de Simone G, Devereux R B, Mureddu G F, Roman M J, Ganau A, Alderman M H, Contaldo F, Laragh J H
Division of Cardiology, New York Hospital-Cornell Medical Center, NY 1002, USA.
Hypertension. 1996 Aug;28(2):276-83. doi: 10.1161/01.hyp.28.2.276.
The evaluation of the effect of obesity on left ventricular systolic performance may differ in relation to the method used to measure left ventricular function and to the type of study population. Whether obesity worsens left ventricular midwall mechanics in arterial hypertension has never been investigated. Accordingly, we assessed echocardiographic left ventricular midwall shortening-circumferential end-systolic stress relations in 156 normotensive and normal-weight (reference) adults, 94 normotensive and overweight (1985 National Institutes of Health partition values) to obese (body mass index > 30 kg/m2) adults, 263 hypertensive and normal-weight adults, and 224 hypertensive and overweight-to-obese adults. There was an inverse relation of midwall shortening to circumferential end-systolic stress in all groups (all P < .005). Left ventricular performance as a ratio of observed to predicted midwall shortening fell below the fifth percentile in 4 of 94 (4%) of overweight-to-obese normotensive individuals. Eighty-eight of 487 hypertensive subjects (18.1%) exhibited depressed midwall shortening as a percentage of the value predicted from wall stress, with no difference between normal-weight (50 of 263 [19%]) and overweight (38 of 224 [17%]) subjects. Sixty-one normotensive and 131 hypertensive subjects were frankly obese. After adjustment for sex and age, midwall shortening, as either absolute values or a percentage of predicted, was not statistically different among obese, overweight, and normal-weight subjects in both normotensive and hypertensive groups. For each quartile of observed-to-predicted midwall shortening ratio, obese subjects had greater left ventricular end-diastolic volume than normal-weight subjects among both normotensive and, more evidently, hypertensive subjects. A predicted midwall shortening was generated from both wall stress and left ventricular volume with the use of multiple regression analysis. High body mass index, mean blood pressure, aging, and male sex independently predicted low afterload and left ventricular volume-independent midwall left ventricular performance (multiple R = .31, P < .0001). Thus, (1) midwall left ventricular systolic performance in asymptomatic overweight or frankly obese individuals is comparable to that in normal-weight individuals in both the presence and absence of arterial hypertension; (2) however, maintenance of normal life ventricular performance in obese individuals is associated with the use of Starling reserve; and (3) this compensatory mechanism is especially evident when arterial hypertension and obesity coexist.
肥胖对左心室收缩功能影响的评估可能因测量左心室功能的方法以及研究人群的类型不同而有所差异。肥胖是否会使动脉高血压患者的左心室中层心肌力学恶化，此前从未有人进行过研究。因此，我们评估了156名血压正常且体重正常（作为参照）的成年人、94名血压正常且超重（采用1985年美国国立卫生研究院的划分标准）至肥胖（体重指数>30kg/m²）的成年人、263名高血压且体重正常的成年人以及224名高血压且超重至肥胖的成年人的超声心动图左心室中层心肌缩短与收缩末期圆周应力的关系。所有组中，中层心肌缩短与收缩末期圆周应力均呈负相关（所有P<.005）。在94名超重至肥胖的血压正常个体中，有4名（4%）的左心室功能（以观察到的与预测的中层心肌缩短比值表示）低于第五百分位数。487名高血压患者中有88名（18.1%）的中层心肌缩短低于根据壁应力预测值的百分比，体重正常者（263名中的50名[19%]）与超重者（224名中的38名[17%]）之间无差异。61名血压正常和131名高血压患者为明显肥胖。在对性别和年龄进行校正后，血压正常组和高血压组中，肥胖、超重和体重正常的受试者之间，中层心肌缩短的绝对值或预测值的百分比在统计学上无差异。对于观察到的与预测的中层心肌缩短比值的每个四分位数，在血压正常以及更明显的高血压受试者中，肥胖受试者的左心室舒张末期容积均大于体重正常的受试者。利用多元回归分析，根据壁应力和左心室容积生成了预测的中层心肌缩短值。高体重指数、平均血压、衰老和男性性别独立预测低后负荷和与左心室容积无关的左心室中层心肌功能（复相关系数R=.31，P<.0001）。因此，（1）无症状超重或明显肥胖个体的左心室中层心肌收缩功能在有或无动脉高血压的情况下均与体重正常个体相当；（2）然而，肥胖个体维持正常的左心室功能与利用Starling储备有关；（3）当动脉高血压和肥胖并存时，这种代偿机制尤为明显。
