Many studies have demonstrated that reduced left ventricular (LV) diastolic distensibility plays a key role in the pathophysiology of hypertrophic cardiomyopathy (HCM). However, the relation'/> Relationship Between Exercise-Induced Myocardial Ischemia and Reduced Left Ventricular Distensibility in Patients with Nonobstructive Hypertrophic Cardiomyopathy
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Relationship Between Exercise-Induced Myocardial Ischemia and Reduced Left Ventricular Distensibility in Patients with Nonobstructive Hypertrophic Cardiomyopathy

机译:运动性心肌缺血与非阻塞性肥厚性心肌病患者左室扩张性降低之间的关系

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id="p-1">Many studies have demonstrated that reduced left ventricular (LV) diastolic distensibility plays a key role in the pathophysiology of hypertrophic cardiomyopathy (HCM). However, the relationship between myocardial ischemia and reduced LV distensibility in HCM remains unclear. We aimed to clarify the relationship between exercise-induced ischemia and reduced LV distensibility in patients with HCM. >Methods: Twenty patients with HCM and 5 age-matched control subjects underwent stress-redistribution 201Tl myocardial scintigraphy and biventricular cardiac catheterization and echocardiography at rest and during exercise. Scintigraphic defect analysis was interpreted using Bermana€?s 20-segment model. The summed stress score (SSS) was calculated as the sum of scores of the 20 LV segments and the summed difference score (SDS) was calculated as the sum of differences between each of the 20 LV segments on stress and rest images. >Results: Patients were divided into 2 groups according to the 201Tl defect as follows: 9 patients with an SSS on 201Tl of a‰¥10 and an SDS on 201Tl of a‰¥5 (ischemic group) and 11 patients with an SSS of 10 or an SDS of 5 (nonischemic group). The absolute increases from rest to peak exercise in LV end-diastolic pressure (LVEDP) and pulmonary artery wedge pressure were significantly greater (15.5 ?± 5.2 vs. 7.6 ?± 5.5 mm Hg and 17.3 ?± 5.0 vs. 8.9 ?± 5.0 mm Hg, P 0.01, respectively), and the percentage changes from rest to peak exercise in the maximum first derivative of LV pressure and LV pressure half-time were significantly smaller in the ischemic HCM group compared with the nonischemic HCM group (70% ?± 24% vs. 123% ?± 43% and a?’32% ?± 6.4% vs. a?’44% ?± 9.4%, P 0.01, respectively). However, the end-diastolic dimensions did not differ between the 2 HCM groups. One of the 9 patients in the ischemic group, as revealed by fill-in on 201Tl scintigraphy, showed increased 18F-FDG uptake in the anteroseptal wall. >Conclusion: Some HCM patients show a significant increase in LVEDP without chamber dilatation, indicating reduced LV diastolic distensibility. Myocardial ischemia may at least in part contribute to this condition.
机译:id =“ p-1”>许多研究表明,左心室(LV)舒张性舒张性降低在肥厚型心肌病(HCM)的病理生理中起关键作用。但是,尚不清楚心肌缺血与HCM左室扩张性降低之间的关系。我们旨在阐明运动诱发的缺血与HCM患者左室扩张性降低之间的关系。 >方法: 20例HCM患者和5名年龄匹配的对照受试者在休息和运动过程中进行了应力分布 201 Tl心肌闪烁显像,双心室导管和超声心动图检查。闪烁缺陷分析是使用Bermana的20段模型进行解释的。计算应力总和(SSS)作为20个LV片段的分数之和,计算差异总和(SDS)作为20个LV片段在压力和静止图像上的差异之和。 >结果:根据 201 T1缺陷将患者分为2组:9位患者在 201 Tl上的SSS≥¥ 10和 201 T1上的SDS≥5(缺血组),11例SSS <10或SDS <5(非缺血组)。从静息运动到高峰运动的绝对舒张末期压力(LVEDP)和肺动脉楔压的绝对增加幅度更大(15.5±±5.2 vs. 7.6±±5.5 mm Hg和17.3±±5.0 vs. 8.9±±5.0 mm Hg, P <0.01),并且缺血性HCM组的LV压力和LV压力半衰期的最大一阶导数从静息运动到峰值运动的百分比显着小于缺血性HCM组。非缺血性HCM组(70%±24%vs.123%±43%和a?'32%±±6.4%vs. a?'44%±±9.4%, P <0.01 , 分别)。但是,两个HCM组之间的舒张末期尺寸没有差异。在 201 T1闪烁显像仪上进行的填入显示,缺血组的9例患者中有1例显示前房壁的 18 F-FDG摄取增加。 >结论:一些HCM患者的LVEDP显着增加,而没有房室扩张,表明LV舒张扩张性降低。心肌缺血可能至少部分促成这种状况。

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