Giorgio Baroldi

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.

Focal lymphocytic myocarditis in acquired immunodeficiency syndrome (AIDS): A correlative morphologic and clinical study in 26 consecutive fatal cases

In 26 consecutive cases with acquired immunodeficiency syndrome (AIDS) the main cardiac findings were Kaposis sarcoma in 2 cases, microfocal myocardial abscess in 1, subendocardial infarct necrosis in 2, contraction band necrosis in 13, lymphocytic myocarditis in 9, intramyocardial lymphocytic infiltrates without myocell necrosis in 7 and epicardial lymphocytic infiltrates in 4. No patient had congestive heart failure. However, two-dimensional echocardiography performed in eight patients demonstrated functional abnormalities in six (fractional shortening ranging from 18 to 30%, globular shape, hypokinesia, mild ventricular dilation). Four of these six patients had lymphocytic myocarditis and two had lymphocytic infiltrates in the myocardium and epicardium without myocell necrosis. No lymphocytic infiltrates were seen in the two cases with a normal echocardiogram. Quantitative analysis indicated that involvement of the heart by lymphocytic myocarditis is inadequate in itself to explain dysfunction. It remains to be established 1) whether lymphocytic myocarditis is a possible indication of a more widespread molecular disorder, and 2) what its eventual relation with dilated cardiomyopathy will be.

Markers of cardiac oxidative stress and altered morphology after intraperitoneal cocaine injection in a rat model

Abstract This study was designed to assess the parameters of myocardial oxidative stress and related cardiac morphological changes following intraperitoneal cocaine exposure in rats. The cardiac levels of reduced glutathione(GSH), oxidised glutathione(GSSG), ascorbic acid (AA), and the production of malondialdehyde (MDA) were measured, as well as the variations of activity in the enzyme systems involved in cell antioxidant defence, glutathione peroxidase (GSH-Px), glutathione reductase (GR) and superoxide dismutase (SOD). After chronic cocaine administration for 30 days GSH was significantly depleted in the heart from 30 min (P < 0.001) to 24 h (P < 0.001) after exposure, and GSSG was increased for a similar time (P < 0.05 at 30 min and P < 0.01 at 24 h). SOD increased during the first hour (P < 0.001), GR and GSH-Px both increased from 30 min to 24 h, and these increases were statistically significant (P < 0.01 and P < 0.001 at 30 min and P < 0.01 and P < 0.001 at 24 h, respectively). The AA levels increased after 1 h (P < 0.01), remaining significantly so for 24 h (P < 0.001) and MDA increased from 30 min to 24 h, all values being highly significant (P < 0.001). The body weight was significantly (P < 0.001) reduced in both cocaine groups (40 mg/kg × 30 days and 40 mg/kg × 10 days + 60 mg/kg × 20 days). The heart weight (P < 0.01) and its percentage of the body weight (P < 0.001) were significantly higher in these two groups than in the controls. Similarly, in the noradrenaline 4 mg/ kg × 30 days group, the body weight was significantly (P < 0.001) reduced and the heart weight (P < 0.01) and its percentage of body weight (P < 0.001) were significantly higher than in the controls. In comparing the cocaine and noradrenaline experiments, the frequency and extent of cardiac lesions obtained with 40 mg/kg × 10 days + 60 mg/kg × 20 days of cocaine were similar to those with 8 mg/kg of noradrenaline at 24 h. In this experimental model, cocaine administration compromised the antioxidant defence system of the heart associated with a significant increase of heart weight and the percentage of body weight.

Lysosomal glycogen storage with normal acid maltase: A familial study with successful heart transplant

Lysosomal glycogen storage in muscle with normal acid maltase activity is a rare inherited condition characterized by cardiomyopathy, mental retardation and mild myopathy in males, but generally only cardiomyopathy in females. Three cases (index case, his sister and her son) are described in a family with at least two other affected members. The index case underwent a successful heart transplant. The sister has cardiac involvement, myopathic changes and mental impairment--to our knowledge the first report of multisystem involvement in a female. We propose that skeletal muscle should be examined in young patients with hypertrophic cardiomyopathy. Furthermore, female relatives of males with the disease should be investigated for cardiomyopathy; they would be excellent candidates for life-saving heart transplant, since myopathy and mental retardation, if clinically evident, are mild.

