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Time course of reduction in left ventricular mass during long-term antihypertensive therapy
I W Franz1, R Ketelhut, U Behr
1Klinik Wehrawald der BfA, Todtmoos, Germany.
Insights
Long-term antihypertensive therapy significantly reduces left ventricular mass index (LVMI) in patients with hypertension. Maximum regression of left ventricular hypertrophy (LVH) depends on treatment duration and initial LVMI.
Area of Science:
- Cardiology
- Hypertension Management
- Cardiac Remodeling
Background:
- Left ventricular mass (LVM) reduction during hypertension treatment is inconsistent.
- Long-term effects of antihypertensive therapy on left ventricular hypertrophy (LVH) are not well-established.
Purpose of the Study:
- To prospectively investigate the long-term effects of antihypertensive therapy on echocardiographically-proven LVH.
- To assess the regression of left ventricular mass index (LVMI) over extended treatment periods.
Main Methods:
- 117 previously untreated hypertensive patients were enrolled.
- Patients received various antihypertensive drug regimens (gallopamil, metoprolol, atenolol/nifedipine, acebutol/nifedipine, atenolol/enalapril).
- Left ventricular mass index (LVMI) was measured blindly by two observers over one to five years.
Main Results:
- A significant decrease in LVMI of 24.5% after one year and 44.1% after five years was observed (P < 0.001).
- A significant correlation (r = 0.61, P < 0.001) existed between baseline LVMI and the percentage of LVMI regression.
- Almost complete regression of LVH was achieved in 82% of patients; fractional shortening increased by 16% (P < 0.001).
Conclusions:
- Achieving maximum LVH regression in hypertensive patients requires long-term antihypertensive therapy.
- The extent of regression depends on treatment duration and baseline left ventricular mass.
- Antihypertensive therapy can lead to significant cardiac remodeling, improving ventricular function.
Abstract:
Left ventricular mass sometimes decreases during treatment of hypertension but the effects are inconsistent and the response to long-term treatment is unknown. Therefore the long-term effects of antihypertensive therapy on echocardiographically-proven left ventricular hypertrophy (LVH) were prospectively investigated in 117 previously untreated hypertensive patients (mean age 46 +/- 9 years; 15 women and 102 men). Twenty-two patients received 100 mg of gallopamil daily, 24 patients received 200 mg of metoprolol, 35 patients received both 50 mg of atenolol and 20 mg of nifedipine (follow-up five years), 14 patients received 200 mg of acebutol plus 20 mg of nifedipine, and 21 patients received 50 mg of atenolol and 10 mg of enalapril daily (follow-up of four years). For the entire population, there was a significant (P < 0.001) decrease in left ventricular mass index (LVMI; measurements were performed blind by two observers) of 24.5% after one year, with a further continuous and significant (P < 0.001) reduction of 44.1% after five years of treatment. There was a significant (r = 0.61, P < 0.001) correlation between the extent of LVMI before therapy and the percentage of regression of LVMI after five years of treatment. In 82% of the patients, almost complete regression of LVH was achieved. Nevertheless, there was no significant change in ventricular end-diastolic dimension but fractional shortening increased by 16% (P < 0.001). It can be concluded that achieving maximum regression of LVH by antihypertensive therapy in previously untreated hypertensives takes a long time and depends not only on the drug regimen chosen but especially on the duration of treatment and the extent of pretreatment left ventricular mass.