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Published on: January 28, 2020
The Coronary Circulation as a Target of Cardioprotection
1From the Institute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, University of Essen, Essen, Germany. gerd.heusch@uk-essen.de.
Insights
Coronary vascular injury during myocardial ischemia/reperfusion involves increased permeability and dysfunction. Animal studies show conditioning reduces this injury, but clinical translation remains challenging.
Area of Science:
- Cardiovascular Science
- Vascular Biology
- Myocardial Infarction Research
Background:
- The coronary vasculature is both a cause and a victim of myocardial ischemia/reperfusion (I/R) injury.
- I/R injury manifests as increased vascular permeability, endothelial dysfunction, microembolization, and capillary destruction.
Purpose of the Study:
- To review the manifestations of coronary vascular injury during myocardial I/R.
- To discuss the efficacy of ischemic conditioning and pharmacological interventions in mitigating I/R injury.
- To highlight the challenges in translating cardioprotective strategies to clinical practice.
Main Methods:
- Review of animal experimental data on ischemic pre- and postconditioning.
- Analysis of clinical observations regarding no-reflow phenomenon post-intervention.
- Examination of current pharmacological treatments for reperfused myocardial infarction.
Main Results:
- Ischemic conditioning in animals reduces infarct size and coronary vascular injury.
- The no-reflow phenomenon in clinical settings is associated with poor prognosis.
- Limited clinical evidence exists for drugs impacting the coronary circulation during I/R.
Conclusions:
- Coronary vascular injury is a critical component of myocardial I/R.
- While animal models show promise, clinical translation of cardioprotective interventions is difficult.
- Further research is needed to understand and improve the coronary vascular response to I/R in patients.
Abstract:
The atherosclerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/reperfusion injury. Manifestations of such injury are increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell aggregates, and finally, in its most severe form, capillary destruction with hemorrhage. In animal experiments, local and remote ischemic pre- and postconditioning not only reduce infarct size but also these manifestations of coronary vascular injury, as do drugs which recruit signal transduction steps of conditioning. Clinically, no-reflow is frequently seen after interventional reperfusion, and it carries an adverse prognosis. The translation of cardioprotective interventions to clinical practice has been difficult to date. Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardial infarction; unfortunately, for these drugs, no information on their impact on the ischemic/reperfused coronary circulation is available.
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