Coronary Artery Disease

Coronary Artery Disease



Curtis M. Rimmerman



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).


image

Figure 1 A 12-lead electrocardiogram example of ischemic anterolateral ST-segment depression in a patient with known coronary artery disease.



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).


image

Figure 2 Computed tomography angiogram of the right coronary artery.


1, Mild proximal stenosis with expansive remodeling and predominantly nonexpansive plaque. 2, Partially calcified advanced mid to distal stenosis.



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*

image

Related posts:

  1. Anaphylaxis
  2. Sleep-Disordered Breathing
  3. Nontuberculous Mycobacterial Disorders
  4. Systemic Scleroderma

Stay updated, free articles. Join our Telegram channel
Tags:
Jul 18, 2017 | Posted by in GENERAL SURGERY | Comments Off on Coronary Artery Disease

Full access? Get Clinical Tree
Get Clinical Tree app for offline access