Soliman Elsayed Z, Ambrosius Walter T, Cushman William C, Zhang Zhu-Ming, Bates Jeffrey T, Neyra Javier A, Carson Thaddeus Y, Tamariz Leonardo, Ghazi Lama, Cho Monique E, Shapiro Brian P, He Jiang, Fine Lawrence J, Lewis Cora E
From Epidemiological Cardiology Research Center, Department of Epidemiology and Prevention, Division of Public Health Sciences (E.Z.S., Z.-M.Z.), Department of Medicine, Section on Cardiology (E.Z.S.), and Department of Biostatistical Sciences, Division of Public Health Sciences (W.T.A.), Wake Forest School of Medicine, Winston-Salem, NC; Preventive Medicine Section, Medical Service, Veterans Affairs Medical Center, Memphis, TN (W.C.C.); Michael E. DeBakey VAMC and Baylor College of Medicine, Houston, TX (J.T.B.); Division of Nephrology, Bone and Mineral Metabolism, Department of Internal Medicine, University of Kentucky, Lexington (J.A.N.); Charles and Jane Pak Center for Mineral Metabolism and Clinical Research and Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas (J.A.N.); Department of Internal Medicine, Division of General Internal Medicine, Augusta University, GA (T.Y.C.); Division of Population Health and Computational Medicine, University of Miami, and Geriatric Research Education and Clinical Center, FL (L.T.); Department of Epidemiology, Division of Public Health, University of Minnesota, Minneapolis (L.G.); Division of Nephrology and Hypertension, University of Utah, Salt Lake City (M.E.C.); Department of Cardiovascular Diseases, Mayo Clinic, Jacksonville, FL (B.P.S.); Department of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA (J.H.); Clinical Applications and Prevention Branch, Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD (L.J.F.); and Division of Preventive Medicine, Department of Medicine, University of Alabama at Birmingham (C.E.L.).
Circulation. 2017 Aug 1;136(5):440-450. doi: 10.1161/CIRCULATIONAHA.117.028441. Epub 2017 May 16.
It is currently unknown whether intensive blood pressure (BP) lowering beyond that recommended would lead to more lowering of the risk of left ventricular hypertrophy (LVH) in patients with hypertension and whether reducing the risk of LVH explains the reported cardiovascular disease (CVD) benefits of intensive BP lowering in this population.
This analysis included 8164 participants (mean age, 67.9 years; 35.3% women; 31.2% blacks) with hypertension but no diabetes mellitus from the SPRINT trial (Systolic Blood Pressure Intervention Trial): 4086 randomly assigned to intensive BP lowering (target SBP <120 mm Hg) and 4078 assigned to standard BP lowering (target SBP <140 mm Hg). Progression and regression of LVH as defined by Cornell voltage criteria derived from standard 12-lead ECGs recorded at baseline and biannually were compared between treatment arms during a median follow-up of 3.81 years. The effect of intensive (versus standard) BP lowering on the SPRINT primary CVD outcome (a composite of myocardial infarction, acute coronary syndrome, stroke, heart failure, and CVD death) was compared before and after adjustment for LVH as a time-varying covariate.
Among SPRINT participants without baseline LVH (n=7559), intensive (versus standard) BP lowering was associated with a 46% lower risk of developing LVH (hazard ratio=0.54; 95% confidence interval, 0.43-0.68). Similarly, among SPRINT participants with baseline LVH (n=605, 7.4%), those assigned to the intensive (versus standard) BP lowering were 66% more likely to regress/improve their LVH (hazard ratio=1.66; 95% confidence interval, 1.31-2.11). Adjustment for LVH as a time-varying covariate did not substantially attenuate the effect of intensive BP therapy on CVD events (hazard ratio of intensive versus standard BP lowering on CVD, 0.76 [95% confidence interval, 0.64-0.90] and 0.77 [95% confidence interval, 0.65-0.91] before and after adjustment for LVH as a time-varying covariate, respectively).
Among patients with hypertension but no diabetes mellitus, intensive BP lowering (target systolic BP <120 mm Hg) compared with standard BP lowering (target systolic BP <140 mm Hg) resulted in lower rates of developing new LVH in those without LVH and higher rates of regression of LVH in those with existing LVH. This favorable effect on LVH did not explain most of the reduction in CVD events associated with intensive BP lowering in the SPRINT trial.
URL: http://www.clinicaltrials.gov. Unique identifier: NCT01206062.
目前尚不清楚强化降压至超出推荐水平是否会进一步降低高血压患者左心室肥厚(LVH)的风险,以及降低LVH风险是否能解释强化降压在该人群中所报告的心血管疾病(CVD)获益。
本分析纳入了SPRINT试验(收缩压干预试验)中8164例患有高血压但无糖尿病的参与者(平均年龄67.9岁;35.3%为女性;31.2%为黑人):4086例被随机分配至强化降压组(目标收缩压<120 mmHg),4078例被分配至标准降压组(目标收缩压<140 mmHg)。在中位随访3.81年期间,比较了治疗组之间根据基线及每半年记录的标准12导联心电图得出的康奈尔电压标准所定义的LVH进展和逆转情况。将LVH作为时变协变量进行调整前后,比较了强化(与标准)降压对SPRINT主要CVD结局(心肌梗死、急性冠状动脉综合征、中风、心力衰竭和CVD死亡的复合结局)的影响。
在无基线LVH的SPRINT参与者中(n = 7559),强化(与标准)降压与发生LVH的风险降低46%相关(风险比=0.54;95%置信区间,0.43 - 0.68)。同样,在有基线LVH的SPRINT参与者中(n = 605,7.4%),被分配至强化(与标准)降压组的患者LVH逆转/改善的可能性高66%(风险比=1.66;95%置信区间,1.31 - 2.11)。将LVH作为时变协变量进行调整并未显著减弱强化降压治疗对CVD事件的影响(在将LVH作为时变协变量调整前后,强化与标准降压对CVD的风险比分别为0.76 [95%置信区间,0.64 - 0.90]和0.77 [95%置信区间,0.65 - 0.91])。
在患有高血压但无糖尿病的患者中,与标准降压(目标收缩压<140 mmHg)相比,强化降压(目标收缩压<120 mmHg)使无LVH者发生新发LVH的比率更低,使已有LVH者LVH逆转的比率更高。在SPRINT试验中,这种对LVH的有利影响并不能解释与强化降压相关的CVD事件减少的大部分原因。