The muscular layer of the artery is termed the media and is composed of smooth muscle cells. These smooth muscle cells normally exist in a quiescent state and exhibit a contractile phenotype that is capable of altering blood vessel tone. Like endothelial cells, these smooth muscle cells exhibit LDL receptors and are capable of lipoprotein modification and presentation to macrophages. With overlying endothelial denudation or injury, medial smooth muscle cells are capable of responding to a variety of mitogens and chemoattractants. The quiescent contractile smooth muscle cell can then be stimulated to differentiate into a proliferative phenotype that can migrate into the intima, divide, and secrete extracellular matrix (Krieger, 1995; Ross, 1993; Zhao, 2013).

The outermost layer of the vessel wall, the adventitia, is composed of a thin layer of collagen and fibroblasts. Although once thought to be a biologically inactive layer, it is now recognized that adventitial fibroblasts participate in the processes of atherogenesis and arterial restenosis. Differentiation of adventitial fibroblasts into myofibroblasts can result in remodeling of the vessel wall. Adventitial myofibroblasts may serve to decrease vessel size in the process of atherogenesis and arterial restenosis, not unlike their role in wound contraction during wound healing (Gibbons & Dzau, 1994).

Process of Atherogenesis

Endothelial injury is the inciting event in the generation of luminal stenosis. Disruption of the endothelial lining exposes the circulating blood elements to the underlying thrombogenic surface of the media. Platelets readily adhere to this surface and release mitogens and growth factors. Medial smooth muscle cells are stimulated to migrate into the intima, proliferate, and secrete extracellular matrix, resulting in intraluminal stenosis. Lymphocytes are also attracted to the site of injury, resulting in continued cytokine release and antigen presentation. This response to the injury process is responsible for restenosis after angioplasty and coronary artery bypass grafting (CABG), as well as the transplant atherosclerosis seen in immunologically injured endothelium of heart transplants (Badimon, Fuster, Chesebro, & Badimon, 1993; Gibbons & Dzau, 1994; Ross, 1993).

The cause of endothelial injury in primary atherosclerosis is most commonly secondary to hyperlipidemia (Gibbons & Dzau, 1994; Ross, 1993). Circulating lipoproteins, especially LDLs, can be taken up by endothelial cells and medial smooth muscle cells. After modification and presentation, resident macrophages scavenge the modified LDLs and oxidize them on the luminal aspect of the artery. This fatty streak can be seen as early as late childhood and young adulthood and is anatomically distributed in areas ultimately affected with progressive atherosclerosis.

Oxidation of LDLs by macrophages leads to toxic injury to the endothelium through generation of superoxide radicals. This endothelial injury, together with secretion of numerous growth factors by these activated macrophages, sets into motion the cascade of smooth muscle cell activation. The resulting lesion is a fibrous plaque composed of large numbers of intimal smooth muscle cells, collagen fibers, macrophages, and lymphocytes. Continued lipid uptake results in intracellular and extracellular accumulations of cholesterol esters. Progressive growth of the fibrous plaque results in slow stenosis of the arterial lumen and eventual occlusion.

Endothelial injury in atherogenesis may also occur in response to flow dynamics associated with hypertension, glycosylation associated with diabetes, superoxide production involved in cigarette smoking, and primary viral injury from cytomegalovirus infection (Badimon et al., 1993). Multidetector computed tomography (CT) has emerged as a means of measuring luminal stenosis, coronary calcium, and even the extent of noncalcified coronary plaque volume. The future holds the possibility of molecular imaging based on the knowledge of molecular mechanisms involved in the development and progression of atherosclerotic plaques and a contrast agent that is able to identify different molecules and/or cells in the target zone (Badimon, Ibanez, & Cimmino, 2009).

Continued injury to the endothelium results in worsening endothelial dysfunction. The permeable barrier created by the endothelium is lost, and the balance between intraluminal anticoagulant and procoagulant properties is disrupted (Loscalzo, 1992). Rupture of the endothelial lining of an atherosclerotic plaque can result in intramural hemorrhage, exposure of subintimal collagen, and intraluminal thrombosis. In contrast to the slow luminal reduction caused by the progressing atherosclerotic plaque, plaque rupture and thrombosis result in acute vessel closure. Without the time necessary for compensatory collateral formation and angiogenesis, plaque rupture results in acute myocardial ischemia and potential myocardial cell death. Tissue factor content is increased in unstable angina and correlates with areas of macrophages and smooth muscle cells, suggesting a cell-mediated thrombogenicity in patients with ACS (Moreno et al., 1996).

