Cardiovascular Effects of Growth Hormone: From Deficiency to Acromegaly

Growth hormone (GH) and insulin-like growth factor-1 (IGF-1) form an endocrine axis with broad cardiovascular relevance because their receptors in cardiomyocytes and vascular cells link hormonal signaling to myocardial growth and performance, vascular tone, endothelial nitric oxide biology, and cardiometabolic risk. This review synthesizes mechanistic, clinical, and epidemiologic evidence to clarify cardiovascular effects across GH/IGF-1 deficiency and excess, and to highlight implications for therapeutic decision making. Key themes include receptor-driven pathways, imaging, and functional phenotyping that distinguishes a "small-heart" pattern with microvascular and endothelial dysfunction in adult GH deficiency from concentric remodeling, diastolic impairment, arrhythmias, and a stiffness/volume-expanded hemodynamic profile in acromegaly, and evidence that timely endocrine control or replacement can yield partial reverse remodeling while residual abnormalities may persist with longer disease duration. Clinically, the review emphasizes that cardiometabolic tradeoffs differ across GH-directed therapies, so biochemical control alone may not capture risk. Major gaps include heterogeneous cohorts, confounding by comorbidities and concurrent hormone replacement, variable endpoints, and limited event-driven prospective data, motivating standardized phenotyping, hard-outcome studies, and validation of IGF-system biomarkers for risk stratification and treatment selection.