SPC365

Impact of subclinical primary aldosteronism on valvular, coronary and aortic calcification: a population-based cohort study

Session: SESSÃO DE POSTERS 09 - OBESIDADE E HIPERTENSÃO: VELHOS CONHECIDOS, NOVAS FERRAMENTAS
Speaker: António Afonso Angélico Gonçalves

Congress: CPC 2025
Topic: J. Preventive Cardiology
Theme: 28. Risk Factors and Prevention
Subtheme: 28.2 Risk Factors and Prevention – Cardiovascular Risk Assessment
Session Type: Cartazes
FP Number: ---
Authors: António Afonso Angélico Gonçalves; Ana Rita Ferreira Leite; João Pedro Ferreira; João Sérgio Neves; Adelino Leite Moreira

<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">Introduction</span></span></strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">: Primary aldosteronism (PA) is a state of autonomous, renin-independent aldosterone production, which elevates cardiovascular risk. </span></span><br />
<span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">Subclinical forms of PA are prevalent in the general population and increase the risk for incident 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,&nbsp;it is unknown whether subclinical forms of PA increases calcification in heart valves and great vessels.</span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">Aims: </span></span></strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">Explore the association of the spectrum of PA with aortic, coronary and valvular calcification in individuals included in the Framingham Heart Study cohort.</span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">Methods</span></span></strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">: We assessed participants from the Generation 3 cohort of the Framingham Heart Study,&nbsp;in which aldosterone and renin levels were measured and&nbsp;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.</span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">Results</span></span></strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">: We included 4573 individuals (mean age 40.9&plusmn;10.1 years; 54% female; mean body mass index [BMI] 26.9 kg/m<sup>2</sup>; mean systolic blood pressure 117&plusmn;0.21 mmHg; mean diastolic blood pressure 75.3&plusmn;9.7), of whom 1566&nbsp;(34%) underwent cardiac CT. A higher aldosterone-to-renin ratio, reflecting increased aldosterone production independent of renin, was not associated with a higher MAC (</span><span style="font-family:Symbol">b</span></span><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">=0.20, 95% CI -0.13-0.53; p=0.22), AVC (</span></span><span style="font-size:11.0pt"><span style="font-family:Symbol">b</span></span><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">=-0.21, 95% CI -0.15 &ndash; 0.11; p=0.75), CAC (</span></span><span style="font-size:11.0pt"><span style="font-family:Symbol">b</span></span><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">=0.01, 95% CI -0.04 &ndash; 0.06; p=0.61) nor TAC (</span></span><span style="font-size:11.0pt"><span style="font-family:Symbol">b</span></span><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">=-0.02, 95% CI -0.07 &ndash; 0.04; p=0.56) scores.</span></span></span></span></p>

<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">Conclusions</span></span></strong><span style="font-size:11.0pt"><span style="font-family:&quot;Arial&quot;,sans-serif">: 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.</span></span></span></span></p>