Coronary Blood Flow and Myocardial Ischemia

Ischemia refers to the inadequate delivery of oxygen to the myocardium, accompanied by an inadequate removal of metabolites consequent to reduced perfusion. Myocardial ischemia is the result of an imbalance between myocardial oxygen demand and myocardial oxygen supply. The therapies for CAD are aimed at reestablishing this balance by decreasing myocardial oxygen consumption, increasing coronary blood flow, or both.

DETERMINANTS OF MYOCARDIAL OXYGEN CONSUMPTION

Cardiac energy generation is primarily aerobic, and therefore, myocardial oxygen consumption is an accurate measure of total cardiac metabolism. Increases in cardiac oxygen consumption are primarily affected by changes in systolic wall tension, contractility, and heart rate (Ardehali & Ports, 1990; Graham, Covell, Sonnenblick, Ross, & Braunwald, 1968; Rooke & Fiegel, 1984).

Systolic wall tension is determined by both stroke volume and systolic pressure generation. These determinants of wall tension have their clinical correlates in preload and afterload. Increases in either parameter result in a greater overall external workload and an increase in myocardial wall tension (Rooke & Fiegel, 1984). By the Laplace relation, myocardial wall tension decreases with decreasing ventricular size and increases with ventricular dilatation.

Changes in contractility increase both systolic pressure generation and time to peak pressure generation; without significant changes in ventricular volume, these translate into increased myocardial wall tension and increased myocardial oxygen consumption (Ardehali & Ports, 1990; Graham et al., 1968; Rooke & Fiegel, 1984). Positive inotropic agents also enhance excitation–contraction coupling. Increased oxygen requirements then result from greater and more rapid calcium uptake by the sarcoplasmic reticulum. Finally, acceleration of the heart rate increases myocardial oxygen demand by increasing the frequency of tension development per unit of time and simultaneously by increasing contractility (Ardehali & Ports, 1990; Rooke & Fiegel, 1984). Myocardial ischemia is the result when any of these determinants causes increased myocardial metabolic demands without concomitant regulation of oxygen delivery.

DETERMINANTS OF MYOCARDIAL OXYGEN DELIVERY

Coronary blood flow is the major determinant of myocardial oxygen delivery. Perfusion of the coronary arteries occurs primarily during diastole because of myocardial compression of the intramyocardial and subendocardial arterioles during systole. Approximately 80% of coronary flow to the left ventricle and 50% of flow to the right ventricle occur during diastole. Coronary perfusion pressure, therefore, is determined by both mean aortic pressure and left ventricular end-diastolic pressure.

Autoregulation of the coronary circulation via neurohumoral mechanisms serves to maintain coronary flow fairly constant over a wide range of perfusion pressures. In the presence of fixed coronary stenosis, however, autoregulation cannot further increase regional blood flow to accommodate increases in myocardial oxygen demand. Coronary vessels with atherosclerotic lesions are maximally dilated to augment distal flow in the setting of luminal obstruction. With further metabolic demands, autoregulation is not possible and regional myocardial ischemia with resultant myocardial dysfunction occurs. Furthermore, in the setting of atherosclerosis, endothelial dysfunction results in impaired ability to generate vasoactive substances such as endothelial-derived relaxing factor and prostacyclin. This results in further impairment of smooth muscle relaxation as well as a loss of platelet aggregation inhibition.

EPIDEMIOLOGY

An estimated 15.4 million Americans have CAD (Go et al., 2014). Among adults 30 to 74 years of age, the average 10-year risk for developing CAD is 6.5%. A person’s lifetime risk varies as a result of his or her risk factor profile. For someone with no CAD risk factors, the lifetime risk for developing CAD is 3.6% for men and <1% for women; but with two or more CAD risk factors (e.g., hypertension, hyperlipidemia, diabetes, or smoking), that risk increases to 37.5% for men and 18.3% for women (Go et al., 2014).

Risk Factors

Obesity is measured by the size of the waist, the ratio of the waist to the hips, and the relationship between height and weight. The last measurement is known as the body mass index (BMI). It is not a perfect way of checking the cardiovascular risk but as the BMI increases, so does the risk of heart disease and stroke. The BMI is calculated by dividing the weight in kilograms by the square of the height in meters (kg/m²). A BMI between 25 and 29.9 kg/m² is considered overweight. Obesity is defined as a BMI >30 kg/m². A BMI >22 kg/m² in persons of South Asian origin may be considered overweight. Women with a BMI >21 kg/m² may be associated with an increased risk for CAD. Underweight is defined as a BMI below 18.5 kg/m².

