Coronary Artery Disease

Curtis M. Rimmerman

CHAPTER SECTION LINKS

Definition
Prevalence
Pathophysiology
Signs and symptoms
Diagnosis

Treatment
Outcomes
Summary

Definition

Coronary artery disease is characterized by atherosclerosis in the epicardial coronary arteries. Atherosclerotic plaques, the hallmark of atherosclerosis, progressively narrow the coronary artery lumen and impair antegrade myocardial blood flow. The reduction in coronary artery flow may be symptomatic or asymptomatic, occur with exertion or at rest, and culminate in a myocardial infarction, depending on obstruction severity and the rapidity of development.

Prevalence

According to the American Heart Association and American Stroke Association's 2006 publication on heart disease and stroke statistics, cardiovascular disease (CVD) remains the leading cause of mortality in the United States in men and women of every major ethnic group. It accounts for nearly 1.4 million deaths per year as of 2002 and was responsible for one in almost three deaths in the United States in 2003. Approximately 13 million persons have a history of coronary artery disease and 7.2 million have suffered a myocardial infarction. Almost 2500 Americans die of CVD each day, an average of one death every 35 seconds. CVD claims more lives each year than the next four leading causes of death combined—cancer, chronic lower respiratory diseases, accidents, and diabetes mellitus.

Pathophysiology

Coronary artery disease is a chronic process that begins during adolescence and slowly progresses throughout life. Independent risk factors include a family history of premature coronary artery disease, cigarette smoking, diabetes mellitus, hypertension, hyperlipidemia, sedentary lifestyle, and obesity. These risk factors accelerate or modify a complex and chronic inflammatory process that ultimately manifests as fibrous atherosclerotic plaque.

The most widely accepted theory of atherosclerosis states that the process represents an attempt at healing in response to endothelial injury. The first step in the atherosclerotic process is the development of fatty streaks, which contain atherogenic lipoproteins and macrophage foam cells. These streaks form between the endothelium and internal elastic lamina. Over time, an intermediate lesion made up of an extracellular lipid core and layers of smooth muscle and connective tissue matrix eventually forms a fibrous cap. The edge of the fibrous cap (the shoulder region) plays a critical role in the development of acute coronary syndromes. The shoulder region is the site where most plaques lose their integrity, or rupture. Plaque rupture exposes the underlying thrombogenic core of lipid and necrotic material to circulating blood. This exposure results in platelet adherence, aggregation, and progressive luminal narrowing, which are associated with acute coronary syndromes.

Inflammation is emerging as a critical component of atherosclerosis genesis, activity, and potential plaque instability. Patients with established coronary artery disease who possess a confluence of risk factors known as the metabolic syndrome remain at particularly high risk for a future vascular event, such as an acute myocardial infarction or cerebrovascular accident. Biochemical markers such as elevated levels of C-reactive protein signal a higher likelihood of vascular inflammation and portend a higher risk of vascular event rates. This marker may also signal more rapidly advancing coronary artery disease and the need for aggressive preventive measures.

Signs and symptoms

Patients with coronary artery disease present with stable angina pectoris, unstable angina pectoris, or a myocardial infarction. They may seek medical attention with their first symptomatic episode of chest discomfort. Many of these patients suffer from unrecognized coronary artery disease and may experience an acute plaque rupture or acute myocardial infarction. Electrical instability can ensue, including potentially lethal cardiac dysrhythmias. Identifying high-risk persons before their first myocardial event is a multifaceted process that involves patient and physician education efforts. Screening for coronary artery disease is not sufficient. Risk factor modification, from an early age, inititates primary prevention efforts, forestalling the development of symptomatic coronary artery disease. Severe coronary artery disease can be detected before a patient develops symptoms.

Angina pectoris is a perceived symptom resulting from a mismatch of myocardial supply and demand. The compromised myocardial blood flow caused by obstructive coronary artery disease is not able to meet the metabolic demands of the myocardial tissue. The anaerobic threshold is crossed and the patient develops symptomatic angina pectoris. Angina pectoris is typically categorized according to the Canadian Cardiovascular Society's functional classification system (Table 1).

