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Biomedical subjects

S B Karch

Publications and source records attributed to S B Karch.

52 records · Page 3Linked to original sources

The pathology and etiology of cocaine-induced heart disease.

During the last two years, reports have appeared linking cocaine use to virtually every type of heart disease. Ischemic events have been reported regularly, and there appears to be a strong relationship between cocaine use, contraction bands, and sudden arrhythmic death. The evidence concerning cocaine-induced myocarditis, cardiomyopathy, and valvular heart disease is less clear. In this article, we review the currently known morphological changes induced by cocaine and discuss the possible mechanisms of action leading to these changes.

Adult↗

Cocaine and the heart.

There is increasing evidence that cocaine can have serious adverse effects on the heart. Angina, myocardial infarction, coronary artery spasm, arrhythmia, and sudden death have been reported in association with its use. There have been only two reports of actual myocardial pathology. In an attempt to clarify the pathophysiology of cocaine-associated cardiotoxicity and to search for pathologic changes that might be useful forensically, we reviewed random microscopic sections of hearts from 30 cases of cocaine-associated death seen by the San Francisco Medical Examiner. The age of the patients at death ranged from 25 to 74 years (mean 33.9 years). Pathologic findings included the presence of mild atherosclerotic coronary artery disease without evidence of thrombosis in three cases, associated with mild interstitial fibrosis in one case as well as mild focal myocardial fibrosis without coronary disease in four other cases. The most notable abnormality was the presence of myocardial contraction bands in 28 (93 per cent) cases. In comparison to 20 control cases of death secondary to sedative-hypnotic overdose, the hearts from the cases of cocaine-associated contained significantly more myocardial contraction bands (P less than .001; two-sided). The diffuseness of the contraction bands correlated directly with the level of cocaine found in the urine and blood at autopsy during routine screening. The presence and number of contraction bands in these cases was independent of other drugs found in the urine and blood, the number of sections of myocardium examined, and a history of attempted resuscitation. Contraction bands may act to supply the anatomic substrate for the arrhythmias associated with cocaine use. They may also provide a morphologic marker that can be sought in suspected cases of lethal cocaine overdose. Their presence may also suggest a cause of death in cases of sudden and unexpected death in which autopsy reveals no other pathology, and a drug screen is positive for cocaine.

Cocaine↗

Resuscitation-induced myocardial necrosis. Catecholamines and defibrillation.

Prolonged resuscitation in adults produces a recognizable pattern of myocardial injury characterized by contraction band necrosis, focal hemorrhage, and coagulation necrosis. To rule out the possibility of these changes being due to ischemia and underlying coronary artery disease, autopsies of 26 children admitted to Stanford from 1981 to 1983 were reviewed. Seventeen had attempted resuscitation with catecholamines and defibrillation; the remainder did not. Sections of myocardium were graded by two observers. For controls, brain-dead heart donors otherwise disease-free and essentially untreated with either defibrillation or beta-active catecholamines were used. Defibrillation alone and catecholamines alone each produced equal amounts of destruction, but using these together resulted in a statistically significant increase in tissue destruction. This suggests that the damaging effects of these agents are synergistic, not additive.

Adolescent↗

Pathology of the lung in near-drowning.

In order to study the initial pathological changes that occur in drowning, the authors developed an experimental model that closely simulates the actual changes in the nearly drowned patient. Adult male rabbits were anesthetized and intubated, and 6 ml/kg of fresh or salt water was instilled directly into the endotracheal tube. The animals were killed after 29 minutes, and the heart and lungs were then examined microscopically. The authors found that in the first 30 minutes, the brunt of the damage is borne by the vascular endothelium and not the alveolar cells.

Animals↗

Pathology of the heart in drowning.

Although ventricular fibrillation is a frequent cause of death in nearly drowned animals, the heart itself has never been studied in this condition. Working with a rabbit model, we have simulated the "near drowning" state and found that the heart undergoes some pathologic changes, including myocyte hypercontraction and hypereosinophilia. These changes may well account for the variety of arrhythmic disturbances that have been observed.

Animals↗

Cyclosporine induced myocardial fibrosis: a unique controlled case report.

Many patients treated with cyclosporine in the Stanford Heart Transplant Program have exhibited perimyocytic fibrosis in the donor heart, seen on endomyocardial biopsy specimen. Although restrictive hemodynamic effects have not been observed up to three years after transplantation, there is a possibility that such changes could become a problem. With the increasing use of cyclosporine in non-cardiac organ transplantation, it is of interest to examine the effect of this drug upon the non transplanted heart. This was possible in a man who underwent a heterotopic heart transplantation 3 1/2 years ago, and who has been followed with serial endomyocardial biopsies from both hearts. Although there were no episodes of rejection the donor heart developed significant perimyocytic fibrosis which was not seen in the native heart. This study suggests that cyclosporine induced fibrosis only occurs in the transplanted heart.

Adult↗

Morphologic effects of defibrillation: a preliminary report.

A 72-yr-old man receiving more than 300 separate DC countershocks in 2 wk exhibited morphologic heart changes, including areas of coagulation necrosis in the subepicardium and areas of frank hemorrhage. In other sites the myocytes were pathologically contracted, a finding previously demonstrated in experimental animals as a result of defibrillation but not seen in man. We suggest that these changes may occur more often than has been previously supposed and thus may be of clinical importance.

Aged↗

Infantile polyneuropathy with defective myelination: an autopsy study.

A case is reported of a boy who developed a severe polyneuropathy in early infancy and died of respiratory failure at the age of 18 months. Autopsy revealed almost total lack of myelin sheaths in the cranial, spinal and peripheral nerves. The defect involved the entire peripheral nervous system and was confined to it, central myelination being normal. It is suggested that this case is another example of the condition described by Lyon (1969) and by Kennedy et al. (1971) in which pathological observations were confined to biopsy material. In spite of some similarities between these cases and those of hypertrophic neuropathy reported by Déjerine and Sottas in 1893, they seem to form a distinct sub-group, possibly even a separate entity: infantile polyneuropathy with defective myelination.

Autopsy↗