主动脉瓣反流时的心室与心肌功能（作者译）

[Ventricular and myocardial function in aortic regurgitation (author's transl)].

作者信息

Ferwer E, Benn M, Neuhaus K L, Spiller P

出版信息

Z Kardiol. 1979 May;68(5):351-6.

Abstract

The influence of chronic volume load on ventricular function and myocardial load and shortening was investigated in 10 patients with chronic aortic regurgitation by means of biplane ventriculography and simultaneous pressure measurements. The regurgitant fraction was 63 +/- 15 per cent. Enddiastolic volume (EDVI 227 +/- 37 ml/m2), systolic (161 +/- 18 mm Hg) and enddiastolic ventricular pressure (30 +/- 12 mm Hg) were elevated, ejection fraction was reduced (54 +/- 7 per cent). Myocardial mass related to EDV was normal (1.2 +/- 0.2 g/ml). Contractility as measured from dp/dt max (1736 +/- 492 mm Hg s-1) and dp/dtmax/PI (22.2 +/- 4.3 s-1) was slightly reduced. Mean velocity of equatorial midwall fiber shortening VMW 0.45 +/- 0.13 cir X s-1) was significantly diminished, equatorial midwall fiber stress during ejection (sigma tej 267 +/- 44.5 X 10(3) dyn X cm-2) was elevated. In spite of a very high enddiastolic stress (sigma ED 96 +/- 36 X 10(3) dyn X cm-2) mean systolic power (sigma tej X VMX 123 +/- 43.2 X 10(3) dyn X cm-2 X s-1) was normal. Compensation of chronic volume load in aortic regurgitation is not compensated by an increased contractility but by ventricular enlargement and a pronouned increase in preload. Myocardial load and shortening in chronic aortic regurgitation are altered in the same way (increased stress and reduced shortening) as in chronic pressure overload.

摘要

通过双平面心室造影和同步压力测量，对10例慢性主动脉瓣反流患者进行了慢性容量负荷对心室功能、心肌负荷及缩短情况的影响研究。反流分数为63±15%。舒张末期容积（EDVI 227±37 ml/m²）、收缩压（161±18 mmHg）和舒张末期心室压力（30±12 mmHg）升高，射血分数降低（54±7%）。与舒张末期容积相关的心肌质量正常（1.2±0.2 g/ml）。从dp/dt max（1736±492 mmHg s⁻¹）和dp/dtmax/PI（22.2±4.3 s⁻¹）测得的收缩性略有降低。赤道中壁纤维缩短的平均速度VMW（0.45±0.13 cir X s⁻¹）显著降低，射血期间赤道中壁纤维应力（σtej 267±44.5×10³ dyn X cm⁻²）升高。尽管舒张末期应力非常高（σED 96±36×10³ dyn X cm⁻²），但平均收缩功率（σtej×VMX 123±43.2×10³ dyn X cm⁻² X s⁻¹）正常。主动脉瓣反流中慢性容量负荷的代偿并非通过增加收缩性，而是通过心室扩大和明显增加前负荷来实现。慢性主动脉瓣反流时的心肌负荷和缩短情况与慢性压力超负荷时的改变方式相同（应力增加和缩短减少）。