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Since initial reports that regional myocardial dysfunction is not always irreversible, the assessment of whether dysfunctional myocardial tissue or regions contain predominantly viable myocytes has become an important research and clinical issue for noninvasive imaging. Imaging of myocardial perfusion, myocyte cell membrane integrity, regional myocardial metabolism, and contractile reserve has provided important insights into the pathophysiology of hibernating and stunned myocardium. From a clinical perspective, the wealth of data built by many clinical investigators over the years has made noninvasive imaging of myocardial viability an important factor in treatment decisions for patients with heart failure, chronic coronary artery disease (CAD), and left ventricular (LV) dysfunction. Some of the historical milestones in this field are listed in Table 21.1.

Involvement of the sympathetic nervous system in congestive heart failure is characterized by a vicious circle, where reduced cardiac output results in neurohumoral activation. The hyperadrenergic state in turn causes desensitization and downregulation of cardiac β-adrenergic receptors and alterations of postsynaptic signal transduction, which further impair myocardial performance. Alterations of presynaptic cardiac sympathetic innervation are also involved in this pathophysiologic process. Reduction of presynaptic catecholamine reuptake increases overexposure to catecholamines further and thereby contributes to disease progression.

Is it estimated that approximately 19 million people around the world suffer from either acute coronary syndrome (ACS) or sudden cardiac death (SCD).In the United States, approximately 540,000 individuals experience a myocardial infarction, and more than 515,000 deaths are caused by coronary artery disease (CAD) each year. A large proportion of these patients are asymptomatic and without clinically overt cardiovascular disease. These data underscore the significance of early identification and treatment of these high-risk patients.

Despite important clinical advances in prevention and treatment of atherosclerosis during the past 20 years, coronary artery disease remains the first cause of mortality in industrialized countries. Atherosclerosis affects medium- and large-diameter arteries and is characterized by a thickening of the arterial intima typically composed of a lipid core with an overlying fibrous cap. Angiography remains the gold standard for diagnosis and quantification of atherosclerotic plaques that result in flow-limiting arterial stenoses but offers only an indirect view of atherosclerosis burden. Positive remodeling of the arterial wall—a process in which the vessel dilates to limit the narrowing of the lumen in presence of atherosclerotic plaques—leads to a clear underestimation of the true extension of atherosclerosis disease with angiography.

Cardiac imaging modalities such as computed tomography (CT), magnetic resonance imaging (MRI), single photon emission computed tomography (SPECT), positron emission tomography (PET), and ultrasound have seen major advances over the past 3 decades. In the clinical setting, these modalities can provide outstanding data regarding organ structure and physiologic function. However, as molecular medicine transitions from bench to bedside in the forms of gene and cellular therapies, novel, noninvasive imaging technologies need to be developed to monitor and evaluate the efficacy of these treatments at the genetic and biochemical levels. This need has given rise to a new and rapidly evolving discipline called “molecular imaging.”

Since recognition of the key role of angiogenic factors in tumor growth more than 3 decades ago, physiological and pathological vascular development has been implicated in a number of pathological states including inflammation (e.g., coronary atherosclerotic plaque), diabetic retinopathy, peripheral vascular disease, and ischemic heart disease.

A 52-year-old female with dyslipidemia and a family history of ischemic heart disease was referred for evaluation of nonanginal chest pain.