Angina pectoris occurs when an oxygen demand-supply mismatch occurs in the myocardium. The most common cause of typical angina pectoris is atherosclerotic disease of the epicardial coronary arteries. Other, less common, causes include epicardial coronary spasm, Kawasaki disease, microvascular coronary disease, aortic stenosis, hypertrophic cardiomyopathy, coronary fistulas, anomalous coronary origins, and intramyocardial location (bridging) of epicardial coronary vessels.
PRESENTING SYMPTOMS AND SIGNS
The definition of typical angina pectoris has three components: (a) substernal chest discomfort with a characteristic quality and duration that is (b) provoked by exertion or emotional stress and (c) relieved by rest or nitroglycerin (NTG). Atypical angina meets two of the three criteria, and noncardiac chest pain meets one or none of the criteria.
Typical angina pectoris is characterized as a feeling of constricting, squeezing, burning, or heaviness. The location of the discomfort may be substernal or interscapular, and it may radiate to the neck, jaw, shoulders, or arms. The typical duration of discomfort is 2 to 10 minutes. Discomfort that lasts less than 1 minute is unlikely to be angina. Pain that lasts longer than 10 minutes may be indicative of unstable angina, myocardial infarction (MI), or noncardiac chest pain. Some patients may have dyspnea as an anginal equivalent. Typical angina may be provoked by physical exertion, emotional stress, cold weather, or heavy meals.
The elderly, and women in particular, are first seen more often with atypical symptoms. Coronary angiography may show insignificant disease, but reduced coronary flow reserve is the cause for inducible ischemia (1,2,3). Diabetics are more prone to have episodes of silent ischemia and need intense care and evaluation. The Canadian Cardiovascular Society Classification System (CCS) is used to grade angina pectoris (Table 9.1) (4). The physical examination findings at rest are usually normal in patients with a history compatible with angina caused by chronic coronary artery disease (CAD). Patients with angina due to aortic stenosis or hypertrophic cardiomyopathy have a characteristic systolic ejection murmur. Auscultation during chest pain may reveal an S3 gallop or a systolic murmur of mitral regurgitation secondary to papillary muscle dysfunction.
PATHOPHYSIOLOGY
Angina occurs with imbalance between oxygen demand and supply. Atherosclerotic plaque causing an important restriction to flow may occur when luminal obstruction by the plaque is greater than 50% for the left main artery or greater than 70% for the remaining coronary arteries. Endothelial dysfunction and altered vasomotor reactivity is also present in coronary arteries affected with atherosclerosis. This leads to impaired vasodilation or even vasoconstriction in response to various stimuli, including exercise (5,6).
TABLE 9.1.Grading of angina pectoris by the Canadian Cardiovascular Society Classification system
Class I
Ordinary physical activity, such as walking or climbing stairs, does not cause angina
Angina (occurs) with strenuous, rapid, or prolonged exertion at work or recreation
Class 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, under emotional stress, or only during the few hours after awakening
Angina occurs on walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace and in normal condition
Class III
Marked limitations of ordinary physical activity; angina occurs on walking one to two blocks on the level and climbing one flight of stairs in normal conditions and at a normal pace
Class IV
Inability to carry on any physical activity without discomfort; anginal symptoms may be present at rest
HELPFUL TESTS
The recommended indications for noninvasive testing and coronary angiography fall into two categories: to establish a diagnosis in patients with suspected angina and to risk-stratify patients with chronic stable angina. Left ventricular (LV) function, the presence of inducible ischemia (Table 9.2), and the anatomic extent and severity of CAD are key predictors of long-term survival of patients with chronic stable angina, and they influence decisions regarding revascularization. Left ventricular ejection fraction (LVEF) may be assessed noninvasively with echocardiography, radionuclide techniques, cardiac magnetic resonance angiography (MRA), and cardiac CT angiography or invasively with contrast-enhanced ventriculography during cardiac catheterization. Exercise testing provides additional prognostic information. For example, a low Duke Treadmill score, which combines parameters reflecting exercise capacity and ischemia, is predictive of 4-year survival in 99% of patients tested (4).
The guidelines recommend the inclusion of either an echocardiographic or radionuclide imaging technique in patients with resting ST-segment depression, left bundle-branch block, ventricular paced rhythm, ventricular pre-excitation, or replorization changes from digoxin therapy. Patients with physical limitations, such as severe lung disease, arthritis, or peripheral vascular disease, should undergo pharmacologic stress testing in combination with an imaging modality.
