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Effect of carvedilol on coronary flow reserve in patients with hypertensive left-ventricular hypertrophy
Huang Xiaozhen1, Zhang Yun, Zhang Mei
1The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Shandong University Qilu Hospital, Jinan, Shandong, PR China.
Insights
Carvedilol therapy significantly improved coronary flow reserve (CFR) in patients with hypertensive left-ventricular hypertrophy (LVH). This beta-blocker reduced left-ventricular mass index and enhanced endothelial function, offering a potential treatment benefit.
Area of Science:
- Cardiology
- Pharmacology
- Hypertension Research
Background:
- Hypertensive left-ventricular hypertrophy (LVH) is associated with reduced coronary flow reserve (CFR).
- The impact of carvedilol on CFR in patients with hypertensive LVH remains unclear.
Purpose of the Study:
- To investigate the effects of carvedilol on CFR in patients diagnosed with hypertensive LVH.
- To compare carvedilol's efficacy against metoprolol in improving cardiovascular parameters.
Main Methods:
- A randomized trial involving 63 patients with hypertensive LVH, treated with either carvedilol or metoprolol for 6 months.
- Coronary flow velocity, left-ventricular mass index (LVMI), and brachial artery reactivity were assessed using echocardiography and other methods.
- Plasma levels of endothelin-1 (ET-1) and nitric oxide (NO) were monitored.
Main Results:
- Both carvedilol and metoprolol reduced blood pressure and heart rate.
- Carvedilol treatment led to a significant increase in CFR, a decrease in LVMI, and improved endothelial function compared to metoprolol.
- Carvedilol therapy also favorably altered plasma ET-1 and NO levels.
Conclusions:
- Six-month carvedilol therapy can increase CFR in patients with hypertensive LVH without coronary artery disease.
- Carvedilol demonstrates superior effects on LVMI and endothelial function compared to metoprolol in this patient group.
Objective:
Patients with hypertensive left-ventricular hypertrophy (LVH) have lower coronary flow reserve (CFR). Whether carvedilol can improve CFR of patients with hypertensive LVH is unknown. We aimed to investigate the effects of carvedilol on CFR in patients with hypertensive LVH.
Methods:
Sixty-three patients were randomly divided into two groups for treatment with carvedilol or metoprolol. The peak diastolic coronary flow velocity in the left anterior descending coronary artery at rest and at maximal vasodilation with dipyridamole infusion was recorded by transesophageal echocardiography (TEE), then CFR was calculated at baseline and at the end of 6 months of therapy. Left-ventricular mass index (LVMI) was calculated by 2-D echocardiography. Endothelium-dependent and -independent reactivity of the brachial artery was measured. Levels of plasma endothelin-1 (ET1), nitric oxide (NO) and other metabolites were monitored and analyzed before and after 6-month therapy.
Results:
Both blood pressure and heart rate decreased significantly in the two treatment groups after therapy (p<0.05). With carvedilol treatment, LVMI was lower (p<0.05), endothelium function of the brachial artery was higher (p<0.05), and peak diastolic coronary flow velocity at rest and at maximal vasodilation after dipyridamole infusion was significantly higher (p<0.05) than with metoprolol treatment, which led to a significantly higher CFR (p<0.05). Changes in CFR and LVMI with carvedilol treatment were inversely correlated (R(2)=0.474, p=0.036). With carvedilol treatment, plasma level of ET-1 was lower, but that of NO was significantly higher than with metoprolol treatment (both p<0.05).
Conclusions:
The CFR of patients with hypertensive LVH but not coronary artery disease could increase with 6-month carvedilol therapy.
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