Fat, especially intra-abdominal fat, has a significant impact on metabolism. Intra-abdominal fat can affect BP and cholesterol levels. It also interferes with the body’s ability to use insulin effectively, which can result in the development of diabetes, a major risk factor for CAD. The risk of developing type 2 diabetes and hypertension rises as weight increases. Evidence shows that, globally, 58% of diabetes and 21% of ischemic heart diseases can be attributed to a BMI >21 kg/m² (WHO, 2002).

Physical Activity • The role of physical activity in the prevention of CAD remains controversial. The exact mechanism of protection is multifactorial. Exercise is important in maintaining ideal body weight, muscle mass, and normal BP, as well as optimizing lipid levels. Regular aerobic exercise decreases both systolic and diastolic pressures, improves the myocardial oxygen supply/demand ratio, lowers triglycerides, raises HDL levels, and decreases platelet aggregation.

The greatest risk reduction is achieved in nonactive and moderately active persons. Intense exercise is associated with decreases in total and LDL cholesterol and increases in HDL cholesterol (Fowler, 2012). Patients who exercise regularly have a decreased incidence of sudden death, although sedentary patients who begin an exercise regimen may be at increased risk of acute MI or malignant ventricular arrhythmia. Therefore, a thorough physical examination is recommended for people older than 40 years before initiating a vigorous exercise program. Likewise, younger patients with hypertension, diabetes, and other associated CAD risk factors should undergo a thorough assessment before undertaking an aggressive exercise regimen, including a baseline ECG. A history of angina or an abnormal ECG should prompt further diagnostic testing before initiating an intensive exercise program.

Alcohol • Patients should be advised that if they drink alcohol they should do so in moderation. This means an average of one to two drinks per day for men and one drink per day for woman (a drink is 12 oz. of beer, 4 oz. of wine, 1.5 oz. of 80 proof spirits, or 1 oz. of 100 proof spirits). Heavy alcohol consumption is associated with a number of health risks such as hypertension, hypertriglyceridemia, obesity, stroke, and breast cancer, as well as cardiomyopathy, cardiac arrhythmias, and sudden cardiac death. There is no evidence that drinking wine or any other alcoholic beverages can replace lowering cholesterol, lowering BP, controlling weight, physical activity, and following a healthy diet. The AHA does not recommend drinking alcohol to prevent CAD (American Heart Association, 2014).

Psychosocial Factors • Psychosocial factors may affect a person’s risk of developing CAD and the course of CAD in patients who already have atherosclerosis. People who are said to have a “type A personality” are characterized as highly competitive, ambitious, and in constant struggle with their environment. Although early studies suggested a link between type A personality and CAD risk, a systematic review has found less consistent evidence linking type A personality to CAD risk (Kuper, Marmot, & Hemingway, 2002). Acute stress from life events such as bereavement or natural disasters has been known to trigger CAD events (Rozanski, Blumenthal, & Kaplan, 1999). In patients with atherosclerosis, acute stress causes vasoconstriction, which can induce angina or an MI. Chronic stresses may also play a role in CAD risk. Chronic stressors such as social isolation and lack of social supports, low socioeconomic status, and work stress have been linked to adverse clinical outcomes (Rozanski, Blumenthal, Davidson, Saab, & Kubzansky, 2005).

A comprehensive review of the literature evaluating the relationship between depression and CAD concluded that depression and CAD have a bidirectional relationship; in other words, CAD can cause depression and depression is an independent risk factor for CAD and its complications (Khawaja, Westermeyer, Gajwani, & Feinstein, 2009). Depression may contribute to sudden cardiac death and increase all causes of cardiac mortality. Depression contributes to an unhealthy lifestyle and poor adherence to treatment (Hance, Carney, Freedland, & Skala, 1996; Khawaja et al., 2009). Because of this correlation, primary care providers should screen all patients at risk of CAD for depression and refer patients for treatment when indicated (Fihn et al., 2012).

Homocysteinurea is a rare autosomal recessive disorder of methomine metabolism. Untreated homocysteinurea may be complicated by CAD. Therefore, vitamin B₆, folate, and vitamin B₁₂ may be used to lower homocysteine and may be of benefit in those with this rare disorder (Kazemi, Eshraghian, Omrani, Lankarani, & Hosseini, 2006).

