Clinical & Experimental Cardiology
Open Access

Synoptic Specifications of Myocardial Infarction and Ischemic Attack

Annie Feng^{* *}Correspondence: Annie Feng, Division of Cardiothoracic Surgery, Harvard University, Massachusetts, USA, Email:

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Description

Myocardial infarction is a common major cardiovascular event caused by ischemia with or without reperfusion, and more fundamental and translational research is needed to better understand the underlying processes and repercussions for heart structure and function. Ischemia underlies a wide range of clinical conditions, from angina to hibernation to permanent blockage, and while reperfusion is required for ischemic trauma to be salvaged, it also causes injury. We give guidelines for animal models of myocardial ischemia and infarction in this consensus statement. The purpose of this study is to present best practise information on cardiac ischemia-reperfusion and infarction models, with an increased awareness of the need for rigour and reproducibility in designing and performing scientific research to ensure that results are substantiated.

When blood vessels to the myocardium is reduced, ischemia occurs. Myocardial infarction is caused by long-term ischemia, and MI is a major cause of heart failure. Ischemic cardiomyopathy is the most prevalent cause of heart failure, and it can develop as a result of remodelling following an acute ST segment elevation myocardial infarction (STEMI), many minor nontransmural infarctions, or chronic recurrent ischemia in the absence of infarction. Ischemia can vary in severity from low flow to total coronary blockage, can last for a short or long time, can be effectively reversed by early reperfusion or not at all, and can cause harm or give cardioprotection. Similarly, there are a wide range of animal models available to study each form of ischemia occurring within this spectrum.

Ischemic cardiomyopathy

In two out of every three patients with heart failure, ischemic cardiomyopathy is the main cause of LV dysfunction. In humans, ischemic cardiomyopathy can emerge from LV remodelling following a massive myocardial infarction, but it is most typically caused by severe multivessel coronary artery disease with mild degrees of diffuse fibrosis and patchy infarction in several coronary artery distributions. Preclinical investigations have shown that when the region at risk is large, persistent coronary artery stenosis can cause considerable mycotic loss with only minor global replacement fibrosis, resulting in worldwide LV dysfunction and different degrees of congestive heart failure.

The stenosis does not restrict blood flow at rest in concept. Rather, it sets the stage for repeated episodes of subendocardial ischemia by lowering maximum perfusion in response to stress.

The myocardial at risk of repeated ischemia constitutes a considerable percentage of the LV (>70 percent of LV mass) in all animal models of ischemic cardiomyopathy. This has been accomplished in rodents with stenosis of the left major coronary artery and in big animals with multivessel coronary artery stenosis. Because of the huge region at risk, both ischemia and mycotic stretch and slippage from increased LV end-diastolic pressure cause mycotic cell death (possibly also reflecting transient ischemia).

While left main coronary stenosis is feasible in large animals, multivessel coronary stenosis can produce a significant ischemia risk region and mimic ischemic cardiomyopathy. When fixed diameter occludes are implemented on both the proximal LAD and circumflex arteries in developing farm-bred pigs, LV ejection fraction decreases with increased resting LV end-diastolic pressure, indicating compensatory LV dysfunction but no overt symptoms of heart failure. Primary myocyte loss is also seen in these animals, despite just a twofold increase in extracellular matrix buildup. In dogs, multivessel ameroid occludes have been used to create a similar situation.

Ischemic cardiomyopathy may be induced in mice by repeated short coronary occlusions, and this model is linked to significant but reversible fibrosis of the cardiac area exposed to repetitive ischemia.