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Imaging plays a critical role in the diagnosis of heart disease. In the past 25 to 30 yr, advanced imaging modalities such as digital angiography, echocardiography, magnetic resonance imaging (MRI), computed tomography (CT), and nuclear cardiology have become important in the evaluation of the heart. However, the conventional radiographic examination remains the mainstay of cardiac imaging. This chapter will discuss the role of the chest radiograph in the diagnosis of cardiac disease in adults, with an emphasis on both normal cardiovascular anatomy and pathoanatomy in a variety of diseases. Correlation will be made with cross-sectional imaging in order to illustrate important anatomic points.

In 1929, Werner Forssman performed the first human cardiac catheterization when he passed a urethral catheter from his left antecubital vein into the right side of his heart (). The introduction of left heart catheterization by Zimmerman () and Limon Lason () and selective coronary arteriography by Sones in the 1950s (,) began the modern era of coronary artery disease management and revascularization. In each of the decades subsequent to the introduction of coronary arteriography, major advances in revascularization therapy were introduced: coronary artery bypass graft surgery by Favolaro in the late 1960s (), percutaneous balloon coronary angioplasty by Gruentzig in the late 1970s (,), and coronary stent implantation by Sigwart in the late 1980s ().

Nuclear imaging harnesses the unique properties of radiopharmaceuticals in allowing us to non-invasively image physiological phenomena, anatomical structures, and metabolic reactions, as well as various physiological spaces and compartments in patients (). Nuclear imaging plays an important role in the noninvasive evaluation of patients with established or suspected coronary artery disease. A number of different radiopharmaceuticals and scintigraphic imaging techniques are available for obtaining important diagnostic and prognostic information about myocardial per-fusion, metabolism, cardiac function, and myocardial necrosis in patients with cardiovascular disorders. This chapter briefly describes various cardiac nuclear imaging techniques, their applications in clinical practice, and the recent developments in this field.

There have been considerable advances in cardiovascular cross-sectional imaging techniques. These include cardiac magnetic resonance imaging (CMR) and computed tomography (CT)—electron beam CT (EBCT) and multidetector CT (MDCT). EBCT generates a cross-sectional scan through the chest within a fraction of a second. It is widely used as a means of detecting calcium in the coronary arteries and providing evidence of atherosclerotic disease. This application is presently controversial, as to date, the available data do not yet support the utility of EBCT-detected coronary artery calcium as a diagnostic or prognostic indicator of ischemic heart disease. EBCT has several other potential uses, however, which will be discussed in this chapter.

In this chapter, a logical approach to choosing among the various cardiac imaging techniques is proposed. Imaging modalities most commonly employed in the evaluation of cardiac disease are chest roentgenography, cardiac angiography, radionuclide imaging, ultrasonography, computed tomography, and magnetic resonance imaging. Electrocardiography and electrophysiologic studies, though crucial in the evaluation of cardiac electrical abnormalities, are technically not imaging modalities. The decision algorithm requires a basic knowledge of the imaging modalities themselves, including their indications and contraindications, which have been described in the preceding chapters. Most important, however, the treating physician should formulate a clear clinical question which will guide selecting an appropriate imaging test. Most cardiac clinical scenarios can be thought of in terms of questions of structure, function, or both.

The normal cardiac cycle is initiated by electrical events that precede cardiac contraction. Abnormalities in the initiation and propagation of cardiac impulses may result in a variety of arrhythmias. The purpose of this chapter is to highlight the cellular mechanisms responsible for normal impulse formation and conduction, and to review the clinical consequences when these mechanisms are perturbed.

The management of cardiac arrhythmias has been revolutionized by the use of new diagnostic and therapeutic modalities. The development and advancement of both pharmacologic and nonpharmacologic therapies, particularly radiofrequency catheter ablation and new implantable devices, have resulted in better treatment, suppression, and frequently cure of otherwise recalcitrant and life-threatening cardiac arrhythmias. Furthermore, catheter ablation has also helped to better elucidate the pathophysiology of these arrhythmias. For the purpose of this chapter, the management of cardiac arrhythmias is divided into that of tachyarrhythmias and bradyarrhythmias. Tachyarrhythmias are managed by antiarrhythmic drugs, radiofrequency catheter ablation, and implantable devices. Bradyarrhythmias are treated mainly by pacemakers.

Syncope is a syndrome consisting of a relatively short period of temporary and self-limited loss of consciousness caused by transient diminution of blood flow to the brain (,). In the absence of complete loss of consciousness, the individual is considered to have experienced a near-faint or near-e, or presyncope.

Heart failure is a clinical syndrome initiated by abnormal function of the heart. Until recently our understanding of this condition has centered on various pathological insults to the heart that lead to abnormal function, usually in the form of contractile dysfunction. One of the earliest terms used to describe heart failure syndrome was “hydrops,” which has its origins in the observation that salt and water retention was a common feature of the condition. Despite this obvious systemic manifestation, heart failure was still considered primarily a disease of the heart. In recent years advances have been made in our understanding of the pathophysiology of heart failure; key to these has been the realization that heart failure is a multisystem disorder in which abnormalities of the heart, vasculature, skeletal muscle, and kidneys all combine with various neurohormonal derangements to produce the heart failure syndrome. Of particular importance has been the emerging concept that many of the compensatory mechanisms designed to overcome the initial insult to the heart are the very same processes that paradoxically set in motion a variety of detrimental consequences for cardiac function, gradually worsening the heart failure syndrome further. Our increasing understanding of these concepts has resulted in a rapid advancement in drug development and many new therapeutic targets continue to emerge. In this chapter we summarize the pathophysiology of heart failure, beginning with the specific insults that initiate heart failure and continuing with a discussion of the body’s responses to such insults, and how compensatory mechanisms ultimately cause further deterioration in cardiac function.

The goals of heart failure treatment include both symptomatic improvement and prolongation of life. These goals are not necessarily concordant. Related to this problem is the observation that the acute actions of an intervention may be very different from the chronic effects. When treating heart failure, therefore, one must understand the immediate and long-term desires of a particular patient and the immediate and long-term consequences of one’s therapy. The result is an uncomfortable use of acute treatments known to have adverse consequences when given for a prolonged period and chronic treatments that are counterintuitive. Fortunately, however, congestive heart failure has been well investigated, with multiple large studies demonstrating the multiple consequences of many of our standard interventions.