DIAGNOSTIC CRITERIA

The diagnosis of CAD is based on a history of chest pain or anginal equivalent pain together with diagnostic studies that demonstrate either functional or anatomic coronary obstruction. New wall motion abnormalities on echocardiography may also be used as soft criteria for recent myocardial injury. The diagnosis of MI is based on history, ECG changes, and myocardial markers. The two markers utilized to diagnosis MI are creatine kinase MB (CK-MB) and troponin levels.

The CK-MB test is a relatively specific cardiac marker when skeletal muscle damage is not present. The level peaks in 10 to 24 hours. Because it has a short duration, it cannot be used for late diagnosis of acute MI, but it can be used to suggest infarct extension if levels rise again. The CK-MB level is usually back to normal within 2 to 3 days.

The troponin I test is the most sensitive and specific test for myocardial damage. It has increased specificity compared with the CK-MB test; therefore, troponin is a superior marker for myocardial injury. Differential diagnoses of troponin elevation include acute MI, severe pulmonary embolism causing acute right heart overload, heart failure, or myocarditis. Troponins can also be used to calculate infarct size, but the peak must be measured on the third day. After myocyte injury, troponin is released in 2 to 4 hours and persists for up to 7 days.

HISTORY AND PHYSICAL EXAMINATION

History

The diagnosis of CAD is based on a careful, skillful clinical history. The patient should be assessed for a history of CAD risk factors, including diabetes mellitus, smoking, hypertension, hyperlipidemia, and family history of CAD. Patients with cerebrovascular or peripheral arterial disease are more likely to have concurrent CAD. Within the current atmosphere of health care cost containment, a concisely focused outlined history will obviate the need for more costly testing.

Typical stable angina pectoris is described as a viselike, constrictive, crushing, or squeezing type of retrosternal chest pain induced by exertion. In some patients, the quality of discomfort is described as mild pressure or substernal burning. In each instance, the symptoms reach their maximal intensity in a few minutes and then dissipate with the cessation of exercise. Typical angina pectoris is relieved within minutes of rest or by using nitroglycerin. The response to nitroglycerin usually occurs within 3 to 5 minutes and can be a very useful diagnostic test. Nonetheless, it has been clearly established that esophageal pain and other syndromes may also respond to nitroglycerin.

Typical angina may be induced by exertional activities such as walking against the wind, climbing stairs or hills, vigorous arm work, and sexual intercourse. The discomfort can likewise be incited by emotional stress (panic, fear, anger, or anxiety), or it may follow a heavy meal. Anginal pain may even occur nocturnally after lying down (angina decubitus) secondary to increased ventricular filling pressure. The duration of discomfort and its cessation are reproducible for each typical anginal syndrome.

Although the area of discomfort is classically retrosternal, radiation is very common. The regions of discomfort may manifest themselves anywhere between the mandible and the epigastrium. Discomfort can radiate to the shoulders, the jaw, the ulnar surface of the left arm, the right arm, or the outer surface of both arms.

Symptoms of myocardial ischemia other than typical anginal discomfort, such as dyspnea with minimal exertion, fatigue, and faintness, are referred to as anginal equivalents. These symptoms are common in the elderly and in patients at high risk of CAD. The symptoms may be caused by elevation of the left ventricular filling pressure and despite a normal ECG should alert the provider to probable severe ischemic heart disease.

In women, while the most common heart attack symptom is some type of pain, pressure, or discomfort in the chest, it is not always severe nor is it the most prominent symptom. It usually is not the crushing chest pain people associate with a heart attack. Women more commonly have heart attack symptoms unrelated to chest pain, such as neck, shoulder, upper back or abdominal discomfort, shortness of breath, nausea or vomiting, sweating, lightheadedness or dizziness, or unusual fatigue. This may be because women are more prone to the development of microvascular disease, a narrowing of the smaller arteries that supply blood to the heart.

Stable angina is a predictable pattern of chest discomfort with a similar degree of severity and classic precipitating factors occurring either recently or over several months. It maintains a constant threshold in severity and relief over time. The corresponding lesion is usually a stable, fixed atherosclerotic lesion that is flow-limiting only when myocardial metabolic demands reach a threshold.

