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Over the past two decades, the experimental and clinical use of positron emission tomography (PET) has significantly contributed to the knowledge of cardiac physiology and metabolism. Positron tomography has emerged from the experimental arena and currently plays an important role in clinical cardiology.

Estimates of regional myocardial blood flow contain information on morphologic alterations of the myocardium itself but also, and importantly, on the structure and function of the upstream coronary circulation. Loss of myocytes, replacement fibrosis, and scar tissue formation are associated with regional reductions of blood flow at rest per unit mass. Conversely, regional flow at rest may also be diminished in the absence of structural alterations but in the presence of, for example, a high-grade stenosis of the epicardial conduit vessel that impinges on flow. Such flow reductions then reflect structural or functional disturbances of the upstream coronary circulation. Myocardial blood flow depends on a complex interplay between the coronary driving pressure (the pressure gradient from the aorta to the right atrium) and resistance forces that adjust the supply of blood to the energy needs of the myocardium. Besides extravascular resistive forces due to intramyocardial and intracavitary pressures and their cardiac cycle-related changes, most of the resistance to flow and its regulation resides at the level of the coronary resistance vessels. Vascular smooth muscle relaxation or constriction in the resistance vessels mediated by metabolic, neuronal, and endocrine mechanisms raises or lowers coronary and, accordingly, myocardial blood flow. The vascular-smooth-muscle-initiated changes in blood flow are modulated by endothelium-related factors that depend on flow-velocity-related shear stresses as well as on neuronal, endocrine, and paracrine factors.

Computed tomography (CT) has long been used for the evaluation of both normal and pathologic human anatomy. In the setting of atherosclerosis (AS) and cardiovascular disease (CVD), CT angiography has a well-established role for the detection of luminal stenoses and aneurysms in various vascular territories such as the aorta, carotid, renal, and lower-extremity arteries. Although of indisputable value in clinical practice, such findings reflect an already advanced stage of the disease. The atherosclerotic changes of the arterial wall in fact commence much earlier, as microscopic lesions progressing slowly into macroscopic plaques that often grow eccentrically without compromising the vessel lumen. Reliance on changes in luminal caliber is therefore insufficient for estimating the extent and severity of atherosclerotic burden. In fact, clinical events are often caused by acute complications (rupture and thrombosis) of specific plaques that may not produce a significant luminal narrowing, particularly in the coronary tree. Because AS is a systemic disorder involving multiple vascular territories, it is important not to restrict the evaluation to a single arterial system. The visualization of the coronary arteries with CT has, however, been traditionally limited by their continuous motion from both cardiac and respiratory origins.

Direct visualization of the epicardial coronary arteries is currently the reference standard to confirm the presence or focal severity of coronary luminal disease, or both. For more than 50 years the coronary angiogram has been used to define epicardial coronary disease. While conventional coronary arteriography provides exceptional spatial resolution and a general road map of the coronary system for catheter-based or surgical intervention to the heart, its chambers, and the individual arteries, it is expensive, has a small but definite risk of complications, and requires either a brief hospitalization or a period of observation for several hours after the procedure in a specialized monitored unit. When it is used for diagnosis of coronary disease, a mechanical intervention is required only about half the time.

Computed tomography angiography (CTA) and magnetic resonance imaging (MRI) and angiography (MRA) have now replaced x-ray angiography for many vascular beds, but only recently has the technology advanced sufficiently for these modalities to interrogate and display coronary artery morphology.

The integration of positron emission tomography (PET) and multidetector CT (PET/CT) technology provides a potential opportunity to delineate the anatomic extent and physiologic severity of coronary atherosclerosis and obstructive disease in a single setting. It allows detection and quantification of the burden of the extent of calcified and noncalcified plaques, quantification of vascular reactivity and endothelial health, and identification of flow-limiting coronary stenoses. PET/CT also has the potential to identify high-risk plaques in the coronary and other arterial beds. Together, by revealing the degree and location of anatomic stenoses and their physiologic significance, and the plaque burden and its composition, integrated PET/CT can provide unique information that may improve noninvasive diagnosis of coronary artery disease (CAD) and the prediction of cardiovascular risk. In addition, this approach expands the diagnostic capability of nuclear cardiology to include atherosclerosis and may facilitate further study of atherothrombosis progression and its response to therapy, thus allowing assessment of subclinical disease.

There is growing evidence that perturbations in myocardial substrate use play a key role in a variety of normal and abnormal cardiac states. A decline in myocardial fatty acid metabolism and a preference for glucose as an energy substrate characterize pressure-overload left ventricular hypertrophy. Conversely, an overdependence on myocardial fatty acid metabolism with a parallel decline in carbohydrate use is characteristic of the myocardial metabolic adaptation in diabetes mellitus. What is unclear is the extent to which these metabolic switches are adaptive and to what extent they have the propensity to become maladaptive.

Left ventricular (LV) function is a well-established and powerful predictor of outcome after myocardial infarction (MI). Indeed, the occurrence of severe LV systolic dysfunction (i.e., LV ejection fraction <35%) post-MI, especially when combined with heart failure, is associated with very poor survival if treated with medical therapy alone. In selected patients, high-risk surgical revascularization appears to afford long-term survival benefit. However, selection of patients with severe LV dysfunction for high-risk revascularization remains controversial.

Computed tomography (CT) can acquire high-resolution cross-sectional images of geometrically precise tomographic sections of the whole heart and thorax during one breath hold. It has the potential not only for measuring cardiac chamber size, shape, and dynamics but also for displaying the myocardial wall itself and providing estimates of myocardial wall dimensions including wall thickness, thickening, mass, and integrity on a regional and global basis. Consequently, contrast cardiac CT can provide useful information regarding myocardial viability and LV remodeling that could be of clinical value in the management of patients with heart failure.

Current clinical magnetic resonance imaging (MRI) techniques are based on detection of protons (H) that are bound to mostly water and macromolecules (such as in fat or protein) of the body. H is very abundant in the body, and this property provides adequate signal-to-noise ratio for image generation at the magnetic field strengths (B) of current clinical MRI scanners (1.5 Tesla). The single positively charged proton itself functions much like a tiny tissue magnet inside a magnetic field. When a patient is placed in an MRI scanner, each proton aligns with the magnetic field and spins around its axis (a process known as precession) at a frequency defined by the magnitude of the magnetic field in Tesla. When a given direction and magnitude of the B magnetic field are manipulated by applying a secondary magnetic field (radiofrequency pulse), the protons within a part of the body of imaging interest can then be “excited.” These excited protons release a specific magnetic resonance signal (known as free induction decay) that contains structural and physical information on the tissues being imaged. To create an MR image, a set of gradient coils in the MRI provides the relevant three-dimensional spatial coordinates (, and ) and detects the intensity of the magnetic resonance signal in each of the coordinates. Utilizing the fast speed of modern computers for data acquisition and digital processing, static or dynamic magnetic resonance images that provide crucial information of tissue functions can be rapidly acquired.