CORONARY BLOOD FLOW IN SUB CORONARY AORTIC STENOSIS

冠状动脉瓣下狭窄的冠状动脉血流

• 批准号: 3352302
• 负责人: BLASE A CARABELLO
• 金额: $ 7.69万
• 依托单位: MEDICAL UNIVERSITY OF SOUTH CAROLINA
• 依托单位国家: 美国
• 财政年份: 1985
• 资助国家: 美国
• 起止时间: 1985-12-01 至 1986-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3352302
• 关键词: aortic valve stenosis; heart circulation; heart contraction; heart dimension /size; intracardiac pressure; ventricular hypertrophy

Aortic stenosis in man, which produces pressure overload hypertrophy of the left ventricle, is often associated with angina pectoris. This suggests myocardial ischemia and occurs even in the presence of normal coronary arteries. An abnormality in coronary blood flow associated with hypertrophy has been proposed as a cause of such ischemia. Experimental studies of coronary blood flow in pressure overload hypertrophied ventricles have shown reduced subendocardial blood flow. These experiments, however, used supracoronary banding techniques to simulate aortic stenosis. These models produce severe pressure overload hypertrophy of the ventricle but differ from true aortic stenosis in that the coronaries are exposed to higher than normal systolic pressure. Coronary hypertension could affect coronary blood flow. Indeed, anatomic alterations of the coronary arteries in supracoronary models have been shown. The effects of such alteration on blood flow in unknown. It is possible that changes in blood flow in experimental supracoronary aortic stenosis may not reflect those seen in subcoronary aortic stenosis in patients. Contractile function may be depressed in some patients with aortic stenosis. Experimental studies of this issue in animals have yielded conflicting results. One source of conflict is that most experimental models have imposed a sudden pressure overload on the ventricle. This is not analogous to gradually occurring pressure overload ot human aortic stenosis and may damage the myocardium. Thus, interpretation of results obtained from sudden pressure overload models are difficult to evaluate. Knowledge of coronary blood flow and muscle contractile function in aortic stenosis would be advanced by study of a model in which a subcoronary stenosis produced gradual but severe pressure overload hypertrophy. This would obviate the confounding influences of coronary artery systolic hypertension seen in supracoronary models as well as possible myocardial damage created by suddenly imposed pressure overload. We propose to study coronary blood flow and ventricular muscle contractile function in a dog model of gradually applied subcoronary aortic stenosis.

人体主动脉瓣狭窄，导致主动脉压力超负荷肥大 左心室，常伴有心绞痛。 这表明 心肌缺血，甚至在存在正常冠状动脉的情况下也会发生 动脉 冠状动脉血流异常与 已经提出肥大是这种局部缺血的原因。 实验 压力超负荷性肥厚患者冠状动脉血流的研究 心室显示出减少的内膜下血流。 这些 然而，实验使用冠状动脉上带技术来模拟 主动脉瓣狭窄 这些模型产生严重的压力超负荷肥大 但不同于真正的主动脉瓣狭窄， 冠状动脉暴露于高于正常的收缩压。 冠状 高血压可影响冠状动脉血流量。 事实上，解剖学 冠状动脉模型中冠状动脉的改变已经被 示出了 这种改变对血流的影响尚不清楚。 是 实验性冠状动脉上主动脉血流量的变化 冠状动脉下主动脉瓣狭窄可能不能反映这些情况， 患者 主动脉瓣狭窄患者的收缩功能可能受到抑制， 狭窄。 在动物身上对这个问题的实验研究已经产生了 矛盾的结果。 冲突的一个来源是， 模型已经在心室上施加了突然的压力过载。 这是 不类似于人主动脉逐渐发生的压力超负荷 狭窄并可能损害心肌。 因此，结果的解释 从突然的压力过载模型获得的结果难以评估。 对冠状动脉血流量和主动脉肌收缩功能的认识 通过研究冠状动脉下 狭窄导致逐渐但严重的压力超负荷肥大。 这 将排除冠状动脉收缩压的混杂影响， 在冠状动脉上模型中观察到的高血压以及可能的心肌 突然施加的压力过载造成的损坏。 我们建议研究 犬冠状动脉血流量和心室肌收缩功能 逐渐应用的冠状动脉下主动脉瓣狭窄模型。