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CORONARY FLOW RESERVE IN DILATED CARDIOMYOPATHY

CORONARY FLOW RESERVE IN DILATED CARDIOMYOPATHY
扩张型心肌病中的冠状动脉血流储备
批准号:
3942931
负责人:
R O CANNON
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
大多数扩张型心肌病患者, 病因不明。 许多扩张型心肌病患者 尽管血管造影正常,但主诉心绞痛型疼痛 心外膜冠状动脉 检查是否有异常 扩张型心肌病存在冠状动脉血流,26例患者 扩张型心肌病和正常的心外膜冠状动脉 动脉,其中12人有经常胸痛的历史, 测量心大静脉血流量, 静息时和起搏至心率期间的心肌代谢 在150 在麦角新碱给药后起搏期间,所有 12例有胸痛史的患者经历了典型的 痛苦 与没有胸痛的患者相比, 血流较低,冠状动脉阻力较高, 心肌氧摄取提示心肌缺血。 此外,左心室 这一组的填充压力。 无明显变化 心电图或心外膜冠状动脉管腔直径。 静脉内给予双嘧达莫0.5至0.75 mg, 20例患者证实,7例有 心绞痛也损害了透壁冠状动脉血流 储备相比,13例患者没有胸痛。 因此,在本发明中, 按病史列出的扩张型心肌病和胸痛患者 冠状血管扩张储备有限,尤其是在 血管收缩刺激 这是否有助于 扩张型心肌病的心肌损害, 一个不相关的病因学的副现象,仍然是 测定
英文摘要
In the majority of patients with dilated cardiomyopathy the etiology is unknown. Many patients with dilated cardiomyopathy complain of anginal-type pain despite angiographically normal epicardial coronary arteries. To examine whether abnormalities in coronary flow exist in dilated cardiomyopathy, 26 patients with dilated cardiomyopathy and normal epicardial coronary arteries, 12 of whom had frequent chest pain by history, underwent measurement of great cardiac vein flow and myocardial metabolism at rest and during pacing to a heart rate of 150. During pacing following administration of ergonovine, all 12 patients with a history of chest pain experienced their typical pain. Compared to patients without chest pain, their coronary flow was lower and coronary resistance higher, with increased myocardial oxygen extraction suggestive of myocardial ischemia. Additionally, there was a greater increase in left ventricular filling pressures in this group. There was no significant change in EKG or epicardial coronary luminal diameter by angiography. Administration of dipyridamole 0.5 to 0.75 mg intravenously to 20 patients demonstrated that those 7 patients with a history of angina pectoris also had impairment in transmural coronary flow reserve compared to the 13 patients without chest pain. Thus, patients with dilated cardiomyopathy and chest pain by history may have limited coronary vasodilator reserve, especially after vasoconstrictor stimulus. Whether this contributes to myocardial damage in dilated cardiomyopathy or is an epiphenomenon of an unrelated etiology, remains to be determined.
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