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Biomedical subjects

G Baroldi

Publications and source records attributed to G Baroldi.

At least 55 records · Page 3Linked to original sources
PubMed1988

The usefulness of the resting electrocardiogram for characterizing acute Chagas' heart disease in the rat.

The present experiment was undertaken to characterize the resting electrocardiogram of rats in the acute stage of experimental T. cruzi infection. One-hundred-and-eighty-seven newly-weaned male albino rats were infected intraperitoneally with 1000 parasites/g body weight. Thirty-two similar but non-infected rats served as controls. Groups of eight randomly chosen rats were killed on day 8, and on days 15, 18, 22, 25 and 29 after infection. Groups of 8 control rats were killed on days 8, 15 and 22. Electrocardiographic changes were observed in 25 of 48 (52%) infected rats. P wave abnormalities indicating atrial chamber dilatation, QRS axis deviation, QRS complex changes compatible with left ventricular hypertrophy or myocardial damage, increased PR interval and ventricular repolarization alteration were detected in 24, 27, 18, 10, and 6% of infected rats, respectively. A mononuclear cell infiltrate and pseudocysts of amastigote forms of T. cruzi were found in 91, and 56% of infected animals, respectively. The sensitivity and the positive predictive value of the electrocardiographic changes were 66, 91, and 96%, respectively. Thus, the resting electrocardiogram is a reliable method for detecting myocardial lesions in the rat with acute Chagas' heart disease.

Animals↗
PubMed1988

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 Kaposi's 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.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Echocardiography detects myocardial damage in AIDS: prospective study in 102 patients.

Few data are available about cardiac involvement in AIDS. We examined 102 consecutive patients with AIDS diagnosed clinically and serologically (Walter Reed Stage 5 and 6), by means of TM and cross-sectional echocardiography with the aim of detecting cardiac abnormalities. None of the patients had overt clinical signs of heart failure. Fifty-five (54%) patients showed persistent tachycardia, diminished left ventricular (LV) wall thickness (mean 7.6 +/- 0.2 mm) and decreased percentage LV fractional shortening (27 +/- 5). In 42 (41%) there was a globular and poorly contracting LV. Thirty-nine (38%) patients had pericardial effusion which was moderate in 30 and small in nine. In four patients, valvular endocarditic vegetation was shown--on the tricuspid valve in three, on the aortic valve in one: all of them were drug addicts; in three (2.9%) patients a cardiac mass was found which proved to be a localization of Kaposi's sarcoma in two. Twenty-five (24.5%) patients died; necropsy showed cardiac chamber dilation, and thin LV walls in 18. On microscopic examination, myocardial fibrosis and lymphocyte infiltration with cell necrosis were observed. We conclude that cardiac abnormalities are common in AIDS. Impairment in LV contractility as assessed from fractional shortening appears to be the most common echocardiographic finding, followed by LV wall thinning, pericardial effusion and eventually by LV cavity dilation. This evolution is suggestive of myocardial damage and supports the hypothesis that dilated cardiomyopathy may be a cardiac complication of AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Anatomy and quantification of myocardial cell death.

Irreversible damage of the myocardial cells may show different morphologic aspects in relation to the type of dysfunction of their contraction-relaxation cycle. Attenuation of the muscle fibers with elongation of the sarcomeres and nuclei are the earliest modifications (systolic paradoxical bulging and stretching by the intraventricular pressure) when the myocells stop their function in irreversible relaxation. This 'atonic' death is pathognomonic of myocardial infarction (infarct or coagulation necrosis) and the lesion evolves with typical structural changes. An opposite and entirely different morphologic pattern is seen in the 'tetanic' death in which the myocardial cells arrest in irreversible contraction (coagulative myocytolysis or contraction band necrosis). Segmental (paradiscal bands) or pancellular hypercontraction with extreme shortening of the sarcomeres and subsequent myofibrillar rhexis alternated with irregular cross band formations (holocytic bands) are characteristic of this necrosis seen in numerous human and experimental conditions and specific of catecholamine toxicity. The third type of damage is observed in low output syndromes in which increasing edematous vacuolization and disappearance of the myofibrils (colliquative myocytolysis) are the main structural alterations. They are suggestive of progressive functional reduction leading to dilatative insufficiency ('failing' death). These clear-cut morphofunctional patterns indicate distinctive biochemical impairments and pathogenesis. In particular their frequent presence in and possible association with the different aspects of the ischemic heart disease presuppose other non-ischemic mechanisms responsible for complications and death in this modern epidemic.

Animals↗
PubMed1988

Correlation of morphological variables in the coronary atherosclerotic plaque with clinical patterns of ischemic heart disease.

