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Published on: September 17, 2015
Losartan reduces left ventricular hypertrophy proportionally to blood pressure reduction in hypertensives, but does
E Zakynthinos1, Ch Pierutsakos, K Konstantinidis
1Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece. ezakynth@yahoo.com
Insights
Losartan treatment reduced blood pressure and left ventricular hypertrophy (LVH) in hypertensive patients. However, LVH regression was linked to blood pressure reduction, not a direct drug effect on the heart, and diastolic function remained impaired.
Area of Science:
- Cardiology
- Pharmacology
Background:
- The impact of angiotensin II type I (AT1)-receptor blockade on left ventricular hypertrophy (LVH) is debated, with limited data on its effects on cardiac diastolic function.
- Angiotensin-converting enzyme inhibition is known for its beneficial effects, but AT1-receptor blockers' role in managing LVH requires further clarification.
Purpose of the Study:
- To investigate the effects of losartan, an AT1-receptor blocker, on left ventricular hypertrophy (LVH) and cardiac diastolic function in patients with moderate primary hypertension.
- To determine if losartan treatment leads to regression of LVH and improves diastolic function in hypertensive individuals.
Main Methods:
- Thirty-nine patients with hypertension and LVH underwent treatment with losartan (50-100 mg daily) for six months.
- Transthoracic echocardiography was performed at baseline and after treatment to assess blood pressure, LVH parameters (including left ventricular mass index), and diastolic function (using Doppler parameters).
- Patients were categorized into responders (mean blood pressure decrease > 5 mm Hg) and non-responders based on their blood pressure response to losartan.
Main Results:
- Losartan treatment significantly reduced blood pressure (BP) and left ventricular mass index (LVMI) in the study group.
- LVH regression was observed in patients who responded to losartan with a significant decrease in BP; non-responders showed no change in LVH.
- Cardiac diastolic function parameters remained abnormal after six months of losartan treatment, and left atrial size increased.
Conclusions:
- A six-month course of losartan effectively decreased blood pressure and reduced left ventricular hypertrophy in hypertensive patients.
- The regression of LVH appeared to be primarily due to the reduction in hemodynamic load rather than a direct trophic effect of losartan on the myocardium.
- Losartan treatment did not improve the abnormal cardiac diastolic function in this patient cohort.
Abstract:
In contrast to the well-recognized salutary effects of angiotensin-converting enzyme inhibition, the value of angiotensin II type I (ATl)-receptor blockade on left ventricular hypertrophy (LVH) is controversial. In addition, the data on the influence of this therapy on cardiac diastolic function are scarce. Thirty-nine patients with moderate primary hypertension, LVH, and normal systolic function received losartan, 50 to 100 mg daily. Transthoracic echocardiography was performed at baseline and after 6 months of treatment. Thirty-one patients completed and were included in the study (16 males, 61.1 +/- 1.0 years). The patients were divided into responders if mean blood pressure (BP) decreased > 5 mm Hg at the end of the study (20 patients) and non-responders (mean BP decrease < or = 5 mm Hg, 11 patients). The BP and the LVH were significantly reduced (systolic BP by 10.0%, diastolic BP 6.5%, mean BP 8.2%, left ventricular mass index [LVMI] 6.2%, interventricular septum 5.8%, posterior wall 3.0%) (p< or =0.02), attributed to the reduction of BP and LVH in responders; the LVH in non-responders did not alter with treatment. A significant correlation was noted between changes in BP and LVMI (r=0.60, p<0.001). The systolic cardiac function remained normal. The Doppler parameters usually used to assess the diastolic function of the LV (early diastolic filling velocity [E wave], late diastolic filling velocity [A wave], ratio of E/A waves, isovolumic relaxation time), which were abnormal at baseline, did not change with treatment. The size of the left atrium increased (p<0.05) at the end of the study. In conclusion, a 6-month course with losartan decreased BP and LVH. However, the LVH regression was rather associated with the reduction of the hemodynamic stimulus per se, than any trophic effect of the drug in the myocardium. The diastolic cardiac function remained abnormal with treatment.
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