TABLE 9.2.Noninvasive risk stratification
High risk (>3% annual mortality)
Resting or exercise LVEF <35%
Duke treadmill score ≤11
Large or multiple stress-induced perfusion defects
Stress-induced LV dilation or increased lung uptake of thallium 201
Echocardiographic evidence of ischemia involving more than two segments at HR <120 or dobutamine infusion ≤10 µg/kg/min
Intermediate risk (1%-3% annual mortality)
LVEF 35%-49%
Duke treadmill score <5 and >11
Moderate stress-induced perfusion defect without LV dilation or increased lung uptake of thallium 201
Echocardiographic evidence of ischemia involving two or fewer segments at dobutamine infusion >10 µg/kg/min
Low risk (<1% annual mortality)
Duke treadmill score ≥5
No or small perfusion defect at rest or with stress
No stress-induced wall-motion abnormalities
HR, heart rate; LV, left ventricular; LVEF, left ventricular ejection fraction.
Electrocardiography
A resting 12-lead electrocardiogram (ECG) should be obtained in all patients with symptoms suggestive of angina pectoris. The resting ECG is normal in approximately 50% of patients with chronic stable angina. ST-T changes are usually nonspecific. Q waves may indicate previous MI. LV hypertrophy may be caused by hypertension, aortic stenosis, or hypertrophic cardiomyopathy. A Holter monitor or event recorder in patients with suspected vasospastic angina may be helpful, as these patients may have symptomatic or silent episodes of ischemia.
Echocardiography
The resting echocardiogram (Table 9.3) is useful for evaluating global and regional LV systolic function and regional wall motion, as well as identification of any underlying structural heart disease, such as aortic stenosis or hypertrophic cardiomyopathy.
Computed Tomography
Electron-beam computed tomography (EBCT) is a highly sensitive technique for detecting coronary artery calcification, an abnormality found in atherosclerotic arteries but not in normal arteries. An ACC/AHA Expert Consensus Document concluded that (a) EBCT has a high sensitivity, a much lower specificity, and overall predictive accuracy of 70% in a typical CAD patient population; (b) the predictive accuracy of EBCT is equivalent to alternative methods for diagnosing CAD; and (c) EBCT is not ideal for diagnosing CAD because of its low specificity (7). The totality of evidence from the literature indicates that the total amount of coronary calcium predicts CAD events beyond standard risk factors. Calcium scoring may be useful in refining clinical risk in some patients with intermediate risk for CAD [i.e., individuals with a 10% to 20% 10-year risk on the Framingham Risk Score (FRS)]. Patients in this latter category who have high calcium scores may thus qualify for more-aggressive target values for lipid-lowering therapies (8). Coronary calcium assessment may also be reasonable in evaluation of (a) symptomatic patients who have equivocal stress tests, (b) patients with a cardiomyopathy of unknown etiology, and (c) patients with chest pain, negative cardiac enzyme results, and negative or equivocal ECGs. Asymptomatic persons with low risk scores on conventional risk-stratification tools probably do not benefit from coronary calcium assessment. Current data do not support serial EBCT studies to assess progression of coronary calcification.
TABLE 9.3.Indications for echocardiography or radionuclide ventriculography to establish diagnosis and to stratify risk according to Canadian Cardiovascular Society Classification system
Class I
Resting echocardiogram in patients with a systolic murmur suggestive of mitral regurgitation, aortic stenosis, or hypertrophic cardiomyopathy
Resting echocardiogram or radionuclide ventriculogram to assess LV function in patients with history of MI, Q waves, complex ventricular arrhythmias, or symptoms suggestive of congestive heart failure
Class IIb
Resting echocardiogram to diagnose mitral valve prolapse in patients with a click or murmur or both
Class III
Resting echocardiogram in patients with a normal ECG, no history of MI, and no symptoms or signs of heart failure, valvular heart disease, or hypertrophic cardiomyopathy
ECG, electrocardiogram; LV, left ventricular; MI, myocardial infarction.
