Left Ventricular Mass Regression With Antihypertensive Therapy: Cardiac Magnetic Resonance...

Background: Left ventricular (LV) hypertrophy is an independent predictor of cardiovascular morbidity and mortality. While LV mass regression via antihypertensive therapy improves outcomes, existing meta-analyses rely predominantly on echocardiography, which is limited by acoustic windows and geometric assumptions. We aimed to pool the effect of antihypertensives on systolic and diastolic blood pressure (SBP and DBP) and subsequent LV mass index (LVMI) remodeling derived by cardiac magnetic resonance (CMR), the current reference standard. Methods: A PRISMA-compliant systematic search of PubMed, Embase, Scopus, and the Cochrane Library was performed without date restriction. Eligible studies enrolled hypertensive adults treated with ≥1 antihypertensive agent and reported baseline and follow-up LVMI by CMR. Each treatment arm was an independent unit of analysis. The primary outcome (ΔLVMI) and primary predictor (change in systolic blood pressure, ΔSBP) were assessed using a DerSimonian-Laird random-effects model with inverse-variance weighting and meta-regression. Subgroup analyses examined drug class, study design, and follow-up duration. Robustness and publication bias were also assessed. Results: Twenty-eight studies contributed 43 active treatment arms (n = 2,275) and 9 control or placebo arms (n = 404). Active treatment yielded a pooled LVMI reduction of 7.33 g/m 2 (95% CI 5.80-8.87; p < 0.0001) compared to 0.58 g/m 2 (95% CI –0.55 to 1.71) in control arms, though heterogeneity was substantial (I 2 = 86.7%). Meta-regression revealed a significant dose-response: each 10 mmHg reduction in SBP and DBP corresponded to 2.54 g/m 2 (R 2 = 0.33; p < 0.001) and 4.17 g/m 2 (R 2 = 0.28; p < 0.001) of LVMI reduction, respectively. Among drug classes, angiotensin converting enzyme inhibitors produced the greatest pooled reduction (16.1 g/m 2 ), followed by calcium channel blockers (9.3 g/m 2 ), angiotensin receptor blockers (8.2 g/m 2 ), combination regimens (6.1 g/m 2 ), and mineralocorticoid receptor antagonists (5.2 g/m 2 ). Findings remained robust across leave-one-out and imputation sensitivity analyses with no evidence of publication bias (Egger’s p=0.88). Conclusions: Antihypertensive therapy produced a clinically meaningful pooled reduction in CMR-derived LVMI, with a clear dose-response relationship. To our knowledge, this is the first pooled CMR-specific estimate of antihypertensive-induced LVMI reduction and provides a benchmark for future trials of myocardial reverse remodeling.