Table 1: Canadian Cardiovascular Society Functional Classification of Angina Pectoris

Class	Definition	Specific Activity Scale
I	Ordinary physical activity (e.g., walking and climbing stairs) does not cause angina; angina occurs with strenuous, rapid, or prolonged exertion at work or recreation.	Ability to ski, play basketball, jog at 5 mph, or shovel snow without angina
II	Slight limitation of ordinary activity. Angina occurs on walking or climbing stairs rapidly, walking uphill, walking or stair climbing after meals, in cold, in wind, or under emotional stress, or only during the few hours after awakening, when walking more than two blocks on level ground, or when climbing more than one flight of stairs at a normal pace and in normal conditions.	Ability to garden, rake, roller skate, walk at 4 mph on level ground, have sexual intercourse without stopping
III	Marked limitation of ordinary physical activity. Angina occurs on walking one to two blocks on level ground or climbing one flight of stairs at a normal pace in normal conditions.	Ability to shower or dress without stopping, walk 2.5 mph, bowl, make a bed, play golf
IV	Inability to perform any physical activity without discomfort.	Anginal symptoms may be present at rest. Inability to perform activities requiring 2 or fewer metabolic equivalents without angina

Adapted from Goldman L, Hashimoto B, Cook EF, Loscalzo A: Comparative reproducibility and validity of systems for assessing cardiovascular functional class: Advantages of a new specific activity scale. Circulation 1981;64:1227-1234.

Stable Angina

Angina pectoris is said to be stable when its pattern of frequency, intensity, ease of provocation, or duration does not change over several weeks. Identification of activities that provoke angina and the amount of sublingual nitroglycerin required to relieve symptoms are helpful indicators of stability. A decrease in exercise tolerance or an increase in the need for nitroglycerin suggests that the angina is progressing in severity or accelerating.

Accelerating Angina

Angina pectoris is said to be accelerating when there is a change in the pattern of stable angina. This may include a greater ease of provocation, more prolonged episodes, and episodes of greater severity, requiring a longer recovery period or more frequent use of sublingual nitroglycerin.

Unstable Angina

Unstable angina pectoris occurs when the pattern of chest pain changes abruptly. Signs of unstable angina are pains at rest, a marked increase in the frequency of attacks, discomfort that occurs with minimal activity, and new-onset angina of incapacitating severity. Unstable angina usually is related to the rupture of an atherosclerotic plaque and the abrupt narrowing or occlusion of a coronary artery, representing a medical emergency.

Diagnosis

The initial diagnostic approach for coronary artery disease encompasses a detailed patient history, a complete physical examination, and an electrocardiogram. Once the initial evaluation is performed, laboratory blood tests, stress testing, and cardiac catheterization may be necessary to obtain further diagnostic insight.

History

The history should include any current symptoms, a complete inventory of comorbid conditions, including cardiac risk factors, and a complete family history. The history should include information about the character and location of discomfort, radiation of discomfort, associated symptoms, and precipitating, exacerbating, or alleviating factors.

Physical Examination

The results of the physical examination of a patient with stable or unstable angina may be entirely normal. The presence of multiple risk factors or atherosclerosis in the carotid or peripheral arteries increases the likelihood that a chest pain syndrome is related to myocardial ischemia. Evaluation should include measurements of blood pressure and the ankle–brachial index. Examination of the carotid arteries should evaluate upstrokes and auscultation for bruits. Examination of the chest wall, neck, and shoulders for deformities and tenderness may be helpful in diagnosing musculoskeletal chest discomfort. Cardiac auscultation may detect murmurs caused by aortic stenosis or hypertrophic cardiomyopathy, either of which can cause angina in the absence of coronary artery disease. Assessment of the abdominal aorta for an aneurysm or bruits and palpation of lower extremity pulses are necessary to rule out peripheral vascular disease. Careful palpation of all peripheral pulses and assessment of symmetry versus diminution are also valuable noninvasive approaches for assessing the integrity of the arterial circulation. Finally, examination for xanthelasmas, tendon xanthomas, retinal arterial abnormalities, and peripheral neuropathy can be helpful.

Diagnostic and Imaging Studies

Electrocardiography

A resting 12-lead electrocardiogram should be obtained on all patients with suspected coronary artery disease. Electrocardiographic results are normal in approximately 50% of patients with chronic stable angina, and they can remain normal during an episode of chest discomfort. Importantly, a normal electrocardiogram does not exclude coronary artery disease (Fig. 1).

Figure 1: Click to Enlarge

Chest Radiography

The usefulness of a routine chest radiograph in a patient with chest discomfort has not been established. Calcification of the aortic knob is a common finding in older patients and is a nonspecific indicator of flow-limiting obstructive coronary disease. Infrequently, coronary calcification is present.

