Specific microbial infections of the myocardium and pericardium. A study of 82 patients.
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The first 100 consecutive patients to undergo right ventricular endomyocardial biopsy at the Mayo Clinic were divided retrospectively into five groups, depending on the prebiopsy clinical diagnosis, and the biopsies were review histologically in a single-blind format. Group 1 consisted of 34 patients with a diagnosis of unexplained congestive heart failure and a dilated heart; of these, 4 (12%) had active myocarditis by biopsy. Of the six patients in group 2 with a clinical diagnosis of myocarditis, only one (17%) had biopsy evidence of inflammation, but two (33%) had changes that, in the clinical setting, were suggestive of cardiomyopathy. Group 3 consisted of 27 patients with dysrhythmia, syncope, or cardiac arrest but without congestive heart failure; of these, 4 (15%) had active myocarditis by biopsy, and 8 (30%) had changes that, with the clinical history, were consistent with cardiomyopathy. Group 4 included 19 patients with unexplained congestive heart failure and a nondilated heart; 4 (21%) had cardiac amyloid on biopsy. Group 5 was a diverse group of 14 patients with possible cardiac involvement by a known systemic disease; myocardial disease was documented by biopsy in 7 (50%). On the basis of these findings, we recommend endomyocardial biopsy (1) in patients with dilated cardiomyopathy in whom myocarditis is suspected, (2) in patients with the clinical diagnosis of active myocarditis in whom tissue documentation is indicated before treatment with anti-inflammatory or immunosuppressive drugs, (3) in patients with clinically unexplained life-threatening dysrhythmias in whom myocarditis or cardiomyopathy may be present, and (4) in patients with apparent hypertrophic or restrictive cardiomyopathy in whom cardiac amyloid may be present.
Some reactions and their components at a microscopical level in myocardium are described using evidence obtained from natural and experimental cardiac conditions. Necrosis of different types, hypertrophy, mineralization, and other changes in myocytes, changes in myocarditis, and patterns involving conductive tissue are considered. A short summary of some collected values concerning the chronology of myocardial reactions is presented. The pathogenesis of myocardial reactions is complex and is influenced by diverse factors. Although certain patterns are recognizable, firm aetiological interpretation from the pattern alone is rarely justifiable.
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Cardiopulmonary bypass (CPB) may be a cause of myocardial damage in a small number of patients undergoing valve replacement (4 out of 1576 valve replacements). The responsibility of CPB can only be presumed when: the degree of myocardial dysfunction after surgery can be quantified, other causes of myocardial dysfunction are excluded. the type of valvular disease is taken into consideration. Variations in load after correction of certain lesions (mitral regurgitation) makes changes of LV systolic function difficult to interpret. The first case concerned a 23 year old patient operated for aortic regurgitation (Björk prosthesis) under local and general hypothermia and followed-up for 1 year after surgery. Ventricular extrasystoles and left bundle branch block were observed during surgery and radiological and echocardiographic LV dilatation persisted with deterioration of echographic, isotopic, haemodynamic and angiographic parameters of LV function: ejection fraction fell from 62% before surgery to 35% with diffuse hypokinesia and persistent LV dilatation (191 vs 188 ml). In the absence of prosthetic valve dysfunction, associated valve lesions or coronary artery disease, LV deterioration was attributed to CPB and inadequate myocardial protection. In two other cases (60 and 62 years) correction of aortic stenosis (Starr 1260) with coronary perfusion was followed by cardiac failure with left bundle branch block, deterioration of LV function, and death after 3 years in one case and precarious survival at 10 years in the other. In a fourth case (mixed mitral valve disease corrected by a Starr prosthesis under aortic clamping), the variation of cardiac load before and after surgery made changes in LV function difficult to interpret. (ABSTRACT TRUNCATED AT 250 WORDS)
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A 6 years old girl presented with hypereosinophilia of 7 months duration and cardiac failure from restrictive myocardiopathy, leading to death in 3 years 6 months. Transient blast cells were found. Sixteen previously reported pediatric cases of hypereosinophilia of unknown cause with cardiac involvement are studied. The meaning of eosinophilic leukemia is discussed, the frequency of cardiac damage and the role of hypereosinophilia in the mechanism of cardiac injury are emphasized. Therapy may stabilize or reverse cardiac involvement. In the cases with intractable congestive failure, surgical treatment must be recommended.
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Acute rat experiments have demonstrated that ethanol and acetaldehyde can produce cardionecrotic affect, provided they are maintained at high levels in the blood via inhalation intragastric (for ethanol) or repeated intraperitoneal (for acetaldehyde) administration. Teturam in doses producing blood acetaldehyde rise has similar effect. No alterative effects of ethanol and acetaldehyde could be demonstrated in isolated perfused hearts. The fact that this necrogenic effect is present in in-vivo experiments and absent in the isolated heart suggests that the action of ethanol and acetaldehyde may be mediated.
Eighteen observations of large-focal damage of the myocardium are analysed which macroscopically simulated myocardial infarction. Histologically the foci were represented by confluent areas of fatty and albuminous degeneration alternating with necrosis of individual cardiomyocytes. This condition is a complication of diseases having signs of intoxication, anemia, disorders of lipid metabolism and water-electrolyte balance combined with ischemic heart disease. The degree of heart function disturbance correlated with both the severity of concurrent diseases and the depth and size of cardiomyocyte damage.
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