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Corticosteroid excess is associated with adverse cardiovascular outcomes. Patients with Cushings's syndrome, either caused by endogenous or exogenous glucocorticoid excess, and patients with primary aldosteronism have increased cardiovascular risk. The increase in risk is mediated partly by traditional cardiovascular risk factors including hypertension and metabolic syndrome but also by other, less well-characterized mechanisms. Experimental and human studies have shown that target organ deterioration induced by aldosterone depends on concomitant high dietary salt intake. Key ongoing research questions that warrant further study by both clinical and experimental approaches include the following: 1) beyond inducing the metabolic syndrome, what are the mechanisms by which glucocorticoids are associated with excess cardiovascular risk, 2) what are the cellular pathways by which excessive mineralocorticoid receptor activation brings about cardiovascular and renal damage, and 3) why is salt critical in this process?

Adverse Cardiovascular Outcomes of Corticosteroid Excess