A higher aldosterone-to-renin ratio in subclinical primary aldosteronism was not associated with increased valvular, coronary, or aortic calcification in 4573 participants.
Does a higher aldosterone-to-renin ratio increase valvular, coronary, or aortic calcification in the general population?
Subclinical primary aldosteronism (elevated aldosterone-to-renin ratio) is not associated with increased valvular, coronary, or aortic calcification in the general population.
Absolute Event Rate: 0% vs 0%
Abstract Introduction Primary aldosteronism (PA) is a state of autonomous, renin-independent aldosterone production, which elevates cardiovascular risk. Subclinical forms of PA are prevalent in the general population and increase the risk for hypertension and cardiovascular events. Data from preclinical and clinical studies showed that aldosterone is involved in atherosclerosis by contributing to vascular calcification and plaque inflammation. However, it is unknown whether subclinical forms of PA increase vascular and valvular calcification. Purpose Explore the association of PA with aortic, coronary and valvular calcification in individuals included in the Framingham Heart Study cohort. Methods We assessed participants from the Generation 3 cohort of the Framingham Heart Study, where aldosterone and renin levels were measured and cardiac computerized tomography (CT) was performed. Individuals taking angiotensin converting enzyme inhibitors, angiotensin receptor blockers or mineralocorticoid blockers were excluded. Linear regressions adjusted for relevant covariates were performed to evaluate the association of the aldosterone-to-renin ratio with mitral annulus calcium (MAC), aortic valve calcium (AVC), coronary artery calcium (CAC) and thoracic aorta calcium (TAC) scores. Results We included 4573 individuals (mean age 40.9±10.1 years; 54% female; mean body mass index BMI 26.9 kg/m2; mean systolic blood pressure 117±0.21 mmHg; mean diastolic blood pressure 75.3±9.7), of whom 1566 (34%) underwent cardiac CT. A higher aldosterone-to-renin ratio, reflecting increased aldosterone production independent of renin, was not associated with a higher MAC (b=0.20, 95% CI -0.13-0.53; p=0.22), AVC (b=-0.21, 95% CI -0.15 – 0.11; p=0.75), CAC (b=0.01, 95% CI -0.04 – 0.06; p=0.61) nor TAC (b=-0.02, 95% CI -0.07 – 0.04; p=0.56) scores. Conclusions In the general population, a biochemical phenotype of subclinical primary aldosteronism did not correlate with meaningful valvular, coronary or aortic calcification, suggesting that pathophysiological mechanisms other than mineralocorticoid receptor overaction are responsible for the calcification of these structures.
Adão et al. (Sat,) reported a other. A higher aldosterone-to-renin ratio in subclinical primary aldosteronism was not associated with increased valvular, coronary, or aortic calcification in 4573 participants.