Variant angina, originally described by Prinzmetal, refers to chest pain occurring almost exclusively at rest, not precipitated by physical exertion or emotional stress. It is associated with ECG ST-segment elevation. It has been demonstrated that variant angina is related to coronary artery spasm with subsequent myocardial ischemia. In addition, it may be associated with MI, ventricular tachycardia, and ventricular fibrillation as well as sudden death (Keller & Lemberg, 2004).

Angina can also be a symptom of coronary microvascular disease, also called cardiac syndrome X or nonobstructive CAD. This is a heart disease that affects the heart’s smallest coronary arteries and is more likely to affect women than men.

Silent myocardial ischemia can occur in patients with angina at rest, unstable angina, and chronic stable angina. It has been clearly established that patients who are at high risk of CAD can be evaluated by stress testing for silent but significant ECG ST-segment changes (Cohn, Fox, & Daly, 2003). Prognostically, this may be the only way to limit sudden death from MI as well as to identify and avoid an initial or subsequent MI.

The cardiac examination may be most helpful during an episode of symptomatic angina because ischemia may produce transient left ventricular dysfunction with a third heart sound and bibasilar pulmonary rales. A softened mitral component of the first heart sound and paradoxical splitting of the second heart sound may occur during an anginal attack. A mid-systolic click followed by a late systolic murmur may occur in patients with CAD related to transient papillary muscle dysfunction with alteration in the alignment of the papillary muscles.

DIAGNOSTIC STUDIES

Noninvasive Testing

ELECTROCARDIOGRAPHY

Patients with chronic stable angina have normal ECG tracings at rest, but they may have severe CAD. However, the 12-lead ECG during a provoked episode of substernal chest pain or during an attack of angina may reveal downward or horizontal sloping depression of the ST-segment, T-wave peaking, or T-wave inversion. These ECG changes accompanied by chest discomfort may signal the possibility of coronary stenosis. ECG findings that indicate a poorer prognosis include evidence of a prior MI with Q waves in multiple leads, as well as the presence of a left bundle branch block, a second- or third-degree atrioventricular block, ventricular arrhythmias, or left ventricular hypertrophy (Fihn et al., 2012).

There are no specific guidelines for ECG follow-up, particularly if the initial ECG is normal. Naturally, there are exceptions. Poorly controlled BP, a family history of premature cardiovascular death, high lipids, or glucose abnormalities, for example, warrant repetition of ECGs on an individual basis (Townsend, 2001).

EXERCISE ECG

Exercise treadmill ECG has been the most studied noninvasive test for the evaluation of CAD in both men and women. Stress testing increases overall cardiac work and heart rate. This increased work results in an increase in myocardial oxygen demand and a subsequent requirement for increased oxygen delivery via an increase in coronary blood flow. If narrowed or obstructed lesions prevent the required increase in coronary blood flow, chest pain or ECG changes may arise. In both sexes, the exercise ECG is most accurate in patients who are able to exercise to 85% of their maximal predicted heart rates (Banerjee, Newman, Van den Bruel, & Heneghan, 2012). However, this goal can be modified based on the characteristics of the patient being evaluated. Younger patients with a low risk of CAD will have a much more sensitive result should they reach their maximal heart rate target or exercise to exhaustion. Older, high-risk patients, in contrast, may reveal clinically meaningful information at lower cardiac workloads. Ischemia is also dependent on the severity of obstruction, as coronary artery stenoses of <70% are frequently undetected by functional testing (Fihn et al., 2012).

ECG, electrocardiogram.

PHARMACOLOGICAL STRESS TESTS

Pharmacological stress tests are inexpensive and safe diagnostic tools with excellent specificity and good sensitivity. They are primarily used in patients who cannot exercise for ECG or imaging stress tests. The choice of a pharmacological agent, either a vasodilator or a positive inotrope, is dependent on patient characteristics, the type of stress test, and provider preference.

Vasodilating agents include dipyridamole, adenosine, and regadenoson. They work by increasing intracellular cyclic adenosine monophosphate levels and inhibiting the formation of thromboxane A₂, a potent vasoconstrictor. When injected, they act as coronary vasodilators. Stenotic coronary lesions are already maximally dilated and cannot respond to vasodilating agents. Nonstenotic coronary arteries maintain their ability to vasodilate, and preferential flow down these newly dilated vessels results in coronary steal from the stenotic arteries. Infusion of a vasodilating agent is contraindicated in patients with bronchospastic pulmonary disease, those with significant hypotension, or patients with sick sinus syndrome and high-degree heart block. Theophylline and caffeine should be avoided for 48 to 72 hours prior to a pharmacological stress test with a vasodilator, as these agents may decrease the effectiveness of the vasodilating agent.

