illustrative entities. An analysis of this particular aspect of scar formation on diverse aneurismogenic entities with different reactions of collagen and particularly different figures of incidence of aneurysmatic formation, show a high correlation with possible alternatives disclosed by this geometrical-dynamical model.

Asunto(s)

Asunto(s)

RESUMEN

We depict the histologic findings of ventricular aneurysms in 8 patients, 5 with Chagas heart disease and 3 secondary to myocardial infarction. Chagas disease and ischemic cardiopathy are the 2 conditions which show the highest incidence of ventricular aneurysms. The first one averages more than 60% in large series. The second one reveals ventricular aneurysms as a complication of myocardial infarction in 20-25% in large series. Both entities share identical hallmarks, and the same frequency of complications related to the presence of the aneurysms: vgr. sudden death, presence of malignant ventricular arrhythmias, thromboembolism, etc. Several histologic findings help to differentiate both conditions. Inflammatory cells, monocytes, eosinophils and lymphocytes interspersed within myocardial fibers, plus diverse lesions of myocytolysis point to a diagnosis of Chagas disease. We consider scar fibrosis as another capital difference to be observed in aneurysms of chagasic or ischemic origin. Fibrosis of ischemic origin is intense and early depending upon a quick stimulation of collagen I and III during the first days of myocardial infarction. Conversely, in Chagas disease the injury to the myofibrils by immunocomplexes is very slow and consequently collagen response will be slower and with lesser fibrotic response. We have previously considered in other publications this phenomenon after a geometrical-dynamical model have been designed for this purpose.

Asunto(s)