Myocardial perfusion and contraction in acute ischemia and chronic ischemic heart disease
- 作者：John M. Canty Jr. ; canty@buffalo.edu ; Gen Suzuki
- 关键词：Myocardial contraction ; Ischemia ; Stunned myocardium ; Hibernating myocardium ; Coronary flow
- 刊名：Journal of Molecular and Cellular Cardiology
- 出版年：2012
- 期刊代码：171_00222828
- 类别：bio
- 出版时间：April, 2012
- 卷：52
- 期：4
- 页码：822-831
- 文件大小：1974 K
摘要
A large body of evidence has demonstrated that there is a close coupling between regional myocardial perfusion and contractile function. When ischemia is mild, this can result in the development of a new balance between supply and energy utilization that allows the heart to adapt for a period of hours over which myocardial viability can be maintained, a phenomenon known as 鈥渟hort-term hibernation鈥? Upon reperfusion after reversible ischemia, regional myocardial function remains depressed. The 鈥渟tunned myocardium鈥?recovers spontaneously over a period of hours to days. The situation in myocardium subjected to chronic repetitive ischemia is more complex. Chronic dysfunction can initially reflect repetitive stunning with insufficient time for the heart to recover between episodes of spontaneous ischemia. As the frequency and/or severity of ischemia increases, the heart undergoes a series of adaptations which downregulate metabolism to maintain myocyte viability at the expense of contractile function. The resulting 鈥渉ibernating myocardium鈥?develops regional myocyte cellular hypertrophy as a compensatory response to ischemia-induced apoptosis along with a series of molecular adaptations that while regional, are similar to global changes found in advanced heart failure. As a result, flow-function relations become independently affected by tissue remodeling and interventions that stimulate myocyte regeneration. Similarly, chronic vascular remodeling may alter flow regulation in a fashion that increases myocardial vulnerability to ischemia. Here we review our current understanding of myocardial flow-function relations during acute ischemia in normal myocardium and highlight newly identified complexities in their interpretation in viable chronically dysfunctional myocardium with myocyte cellular and molecular remodeling. This article is part of a Special Issue entitled 鈥淐oronary Blood Flow鈥?