Cardiac Computed Tomography Angiography

A noninvasive imaging assessment of coronary atherosclerosis is now possible. When negative, this test possesses a high negative predictive value. The positive predictive value is also high, but exact stenosis quantification can be complicated. Associated calcification can cause a blooming artifact, resulting in an overestimation of stenosis severity (Fig. 2).

Figure 2: Click to Enlarge

Echocardiography

Echocardiography is recommended for patients with stable angina and physical findings suggesting concomitant valvular heart disease. It is invaluable for assessing the patient with suspected hypertrophic cardiomyopathy. It is also recommended for the assessment of global and regional left ventricular systolic function in patients who have congestive heart failure, complex ventricular arrhythmias, or a history of a past myocardial infarction.

Laboratory Studies

Routine laboratory measurements recommended as a part of the initial evaluation of patients with coronary artery disease should include determination of fasting glucose and fasting lipid levels (total cholesterol, high-density lipoprotein [HDL] cholesterol, triglycerides, and calculated low-density lipoprotein [LDL] levels). Other markers such as lipoprotein(a) (Lp[a]) and high-sensitivity C-reactive protein, may be useful in assessing cardiac risk. High-sensitivity C-reactive protein is gaining greater prominence in assessing the inflammatory level of vascular disease and predicting future risk of vascular events, such as myocardial infarctions and cerebrovascular accidents.

Once all these initial evaluations are complete, it is possible to estimate a patient's probability of existing coronary artery disease before proceeding with stress testing or coronary angiography (Table 2).

Table 2: Pretest Probability of Coronary Artery Disease (CAD) by Age, Gender, and Symptom Status*

Age, yr†	Gender	Typical or Definite Angina Pectoris	Atypical or Probable Angina Pectoris	Nonanginal Chest Pain	No Symptoms
30-39	Male	Intermediate	Intermediate	Low	Very low
	Female	Intermediate	Very low	Very low	Very low
40-49	Male	High	Intermediate	Intermediate	Low
	Female	Intermediate	Low	Very low	Very low
50-59	Male	High	Intermediate	Intermediate	Low
	Female	Intermediate	Intermediate	Low	Very low
60-69	Male	High	Intermediate	Intermediate	Low
	Female	High	Intermediate	Intermediate	Low

^*High probability, >90%; intermediate, 10%-90%; low, <10%; very low, <5%.
^†No data exist for patients younger than 30 yr or older than 69 yr, but it can be assumed that the prevalence of CAD increases with age. In a few cases, patients at the extremes of each decade may have probabilities slightly outside the high or low range.
Adapted from Gibbons RJ, Balady GJ, Beasley JW, et al: ACC/AHA guidelines for exercise testing: Executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). Circulation 1997;96:345-354.

Stress Testing

Stress testing is another method for determining the presence of flow-limiting, functionally significant coronary artery disease. All stress testing techniques include electrocardiography and blood pressure monitoring. The absolute and relative contraindications to exercise stress testing are outlined in Box 1.

Box 1: Absolute and Relative Contraindications to Exercise Stress Testing
Absolute Contraindications
Acute MI within 2 days Symptomatic or severe aortic stenosis Decompensated heart failure Symptomatic or hemodynamically significant cardiac arrhythmias Unstable angina not previously stabilized by medical therapy Acute aortic dissection Acute myocarditis or pericarditis Acute pulmonary embolus or pulmonary infarction
Relative Contraindications
Left main coronary artery stenosis Electrolyte imbalance Systolic blood pressure ≥200 mm Hg Diastolic blood pressure ≥110 mm Hg Tachyarrhythmias or bradyarrhythmias Hypertrophic cardiomyopathy, other forms of outflow tract obstruction High-degree atrioventricular block Moderate stenotic valvular heart disease Mental or physical impairment leading to inability to exercise adequately MI, myocardial infarction.

Adapted from Gibbons RJ, Balady GJ, Beasley JW, et al: ACC/AHA guidelines for exercise testing: Executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). Circulation 1997;96:345-354.

