Villari B, Vassalli G, Betocchi S, Briguori C, Chiariello M, Hess O M
Department of Internal Medicine, Cardiology, University Hospital, Zurich, Switzerland.
Am J Cardiol. 1996 Jul 1;78(1):66-71. doi: 10.1016/s0002-9149(96)00229-9.
The aim of the present study was to evaluate nonuniformity in pressure overload hypertrophy due to aortic stenosis. Twenty patients were included in the present analysis. Ten patients with severe aortic stenosis were studied preoperatively as well as early (21 +/- 8 months) and (89 +/- 21 months) after aortic valve replacement (AVR) using left ventricular biplane angiograms, high-fidelity pressure measurements and endomyocardial biopsies. Ten normal subjects served as controls. LV systolic function was assessed from biplane ejection fraction, and diastolic function from the time constant of relaxation, the peak filling rate and the constant of myocardial stiffness. Nonuniformity was evaluated from the coefficient of variation of the time to end-systole (systolic asynchrony) and peak filling rate (diastolic asynchrony) of 12 regions in right anterior oblique and left anterior oblique projection. Ejection fraction was comparable in patients with aortic stenosis and in controls, whereas preoperatively diastolic dysfunction with prolonged relaxation and increased stiffness was present in patients with aortic stenosis and was normalized late after AVR. LV systolic asynchrony was present (>25D of controls) in 7 and diastolic asynchrony in 10 of 10 patients with aortic stenosis. Early as well as late after AVR systolic asynchrony was normalized in 9 of 10 patients. Diastolic asynchrony was present early AVR in all but one patient, although there was a significant improvement with respect to the preoperative evaluation. Late after AVR there was a normalization of diastolic asynchrony in 9 of 10 patients with aortic stenosis. Thus, it is concluded that systolic asynchrony is normalized early after AVR probably due to its load-sensitivity, whereas diastolic asynchrony persists probably due to residual LV hypertrophy with increased interstitial fibrosis and myocardial stiffness. Late after AVR, diastolic asynchrony is normalized due to structural remodeling with regression of both myocardial hypertrophy and interstitial fibrosis.
本研究的目的是评估主动脉瓣狭窄所致压力超负荷性肥厚中的不均一性。本分析纳入了20例患者。对10例重度主动脉瓣狭窄患者在术前以及主动脉瓣置换术（AVR）后早期（21±8个月）和晚期（89±21个月）进行研究，采用左心室双平面血管造影、高保真压力测量和心内膜心肌活检。10名正常受试者作为对照。通过双平面射血分数评估左心室收缩功能，通过舒张时间常数、峰值充盈率和心肌僵硬度常数评估舒张功能。从右前斜位和左前斜位投影的12个区域的收缩末期时间（收缩不同步）和峰值充盈率（舒张不同步）的变异系数评估不均一性。主动脉瓣狭窄患者和对照组的射血分数相当，而主动脉瓣狭窄患者术前存在舒张功能障碍，表现为舒张时间延长和僵硬度增加，AVR术后晚期恢复正常。10例主动脉瓣狭窄患者中，7例存在左心室收缩不同步（>对照组25%），10例中有10例存在舒张不同步。AVR术后早期和晚期，10例患者中有9例收缩不同步恢复正常。除1例患者外，AVR术后早期所有患者均存在舒张不同步，尽管与术前评估相比有显著改善。AVR术后晚期，10例主动脉瓣狭窄患者中有9例舒张不同步恢复正常。因此，得出结论：AVR术后早期收缩不同步可能因其对负荷敏感而恢复正常，而舒张不同步可能持续存在，原因是左心室残余肥厚伴间质纤维化和心肌僵硬度增加。AVR术后晚期，由于心肌肥厚和间质纤维化消退的结构重塑，舒张不同步恢复正常。
