Echocardiography for the Assessment of Myocardial Viability in Ischemic Cardiomyopathy

Introduction and General Concepts

There has been a dramatic change in the acute presentation, chronic consequences, and mode of death related to coronary artery disease (CAD) in the past few decades. The rapid recognition of acute coronary syndromes and increased availability and utilization of percutaneous coronary interventions have led to a reduction in sudden cardiac death and early in-hospital mortality rates, with a resulting increase in the prevalence of chronic left ventricular (LV) systolic dysfunction and in the presentation of heart failure in patients with ischemic cardiomyopathy. ^, Accordingly, there has been increasing interest in the mechanisms that determine LV dysfunction in these patients with a focus on the possibility of its reversal with revascularization. In this regard, impaired myocardial contraction in patients with CAD may be either a consequence of irreversibly damaged myocardium—as a result of previous infarction—or an expression of viable but dysfunctional myocardium that has the potential to recover its contractility with revascularization.

Two basic mechanisms of chronic systolic dysfunction in myocardial segments with underlying viability have been proposed. ^, The term myocardial stunning refers to myocardium that has suffered an acute ischemic insult with subsequent restoration of blood flow is still “alive” and will therefore recover its force of contraction unless another ischemic insult ensues. Although typically this mechanism applies to acute coronary syndromes with rapid reperfusion, the possibility of chronic systolic dysfunction as a consequence of repeated episodes of ischemia in myocardial segments with preserved resting blood flow but critically reduced flow reserve has been described as repetitive stunning . The term myocardial hibernation , on the other hand, has been used to describe a more chronic state of decreased myocardial contraction accompanying a critical reduction in myocardial blood flow. In this paradigm, systolic dysfunction is an adaptive process to reset the degree of contraction to match the level of reduced myocardial blood flow. As a result, there is a steady state of matched myocardial perfusion and function that allows the myocyte to remain viable. The ischemic myocardium presents various tissue abnormalities that can result in impaired contractile function: damaged contractile apparatus, decreased myocardial metabolism, impaired mitochondrial or membrane integrity, or even replacement of myocardial tissue by fibrosis after myocardial cell death.

Importantly, both described mechanisms of chronic systolic dysfunction in the presence of viable myocardium (i.e., repetitive stunning and hibernation) are amenable to improvement with revascularization. Thus, in the case of repetitive stunning, successful revascularization would lead to increase in the coronary flow reserve, hence abating the episodes of myocardial ischemia and allowing for recovery of contractile function. On the other hand, restoration of resting myocardial blood flow with revascularization would similarly allow for restoration of systolic dysfunction in the paradigm of hibernating myocardium.

As can be surmised from the description of these proposed mechanisms, the concept of myocardial viability in ischemic cardiomyopathy is tightly linked to reduced coronary perfusion and to the potential for recovery of systolic function with successful revascularization. It is this potential that has led to the concept that unveiling myocardial viability in segments with systolic dysfunction is necessary to identify patients with ischemic cardiomyopathy that are most likely to benefit from revascularization. Because clinical and electrocardiographic criteria to detect myocardial viability have limited accuracy, ^, the in-depth assessment of dysfunctional but viable myocardium requires dedicated tests.

Assessment of Myocardial Viability by Echocardiography

Myocardial segments that are akinetic or dyskinetic, thinned (<5 mm of wall thickness), and hyperechogenic (bright by ultrasound) in a resting echocardiogram are likely to be scarred and therefore unable to recover their function. In the absence of these features, more specific testing can be done with dobutamine echocardiography (DE), myocardial strain, myocardial perfusion with ultrasound-enhancing agents, or a combination of them to distinguish myocardial scar from viable but dysfunctional myocardium.