Given the invasive nature of cardiac catheterization and the significant number of patients referred for catheterization who have no or minimal epicardial coronary disease, an impetus exists to explore alternative ways of defining the lumen and walls of the coronary vasculature. Therefore interest in and use of multidetector cardiac CT (MDCT) angiography has increased dramatically over the last few years. CT angiography is a reasonable tool to rule out obstructive epicardial coronary disease in symptomatic patients with a low-to-intermediate pretest likelihood of disease. Use of CT angiography is currently not deemed “appropriate” when used in asymptomatic persons for the detection of occult disease (8). A significant limitation of CT angiography is variability in image quality due to motion artifacts (heart rate, ectopy, patient breathing), patient girth, and calcification. Another concern with MDCT is the high radiation dose associated with these studies. It is expected that the evolution of hardware programs and imaging protocols will lead to lower patient radiation exposure with future application of MDCT.
TABLE 9.4.Selected indications for noninvasive stress testing to establish diagnosis and to stratify risk according to Canadian Cardiovascular Society Classification system
Class I
Exercise ECG without imaging in patients with an intermediate pretest probability of CAD (see exceptions listed in classes II and III)
Exercise myocardial perfusion imaging or echocardiography in patients who are able to exercise, have an intermediate pretest probability of CAD, and one of the following baseline ECG abnormalities: Pre-excitation (Wolff-Parkinson-White) syndrome >1-mm resting ST depression
Exercise myocardial perfusion imaging or echocardiography in patients with prior PCI or CABG
Adenosine or dipyridamole myocardial perfusion imaging in patients with an intermediate pretest probability of CAD and one of the following baseline ECG abnormalities:
Electronically paced ventricular rhythm
Left bundle-branch block (LBBB)
Stress myocardial perfusion imaging or echocardiography to identify the extent, severity, and location of ischemia in patients who do not have LBBB or electronically paced ventricular rhythm, or to assess the functional significance of coronary lesions in planning PCI
Class IIa
Patients with suspected vasospastic angina
Class IIb
Exercise ECG in patients with high or low pretest probability of CAD
Exercise ECG in patients taking digitalis or with left ventricular hypertrophy and <1-mm ST-segment depression
Exercise or dobutamine echocardiography in patients with LBBB
Class III
Exercise ECG without imaging in patients with the following baseline ECG abnormalities:
Pre-excitation (Wolff-Parkinson-White) syndrome
Electronically paced ventricular rhythm
>1-mm resting ST depression
Complete LBBB
Patients with severe comorbidity that is likely to limit life expectancy or prevent revascularization
The predictive accuracy of noninvasive stress testing (Table 9.4) depends on the sensitivity and specificity of the test and the prevalence of the disease in the population studied, that is, the pretest probability of CAD. The exercise ECG is useful in patients with a normal resting ECG and an intermediate pretest probability of CAD, whereas it is less useful in patients with an abnormal resting ECG or either a low or high pretest probability of CAD. The inclusion of an imaging technique (i.e., echocardiography or myocardial perfusion imaging) increases the sensitivity and specificity of noninvasive stress testing. Pharmacologic stress testing (e.g., dobutamine echocardiography and adenosine or dipyridamole myocardial perfusion imaging) should be performed in patients who are unable to exercise adequately because of lung disease, peripheral vascular disease, or musculoskeletal disease.
TABLE 9.5.Selected indications for coronary angiography to establish diagnosis and to stratify risk according to Canadian Cardiovascular Society Classification system
Class I
Patients with known or possible angina who have survived sudden death
Patients with CCS class III or IV angina despite medical therapy
Patients with high-risk criteria shown on noninvasive testing regardless of anginal severity
Patients with angina and symptoms or signs of congestive heart failure
Class IIa
Patients with an uncertain diagnosis after noninvasive testing in whom the benefit of a more-certain diagnosis outweighs the risk and cost
Patients who cannot undergo noninvasive testing because of disability, illness, or obesity
Patients with an occupation requirement for a definitive diagnosis
Patients with a high pretest probability of left-main or three-vessel CAD
Patients with LVEF <45%, CCS class I or II angina, and demonstrable ischemia but less than high-risk criteria shown on noninvasive testing
Class IIb
Patients with recurrent hospitalization for chest pain
Patients with greater than a low probability of CAD and an overriding desire for a definitive diagnosis
Patients with LVEF >45%, CCS class I or II angina, and less than high-risk criteria shown on noninvasive testing
Class III
Patients with significant comorbidity in whom the risk outweighs the benefit
Patients with CCS class I or II angina who respond to medical therapy and have no evidence of ischemia on noninvasive testing
Patients who prefer to avoid revascularization
Patients with a personal desire for a definitive diagnosis but a low probability of CAD
CAD, coronary artery disease; CCS, Canadian Cardiovascular Society; LVEF, left ventricular ejection fraction.
