![]() 18– 20 Mitochondrial biogenesis is strictly regulated to maintain the mitochondrial mass and function. 16, 17 Improvement of ETC efficiency appears to reduce mortality in HF patients. 13, 14 The progression of HF has been linked to the faltering energy supply, 15 and suppression of ETC activities. Catecholamine could depress mitochondrial function and subsequent HF. Mitochondria act as the most metabolically active organelle to support the cardiac energy, 11 and to generate energy via electron transport chain (ETC) from mitochondrial respiratory complex I and II to III, which then transfers the electron to IV. 9 Thus, β-blockers have been proposed to possibly relieve substantial symptoms and prevent further adverse cardiac dysfunction by reducing myocardium energy requirement. 1 The underlying mechanism is generally believed to result from excessive NE release caused by a brain lesion with cardiomyocyte apoptosis. 9– 11 Similar to the cardiac histopathology in patients with NE-associated damage, EV-71-complicated myocarditis revealed coagulative myocytolysis, myofibrillar degeneration, and apoptosis of cardiomyocytes, which are the characteristics of catecholamine cardiotoxicity. Many studies have suggested that norepinephrine (NE), released due to infection of the vasomotor center, is able to induce apoptosis in neonatal rat cardiomyocytes and endothelial cells through a β-adrenergic receptor-reactive oxygen species-TNF-caspase signaling pathway. ![]() Despite high mortality in the acute phase, the survivors may develop long-term left ventricular dysfunction and experience poor life quality. 1 The mechanism of disease progression and the most effective therapeutic strategy remain uncertain. 7, 8 Without adequate therapy, most of these involved patients would suddenly die within 4–6 h after the clinical presentation of hypernorepinephrinemia in EV-71-complicated myocarditis. 4 Catecholamine-storm, a status of hypernorepinephrinemia resulting from excessive release of catecholamines in these circumstances may cause hypersympathetic activity including tachycardia and hypertension, consequently leading to myocardial damage, 5 acute fulminant HF, 6 and death. Of note, viral entry-induced angiotensin-converting enzyme 2 downregulation worsens HF via elevated level of angiotensin II and activation of the renin–angiotensin system, which was especially observed in those accompanied with hypercytokinemia. 1– 4 Severe acute respiratory syndrome coronavirus-2 can induce myocarditis via direct invasion of the myocardium and consequent HF. Acute fulminant heart failure (HF) is a critical complication of enterovirus 71 (EV-71) infection-related brainstem encephalitis, pheochromocytoma, and pandemic coronavirus infection disease-2019 (COVID-19).
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