Dobutamine is a synthetic beta-1 and beta-2 agonist with positive inotropic effects. Dobutamine causes myocardial ischemia primarily through a marked increase in myocardial oxygen demand resulting from increased heart rate, BP, and myocardial contractility. The increase in coronary blood flow achieved is comparable to that during physical exercise but slightly less than that with vasodilating agents. Dobutamine stress testing is an appropriate alternative in patients who cannot exercise and who have contraindications to vasodilating agents. Dobutamine stress testing causes ventricular ectopy in 40% to 50% of patients; a recent history of tachyarrhythmias is a relative contraindication.

From a meta-analysis of 82 studies (Kim, Kwok, Heagerty, & Redberg, 2001), it was concluded that the sensitivity of dipyridamole SPECT imaging (89%) was higher than that of dipyridamole echocardiography (80%), but the specificity of dipyridamole SPECT imaging (65%) was lower than that of dipyridamole echocardiography (93%). The sensitivity of dobutamine echocardiography (80%) was similar to that of dobutamine SPECT imaging (82%), but dobutamine echocardiography had a higher specificity (84%) than dobutamine SPECT imaging (75%).

Either vasodilating or positive inotropic agents may be used in stress testing in lieu of treadmill exercise, and they achieve similar sensitivity (Fihn et al., 2012). When coupled with radionuclide imaging, CAD detection is similar to that of exercise radionuclide testing, so pharmacological stress testing is a powerful tool in patients who cannot exercise. Pharmacological stress echocardiography has also been used in the diagnosis and management of CAD with a prognostic value similar to radionuclide testing (Sicari et al., 2008).

CT CORONARY ANGIOGRAM

The 64-multislice CT coronary angiogram is a noninvasive, fast, and accurate procedure that captures three-dimensional (3-D) images of the heart. The results of multiple meta-analyses and clinical trials report a sensitivity ranging from 93% to 97% and a specificity ranging from 80% to 90% for detecting obstructive CAD (Fihn et al., 2012). The coronary artery scan can reveal plaque (CAD) many years before it can be found by physical examination, ECG, or stress testing. If plaque is present, early treatments can help to prevent MI or the need for revascularization. The 64-multislice CT coronary angiogram helps to identify CAD in individuals at risk of the disease and can be useful in patients not diagnosed with CAD but whose symptoms suggest that the condition could be present, in those who have an inconclusive stress test, or those who are having chest pain and have risk factors for developing CAD.

The 64-multislice CT coronary angiogram is an easy and reliable tool for comprehensive in vivo diagnosis of myocardial bridging. Myocardial bridging is a rare cause of chest pain in a subgroup of younger patients with less prevalence of hyperlipidemia and more prevalence of cardiomyopathy than patients with significant atherosclerotic CAD (de Agustín et al., 2012). A myocardial bridge is a band of heart muscle that lies on top of a coronary artery; so part of a coronary artery dips into and underneath the heart muscle and then comes back out again. The band of muscle that lies on top of the coronary artery is called a “bridge,” and this is how the condition gets its name.

As previously stated, CAD is the leading cause of mortality in the United States. While invasive angiography is regarded as the gold standard for the diagnosis of CAD, invasive angiography is not without its potential risks, although, according to ACC/AHA guidelines, the risk of major complications is <2% (Scanlon et al., 1999). At the same time, lingering concerns about radiation safety in CT coronary angiogram exist. It has been unclear what risk of cancer is attributable to CT coronary angiogram scans. A 128-slice CT scan is now available. The 128-slice CT coronary angiogram is ideal because of its high accuracy in the assessment of significant coronary stenosis and significant reduction in radiation exposure (Ghadri et al., 2012).

Cardiac catheterization and selective coronary arteriography is the gold standard for visualization of the in vivo morphological details of the coronary arteries (Fihn et al., 2012). Access to the coronary circulation is usually achieved through the femoral artery. In patients with severe peripheral vascular disease, an alternative arterial entry using the radial or brachial artery can be used. Each coronary ostium is then selectively cannulated and an angiogram of each vessel is taken in several standard views.

Coronary angiography can detect as little as 20% narrowing of the main coronary arteries, as well as a critical stenosis of 70% or greater (de Bono, 1993). The cardiac catheterization can also assess hemodynamic measurements, left ventricular function, valve surface area, and valvular gradients.