Effect of amlodipine on ventricular hypertrophy in hypertension patients: a systematic review and meta-analysis

Abstract

Background: Left ventricular (LV) hypertrophy predicts worse cardiac outcomes. Blood pressure lowering is associated with the reduction of LV hypertrophy. This study evaluated the effect of a calcium channel blocker, amlodipine, on LV hypertrophy in patients with hypertension. Methods: Studies were identified by conducting a literature survey in electronic databases, and study selection was carried out according to precise eligibility criteria. Meta-analyses of mean change between the follow-up and baseline values of systolic/diastolic blood pressure (SBP/DBP) and LV hypertrophy indices were performed. Meta-regression analyses were performed to examine the factors affecting changes in these indices. Results: Twenty-three studies [involving 737 patients; age 56.4 years, 95% confidence interval (CI): 53.5–59.2; females 34%, 95% CI: 25–44%; body mass index 26.4 kg/m2, 95% CI: 24.6–28.1] were included. Amlodipine treatment led to a significant reduction in SBP (−24.9 mmHg; 95% CI: −28.3 to −21.6; P<0.0001) and DBP (−14.8; 95% CI: −16.4 to −13.3; P<0.0001), without affecting the heart rate. Amlodipine treatment also significantly reduced the LV mass index. The mean difference (MD) between the follow-up and baseline LV mass index was −12.9; 95% CI: −15.4 to −10.4 (P<0.001). This decrease in LV mass index was positively associated with the follow-up duration [meta-regression coefficient (MC): 0.392; 95% CI: 0.050–0.733; P=0.026] and baseline LV mass index (MC: 0.139; 95% CI: 0.007–0.271; P=0.040). Amlodipine treatment significantly reduced the LV posterior wall thickness, which was also positively associated with the follow-up duration. There was no significant decrease in the LV end-diastolic diameter following amlodipine treatment. Discussion: Amlodipine treatment in patients with hypertension significantly reduced the LV mass index and LV posterior wall thickness, without notably affecting the LV end-diastolic diameter. Since many of the included studies were non-randomized, open-label, or lacking appropriate comparability, we therefore performed pooled analyses of the changes from baseline, and a comparative account could not be carried out.