在变力状态和心率改变期间，通过应变率和应变定义的心肌功能。

Myocardial function defined by strain rate and strain during alterations in inotropic states and heart rate.

作者信息

Weidemann Frank, Jamal Fadi, Sutherland George R, Claus Piet, Kowalski Miroslaw, Hatle Liv, De Scheerder Ivan, Bijnens Bart, Rademakers Frank E

机构信息

Department of Cardiology, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.

出版信息

Am J Physiol Heart Circ Physiol. 2002 Aug;283(2):H792-9. doi: 10.1152/ajpheart.00025.2002.

DOI:10.1152/ajpheart.00025.2002

PMID:12124229

Abstract

For porcine myocardium, ultrasonic regional deformation parameters, systolic strain (epsilon(sys)) and peak systolic strain rate (SR(sys)), were compared with stroke volume (SV) and contractility [contractility index (CI)] measured as the ratio of end-systolic strain to end-systolic wall stress. Heart rate (HR) and contractility were varied by atrial pacing (AP = 120-180 beats/min, n = 7), incremental dobutamine infusion (DI = 2.5-20 microg. kg(-1). min(-1), n = 7), or continuous esmolol infusion (0.5 mg. kg(-1). min(-1)) + subsequent pacing (120-180 beats/min) (EI group, n = 6). Baseline SR(sys) and epsilon(sys) averaged 5.0 +/- 0.4 s(-1) and 60 +/- 4%. SR(sys) and CI increased linearly with DI (20 microg. kg(-1). min(-1); SR(sys) = 9.9 +/- 0.7 s(-1), P < 0.0001) and decreased with EI (SR(sys) = 3.4 +/- 0.1 s(-1), P < 0.01). During pacing, SR(sys) and CI remained unchanged in the AP and EI groups. During DI, epsilon(sys) and SV initially increased (5 microg. kg(-1). min(-1); epsilon(sys) = 77 +/- 6%, P < 0.01) and then progressively returned to baseline. During EI, SV and epsilon(sys) decreased (epsilon(sys) = 38 +/- 2%, P < 0.001). Pacing also decreased SV and epsilon(sys) in the AP (180 beats/min; epsilon(sys) = 36 +/- 2%, P < 0.001) and EI groups (180 beats/min; epsilon(sys) = 25 +/- 3%, P < 0.001). Thus, for normal myocardium, SR(sys) reflects regional contractile function (being relatively independent of HR), whereas epsilon(sys) reflects changes in SV.

摘要

对于猪心肌，将超声区域变形参数、收缩期应变（ε(sys)）和收缩期峰值应变率（SR(sys)）与每搏输出量（SV）以及作为收缩末期应变与收缩末期壁应力之比测量的收缩性[收缩性指数（CI）]进行比较。通过心房起搏（AP = 120 - 180次/分钟，n = 7）、递增多巴酚丁胺输注（DI = 2.5 - 20μg·kg⁻¹·min⁻¹，n = 7）或持续艾司洛尔输注（0.5mg·kg⁻¹·min⁻¹）+随后的起搏（120 - 180次/分钟）（EI组，n = 6）来改变心率（HR）和收缩性。基线时SR(sys)和ε(sys)平均分别为5.0±0.4s⁻¹和60±4%。SR(sys)和CI随DI呈线性增加（20μg·kg⁻¹·min⁻¹；SR(sys)=9.9±0.7s⁻¹，P<0.0001），并随EI降低（SR(sys)=3.4±0.1s⁻¹，P<0.01）。在起搏期间，AP组和EI组的SR(sys)和CI保持不变。在DI期间，ε(sys)和SV最初增加（5μg·kg⁻¹·min⁻¹；ε(sys)=77±6%，P<0.01），然后逐渐恢复到基线。在EI期间，SV和ε(sys)降低（ε(sys)=38±2%，P<0.001）。起搏也使AP组（180次/分钟；ε(sys)=36±2%，P<0.001）和EI组（180次/分钟；ε(sys)=25±3%，P<0.001）的SV和ε(sys)降低。因此，对于正常心肌，SR(sys)反映区域收缩功能（相对独立于HR），而ε(sys)反映SV的变化。