Dujardin K S, Enriquez-Sarano M, Bailey K R, Seward J B, Tajik A J
Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
Am J Cardiol. 2001 Mar 1;87(5):570-6. doi: 10.1016/s0002-9149(00)01433-8.
The objective of this study was to determine the effect of oral losartan on the degree of mitral regurgitation (MR). The regurgitant volume and effective regurgitant orifice were quantified using 3 methods (flow convergence, quantitative Doppler, and quantitative 2-dimensional echocardiography) in 32 patients (26 men, mean age 67 +/- 14 years) with MR, both at baseline and 4 hours after losartan (50 mg orally). Twenty-eight patients were also reevaluated after 1 month of continued treatment with losartan (50 mg/day). With treatment, systolic blood pressure decreased from 143 +/- 16 to 130 +/- 18 mm Hg and left ventricular end-systolic wall stress from 173 +/- 46 to 156 +/- 44 g/cm2 (both p < 0.001). With treatment, regurgitant volume decreased (from 77 +/- 28 to 64 +/- 26 ml, - 18 +/- 10%; p < 0.001) in direct relation to the effective regurgitant orifice change (from 43 +/- 16 to 37 +/- 15 mm2, -17 +/- 10%; p < 0.001) but without significant change in regurgitant gradient or duration. Wide individual variability in response was observed unrelated to the magnitude of blood pressure changes. Larger reduction in regurgitant volume was observed in patients with a marked decrease in wall stress (r = 0.47, p = 0.01) and higher baseline end-diastolic volume index (r = -0.38, p = 0.03) and regurgitant volume (r = -0.45, p = 0.01). Acute improvements were sustained and unchanged at 1 month (all p > 0.15). Treatment of MR using the angiotensin receptor antagonist losartan produces a significant and sustained decrease in the degree of MR, with decreases in regurgitant volume and effective regurgitant orifice. However, the changes are of modest and variable magnitude.
本研究的目的是确定口服氯沙坦对二尖瓣反流（MR）程度的影响。在32例二尖瓣反流患者（26例男性，平均年龄67±14岁）中，于基线时及口服氯沙坦（50mg）4小时后，使用三种方法（血流会聚法、定量多普勒法和定量二维超声心动图）对反流容积和有效反流口进行定量分析。28例患者在继续服用氯沙坦（50mg/天）1个月后也进行了重新评估。治疗后，收缩压从143±16mmHg降至130±18mmHg，左心室收缩末期壁应力从173±46g/cm²降至156±44g/cm²（均p<0.001）。治疗后，反流容积减少（从77±28ml降至64±26ml，-18±10%；p<0.001），与有效反流口变化直接相关（从43±16mm²降至37±15mm²，-17±10%；p<0.001），但反流压差或持续时间无显著变化。观察到个体反应存在广泛差异，与血压变化幅度无关。壁应力显著降低的患者（r=0.47，p=0.01）、基线舒张末期容积指数较高的患者（r=-0.38，p=0.03）和反流容积较大的患者（r=-0.45，p=0.01），反流容积减少幅度更大。急性改善在1个月时得以持续且无变化（均p>0.15）。使用血管紧张素受体拮抗剂氯沙坦治疗二尖瓣反流可使二尖瓣反流程度显著且持续降低，反流容积和有效反流口减小。然而，这些变化的程度适中且存在差异。
