Haczynski J et al. | ||||||||
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Effect of moxonidine on left ventricular hypertrophy in hypertensive patients Journal of Clinical and Basic Cardiology 2001; 4 (1): 61-65 PDF Summary Figures
Keywords: arterielle Hypertonie, Blutdruck, Echokardiographie, linksventrikuläre Hypertrophie, linksventrikuläre Masse, arterial hypertension, blood pressure, echocardiography, left ventricular hypertrophy, left ventricular mass The objective of the present study was to investigate the effect of moxonidine in left ventricular hypertrophic remodeling and to check the possible association between the moxonidine dose, blood pressure and the decrease in left ventricular mass assessed by transthoracic echocardiography in a nonrandomized prospective study. Twenty patients completed the study (15 males = 75 %, and 5 females, mean age 47 ± 10 years). After the titration period, 8 patients (40 %) were treated with 0.6 mg, 8 patients (40 %) with 0.4 mg and 4 patients (20 %) with 0.2 mg moxonidine daily. After the 9 month therapy period, the systolic blood pressure had decreased from 154.3 ± 10.3 to 136.2 ± 10.3 mmHg (p < 0.001), and the diastolic blood pressure from 99.3 ± 3.6 to 84.1 ± 5.0 mmHg (p < 0.001). The echocardiography showed a significant decrease in interventricular septum thickness (1.38 ± 0.1 vs 1.25 ± 0.05 mm, p < 0.05). The left ventricular posterior wall end-diastolic thickness and the left ventricular end-diastolic diameter did not change. The left ventricular mass decreased significantly during the moxonidine treatment period (309.7 ± 39 vs 264.6 ± 44.9 g, p = 0.006). There was a tendency toward an association between the dose of moxonidine and degree of left ventricular mass decrease, but the level of significance was not attained. Similarly, the decrease in systolic and diastolic blood pressure was not related to the moxonidine dose. In conclusion, we have shown that moxonidine monotherapy effectively reduces the arterial systolic and diastolic pressure and significantly decreases the left ventricular mass. J Clin Basic Cardiol 2001; 4: 61-65. |