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Biomedical subjects

G Baroldi

Publications and source records attributed to G Baroldi.

At least 73 records · Page 4Linked to original sources
PubMed1978

Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of "preinfarction" angina.

To investigate the pathogenesis of myocardial infarction we undertook a systematic study of patients with angina at rest, a syndrome known to evolve frequently into infarction. Among 187 consecutive patients, 37 had infarction, all in the area that showed electrocardiographic changes during angina. In all 76 patients who underwent hemodynamic monitoring, 201thallium myocardial scintigraphy or angiography during angina, a vasospastic origin of the attacks was documented. In six patients with infarction shortly after these studies and in two in whom the infarction developed during hemodynamic monitoring or during angiography the onset of infarction was indistinguishable from the onset of anginal attacks. One patient in whom spasm was observed at the onset of infarction died six hours later; at post-mortem examination, a fresh laminar thrombus was found at the site of the spasm. After infarction, complete thrombotic occlusion of the branch shown to undergo vasospasm was documented in two patients by angiography.

Adult↗
PubMed1975

Different morphological types of myocardial cell death in man.

The evolutive histological stages, the frequency, and the eventual association of the different types of myocardial cell death have been studied in the following human material: acute infarction, sudden "coronary" death, accidental death, pheochromocytoma, transplanted hearts, "stone" heart syndrome, thrombotic thrombocytopenic purpura, and alcoholic cardiomyopathy. Three distinct main histological types of myocardial cell death are recognizable: Coagulation necrosis, the fundamental lesion in infarcts in which the myocardial cell loses its capability to contract and dies in an atonic state with overdistension due to the intraventricular pressure. No early myofibrillar damage is seen. Coagulative myocytolysis, found in all the present cases, always seen in the outer zone of an early infarct and in the surrounding normal myocardium at any stage of the repair process in most of the acute infarcts and in most cases of sudden death. The myocardial cell dies in a hypercontracted state, with early myofibrillar rhexis, and anomalous irregular cross-band formations. This tetanic death is similar to that seen in pheochromocytoma and in experimental catecholamine-induced necrosis. Colliquative myocytolysis, in which edematous vacuolization with dissolution of myofibrils is the main early finding, without hypercontraction, anomalous bands, and myofibrillar rhexis. This pattern, likely related to the low-output syndrome, was often seen in the preserved subendocardial and perivascular muscle fibers of acute infarct cases, in some transplanted hearts, and in all the alcoholic hearts. The different clear-cut morphological patterns of these three types of myocardial necrosis suggest a different pathogenesis and that different pathogenetic mechanisms may act in the same disease.

Acute Disease↗
PubMed1975

The healing of myocardial infarcts in man.

One hundred and fifty hearts of patients who died within 25 days of the onset of a clinically proven myocardial infarct were examined. Three morphologically distinct forms of myocardial necrosis were recognized. In the central and median zones of an infarct the muscle showed coagulation necrosis. Subsequently the dead tissue was obsorbed by macrophages with the preservation of sarcolemmal sheaths. Then fibroblastic collagenization of the preserved stroma occurred. Repair was not achieved by granulation tissue. Coagulative myocytolysis occurred in the outer zone of an infarct and in the non-infarcted myocardium. The dead cells were acidophilic and showed myofibrillary damage characterized by anomalous cytoplasmic band formation. Breakdown of the fibres was followed by macrophage absorption and healing as in the central area of coagulation necrosis. Colliquative myocytolysis was seen in big infarcts. It affected a narrow band of myocardial cells in the subendocardial zone or surrounding blood vessels. The fibres became oedematous and seemed to liquefy.

Autopsy↗