Division of Cardiology, Fatebenefratelli Hospital of Benevento, Benevento, Italy.
Circulation. 2009 Dec 8;120(23):2386-92. doi: 10.1161/CIRCULATIONAHA.108.812685. Epub 2009 Nov 23.
Regression of left ventricular (LV) hypertrophy with normalization of diastolic function has been reported in patients with aortic stenosis late after aortic valve replacement (AVR). The purpose of the present study was to evaluate the effect of AVR on LV function and structure in chronic aortic regurgitation early and late after AVR.
Twenty-six patients were included in the present analysis. Eleven patients with severe aortic regurgitation were studied before, early (21 months) and late (89 months) after AVR through the use of LV biplane angiograms, high-fidelity pressure measurements, and LV endomyocardial biopsies. Fifteen healthy subjects were used as controls. LV systolic function was determined from biplane ejection fraction and midwall fractional shortening. LV diastolic function was calculated from the time constant of LV relaxation, peak filling rates, and myocardial stiffness constant. LV structure was assessed from muscle fiber diameter, interstitial fibrosis, and fibrous content. LV muscle mass decreased significantly by 38% early and 55% late after surgery. Ejection fraction was significantly reduced preoperatively and did not change after AVR (P=NS). LV relaxation was significantly prolonged before surgery (89+/-28 ms) but was normalized late after AVR (42+/-14 ms). Early and late peak filling rates were increased preoperatively but normalized postoperatively. Diastolic stiffness constant was increased before surgery (22+/-6 versus 9+/-3 in control subjects; P=0.0003) and remained elevated early and late after AVR (23+/-4; P=0.002). Muscle fiber diameter decreased significantly after AVR but remained increased at late follow-up. Interstitial fibrosis was increased preoperatively and increased even further early but decreased late after AVR. Fibrosis was positively linearly correlated to myocardial stiffness and inversely correlated to LV ejection fraction.
Patients with aortic regurgitation show normalization of macroscopic LV hypertrophy late after AVR, although fiber hypertrophy persists. These changes in LV myocardial structure late after AVR are accompanied by a change in passive elastic properties with persistent diastolic dysfunction.
主动脉瓣置换（AVR）后晚期，主动脉瓣狭窄患者左心室（LV）肥厚伴舒张功能正常化已见报道。本研究旨在评估 AVR 对慢性主动脉瓣反流早期和晚期 LV 功能和结构的影响。
本分析共纳入 26 例患者。11 例严重主动脉瓣反流患者在 AVR 前、早期（21 个月）和晚期（89 个月）通过 LV 双平面造影、高保真压力测量和 LV 心内膜心肌活检进行研究。15 例健康受试者作为对照。LV 收缩功能通过双平面射血分数和中壁节段缩短率确定。LV 舒张功能通过 LV 松弛时间常数、峰值充盈率和心肌僵硬度常数计算。LV 结构通过肌纤维直径、间质纤维化和纤维含量评估。LV 心肌质量在术后早期显著减少 38%，晚期减少 55%。术前射血分数显著降低，AVR 后无变化（P=NS）。LV 松弛在术前明显延长（89+/-28ms），但在 AVR 后晚期正常化（42+/-14ms）。术前早期和晚期峰值充盈率升高，但术后正常化。舒张僵硬度常数在术前升高（22+/-6 与对照组 9+/-3；P=0.0003），并在 AVR 后早期和晚期持续升高（23+/-4；P=0.002）。AVR 后肌纤维直径明显减小，但在晚期随访时仍升高。间质纤维化在术前增加，早期进一步增加，但 AVR 后早期减少。纤维化与心肌僵硬度呈正线性相关，与 LV 射血分数呈负线性相关。
主动脉瓣反流患者在 AVR 后晚期左心室（LV）宏观肥厚正常化，尽管纤维肥厚持续存在。AVR 后晚期 LV 心肌结构的这些变化伴随着被动弹性特性的改变，伴有持续的舒张功能障碍。
