Contrasting Hemodynamic Mechanisms of Losartan- vs. Atenolol-Based Antihypertensive Treatment: A LIFE Study

被引:9
|
作者
Greve, Anders M. [1 ]
Olsen, Michael H. [2 ]
Bella, Jonathan N. [3 ]
Lonnebakken, Mai T. [4 ,5 ]
Gerdts, Eva [4 ,5 ]
Okin, Peter M. [3 ]
Palmieri, Vittorio [3 ]
Boman, Kurt [6 ]
Nieminen, Markku S. [7 ]
Omvik, Per [4 ]
Dahlof, Bjorn [8 ]
Devereux, Richard B. [3 ]
Wachtell, Kristian [1 ,3 ,9 ]
机构
[1] Rigshosp, Dept Med B, Ctr Heart, DK-2100 Copenhagen, Denmark
[2] Odense Univ Hosp, DK-5000 Odense, Denmark
[3] Weill Cornell Med Coll, New York, NY USA
[4] Univ Bergen, Bergen, Norway
[5] Haukeland Hosp, N-5021 Bergen, Norway
[6] Skelleftea Lasarett & Umea Univ, Skelleftea, Sweden
[7] Univ Helsinki, Cent Hosp, Helsinki, Finland
[8] Sahlgrens Univ Hosp, Gothenburg, Sweden
[9] Gentofte Univ Hosp, Gentofte, Denmark
关键词
blood pressure; hemodynamics; hypertension; left ventricular hypertrophy; LEFT-VENTRICULAR HYPERTROPHY; END-POINT REDUCTION; AMBULATORY BLOOD-PRESSURE; FUNCTION EVALUATION CAFE; HYPERTENSIVE PATIENTS; PULSE PRESSURE; STROKE VOLUME; HEART-RATE; INTERVENTION; REGRESSION;
D O I
10.1038/ajh.2012.81
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
BACKGROUND Pharmaceutical differences in central hemodynamics might influence cardiac response to antihypertensive treatment despite similar lowering of brachial blood pressure (BP). METHODS Data from all patients with at least two echocardiographic examinations in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) echocardiographic substudy (n = 801); high-risk patients on losartan- vs. atenolol-based antihypertensive therapy. Echocardiography was performed annually for 4 years to measure stroke index (SI), heart rate, cardiac index (CI), conduit artery stiffness assessed as pulse pressure/stroke index (PP/SI) and total peripheral resistance index (TPRI). RESULTS Atenolol- and losartan-based therapy reduced BP similarly (cumulative difference in mean brachial blood pressure 0.3 mm Hg, P = 0.65). After 4 years the cumulative means of SI and heart rate were 1.8 ml/m(2) higher and 5.7 beats/min lower on atenolol-based treatment, respectively (both P < 0.001). This kept CI below baseline in atenolol-treated patients, whereas in the losartan group CI was unchanged from baseline throughout the study. TPRI was decreased more and remained lower in the losartan group (cumulative difference in mean TPRI 287 dynes/sec(-5)/cm/m(2), P < 0.001). These findings partly explained univariate differences in systolic- and diastolic function indices between the two treatments; fully adjusted losartan was only associated with a smaller left atrial diameter (cumulative mean difference 0.07 cm; 95% confidence intervals, -0.13 to -0.01, P = 0.03). CONCLUSIONS Contrasting hemodynamics impacted cardiac response to similar reductions in brachial BP on losartan- vs. atenolol-based therapy. The similar reduction of PP/SI suggests that the antihypertensive regimens used in the LIFE study had comparable effects on arterial stiffness (LIFE study; NCT00338260)
引用
收藏
页码:1017 / 1023
页数:7
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