The frequency and severity of "morphological" variables (fibrosis, proteoglycan accumulation, atheroma, intimal vascularization, calcification, acute intimal hemorrhage, and both adventitial and intimal lymphoplasmacellular infiltrates) in atherosclerotic plaques were related to plaque type, percentage of lumen reduction, plaque length, and intimal and medial thickness in 3,640 coronary artery sections sampled at the site of maximal lumen reduction in 8 selected segments from 100 cases of acute myocardial infarct, 50 of chronic angina, 208 of unexpected sudden coronary death with or without prodromata, and from 97 normal subjects dying accidentally. Morphological variables were occasionally observed in 1,519 sections with no lumen reduction. They were found only in sections from ischemic patients. With increasing luminal stenosis and intimal thickness, progression of the coronary plaque seemed to start as a fibrous change followed by proteoglycan accumulation in the deeper portion of the fibrous intima. Proteoglycan deposits appeared as a recurrent phenomenon. In them, atheroma or calcification develop. Intimal hemorrhage was a less frequent variable. It was found mainly in a vessel supplying an infarcted area. Lymphoplasmacellular inflammation correlated mainly with proteoglycan accumulation and atheroma, both showing a parallel increase with increasing intimal thickness and lumen reduction. No correlation was found between plaque variables and sex, age, heart weight, and infarct size. Significant variations in the distribution of plaque variables were observed among hearts of patients in the ischemic groups and between them and controls. In particular, inflammatory reaction was significantly more frequent and severe in ischemic groups than in controls, independent of the degree of coronary stenosis. Coagulative myocytolysis (contraction band necrosis), found in the majority of ischemic patients, correlated with the inflammatory reaction in supplying vessels. A peculiar tropism of mononuclear cell infiltrates for adventitial nerve structures was found. As a result, we question whether this inflammation may trigger coronary spasm and/or coagulative myocytolysis ("active" plaque vs "inactive" plaque).

Arteries↗
PubMed1986

Ischemic heart disease: clinical and pathological mismatch.

Disagreements between dynamic and postmortem morphology arise mainly from different imaging and selection of study population. The high frequency of severe and multivessel atherosclerotic stenosis in non cardiac patients and healthy subjects dying accidentally questions the direct cause-effect relationship between stenosis and ischemic heart disease; supports the view the dramatically enlarged collaterals always found in this condition may have an adequate compensatory role; and suggests the ineffectiveness of occlusion at the site of severe stenosis already bypassed by collaterals. The degree and number of severe stenoses in ischemic heart disease do not predict onset, course, complications, infarct size or death. On the other hand, the presence in this disease of three different types of morpho-functional myocardial damage indicate that different pathogenic mechanisms exist. Complications and death appear related more to metabolic disorders linked with adrenergic unbalance than to ischemia and subsequent expansion of primary infarct necrosis. Finally, postmortem findings show that lympho-plasmacellular inflammation of coronary atherosclerotic plaques is significantly more frequent (100% acute infarct, 88% chronic ischemia, 83% sudden coronary death, 64% healthy controls), severe and diffuse in all plaques in single patients compared to controls. Its preferential location around pericoronary nerves suggests the working hypothesis that it may be the cause of spasm and/or regional alterations of cardiac contractility with extravascular compression of the intramyocardial vasculature. These functional mechanisms could explain the cineangio imaging of coronary cut off rather than thrombus.

Angina Pectoris↗
PubMed1986

Medial hyperplasia obliterans of the intramural coronary arterial vessels.

Primitive structural changes of the tunica media of the intramural coronary small arterial branches have been observed in 52 per cent of 208 unexpected sudden coronary death cases and in 78 per cent of 97 normal subjects dying by accident. These changes consisted in hyperplasia and hypertrophy of the smooth muscle cells with longitudinal and oblique bundle formation, dramatic thickening of the media and fibrous replacement with lumen reduction. No aneurysms, inflammatory reaction or abnormal depositions have been observed. This process, defined as "Medial hyperplasia obliterans", showed a preferential location in the anterior papillary muscles, columnae carneae, superior interventricular septum. When present the number of "hyperplastic" vessels ranged from one to a maximum of forty-four per section. No relation was found with acute or chronic myocardial damage, heart weight, sex and age and sudden death. From the present data these medial structural changes and their aging appear to be a physiological response of the arterial wall to functional factors linked with the regional myocardial contraction. The correct recognition of this overlooked pattern seems important to avoid pathogenic misinterpretations and erroneous diagnosis of small vessel disease in case of endomyocardial biopsy.

Coronary Vessels↗
PubMed1985

Experimental catecholamine-induced myocardial necrosis. II. Temporal development of isoproterenol-induced contraction band lesions correlated with ECG, hemodynamic and biochemical changes.

