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Optimal Control of Blood Pressure can Reverse Left Ventricular Hypertrophy in Uremic Hypertensive Hemodialysis Patients

血壓控制良好可善尿毒高血壓長期透析患者之左心室肥大

摘要


We investigated the effects of antihypertensive treatment on left ventricular hypertrophy (LVH) of long-term hemodialysis patients. In uremic patients, it is still controversial in antihypertensive effect to the regression of LVH. The left ventricular size and function of 39 uremi hypertensive long-term hemodialysis patients (27 men, 12 women, mean age 58.3) was evaluated with M-mode, 2-dimensional and Doppler echocardiography before, and 12months, after, the start of combined anti hypertensive therapy. This therapy included angiotensin II converting enzyme inhibitors, beta-blockers and calcium antagonists. Patients were classified as responders or nonresponders, depending upon whether their systolic blood pressure (SBP) decreased by more than 10 mmHG after antihypertensive treatment for 12 months. Before treatment, 36 (92%) patients had LVH and diastolic dysfunction and three (8%) had systolic dysfunction. At the end of 12 months, only 25 (64%) patients had LVH, 30 (77%) had diastolic dysfunction and 2 (5%) had systolic dysfunction. Left ventricular mass index (LVMI) also decreased from 203.63 ± 70.47 g/m2 to 178.57 ± 67.31 g/m2. LVMI correlated with systolic blood pressure (SBP) but did not correlate with diastolic blood pressure (DBP). There were 26 responders and 13non-responders. Among responders, both the SBP (153.91 ± 13.24 mmHG vs 134.43 ± 14.21mmHG, p<0.01) and DBP (90.39 ± 7.89 mmHG vs 79.98 ± 7.35mmHG, P<0.01) decreased significantly after antihypertensive therapy. Responders also exhibited progressive regression of LVH (LVMI decreased significantly from 208.52 ± 72.03 g/m2 to 168.52 ± 55.53 g/m2, p<0.05). However, LVH regression was not found in nonresponders (LVMI showed 194.84 ± 64.36 g/m2 vs 193.66 ± 77.67 g/m2). We conclude that good control of blood pressure can reverse LVH in hypertensive hemodialysis patients.

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並列摘要


We investigated the effects of antihypertensive treatment on left ventricular hypertrophy (LVH) of long-term hemodialysis patients. In uremic patients, it is still controversial in antihypertensive effect to the regression of LVH. The left ventricular size and function of 39 uremi hypertensive long-term hemodialysis patients (27 men, 12 women, mean age 58.3) was evaluated with M-mode, 2-dimensional and Doppler echocardiography before, and 12months, after, the start of combined anti hypertensive therapy. This therapy included angiotensin II converting enzyme inhibitors, beta-blockers and calcium antagonists. Patients were classified as responders or nonresponders, depending upon whether their systolic blood pressure (SBP) decreased by more than 10 mmHG after antihypertensive treatment for 12 months. Before treatment, 36 (92%) patients had LVH and diastolic dysfunction and three (8%) had systolic dysfunction. At the end of 12 months, only 25 (64%) patients had LVH, 30 (77%) had diastolic dysfunction and 2 (5%) had systolic dysfunction. Left ventricular mass index (LVMI) also decreased from 203.63 ± 70.47 g/m2 to 178.57 ± 67.31 g/m2. LVMI correlated with systolic blood pressure (SBP) but did not correlate with diastolic blood pressure (DBP). There were 26 responders and 13non-responders. Among responders, both the SBP (153.91 ± 13.24 mmHG vs 134.43 ± 14.21mmHG, p<0.01) and DBP (90.39 ± 7.89 mmHG vs 79.98 ± 7.35mmHG, P<0.01) decreased significantly after antihypertensive therapy. Responders also exhibited progressive regression of LVH (LVMI decreased significantly from 208.52 ± 72.03 g/m2 to 168.52 ± 55.53 g/m2, p<0.05). However, LVH regression was not found in nonresponders (LVMI showed 194.84 ± 64.36 g/m2 vs 193.66 ± 77.67 g/m2). We conclude that good control of blood pressure can reverse LVH in hypertensive hemodialysis patients.

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