Patient with ischemic heart failure: Ischemia and viability assessment and management

Introduction

Nuclear cardiology imaging techniques are frequently employed to guide clinical decision making in patients with ischemic heart failure (IHF). Perhaps surprisingly, it is not always straightforward to distinguish whether coronary artery disease (CAD) is indeed causal, coincidental, or a contributor to IHF. Diagnosing the cause of heart failure (HF) is an important step to determining the management strategy, potential urgency, and need for revascularization. Nuclear cardiology—single photon computed tomography (SPECT) and cardiac positron emission tomography (PET)—applications can help determine the presence of ischemia, scar, hibernating myocardium, or sympathetic denervation abnormalities, all of which may help both in diagnosis, prognostication, and prediction of a response to therapy. Despite the clinical observation that cardiac PET and SPECT are useful imaging tools in IHF, clinical evidence to support their use has not been consistent. Although the routine use of viability imaging has been questioned in some clinical studies, there may be specific clinical scenarios where viability and ischemia imaging may aid in decision making. In this chapter, we will consider how ischemia and viability imaging remain valuable techniques to identify those patients in whom CAD is the cause or major contributor to their HF and how this can help in decisions for revascularization therapies. We will consider some of the foundational evidence of the importance of imaging in this area and highlight more recent controversial evidence, some of which supports and some of which is ambivalent toward their utility. We will also provide case vignettes to illustrate graphically how ischemia and viability imaging is used in this patient demographic.

Ischemic heart failure

The burden of ischemic heart disease (IHD) has increased within the past 30 years. Despite the fact that the prevalence of fatal myocardial infarction (MI) has decreased since the 1990s, there is a higher prevalence of IHD. This has been attributed to improvements in the treatment of acute coronary syndrome and stable coronary disease in combination with the increasing aging of the population. IHD is the main cause of HF, a major public health problem with a growing estimated prevalence of over 37 million cases worldwide. ^, HF affects up to 2% of the adult population in the developed world, with estimates of increasing prevalence over time. By 2030, the prevalence of HF is estimated to increase by 46% in the United States. The burden to patients and providers is significant, with an estimated annual cost of treatment exceeding $30 billion in the United States alone, equivalent to more than 10% of the total cardiovascular disease health expenditure, half of which is attributed to hospitalization. Interestingly, the increase in prevalence contrasts with a decline in incidence worldwide, partially attributed to advances in therapy and improvement in diagnostic technologies. In the United States, however, there are still 915,000 new cases of HF per year, corresponding to an incidence of 10 per 1000 subjects after 65 years of age. ^,

Myocardial ischemia results from an imbalance between oxygen supply and demand. It can manifest as an acute coronary syndrome (ACS) or chronic IHD. The severity of inadequate flow will determine myocardial adaptations and the extent of reversibility once flow is restored. In patients with IHD, persistent ventricular dysfunction can result from repeated episodes of stress-induced ischemia with postischemic stunning (repetitive stunning), myocardial hibernation, or scar. Such persistent dysfunctional myocardium is considered viable when the ischemia-related injury (repetitive stunning or hibernation) is not severe or prolonged enough to cause cell death. In this case, cardiomyocyte dysfunction can be reversed (or partly reversed) if flow is restored with revascularization. Prolonged ischemic-related injury results in cell death with attendant scar tissue formation that replaces healthy myocardium. The recovery of is chemically injured myocardium that contains scar depends on the transmural extent of infarcted myocardium ( Table 20.1 ).

Myocardial ischemia, viability, and scar can be identified and quantified with different noninvasive tests, such as echocardiography, cardiac magnetic resonance (CMR), and radionuclide imaging. Each can evaluate different aspects of cellular and myocardial physiology, including perfusion, contractile reserve, cell membrane and mitochondrial integrity, cell metabolism, and fibrosis.

Despite the fact that assessment of ischemia and/or viability in patients with CAD and HF seems to be important, at least one recent report suggests that the use of these tests may be underutilized.

Imaging techniques for the evaluation of ischemia and viability

IHF represents the impairment in contractility of (principally) the left ventricle (LV) due to obstructive CAD. Whether revascularization will improve contractility and/or outcome is determined by the balance of myocardial ischemia and scar to viable cardiomyocytes as well as other factors discussed later in this chapter. Unless stress testing is deemed too high of a risk because of the patient clinical status or coronary anatomy (e.g., critical left main or three-vessel CAD), it is generally reasonable to first assess the presence and magnitude of stress-induced ischemia. Please refer to Chapter 4 for a detailed discussion of radionuclide imaging techniques and protocols for stress radionuclide imaging. In patients without significant inducible ischemia and large apparent areas of scarring, there is a need to determine whether these regions may, in fact, contain significant viable myocardium. Methods to assess viability have nevertheless been established with echocardiography, SPECT or PET imaging, and cardiac magnetic resonance imaging (CMR).