Institute of Medicine, University of Bergen, 5021 Bergen, Norway.
Hypertension. 2012 Jul;60(1):90-7. doi: 10.1161/HYPERTENSIONAHA.112.194878. Epub 2012 May 29.
The impact of hypertension on left ventricular structure and outcome during progression of aortic valve stenosis has not been reported from a large prospective study. Data from 1616 patients with asymptomatic aortic stenosis randomized to placebo-controlled treatment with combined simvastatin and ezetimibe in the Simvastatin Ezetimibe in Aortic Stenosis Study were used. The primary study end point included combined cardiovascular death, aortic valve events, and ischemic cardiovascular events. Hypertension was defined as history of hypertension or elevated baseline blood pressure. Left ventricular hypertrophy was defined as left ventricular mass/height(2.7) ≥ 46.7 g/m(2.7) in women and ≥ 49.2 g/m(2.7) in men and concentric geometry as relative wall thickness ≥ 0.43. Baseline peak aortic jet velocity and aortic stenosis progression rate did not differ between hypertensive (n = 1340) and normotensive (n = 276) patients. During 4.3 years of follow-up, the prevalence of concentric left ventricular hypertrophy increased 3 times in both groups. Hypertension predicted 51% higher incidence of abnormal LV geometry at final study visit independent of other confounders (P<0.01). In time-varying Cox regression, hypertension did not predict increased rate of the primary study end point. However, hypertension was associated with a 56% higher rate of ischemic cardiovascular events and a 2-fold increased mortality (both P<0.01), independent of aortic stenosis severity, abnormal left ventricular geometry, in-treatment systolic blood pressure, and randomized study treatment. No impact on aortic valve replacement was found. In conclusion, among patients with initial asymptomatic mild-to-moderate aortic stenosis, hypertension was associated with more abnormal left ventricular structure and increased cardiovascular morbidity and mortality.
高血压对主动脉瓣狭窄进展过程中左心室结构和结局的影响尚未在大型前瞻性研究中报道。这项研究的数据来自于 1616 例无症状主动脉瓣狭窄患者,他们被随机分配至接受辛伐他汀和依折麦布联合治疗的安慰剂对照组,该研究为 Simvastatin Ezetimibe in Aortic Stenosis Study。主要研究终点包括心血管死亡、主动脉瓣事件和缺血性心血管事件的联合发生。高血压定义为既往高血压病史或基线血压升高。左心室肥厚定义为左心室质量/身高的 2.7 次方≥46.7g/m2.7(女性)和≥49.2g/m2.7(男性),且同心几何结构定义为相对室壁厚度≥0.43。基线时的峰值主动脉瓣射流速度和主动脉瓣狭窄进展率在高血压(n=1340)和正常血压(n=276)患者之间没有差异。在 4.3 年的随访期间,两组患者的同心性左心室肥厚患病率均增加了 3 倍。高血压独立于其他混杂因素预测最终研究访视时异常 LV 几何结构的发生率增加 51%(P<0.01)。在时变 Cox 回归中,高血压并未预测主要研究终点的发生率增加。然而,高血压与缺血性心血管事件发生率增加 56%以及死亡率增加 2 倍(均 P<0.01)相关,与主动脉瓣狭窄严重程度、异常左心室几何结构、治疗中的收缩压和随机研究治疗无关。未发现对主动脉瓣置换有影响。总之,在最初患有无症状轻度至中度主动脉瓣狭窄的患者中,高血压与更多的异常左心室结构以及更高的心血管发病率和死亡率相关。