Catecholamines have been shown to produce irreversible contraction band lesions of myocardial cells. However, little is known about the temporal appearance and correlation of the acute form of coagulative myocytolysis with ECG, hemodynamic and biochemical parameters. Groups of adult mongrel dogs were anesthetized with sodium pentobarbital, infused continuously with isoproterenol (2.5 micrograms/kg/min) and killed after periods of 0, 5, 15, 30, or 60 min. There were two predominant myocardial patterns: 'paradiscal' and 'holocytic' contraction band lesions. Either type of lesion was non-existent or rare in the control hearts. The small 'paradiscal' contraction band lesions were present as early as 5 min of isoproterenol infusion, particularly in the inner myocardial layer. The large 'holocytic' contraction band lesions were present by 15 min, however, they were not produced in any significant numbers before 30 min. Both types of contraction band lesions continued to accumulate up to 60 min. ST segment depression was the predominant ECG change. This occurred as early as 5 min when heart rate, blood pressure and dP/dt values had also significantly changed. The high-energy phosphates, phosphocreatine and ATP, started declining as early as 5 min. Furthermore, these phosphates and lactate were distributed in transmural gradients across the left ventricular wall with the greatest change in the endocardial third. This was also the site of the largest accumulation of each type of contraction band lesion. While the lesions correlated with certain biochemical and hemodynamic changes, the underlying pathophysiology is more complex than ischemia or high-energy phosphate depletion alone.

Adenosine Triphosphate↗
PubMed1985

Experimental catecholamine-induced myocardial necrosis. I. Morphology, quantification and regional distribution of acute contraction band lesions.

Acute histologic and ultrastructural changes, quantification and regional distribution (transmural, circumferential, transaxial) of damaged myocells from anesthetized, open-chested dogs following one hour of intravenous infusions of saline or increasing doses of isoproterenol (0.1, 1.0, 2.5 micrograms/kg/min) or norepinephrine (4.0 micrograms/kg/min) were investigated. Two predominant subsets of acute contraction band lesions were produced: 'paradiscal' involving aggregation of less than 15 sarcomeres adjacent to the intercalated disc and 'holocytic' involving coagulation of groups of adjoining sarcomeres into transverse bands interspersed with areas of myofibrillar rhexis throughout the cell. Both lesions were distributed as isolated cells or as small foci of myocells surrounded by normal myocardium. Quantification of 'paradiscal' and 'holocytic' contraction band lesions/mm2 of area was used as an index of the severity of catecholamine-induced necrosis. Numbers of 'paradiscal' myocells increased with increasing doses of isoproterenol, while 'holocytic' myocells were not present in any significant numbers until 1.0 microgram/kg/min) and increased further at 2.5 micrograms/kg/min. 'Paradiscal' myocells with both isoproterenol (2.5 micrograms/kg/min) and norepinephrine were distributed with the greatest number in the inner third of the free wall. This gradient was not significant for 'holocytic' lesions. There was, generally, no significant difference in distribution of either type of lesion around the circumference. However, transaxially there was a higher frequency of 'paradiscal' lesions at the apex with norepinephrine. The lesions were identical and present in comparable numbers at both the highest dose of isoproterenol and with norepinephrine. Thus, these two catecholamines result in a similar cardiotoxicity, each with two predominant subsets of lesions, despite their hemodynamic diversities.

Animals↗
PubMed1980

[Morphology, frequency and significance of intramural arterial lesions in sudden coronary death (author's transl)].

In 208 selected cases of sudden coronary death (SD) and in 97 normal subjects dying from accident (AD) the intramural arterial vessels have been studied. In only one instance a unique "atheromatous" embolus was found. Arterial platelet aggregates (AP) were seen in 70% of SD and 76% of AD cases. The average number of arteria vessels with AP per section was 2.2 in SD and 2.5 in AD group (the range was 1 to 15 vessels). No correlation was found with the type of blood stasis and with a longer survival time. The conclusion is that AP are a secondary, terminal, non pathogenic phenomenon. This was documented by the findings in 39 cases of thrombotic thrombocytopenic purpura. In the latter, despite severe platelet sequestration and aggregation associated to other severely ischemic or hypoxic factors (obstructive microangiopathy, anemia, hemorrhagic diathesis, convulsive neurologic disorders) no evidence of coronary heart disease was shown. Other pathologic findings were "stenosing myo-fibrous medial hyperplasia" and more rarely intimal thickening, perivascular fibrosis and subintimal nodular hyalinosis. No one of these conditions predominated in SD cases. The conclusion is that the diseases of the small coronary arteries do not play any role in the nautral history of sudden coronary death.

Coronary Disease↗