Myocardial necrosis and cocaine. A quantitative morphologic study in 26 cocaine-associated deaths.

Abstract A quantification of different forms of acute myocardial necrosis, myocardial leukocytic infiltrates and myocardial fibrosis was accomplished in 26 chronic cocaine abusers who died of cocaine intoxication and compared to 45 normal subjects who died from head trauma and 38 who died of acquired immunodeficiency syndrome. The findings were: absence of infarct necrosis, a similar frequency and extent of coagulative myocytolysis (contraction band necrosis) and leukocytic infiltrates in cocaine abusers and normal controls, and an absence of myocardial fibrosis in cocaine abusers. These findings question both the acute and chronic cardiotoxicity of cocaine. The infarct-like pattern in some predisposed subjects may be due to an excess of catecholamine release induced by the drug resulting in coagulative myocytolysis and platelet thrombi.

Myocardial findings in fatal carbon monoxide poisoning: a human and experimental morphometric study.

Abstract The aim of this study was to define the status of the myocardium in selected human cases of acute, fatal carbon monoxide intoxication and the myocardial changes in rats exposed to carbon monoxide in relation to the type of cardiac arrest and the effects of reoxygenation following pre-fatal CO intoxication. The human study consisted of 26 cases (17 accidental and 9 suicide) of acute, fatal CO intoxication, without evidence of obstructive coronary atherosclerosis or history of ischemic heart disease which were compared with 45 cases of fatal head trauma in subjects who died instantaneously (26 cases) or within 1–12 h (19 cases). Inhalation of a lethal dose of CO in rats was compared with sub-lethal doses plus reoxygenation with and without pre-treatment by a betablocker. In all human and experimental histological sections, changes were normalised per mm2 area. In the human cases the myocardium did not show any ischemic types of changes or other lesions. Only in “three accidental” cases a few, small foci of coagulative myocytolysis were detected. In the case of spontaneous death in 31 rats following CO intoxication, no pathological myocardial changes were seen. Of the 15 “reoxygenated” rats, 2 of the 7 spontaneous deaths presented coagulative myocytolysis with 15 ± 6 foci and 381 ± 255 necrotic myocells. All the eight rats sacrificed at 3 h had coagulative myocytolysis with 5 ± 4 foci and ¶60 ± 47 myocells. Of the 24 reoxygenated rats pre-treated with a betablocker, 5 died spontaneously after a short survival and 2 of these showed 11 ± 9 foci and 21 ± 20 myocells. The 19 rats sacrificed after 3 h all presented coagulative myocytolysis with figures of 75 ± 43 and ¶356 ± 301 with 0.5 mg/kg of propranolol hydrochloride and 55 ± 45 and 253 ± 216 with 2 mg/kg, respectively.

CORONARY ARTERY ANEURYSMS IN A YOUNG ADULT : A CASE OF SUDDEN DEATH. A LATE SEQUELAE OF KAWASAKI DISEASE?

Abstract The case concerns the sudden death of a 21-year-old male during a soccer game. The autopsy revealed large, calcified saccular aneurysms at the origins of both the left anterior descending and the right coronary arteries. Histologically, the wall of the aneurysms was thin and composed of an internal fibro-calcified layer and an external thin tunica media. There was no evidence of active inflammation. The autopsy findings and a detailed medical history support the diagnosis of a late fatal sequela of Kawasaki disease.

Ultrasound imaging versus morphopathology in cardiovascular diseases. Coronary atherosclerotic plaque

This review article is aimed at comparing the results of histopathological and clinical imaging studies to assess coronary atherosclerotic plaques in humans. In particular, the gap between the two techniques and its effect on the understanding of the pathophysiological basis of coronary artery disease is critically discussed.

Ultrasound imaging versus morphopathology in cardiovascular diseases. Myocardial cell damage.

This review article summarizes the results of histopathological and clinical imaging studies to assess myocardial necrosis in humans. Different histopathological features of myocardial cell necrosis are reviewed. In addition, the present role of echocardiographic techniques in assessing irreversible myocardial damage is briefly summarized.

Ultrasound Imaging Versus Morphopathology in Cardiovascular Diseases: The Heart Failure

This review article summarizes the results of histopathological studies to assess heart failure in humans. Different histopathological features underlying the clinical manifestations of heart failure are reviewed. In addition, the present role of echocardiographic techniques in assessing the failing heart is briefly summarized.