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Left Ventricular Twist Is Augmented in Hypoxia by β1-Adrenergic–Dependent and β1-Adrenergic–Independent Factors, Without Evidence of Endocardial Dysfunction
Circulation: Cardiovascular Imaging ( IF 7.5 ) Pub Date : 2019-05-01 , DOI: 10.1161/circimaging.118.008455 Alexandra M. Williams 1, 2 , Philip N. Ainslie 1 , James D. Anholm 2 , Chris Gasho 2 , Prajan Subedi 2 , Mike Stembridge 3
Circulation: Cardiovascular Imaging ( IF 7.5 ) Pub Date : 2019-05-01 , DOI: 10.1161/circimaging.118.008455 Alexandra M. Williams 1, 2 , Philip N. Ainslie 1 , James D. Anholm 2 , Chris Gasho 2 , Prajan Subedi 2 , Mike Stembridge 3
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Background:Left ventricular (LV) twist mechanics are augmented with both acute and chronic hypoxemia. Although the underlying mechanisms remain unknown, sympathetic activation and a direct effect of hypoxemia on the myocardium have been proposed, the latter of which may produce subendocardial dysfunction that is masked by larger subepicardial torque. This study therefore sought to (1) determine the individual and combined influences of β1-AR (β1-adrenergic receptor) stimulation and peripheral O2 saturation (Spo2) on LV twist in acute and chronic hypoxia and (2) elucidate whether endocardial versus epicardial mechanics respond differently to hypoxia.Methods:Twelve males (27±4 years) were tested near sea level in acute hypoxia (Spo2=82±4%) and following 3 to 6 days at 5050 m (high altitude; Spo2=83±3%). In both settings, participants received infusions of β1-AR blocker esmolol and volume-matched saline (double-blind, randomized). LV mechanics were assessed with 2-dimensional speckle-tracking echocardiography, and region-specific analysis to compare subendocardial and subepicardial mechanics.Results:At sea level, compared with baseline (14.8±3.0°) LV twist was reduced with esmolol (11.2±3.3°; P=0.007) and augmented during hypoxia (19.6±4.9°; P<0.001), whereas esmolol+hypoxia augmented twist compared with esmolol alone (16.5±3.3°; P<0.001). At 5050 m, LV twist was increased compared with sea level (19.5±5.4°; P=0.004), and reduced with esmolol (13.0±3.8°; P<0.001) and Spo2 normalization (12.8±3.4°; P<0.001). Moreover, esmolol+normalized Spo2 lowered twist further than esmolol alone (10.5±3.1°; P=0.036). There was no mechanics-derived evidence of endocardial dysfunction with hypoxia at sea level or high altitude.Conclusions:These findings suggest LV twist is augmented in hypoxia via β1-AR–dependent and β1-AR–independent mechanisms (eg, α1-AR stimulation), but does not appear to reflect endocardial dysfunction.
中文翻译:
缺乏心律失常的证据表明,左心室扭曲在缺氧时通过β1-肾上腺素依赖性和β1-肾上腺素依赖性因子而增强。
背景:急性和慢性低氧血症都增加了左心室(LV)扭转机制。尽管尚不清楚其基本机制,但已提出了交感神经激活和低氧血症对心肌的直接作用,后者可能会产生心内膜下功能障碍,而后者会被较大的心外膜下扭矩所掩盖。因此,本研究的目的是(1)确定β的单独和组合的影响1 -AR(β 1 -肾上腺素能受体)的刺激和外围ö 2饱和(SP Ò 2)关于急性和慢性低氧时的左心室扭转,(2)阐明心内膜和心外膜力学对低氧的反应是否不同。方法:在急性低氧时,在海平面附近对十二名男性(27±4岁)进行了测试(Sp o 2 = 82±4 %),然后在5050 m(高海拔; Sp o 2 = 83±3%)下进行3至6天。在这两种设置,参与者接收β的输注1 -AR阻断艾司洛尔和体积匹配盐水(双盲,随机化)。通过二维散斑跟踪超声心动图评估LV力学,并进行区域特异性分析以比较心内膜下和心外膜力学。结果:在海平面,与基线相比(14.8±3.0°)esmolol降低了LV扭转(11.2±3.3) °; P= 0.007)并在缺氧时增强(19.6±4.9°; P <0.001),而艾司洛尔+低氧与单独的艾司洛尔相比增加了扭曲(16.5±3.3°; P <0.001)。在5050 m处,LV扭曲与海平面相比有所增加(19.5±5.4°; P = 0.004),而艾司洛尔(13.0±3.8°; P <0.001)和Sp o 2归一化(12.8±3.4°; P < 0.001 0.001)。此外,艾司洛尔+归一化的Sp o 2比单独的艾司洛尔更进一步降低了扭曲(10.5±3.1°;P = 0.036)。在海平面或高海拔地区,没有力学上的证据表明心内膜功能障碍伴有低氧。结论:这些发现表明,低氧会通过β加剧左心室扭转1 -AR依赖性和β 1 -AR无关的机制(例如,α 1 -AR刺激),但是似乎不反映心内膜功能障碍。
更新日期:2019-05-16
中文翻译:
缺乏心律失常的证据表明,左心室扭曲在缺氧时通过β1-肾上腺素依赖性和β1-肾上腺素依赖性因子而增强。
背景:急性和慢性低氧血症都增加了左心室(LV)扭转机制。尽管尚不清楚其基本机制,但已提出了交感神经激活和低氧血症对心肌的直接作用,后者可能会产生心内膜下功能障碍,而后者会被较大的心外膜下扭矩所掩盖。因此,本研究的目的是(1)确定β的单独和组合的影响1 -AR(β 1 -肾上腺素能受体)的刺激和外围ö 2饱和(SP Ò 2)关于急性和慢性低氧时的左心室扭转,(2)阐明心内膜和心外膜力学对低氧的反应是否不同。方法:在急性低氧时,在海平面附近对十二名男性(27±4岁)进行了测试(Sp o 2 = 82±4 %),然后在5050 m(高海拔; Sp o 2 = 83±3%)下进行3至6天。在这两种设置,参与者接收β的输注1 -AR阻断艾司洛尔和体积匹配盐水(双盲,随机化)。通过二维散斑跟踪超声心动图评估LV力学,并进行区域特异性分析以比较心内膜下和心外膜力学。结果:在海平面,与基线相比(14.8±3.0°)esmolol降低了LV扭转(11.2±3.3) °; P= 0.007)并在缺氧时增强(19.6±4.9°; P <0.001),而艾司洛尔+低氧与单独的艾司洛尔相比增加了扭曲(16.5±3.3°; P <0.001)。在5050 m处,LV扭曲与海平面相比有所增加(19.5±5.4°; P = 0.004),而艾司洛尔(13.0±3.8°; P <0.001)和Sp o 2归一化(12.8±3.4°; P < 0.001 0.001)。此外,艾司洛尔+归一化的Sp o 2比单独的艾司洛尔更进一步降低了扭曲(10.5±3.1°;P = 0.036)。在海平面或高海拔地区,没有力学上的证据表明心内膜功能障碍伴有低氧。结论:这些发现表明,低氧会通过β加剧左心室扭转1 -AR依赖性和β 1 -AR无关的机制(例如,α 1 -AR刺激),但是似乎不反映心内膜功能障碍。