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A preventive approach to management of atherosclerotic cardiovascular disease (CVD) is needed because once CVD becomes manifest, it is often immediately lethal and those fortunate enough to survive seldom can be restored to full function. Prevention of the major atherosclerotic CVD events is now feasible because several modifiable predisposing risk factors have been ascertained that when corrected, can reduce the likelihood of such events occurring (,). Multivariate risk formulations for estimating the probability of cardiovascular events conditional on the burden of a number of specified risk factors have been produced to facilitate evaluation of candidates for CVD in need of preventive management (–).

The heart’s pumping action is made possible by interactions between myosin, the major protein of the thick filaments, and actin, which makes up the backbone of the thin filaments. These interactions, which are activated by calcium, are regulated by tropomyosin and troponins C, I, and T that are present along with actin in the thin filaments.

The basic cardiac events of Wiggers’ cycle (Fig. 1) are: (1) left ventricular (LV) contraction, (2) LV relaxation, and (3) LV filling. A natural starting point is with the arrival of calcium ions at the contractile protein that starts actin-myosin interaction and left ventricular contraction. During the initial phase of contraction, the LV pressure builds up until it exceeds that in the left atrium (normally 10 to 15 mmHg), whereupon the mitral valve closes. With the aortic and mitral valves both shut, the LV volume cannot change and contraction must be (iso = the same) until the aortic valve is forced open as the LV pressure exceeds that in the aorta. Once the aortic valve is open, blood is vigorously ejected from the LV into the aorta, which is the phase of . The speed of ejection of blood is determined both by the pressure gradient across the aortic valve and by the elastic properties of the aorta, which undergoes systolic expansion.

All blood vessels have an outer adventitia, a medial layer of smooth muscle cells, and an intima lined by endothelial cells. Contraction of the vascular smooth muscle causes changes in the diameter and wall tension of blood vessels. In the aorta and large arteries vascular smooth muscle contraction affects mainly the compliance (the reciprocal of stiffness) of the vessel. At the precapillary level, contraction of vascular smooth muscle will regulate blood flow to different organs, and contribute to the peripheral resistance. Compliance of large vessels and resistance of arterioles both contribute most of the impedance of the vascular circuit and therefore the afterload of the heart. The capacity of the circulation is determined by the degree of contraction of the veins (“capacitance vessels”) especially in the splanchnic area; this will affect the venous filling pressure, or preload, of the heart.

Thrombosis and hemostasis are similar processes, the former being pathologic and involving intravascular formation of aggregates of platelets and fibrin, and the latter resulting in the cessation of bleeding after external injury to the vasculature. While it is not clear that these processes involve precisely the same biochemical and biophysical events, they appear to be sufficiently similar to be considered as a single process that results in quite different structures owing to the local environment, either within a vessel or at the site of bleeding.

The medical history and physical examination provide the most fundamental information regarding personal health and the need for specific medical care. It is the purpose of this chapter, first, to restate and underscore the objective of the taking of a medical history in general, and then to consider the nature of complaints that may be associated with cardiovascular disease in the adult patient. Specific symptom profiles and presentations are best discussed in association with specific clinical entities, including the chapters on ischemic heart disease, acute myocardial infarction, and congestive heart failure. Symptoms related to congenital malformations with associated cardiac lesions, including “failure to thrive,” cyanosis, and heart failure in the neonate will not be considered in this chapter. The principal symptoms are summarized in tables, followed by a short comment on general issues. The onset and severity of a principal complaint may dominate the initial history taking, and relief of distressing symptoms becomes a first priority. However, it is then essential to return to obtain a complete and comprehensive medical and cardiac history. Because of the overall primacy of atherosclerosis (,) as a cause of vascular and heart disease, specific inquiries must be made to include a risk evaluation for atherosclerosis, not only for the coronary arteries but also for the aorta and its principal branches. (The factors currently deemed most important are listed in Table 1.) Gender offers no specific protection, as heart disease is the most frequent cause of death in women although later in life than men. Women are equally prone to congenital and rheumatic heart disease, arrythmias, and the less common diseases such as cardiac tumor.

The examination of the heart and circulation has a long and rich tradition in clinical medicine. Most of the cardinal signs of cardiovascular disease detectable on the physical examination were described and documented by master physicians during the 19th and early 20th centuries. Subsequently, echocardiography and cardiac catheterization have demonstrated that the presumed pathogenesis of many to most cardiovascular abnormalities on the physical examination were accurately and presciently described before these modern techniques became available. In the past, generations of internists and cardiologists were well trained in the skills of cardiac examination; the absence of our current ultrasound technology providing “immediate” answers contributed to the emphasis of expertise in cardiac physical diagnosis. Unfortunately, clinical skills in this area are no longer emphasized in medical education, in part due to the burgeoning of other aspects of medical science that must be taught in the medical student curriculum. The advent of readily available two-dimensional echocardiography has clearly contributed to the demise of cardiac physical diagnosis capability among physicians, a phenomenon well documented in recent published studies.

The electrocardiogram (ECG) records electric potential changes in the electrical field produced by the heart. Although it records only the behavior of the heart, it can be used to identify numerous metabolic, hemodynamic, and anatomic changes. Electrocardiography is considered a gold standard for the diagnosis of arrhythmias ( Chapter 17). In this chapter, mostly nonarrhythmic ECG changes will be reviewed. Abbreviations and acronyms used in this chapter can be found in Table 1.

Echocardiography is the evaluation of cardiac structures and function utilizing images produced by ultrasound (US) energy. Echocardiography started as a crude one-dimensional technique but has evolved into one that images in two and three dimensions (2-D, 3-D) and that can be performed from the chest wall, from the esophagus, and from within vascular structures. Clinically useful M-mode recordings became available in the late 1960s and early 1970s. In the mid-1970s, linear-array scanners that could produce 2-D images of the beating heart were developed. Eventually, these evolved into the phased-array instruments currently in use. In addition to 2-D imaging, the Doppler examination has become an essential component of the complete echocardiographic evaluation. Doppler US technology blossomed in the early 1980s with the development of pulsed-wave (PW), continuous-wave (CW), and 2-D color-flow imaging. The field of cardiac US continues to grow rapidly: recent clinical additions include 3-D imaging, harmonic imaging, and contrast echocardiography.

Exercise can be considered the true test of the heart because it is the most common everyday stress that humans undertake. The exercise test is the most practical and useful procedure in the clinical evaluation of cardiovascular status.