Optimal control of blood pressure can reverse left ventricular hypertrophy in uremic hypertensive hemodialysis patients.

Optimal control of blood pressure can reverse left ventricular hypertrophy in uremic hypertensive hemodialysis patients.
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最佳控制血压可以逆转尿毒症高血压血液透析患者的左心室肥厚。

DOI:
10.6452/kjms.199902.0062
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发表时间:
1999
期刊:
The Kaohsiung journal of medical sciences
影响因子:
--
通讯作者:
C. Su
C. Su
中科院分区:
--
文献类型:
--
作者:
S. Wu;S. L. Lin;C. M. Wu;F. Jeng;C. Su

文献摘要

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我们研究了降压治疗对长期血液透析患者左心室肥厚(LVH)的影响。在尿毒症患者中,是否能逆转LVH的降压效果仍存在争议。应用M型、二维及多普勒超声心动图对39例尿毒症高血压长期血液透析患者(男27例,女12例,平均年龄58.3岁)在联合降压治疗前及治疗后12个月进行了左室大小及功能的评价。该治疗包括血管紧张素II转换酶抑制剂、β受体阻滞剂和钙拮抗剂。根据降压治疗12个月后收缩压(SBP)下降是否超过10 mmHg,将患者分为应答者或无应答者。治疗前,36例(92%)患者有左室肥厚和舒张功能障碍,3例(8%)有收缩功能障碍。12个月时,仅25例(64%)患者存在LVH,30例(77%)患者存在舒张功能障碍,2例(5%)患者存在收缩功能障碍。左心室质量指数(LVMI)也从203.63 +/- 70.47 g/m2降至178.57 +/- 67.31 g/m2。LVMI与收缩压(SBP)相关,但与舒张压(DBP)无关。有26名应答者和13名无应答者。降压治疗后,有效者的收缩压(153.91 ± 13.24 mmHg vs 134.43 ± 14.21 mmHg,p < 0.01)和舒张压(90.39 ± 7.89 mmHg vs 79.98 ± 7.35 mmHg,p < 0.01)均显著下降。反应者也表现出LVH的进行性消退(LVMI从208.52 +/- 72.03 g/m2显著降低至168.52 +/- 55.53 g/m2,p < 0.05)。然而,在无应答者中未发现LVH消退(LVMI显示194.84 +/- 64.36 g/m2 vs 193.66 +/- 77.67 g/m2)。我们的结论是,良好的血压控制可以逆转高血压血液透析患者的左室肥厚。
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 uremic 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 12 months after, the start of combined antihypertensive 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 13 non-responders. Among responders, both the SBP (153.91 +/- 13.24 mmHg vs 134.43 +/- 14.21 mmHg, p < 0.01) and DBP (90.39 +/- 7.89 mmHg vs 79.98 +/- 7.35 mmHg, 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.