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Is left ventricular diastolic thickening documented during dobutamine and pacing stress echocardiography related to myocardial ischemia? An animal model study.

机译:多巴酚丁胺和起搏应激超声心动图检查期间是否记录了左室舒张期增厚与心肌缺血相关?动物模型研究。

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Transient increase in diastolic wall thickness (pseudohypertrophy) during pacing stress echocardiography has been reported in normal myocardium. To evaluate the occurrence of pseudohypertrophy and to investigate the contribution of myocardial ischemia on its production during pacing and dobutamine stress echocardiography, we produced a physiologically significant coronary stenosis in 14 open chest dogs. The stenosis in the circumflex artery was measured by quantitative coronary angiography (range: 50% to 89% reduction in luminal diameter), and no resting segmental wall-motion abnormalities were observed by epicardial echocardiography (short-axis, papillary level). In each study, dobutamine (5-40 microg/kg/min) and pacing (up to 260 beats/min) were performed randomly. Positivity of stress echocardiography tests was quantitatively determined by a significant (P < 0.05) reduction or failure to increase in absolute and percent systolic wall thickening in the myocardial area supplied by the stenotic artery as compared to the left anterior descending (LAD) artery-related areas. Diastolic wall thickness and left ventricular diastolic area were compared before and after each stress test in the circumflex and LAD artery-related regions. Pseudohypertrophy was observed in 57% and 86% of dogs for pacing and dobutamine, respectively, in the circumflex region, and in 50% and 64% in the LAD region. Despite its increased incidence in the circumflex region, the augmented diastolic wall thickness did not correlate with coronary stenosis severity or stress test positivity, but correlated inversely with changes in left ventricular diastolic area. In addition, it correlated directly with changes in heart rate only for pacing. In conclusion, pseudohypertrophy was a frequent finding during pacing and dobutamine stress echocardiography tests but was not related to myocardial ischemia in this animal model.
机译:在正常心肌中,在起搏应力超声心动图检查中,舒张壁厚度(假性肥大)的短暂增加已有报道。为了评估假性肥大的发生并调查起搏和多巴酚丁胺应激超声心动图检查期间心肌缺血对其产生的贡献,我们在14只开胸犬中产生了具有生理学意义的冠状动脉狭窄。通过定量冠状动脉血管造影(范围:腔直径减小50%至89%)测量了回旋动脉狭窄,通过心外膜超声心动图(短轴,乳头水平)未观察到静止的节段性壁运动异常。在每项研究中,随机进行多巴酚丁胺(5-40微克/千克/分钟)和起搏(最高260次/分钟)。压力超声心动图测试的阳性率是通过与狭窄的左前降支(LAD)动脉相关的狭窄区域显着(P <0.05)减少或无法增加狭窄区域的绝对绝对收缩率和收缩壁增厚百分比来确定的地区。在每个压力测试前后,在回旋支和LAD动脉相关区域比较舒张壁厚度和左心室舒张面积。在回旋支区域起搏和多巴酚丁胺的起搏和多巴酚丁胺分别为57%和86%,在LAD区域为50%和64%,观察到假肥大。尽管其在回旋支区域的发病率增加,但舒张壁厚度的增加与冠状动脉狭窄程度或压力测试阳性无关,但与左心室舒张区域的变化呈反相关。此外,它仅与起搏时的心率变化直接相关。总之,假性肥大是起搏和多巴酚丁胺应力超声心动图检查期间的常见发现,但在该动物模型中与心肌缺血无关。

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