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

Table 1 Cardiac manifestations and pathophysiological mechanisms of endocrine-related cardiomyopathies

Endocrine disorder	Pathophysiological mechanisms	Cardiac manifestations	Distinctive features
Hyperthyroidism	Increased β-adrenergic receptor expression, oxidative stress, mitochondrial dysfunction, impaired calcium handling	High-output heart failure, tachyarrhythmias, systolic dysfunction	Often reversible; leads to tachycardia-induced cardiomyopathy
Hypothyroidism	Myocardial fibrosis, impaired mitochondrial function, altered lipid metabolism, decreased β-adrenergic receptor density	Bradycardia, diastolic dysfunction, pericardial effusion	Slowed myocardial relaxation; TFT recommended in DCM
Acromegaly	IGF-1-mediated myocyte hypertrophy, interstitial fibrosis, altered calcium signaling	Concentric LV hypertrophy, diastolic dysfunction, arrhythmias	May be subclinical for years; improvement with hormonal control
Diabetes mellitus	Activation of renin–angiotensin-aldosterone system (RAAS), increased oxidative stress, lipid accumulation, myocardial inflammation, and interstitial fibrosis	LV hypertrophy, diastolic dysfunction, interstitial fibrosis	Occurs independently of ischemic heart disease; linked to poor glycemic control
Cushing’s syndrome	Cortisol-induced insulin resistance, endothelial dysfunction, RAAS overactivation, myocardial remodeling	LV hypertrophy, diastolic dysfunction, arrhythmias	Cardiovascular risk may persist despite remission
Addison’s disease	Glucocorticoid and mineralocorticoid deficiency: ↓ vascular tone, electrolyte imbalance	Hypotension, arrhythmias, reduced cardiac output	May present with shock or cardiomyopathy; improves with hormone replacement
Primary hyperaldosteronism	Aldosterone-induced myocardial remodeling, oxidative stress, collagen deposition	LV hypertrophy, myocardial fibrosis, arrhythmias	Frequently associated with resistant hypertension; regression with mineralocorticoid receptor antagonists
Primary hyperparathyroidism	Oxidative stress, endothelial dysfunction, inflammatory cytokine release, vascular and myocardial smooth muscle proliferation, hypercalcemia leading to arterial calcification and atherosclerosis	Arrhythmias, vascular calcification, LV structural remodeling	Hypercalcemia and PTH excess cause vascular calcification and myocardial hypertrophy; frequently associated with metabolic comorbidities (e.g., hypertension, obesity, diabetes)
Hypoparathyroidism	Hypocalcemia leading to impaired excitation–contraction coupling and electrophysiological instability	Dilated cardiomyopathy, prolonged QT interval	Often reversible with calcium and vitamin D replacement
Carcinoid heart	Serotonin-induced fibrosis of endocardium and valves, elevated 5-HT and cytokines	Right-sided valvular disease (tricuspid, pulmonary), heart failure	Involves only right heart; associated with neuroendocrine tumors and elevated 5-HIAA
Pheochromocytoma	Catecholamine excess, calcium overload, myofibrillolysis, contraction band necrosis	Takotsubo-like cardiomyopathy, myocarditis, arrhythmias	Acute and reversible; EMB shows characteristic catecholamine toxicity

TFT: Thyroid function tests; DCM: Dilated cardiomyopathy; LV: Left ventricle; IGF-1: Insulin-like growth factor 1; PTH: Parathyroid hormone; 5-HT: 5-Hydroxytryptamine; 5-HIAA: 5-Hydroxyindoleacetic acid; EMB: Endomyocardial biopsy.