Cardiac Catheterization and Coronary Angiography
Direct referral for diagnostic coronary angiography (Table 9.5) may be indicated in patients with chest pain and either a high pretest probability of severe CAD or a contraindication to noninvasive testing. Coronary angiography is usually accompanied by left-sided heart catheterization to rule out aortic stenosis and by contrast-enhanced ventriculography to assess regional and global LV function. Coronary angiography delineates the extent and severity of CAD and may reveal less-common nonatherosclerotic causes of angina, such as Kawasaki disease, vasospasm, coronary dissection, coronary fistulas, or anomalous origin of coronaries. Intracoronary ultrasound studies have demonstrated that diffuse coronary atherosclerosis may exist with a “false-negative” coronary angiogram. The hemodynamic significance of a coronary stenosis can be assessed with a Doppler wire or pressure-sensing wire.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis of chest pain includes numerous cardiac and noncardiac causes. Common cardiac causes of chest pain not attributable to myocardial ischemia are pericarditis and aortic dissection. Pulmonary causes include pulmonary embolism, pulmonary arterial hypertension, pneumothorax, pneumonia, and pleuritis. Gastrointestinal causes are esophagitis, esophageal spasm or reflux, esophageal tears, peptic ulcer disease, pancreatitis, and biliary tract diseases. Musculoskeletal causes of chest pain are muscular strain or spasm, costochondritis, fibromyalgia, rib fractures, cervical radiculopathy, and herpes zoster. Finally, chest pain may occur in patients with various psychiatric conditions, such as anxiety and affective disorders.
COMPLICATIONS
Stable angina can have significant adverse effects on a patients’ quality of life and, in its most severe forms, it negatively affects an individual’s exercise capacity and functional independence. The medical complications of stable angina are primarily those that may ensue from CAD (i.e., progression to unstable angina, myocardial infarction, ischemic cardiomyopathy, congestive heart failure, atrial and ventricular arrhythmias, and sudden death).
THERAPY
The goals of treatment are to relieve symptoms and to reduce the risk of morbidity (e.g., MI) and mortality (4). Ideally, successful treatment results in a functional capacity of CCS class I. Contributing factors, such as anemia, hyperthyroidism, and poorly controlled blood pressure, should be identified and treated. The initial treatment program consists of the following:
C: cigarette-smoking cessation and cholesterol management
D: diet and diabetes therapy
E: education and exercise
Pharmacologic Therapy
Antianginal agents
Nitrates
Parker and Parker (9) published a detailed review of nitrate therapy (Table 9.6). Sublingual NTG tablets and spray are useful both for treating attacks of angina and for preventing episodes of exertional angina. Multiple long-acting nitrate preparations, including transdermal NTG, oral isosorbide dinitrate, and oral isosorbide mononitrate, have been shown to prolong the time to onset of ischemia during exercise testing. Tolerance, the major limitation of nitrate therapy, can be avoided by dosage regimens that provide a nitrate-free interval. Studies have suggested that antioxidant vitamins, such as vitamin C (10) and vitamin E (11), may counteract nitrate tolerance. No published evidence suggests that nitrates change the incidence of death or MI in patients with chronic stable angina.
TABLE 9.6.Recommendations for pharmacotherapy according to Canadian Cardiovascular Society Classification system
Class I
Aspirin
β-Blockers in patients with prior myocardial infarction
Calcium antagonists or long-acting nitrates when β-blockers are contraindicated or cause unacceptable side effects
Sublingual NTG or NTG spray for immediate relief of angina
Lipid-lowering therapy to achieve LDL <100 mg/dL
Class IIa
Clopidogrel when aspirin is contraindicated
Long-acting nondihydropyridine calcium antagonists instead of β-blockers
Class IIb
Low-intensity anticoagulation with warfarin in addition to aspirin
Class III
Dipyridamole
Chelation therapy
LDL, low-density lipoprotein; NTG, nitroglycerin.
