Cardiomyopathies of endocrine origin: A state-of-the-art review

Endocrine disorders are increasingly recognized as potentially reversible causes of secondary cardiomyopathies, yet they often remain underdiagnosed in clinical practice. These conditions-including thyroid dysfunction, acromegaly, pheoch-romocytoma, diabetes mellitus, adrenal disorders, among others-can significantly alter cardiac structure and function through hormonal excess, metabolic remodeling, and neurohumoral activation. Hyperthyroidism may lead to high-output heart failure (HF) and atrial fibrillation, while hypothyroidism is associated with diastolic dysfunction, pericardial effusion, and accelerated atherosclerosis. Acromegaly promotes biventricular hypertrophy and myocardial fibrosis via insulin-like growth factor 1 overproduction. Pheochromocytoma triggers catecholamine-induced cardiomyopathy, resembling Takotsubo syndrome and carrying a high risk of mortality if left untreated. Diabetes induces a distinct phenotype of cardiomyopathy, affecting both systolic and diastolic function through microvascular injury and oxidative stress. Recognizing these endocrine etiologies is crucial, as targeted hormonal therapies-such as antithyroid agents, somatostatin analogs, or adrenalectomy-can reverse or significantly mitigate cardiac dysfunction. Comprehensive endocrine screening in patients with unexplained cardiomyopathy is therefore essential. This review synthesizes current knowledge on the pathophysiological mechanisms, clinical manifestations, and therapeutic strategies for endocrine cardiomyopathies and proposes a diagnostic algorithm for early recognition. Emerging biomarkers, such as galectin-3 in diabetic heart disease, may further enhance diagnostic accuracy and risk stratification. The interplay between endocrine and cardiovascular systems offers a unique opportunity for early intervention, potentially preventing progression to irreversible HF.