PubMed · 5405652
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G Lodi. 1969-11-03. [Functional hypercorticism in school age].. https://pubmed.ncbi.nlm.nih.gov/5405652/
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BACKGROUND: Myocardial disarray is a structural abnormality found in specific zones of the normal heart. In some conditions, such as hypertrophic cardiomyopathy (HCM), its occurrence represents a pathological process leading to myocardial asynergy. The incidence of "pathological" myocardial disarray in humans is still not known. It has been suggested that a link exists between adrenergic overactivity and myocardial disarray. The aim of the present study is to compare heart findings in conditions with and without chronic sympathetic overtone for evidence of possible linkage in humans. MATERIALS AND METHODS: A total of 340 hearts were studied. They were divided into seven groups: sudden/unexpected coronary death; sudden/unexpected death in silent Chagas' disease; brain haemorrhage following berry aneurysm rupture; transplanted hearts; congestive heart failure, AIDS and cocaine abuse. Findings in these hearts were compared with anatomic changes in 92 control hearts, where the decedent had died from head trauma, electrocution, or carbon monoxide intoxication. The frequency and presence of myocardial disarray were recorded and correlated to heart weight, extent of myocardial fibrosis, and contraction band necrosis (CBN). RESULTS: Hearts from patients with conditions that increased sympathetic tone showed an association of myocardial disarray and contraction band necrosis without any relationship to heart weight. CONCLUSIONS: Myocardial disarray was observed in cardiac areas where it is not found normally. It was associated with adrenergic myocardial stress morphologically expressed by a higher number of foci (p<0.01) and myocells (p<0.001) with CBN versus findings in normal subjects. The condition deserves further study as a possible myocardial asynergic and arrhythmogenic factor especially in sudden/unexpected death.
This article emphasizes the disorders caused by mutations and polymorphisms of the alpha form of the glucocorticoid receptor. These disorders usually present with increased circulating cortisol concentrations and must be distinguished from Cushing's syndrome, because the therapies are markedly different. The other disorders present with clinical features limited to a specific organ system. Although they illustrate important physiologic and pathophysiologic principles, they usually are not confused with Cushing's syndrome.
Hypertension is a common complication of canine hyperadrenocorticism. Increased pressor sensitivity to endogenous catecholamines is currently believed to be the main mechanism involved in the development of hypertension in human hyperadrenocorticism. The aim of this study was to evaluate pressor sensitivity to norepinephrine in dogs after induction of iatrogenic hyperadrenocorticism (I-HAC) by serial arterial blood pressure measurements during infusions of increasing dose rates of norepinephrine (0.1, 0.15, 0.2, 0.3, 0.4, 0.6, and 0.8 microg/kg/min) in eight dogs with I-HAC and eight control dogs. Systolic, diastolic, mean blood pressure and heart rate measurements were recorded. The changes in these parameters between the two groups of dogs were compared. Dogs in the I-HAC group had a more pronounced pressor response to norepinephrine infusions than control dogs since the infusions had to be stopped in seven of the dogs due to severe hypertension (>240 mmHg). The mean maximum tolerated dose rate in the control group was 0.6 microg/kg/min with a standard error of 0.0 and 0.34 microg/kg/min with a standard error of 0.08 in the I-HAC group. The study demonstrated the presence of increased pressor sensitivity to norepinephrine in dogs with I-HAC.