β-blockers
The Atenolol Silent Ischemia Study (ASIST) was a double-blind, placebo-controlled, randomized study of atenolol, 100 mg daily, versus placebo in 306 patients with class I or II angina (12). The entry criteria included evidence of ischemia during both exercise testing and Holter monitoring. Treatment with atenolol reduced the number and average duration of ischemic episodes recorded during 48 hours of ambulatory ECG monitoring. The 1-year event-free survival rates were higher among the atenolol recipients than among the placebo recipients. Although ASIST was a relatively small trial, the results suggest that β-blockers may improve the prognosis of patients with chronic stable angina. β-Blockers are relatively contraindicated in patients with vasospastic angina, as unopposed α-receptor activity can induce or exacerbate coronary spasm.
Calcium channel blockers
The largest published placebo-controlled trial of a calcium channel blocker in patients with CAD was the Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial (PREVENT) (13). The trial was designed to determine whether amlodipine retards progression of atherosclerosis in patients with CAD. Coronary angiography and carotid ultrasonography were performed in 825 patients at baseline and after 3 years. Of these patients, 69% had a history of stable angina. During the 3 years of follow-up, fewer hospitalizations occurred for unstable angina and coronary revascularization among the amlodipine recipients. No differences were found in mortality or MI rates. Carotid artery atherosclerosis measured by ultrasonography progressed in the placebo recipients but not in the amlodipine recipients. No effect of amlodipine was noted on progression of coronary atherosclerosis as measured by coronary angiography.
The Angina Prognosis Study in Stockholm (APSIS) was a long-term study of metoprolol or verapamil in 809 patients with stable angina (14). Patients were randomly assigned in a double-blind manner to receive either metoprolol, 200 mg daily, or verapamil, 240 mg twice daily. After a median follow-up period of 3.4 years, no differences were seen in total mortality, cardiovascular mortality, nonfatal cardiovascular events, or combined cardiovascular events.
The Total Ischaemic Burden European Trial (TIBET) was a long-term study of atenolol, nifedipine, and their combination in 682 patients with chronic stable angina (15). Patients were randomly assigned to receive atenolol, 50 mg twice daily; nifedipine, 20 or 40 mg twice daily; or the combination. Exercise parameters improved and ambulatory ischemia decreased in each group, with no differences between the groups. No significant differences were found in the frequency of clinical events.
Heidenreich et al. (16) performed a meta-analysis of trials that compared β-blockers, calcium channel blockers, and nitrates for stable angina. Trials that compared nitrates with either β-blockers or calcium channel blockers were too few to determine their relative efficacy. Although 72 studies that compared β-blockers with calcium channel blockers were identified, the APSIS and TIBET trials discussed previously were the only trials longer than 6 months, and they accounted for 103 of the 116 cardiac events that occurred in all of the trials. Short-acting dihydropyridine Ca+ antagonists should be avoided in patients with angina.
A more recent prospective double-blind randomized study, the CAMELOT trial, compared the effects of enalapril, amlodipine, and placebo on cardiovascular events in patients with established CAD but normal blood pressures (17). Amlodipine, but not enalapril, significantly reduced the incidence of cardiovascular events compared with placebo (HR = 0.69; p = 0.003). The intravascular ultrasound substudy showed a significantly reduced rate of atherosclerosis progression (p = 0.02) in a subgroup of patients with systolic blood pressures greater than the mean (i.e., 129/78 mm Hg).
Ranolazine
Ranolazine is a recently approved drug for treatment of angina in patients whose symptoms are refractory to conventional drugs and in whom the coronary anatomy is unsuitable for revascularization. Two mechanisms of action exist for this drug: (a) prevention of calcium overload in ischemic myocytes and thus prevention of diastolic tension, and (b) altered cardiac energy metabolism with partial inhibition of fatty acid oxidation with switch to glucose oxidation, thus increasing cardiac metabolic efficiency (18). Several large-scale clinical trials have confirmed the efficacy of this drug, either as monotherapy or when added to other antianginal agents (i.e., β-blockers).
