Chen C H, Nakayama M, Nevo E, Fetics B J, Maughan W L, Kass D A
Veterans General Hospital-Taipei and National Yang-Ming University, Republic of China.
J Am Coll Cardiol. 1998 Nov;32(5):1221-7. doi: 10.1016/s0735-1097(98)00374-x.
We tested the hypothesis that age-related arterial stiffening is matched by ventricular systolic stiffening, and that both enhance systolic pressure sensitivity to altered cardiac preload.
Arterial rigidity with age likely enhances blood pressure sensitivity to ventricular filling volume shifts. Tandem increases in ventricular systolic stiffness may also occur and could potentially enhance this sensitivity.
Invasive left ventricular pressure-volume relations were measured by conductance catheter in 57 adults aged 19 to 93 years. Patients had normal heart function and no cardiac hypertrophy and were referred for catheterization to evaluate chest pain. Twenty-eight subjects had normal coronary angiography and hemodynamics, and the remaining had either systolic hypertension or coronary artery disease without infarction. Data recorded at rest and during transient preload reduction by inferior vena caval obstruction yielded systolic and diastolic left ventricular chamber and effective arterial stiffness and pulse pressure.
Left ventricular volumes, ejection fraction and heart rate were unaltered by age, whereas vascular load and stiffening increased (p < 0.008). Arterial stiffening (Ea) was matched by increased ventricular systolic stiffness (Ees): Ees=0.91 x Ea + 0.53, (r=0.50, p < 0.0001), maintaining arterial-heart interaction (Ea/Ees ratio) age-independent. Ventricular systolic and diastolic stiffnesses correlated (r=0.51, p < 0.0001) and increased with age (p < 0.03). Both ventricular and vascular stiffening significantly increased systolic pressure sensitivity to cardiac preload (p < 0.006).
Arterial stiffening with age is matched by ventricular systolic stiffening even without hypertrophy. The two effects contribute to elevating systolic pressure sensitivity to altered chamber filling. In addition to recognized baroreflex and autonomic dysfunction with age, combined stiffening could further enhance pressure lability with diuretics and postural shifts in the elderly.
我们验证了以下假设,即与年龄相关的动脉僵硬度增加与心室收缩期僵硬度增加相匹配,且二者均增强了收缩压对心脏前负荷改变的敏感性。
随着年龄增长,动脉僵硬度增加可能会增强血压对心室充盈量变化的敏感性。心室收缩期僵硬度也可能会同步增加,并可能增强这种敏感性。
采用电导导管测量了57名年龄在19至93岁的成年人的有创左心室压力-容积关系。患者心功能正常,无心肌肥厚,因胸痛接受导管检查。28名受试者冠状动脉造影和血流动力学正常,其余受试者患有收缩期高血压或无梗死的冠状动脉疾病。在静息状态和通过下腔静脉阻塞短暂降低前负荷期间记录的数据得出左心室收缩期和舒张期腔室以及有效动脉僵硬度和脉压。
左心室容积、射血分数和心率不受年龄影响,而血管负荷和僵硬度增加(p < 0.008)。动脉僵硬度(Ea)增加与心室收缩期僵硬度(Ees)增加相匹配:Ees = 0.91×Ea + 0.53,(r = 0.50,p < 0.0001),维持动脉-心脏相互作用(Ea/Ees比值)不随年龄变化。心室收缩期和舒张期僵硬度相关(r = 0.51,p < 0.0001)且随年龄增加(p < 0.03)。心室和血管僵硬度均显著增加收缩压对心脏前负荷的敏感性(p < 0.006)。
即使没有心肌肥厚,随着年龄增长,动脉僵硬度增加也与心室收缩期僵硬度增加相匹配。这两种效应导致收缩压对腔室充盈改变的敏感性升高。除了已知的与年龄相关的压力反射和自主神经功能障碍外,联合僵硬度增加可能会进一步增强老年人使用利尿剂和体位改变时的血压波动。