Cardiovascular stress testing takes two forms, exercise and pharmacologic administration. The preferred method of cardiovascular stress testing is exercise, using a treadmill or bicycle. Through aerobic exercise, a higher rate pressure product (peak systolic blood pressure multiplied by peak pulse rate), and therefore greater cardiovascular stress, can be obtained. This permits an assessment of a patient's functional capacity, providing prognostic data using the sole parameter of attained metabolic equivalents or oxygen uptake. Heart rate recovery—how fast the heart rate decreases after exercise cessation—is also an important prognostic parameter.

The most common pharmacologic agents used for nonexercise stress testing are dobutamine, dipyridamole, and adenosine. Dobutamine echocardiography is useful for determining the presence of functionally significant obstructive coronary artery disease and assessing a post–myocardial infarction patient. Using echocardiography, whether it is combined with exercise or dobutamine, the physician interpreter is focusing on the global and regional endocardial thickening responses to cardiovascular stress.

Figure 3: Click to Enlarge

Nuclear stress testing is an equally important modality for assessing the coronary circulation. Unlike stress echocardiography, in which the endocardial thickening response to cardiovascular stress is the marker for inducible myocardial ischemia, nuclear stress testing relies on the concept of coronary flow reserve and differential myocardial blood flow. In the presence of exercise or the administration of a pharmacologic coronary vasodilator, the normal response is hyperemia, with a significant increase in myocardial blood flow. If there is no coronary obstructive disease, the pattern of hyperemia and blood flow is reflected as a symmetrical increase, with a homogeneous distribution of the blood flow tracer. In the presence of a severe coronary artery stenosis, dipyridamole or adenosine induces coronary macrovascular and microvascular vasodilation, which results in differential myocardial blood flow that can be detected by radionuclide imaging with thallium 201 or technetium 99m (Tc 99m)-labeled radiopharmaceuticals (Tc 99m sestamibi or Tc 99m tetrofosmin). Functionally significant coronary artery disease can be suspected on nuclear perfusion imaging when an area of relative hypoperfusion is detected on peak stress images compared with resting images. Resting nuclear cardiac images may also be abnormal (Fig. 3).

Combining imaging with the electrocardiographic stress test adds approximately 15 percentage points to the sensitivity and specificity. In certain cases, electrocardiographic stress testing is of borderline help, particularly in the presence of an abnormal resting electrocardiogram. The indications for cardiac stress imaging are outlined in Box 2.

Box 2: Indications for Cardiac Stress Imaging
Resting ST-segment depression >1 mm
Complete left bundle branch block
Ventricular paced rhythm
Ventricular pre-excitation syndrome
Previous revascularization with PCI or CABG
Inability to exercise

Cardiac stress imaging is useful for determining the extent, severity, and location of ischemia. The exercise portion of the test also provides prognostic information. Prognostic markers include the Duke treadmill score, heart rate recovery (HRR) score, and the chronotropic response index (CRI). The Duke treadmill scoring system is summarized in Table 3.

Table 3: Duke Treadmill Scoring System*

Risk Group	Annual Mortality Rate
Low (>4)	0.25%
Intermediate (−10 to 4)	1.25%
High (<−10)	5.0%

^*The Duke treadmill score is calculated according to the following formula:

Exercise time min −5 (max ST-segment deviation [in mm, during or after exercise]) −angina score

where the score is 0 if there is no angina, 4 if angina occurs, and 8 if angina is the reason for stopping the test.
Adapted from Mark DB, Shaw L, Harrell FE Jr, et al: Prognostic value of a treadmill exercise score in outpatients with suspected coronary artery disease. N Engl J Med 1991;325:849-853.

The HRR score is calculated according to the following formula:

HRR score = HR (at peak exercise) − HR (1 min postexercise)

where HR is in beats per minute. A normal HRR score (>12 beats/min) is associated with a low risk of death, whereas a low HRR score (<8 beats/min) is associated with a high risk. HRR scores of 8 to 12 beats per minute indicate an intermediate risk.

The CRI is calculated according to the following formula:

(Peak HR – resting HR) / ([220 − patient's age] – resting HR)

where HR is in beats per minute. A normal CRI (>0.8) is associated with a decreased probability of coronary artery disease and a lower risk of death. A low CRI (<0.8) in a patient who is not on beta blocker therapy is associated with an increased likelihood of coronary artery disease and a higher risk of death.

Coronary Arteriography

Cardiac catheterization is currently the gold standard for determining the presence of obstructive coronary artery disease. A cardiac catheterization yields a two-dimensional rendering of the coronary artery circulation. To assist in circumventing the limitations of a two-dimensional depiction of three-dimensional anatomy, multiple views from varying angles are obtained as a standard.