In the ERICA trial, 565 patients with stable angina who were taking amlodipine, 10 mg per day, and were allowed long-acting nitrates, but no β-blockers, were assigned to ranolazine, 1,000 mg per day, or placebo (19). Ranolazine significantly reduced the number of anginal episodes per week to 2.88 compared with 3.31 with placebo. In a larger trial consisting of 823 patients (CARISA) who were taking either atenolol or a calcium channel blocker, ranolazine significantly increased symptom-limited exercise duration and time to ST-segment depression compared with placebo (20). The frequency of anginal episodes was reduced by 0.8 per week with 750 mg twice daily and by 1.2 episodes per week with 1,000 mg twice daily compared with placebo. In the MARISA trial, 191 patients were randomly assigned to placebo or monotherapy with three different doses of ranolazine (500, 1,000, and 1,500 mg twice daily). At all three doses, ranolazine significantly increased exercise duration compared with placebo (21).
Ranolazine can produce QT prolongation and is contraindicated in patients with prolonged QT as well as those taking other drugs that can prolong the QT interval. However, torsades de pointes ventricular tachycardia has not yet been reported. This drug should be used with caution in patients taking digitalis glycosides or simvastatin, as ranolazine may inhibit their metabolism.
Antiplatelet agents
Aspirin
Several clinical trials have demonstrated that aspirin improves outcome in patients with chronic stable angina. The Physicians’ Health Study, a trial of aspirin (325 mg daily) among 22,071 male physicians, included 333 men with chronic stable angina at the time of enrollment (22). After an average follow-up of 60 months, the incidence of MI was seven among 178 patients who received aspirin, in comparison with 20 among 155 patients who received placebo (relative risk, 0.30; confidence interval, 0.04 to 0.42; p < 0.001). The Swedish Angina Pectoris Trial (SAPAT) randomly assigned 2,035 patients with chronic stable angina to receive either aspirin, 75 mg daily, or placebo (23). All patients were treated with sotalol for control of symptoms. After a median-duration follow-up of 50 months, the aspirin recipients had a 34% lower incidence of sudden death and nonfatal MI (p = 0.003). No significant difference was found in major bleeding. The guidelines recommend that aspirin, 75 to 325 mg, should be prescribed to all patients with angina and no contraindications (4).
Clopidogrel
Although no placebo-controlled trials of clopidogrel have been conducted in patients with chronic stable angina, clopidogrel was superior to aspirin in patients with CAD who were enrolled in the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial (24). Therefore patients who are intolerant of or truly allergic to aspirin should be treated with clopidogrel.
Lipid-lowering agents
Statins
The Scandinavian Simvastatin Survival Study (4S) was a randomized trial of simvastatin in 4,444 patients with a history of angina pectoris or MI. Among the 21% of patients who had angina but no history of MI at the time of enrollment, a 26% reduction occurred in the risk of major coronary events (coronary deaths, nonfatal MI, and resuscitated cardiac arrest), but analysis of this subgroup was not prespecified, and the difference did not achieve statistical significance (25). The Regression Growth Evaluation Statin Study (REGRESS) was a randomized trial of the effects of pravastatin on progression and regression of CAD (26). Enrollment included 768 male patients with stable angina, documented CAD, and serum cholesterol levels of 155 to 310 mg per deciliter. Forty-eighthour ambulatory ECGs that were obtained before and after random assignment to receive pravastatin, 40 mg daily, or placebo demonstrated that pravastatin significantly decreased the frequency and duration of ischemic episodes.
The Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial compared intensive lipid lowering with atorvastatin, 80 mg, with moderate lipid lowering with pravastatin, 40 mg, on coronary artery atheroma burden assessed with intravascular ultrasound measurements (27). Patients undergoing diagnostic coronary angiography for a clinical indication were enrolled, in whom intravascular ultrasound study was performed at baseline and after an 18-month period of treatment. Of the 654 patients randomized, 502 had evaluable paired studies. The mean baseline LDL was 150 mg per deciliter in both groups. It was reduced to 110 mg per deciliter in the pravastatin group and to 79 mg per deciliter in the atorvastatin group. Atheroma burden was unchanged in the atorvastatin group, suggesting no disease progression, whereas it increased (+ 2.7%; p < 0.001) in the pravastatin group, suggesting progression of disease. A significant decrease in CRP was observed compared with baseline in high-dose statin patients compared with the moderate-dose group. This latter finding raises the possibility that, to the extent that atherosclerosis is an inflammatory disease, the differences in the atheroma burden in the two groups are largely attributable to the differences in CRP reductions.
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