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Effect of amlodipine on ventricular hypertrophy in hypertension patients: a systematic review and meta-analysis
1Department of Cardiology, China-Japan Union Hospital of Jilin University, Changchun, China; Jilin Provincial International Collaboration Research Center for Precision Medicine, Changchun, China.
Insights
Amlodipine effectively reduces left ventricular (LV) hypertrophy in hypertensive patients by lowering blood pressure. This medication significantly decreases LV mass index and posterior wall thickness, improving cardiac outcomes.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Research
Background:
- Left ventricular (LV) hypertrophy is a significant predictor of adverse cardiac events.
- Blood pressure reduction is a known strategy to mitigate LV hypertrophy.
- This study investigates amlodipine's impact on LV hypertrophy in hypertensive individuals.
Purpose of the Study:
- To evaluate the efficacy of amlodipine, a calcium channel blocker, in reducing left ventricular hypertrophy.
- To assess the effects of amlodipine on blood pressure and cardiac structural parameters in patients with hypertension.
Main Methods:
- A systematic literature review and meta-analysis were conducted on 23 studies involving 737 hypertensive patients.
- Eligibility criteria were applied for study selection.
- Meta-analyses and meta-regression analyses were performed on changes in blood pressure and LV hypertrophy indices.
Main Results:
- Amlodipine significantly reduced systolic blood pressure (SBP) by -24.9 mmHg and diastolic blood pressure (DBP) by -14.8 mmHg.
- LV mass index decreased significantly (MD: -12.9), associated with follow-up duration and baseline LV mass.
- LV posterior wall thickness was reduced, but LV end-diastolic diameter showed no significant change.
Conclusions:
- Amlodipine treatment significantly reduces LV mass index and LV posterior wall thickness in hypertensive patients.
- The observed reductions in LV hypertrophy are linked to blood pressure lowering effects of amlodipine.
- Limitations include the open-label and non-randomized nature of many included studies.
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.
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