Zakynthinos E, Pierutsakos Ch, Konstantinidis K, Zakynthinos S, Papadogiannis D
Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece.
Angiology. 2004 Nov-Dec;55(6):669-78. doi: 10.1177/00033197040550i608.
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.
与血管紧张素转换酶抑制已被充分认识的有益作用形成对比的是，血管紧张素II 1型（AT1）受体阻断对左心室肥厚（LVH）的价值存在争议。此外，关于这种治疗对心脏舒张功能影响的数据很少。39例中度原发性高血压、LVH且收缩功能正常的患者接受氯沙坦治疗，每日50至100毫克。在基线和治疗6个月后进行经胸超声心动图检查。31例患者完成并纳入研究（16例男性，年龄61.1±1.0岁）。如果研究结束时平均血压（BP）下降>5毫米汞柱，则将患者分为反应者（20例患者）和无反应者（平均BP下降≤5毫米汞柱，11例患者）。BP和LVH显著降低（收缩压降低10.0%，舒张压降低6.5%，平均BP降低8.2%，左心室质量指数[LVMI]降低6.2%，室间隔降低5.8%，后壁降低3.0%）（p≤0.02），这归因于反应者中BP和LVH的降低；无反应者的LVH并未随治疗而改变。BP变化与LVMI之间存在显著相关性（r = 0.60，p<0.001）。收缩期心脏功能保持正常。通常用于评估LV舒张功能的多普勒参数（舒张早期充盈速度[E波]、舒张晚期充盈速度[A波]、E/A波比值、等容舒张时间）在基线时异常，并未随治疗而改变。研究结束时左心房大小增加（p<0.05）。总之，氯沙坦6个月疗程降低了BP和LVH。然而，LVH的消退与其本身血流动力学刺激的降低有关，而非药物对心肌的任何营养作用。治疗后舒张期心脏功能仍异常。
