Effect of bariatric surgery on cardiac structure and function in obese patients: Role of the renin-angiotensin system.

Echocardiographic alterations have been described in obesity, but their modifications after bariatric surgery (BS) and mechanisms are little known, mostly in normotensive patients. We aimed to analyze cardiac changes 1 year post-BS and to explore possible mechanisms. A cohort of patients with severe obesity (58% normotensives) were prospectively recruited and examined before surgery and after 12 months. Clinical and echocardiographic data, 24 h BP, renin-angiotensin-aldosterone system (RAAS) components, cytokines, and inflammatory markers were analyzed at these two time points. Overall reduction in body weight was mean (IQR) = 30.0% (25.9-33.8). There were statistically significant decreases in left ventricle mass index (LVMI) , septum thickness (ST), posterior wall thickness (PWT), relative wall thickness (RWT), and E/e', both in the whole cohort and in patients without RAAS blockers (p ≤ .04 for all). Plasma renin activity (PRA) decreased from (median, IQR) = 0.8 (0.3;1.35) to 0.4 (0.2;0.93) ng/ml/h, plasma aldosterone from 92 (58.6;126) to 68.1 (56.2;83.4) ng/dl, and angiotensin-converting enzyme (ACE)-2 activity from 7.7 (5.7;11.8) to 6.8 (5.3;11.2) RFU/µl/h, p < .05. The body weight loss correlated with a decrease in both 24 h SBP and 24 h DBP (Pearson's coefficient 0.353, p = .022 and 0.384, p = .012, respectively). Variation (Δ) of body weight correlated with ΔE/e' (Pearson's coeff. 0.414, p = .008) and with Δ lateral e' (Pearson's coeff. = -0.363, p = .018). Generalized linear models showed that ΔPRA was an independent variable for the final (12-months post-BS) LVMI (p = .028). No other changes in cardiac parameters correlated with ΔBP. In addition to the respective baseline value, final values of PWT and RWT were dependent on 12-month Δ of PRA, ACE, and ACE/ACE2 (p < .03 for all). We conclude that there are cardiac changes post-BS in patients with severe obesity, normotensives included. Structural changes appear to be related to modifications in the renin-angiotensin axis.