Treatment

Once a cardiac catheterization has been performed, the three most common therapeutic options are medical therapy, percutaneous coronary intervention (PCI), and coronary artery bypass grafting (CABG).

Lifestyle Modification

Patients with documented coronary artery disease should actively pursue lifestyle modifications that reduce the risk of future cardiovascular events.

Smoking

Tobacco use is one of the most important contributors to recurrent cardiovascular events. Tobacco use induces endothelial dysfunction, reduces coronary vasoreactivity, increases circulating carbon monoxide levels, impairs functional status, and raises blood pressure.

Exercise

Functional capacity is a strong predictor of major adverse cardiac events. Functional capacity can be improved by following an exercise program that includes at least 30 minutes of exercise 3 or 4 days a week; a daily regimen is optimal.

Weight Control

The best weight management strategy is diet and exercise. Ideal benchmarks are a body mass index between 19 and 25 kg/m² and a waist circumference of no more than 40 inches for men and 35 inches for women. Weight loss has a favorable metabolic syndrome impact on many cardiac risk factors, including hypertension, high LDL level, low HDL level, and glucose intolerance.

Pharmacologic Therapy

Antiplatelet Agents

Aspirin is the mainstay of antiplatelet therapy for patients who have known coronary artery disease or symptoms suggestive of coronary artery disease. Aspirin inhibits both cyclooxygenase and the synthesis of thromboxane A_2.

Clopidogrel (Plavix), a thienopyridine derivative, blocks adenosine diphosphate–induced platelet activation. Clopidogrel is indicated as an alternative for patients who cannot take aspirin.

Antianginal Agents

Beta blockers, calcium channel blockers, and nitrates are the mainstays of antianginal therapy. Unless contraindications exist, all patients who have a history of angina pectoris should carry sublingual nitroglycerin. Beta blockers are recommended as first-line therapy for the management of stable angina in all patients with established coronary artery disease.

Patients who have a history suggestive of vasospastic angina should be treated with a calcium channel blocker or a long-acting nitrate as an initial therapy. Either treatment option can also serve as a substitute for a beta blocker in the presence of traditional angina when intolerable beta blocker effects ensue.

Nitrates improve exercise tolerance and prolong the time to onset of angina in patients with exertional angina. They are contraindicated in patients who have severe aortic stenosis or hypertrophic cardiomyopathy because they can adversely alter hemodynamics and exacerbate symptoms. Ranolazine may be useful for treating refractory angina pectoris.

Risk Factor Management

Hypertension

Management of hypertension in patients with coronary artery disease is exceedingly important. Control of blood pressure reduces myocardial oxygen consumption and thereby reduces angina, and it also lowers the incidence of cardiovascular events.

Beta blockers devoid of intrinsic sympathomimetic activity represent first-line antihypertensive therapy for patients with a history of myocardial infarction or coronary artery disease with angina. Angiotensin-converting enzyme (ACE) inhibitors are indicated for all patients with diabetes mellitus or a history of myocardial infarction, particularly those with impaired left ventricular systolic function. In the Heart Outcomes Prevention Evaluation (HOPE) study, high-risk patients without a history of a myocardial infarction treated with the ACE inhibitor ramipril experienced a significant reduction in major cardiac events.

Calcium channel blockers are useful for patients with hypertension and angina despite maximum tolerable administration of beta blockers. The long-acting dihydropyridines are preferred; short-acting preparations should be avoided because they might increase the risk of cardiac events via precipitous blood pressure reduction and induction of the coronary steal phenomenon, diverting coronary arterial blood flow from flow-limited myocardial regions.

Hyperlipidemia

Guidelines of the National Cholesterol Education Program (NCEP) have recommended an LDL level lower than 70 mg/dL for all patients with coronary artery or other atherosclerotic disease. Patients whose LDL levels are higher than 100 mg/dL should start drug therapy. 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are the recommended first-line agents for patients who have coronary artery disease and elevated total and LDL cholesterol levels.

The NCEP also recommends a target HDL level higher than 45 mg/dL for men with coronary artery disease and higher than 55 mg/dL for women. Patients with the metabolic syndrome (obesity, hypertension, and insulin resistance) often have HDL levels lower than 35 mg/dL. These patients are at especially high risk for arterial vascular disease. Their recommended lifestyle changes include regular exercise and weight loss, which are two of the most effective ways to raise HDL levels. If lifestyle changes fail to increase HDL levels to their target, drug treatment with a fibrate or niacin should be considered, particularly in patients whose triglyceride levels are higher than 200 mg/dL.

