Myocardium at risk: Reasons and methods for measuring the extent

Abstract

See related article, pp. 99-110 MYOCARDIUM AT RISKIf a coronary artery is acutely occluded, the downstream myocardium becomes severely under-perfused and at risk of necrosis. The area of myocardium at jeopardy of infarction is usually referred to as area at risk. It is intuitive that the extent of myocardium at risk downstream from an occluded coronary artery does not have the dimension of an area, but rather that of a volume or a mass. Indeed, the extent of myocardium at risk is usually expressed in grams or in percentage of ventricular myocardium. However, because the initial experiments were carried out by injecting dyes or radionuclide-labeled microspheres upstream from the occluded coronary artery, and because the myocardium at risk was defined postmortem as the non-stained or non-labeled area in cross-sectional slices of the heart, the term area at risk has become common and hence entered the medical dictionary. 1,2 If a flow tracer is injected into a coronary artery proximal to its occlusion, and a second flow tracer is injected after the occlusion upstream the occluded artery, it becomes evident that the extent of myocardium perfused by a given open artery is larger than the myocardium at risk when the same vessel is occluded ( Figure 1A, B). This difference is on average 20% in the canine heart, and is due to the collateral circulation. 3 It has been traditionally assumed that coronary arteries are functional end-arteries under physiological conditions. However, even in the absence of coronary stenoses or in entirely normal hearts, brief periods of coronary occlusion produced by balloon inflation are not followed by electrocardiographic signs of myocardial ischemia in 20%-25% of patients. This is attributed to collateral circulation. 4 This phenomenon is more prominent in the case of preexisting collaterals, as observed in patients with chronic coronary artery disease. Thus, the extent of the area at risk after coronary occlusion is influenced both by an anatomical factor (the size and hierarchy of the occluded vessel) and by a series of functional factors (largely related to the collateral circulation). For this reason, an acute coronary occlusion causes a smaller infarction and a less severe hemodynamic impairment in an older patient with extensive coronary atherosclerosis and well-developed collaterals than in a younger patient without preexisting collaterals. Another functional factor is how rapid is the occlusion. If the occlusion is very slow (as it can be obtained in experimental animals and as it occurs in patients with coronary lesions slowly evolving toward total occlusion), collaterals have the time to develop and to minimize the extent of myocardium at risk. This goes in parallel with the common observation of patients with even complete occlusion of a proximal coronary artery and absence of myocardial infarction. Finally, if the perfusion territory is small, as when a secondary branch is occluded, collateral vessels can totally obscure the area of myocardium at risk. WHY MEASURE THE EXTENT ...

Re-evaluation of the cardioprotective effects of cannabinoids against ischemia-reperfusion injury according to the IMproving Preclinical Assessment of Cardioprotective Therapies (IMPACT) criteria

“…Similarly, a limitation of infarct size was observed after administration of JWH133 ( Yu et al, 2019 ) and HU308 ( Wang et al, 2012 ) after AMI. One should keep in mind, that myocardial infarction is properly expressed as percentage of the area at risk which represents the myocardial perfusion bed distal to an occluded artery ( Gimelli and Rovai, 2013 ; Heusch, 2019 ). Unfortunately, the reduction in infarct size in cannabinoid studies (Tables 3 - 5 ) was not correlated with the reduction of the area at risk (with one exception in the study of Liu et al (2021) .…”

The Never-ending Story: Assessing coronary collateral circulation with myocardial perfusion imaging

“…In the setting of acute coronary syndromes and acute myocardial infarction, it was a well-accepted fact that patients with chronic coronary artery disease and longlasting anginal symptoms could attain better response to primary percutaneous interventions, as it was demonstrated by more limited infarct size according to enzymatic measurements, cardiac magnetic resonance, and myocardial perfusion imaging. 1 In particular, the importance of collaterals in possibly preserving tissue during acute myocardial infarction was proven by means of myocardial perfusion imaging. 2 Thus, it was suggested that coronary collateral circulation could explain the protective role of previous history of stable angina and therefore an assessment of its extent could in theory be helpful to explain part of the variability of the final treatment results that can range from infarct abortion to an extensive myocardial damage.…”

“…2 Thus, it was suggested that coronary collateral circulation could explain the protective role of previous history of stable angina and therefore an assessment of its extent could in theory be helpful to explain part of the variability of the final treatment results that can range from infarct abortion to an extensive myocardial damage. 1,3 However, other studies suggested that the role of collaterals is not crucial, and it is overcome by many other parameters, such as time delay and pre-treatment TIMI flow. 4,5 Moreover, this is not a fundamental issue in the clinical practice since the therapeutic strategy remains in any case to achieve revascularization as early as possible.…”

“…6 Thus, there is presently no actual role for a specific assessment of coronary collateral circulation in acute myocardial infarction patients, although the desirable evaluation of the myocardium at risk could expand the role of myocardial imaging techniques or dedicated angiographic approaches in this setting. 1 Similarly, collateral circulation plays an important role in the setting of chronic total occlusion of a coronary artery. 7 Several studies have explored the capability of coronary collateral circulation to protect from ischemia the myocardium subtended by the occluded vessel, or to sustain viability within it.…”