Diabetes Mellitus

Diabetics with coronary artery disease have a particularly high risk for recurrent cardiovascular events, and they should be targeted for aggressive risk-factor modification. The American Diabetes Association recommends a hemoglobin A_1c level lower than 7%.

Surgical Management: Revascularization

The primary revascularization options are PCI and CABG surgery. The most common PCI techniques are percutaneous transluminal coronary angioplasty and coronary stenting. A major limitation of PCI is restenosis at the intervention site. This represents the body's response to local injury with an exaggerated neointimal proliferative response. The use of stents, aspirin, clopidogrel, and glycoprotein IIb/IIIa inhibitors lowers the rate of restenosis to less than 10% at 6 months in optimal circumstances.

The most common conduits for CABG are the saphenous vein and the internal thoracic (mammary) artery. The long-term patency rates of internal thoracic artery grafts are superior to those of venous grafts.

Outcomes

Percutaneous Coronary Intervention Versus Medical Therapy

Percutaneous coronary intervention is more effective than medical therapy in relieving angina, but it confers no greater survival benefit. Aggressive lipid-lowering therapy appears to be as effective as percutaneous coronary intervention plus usual medical care for preventing ischemic events.

Coronary Artery Bypass Grafting Versus Medical Therapy

CABG produces better survival rates compared with medical therapy and is recommended for symptomatic patients with left main coronary artery disease, three-vessel coronary artery disease, or two-vessel coronary artery disease marked by stenosis of the proximal left anterior descending artery. CABG is more effective than medical therapy for the relief of angina, although this benefit narrows after 5 to 10 years.

Percutaneous Coronary Intervention Versus Coronary Artery Bypass Grafting

Outcomes following percutaneous coronary intervention and coronary artery bypass grafting have been compared in high-risk patients. The two largest studies in the United States were the Emory Angioplasty versus Surgery Trial (EAST) and the Bypass Angioplasty Revascularization Investigation (BARI). In both trials, percutaneous coronary intervention was limited solely to angioplasty. Similarly, current CABG techniques, including the more frequent use of arterial conduits, were not included in either trial. EAST results have demonstrated that the long-term survival rates following percutaneous coronary intervention and coronary artery bypass grafting are comparable. BARI results have indicated that coronary artery bypass grafting produces better long-term survival rates than percutaneous coronary intervention. However, the benefit of CABG in BARI was not apparent until 7 years postoperatively, and it was largely attributable to the significantly higher survival rate in the subgroup of patients with diabetes mellitus. Both trials have shown that CABG is superior to PCI in relieving angina and obviating the need for repeat revascularization procedures. With the introduction of drug-eluting stents, coupled with improved catheterization techniques, coronary artery disease treatment is shifting away from bypass surgery toward a percutaneous approach. Restenosis rates have been lowered significantly and acute thrombotic complications are rare given the advances in antiplatelet therapy.

Summary

The diagnostic and treatment options for coronary artery disease are changing rapidly.

New pharmaceuticals are being developed and introduced into the treatment armamentarium.
Biologic markers are now used to track coronary artery disease activity at the vascular level, guiding medication selection and dose titration.
Procedures are less invasive and offer percutaneous treatment options, such as drug-eluting stents, that were previously unavailable.
Despite these advances, coronary artery disease and its deleterious manifestations represent the number one killer in the United States. This is largely caused by poor dietary choices, sedentary lifestyles, and continuance of tobacco use.
Efforts at primary and secondary prevention of obstructive coronary artery disease among the general public are still lacking.
Public awareness campaigns are a partial success.
It is imperative for the physician to allocate time to address the importance of lifestyle modification efforts.
The genetic basis of coronary artery disease is slowly being unraveled.
In the future, a genetic assessment of a person's risk for developing atherosclerotic vascular disease may be possible at a young age.
These findings can guide lifestyle modification prescription and the choice and dosage of select pharmaceuticals.
A preemptive approach is the best way to tackle the immensity of coronary artery disease.

We must erase the myth that medications, stenting, and bypass surgery are curative approaches. Instead, the patient must meet the health care team at least halfway to achieve a successful health outcome.