A successful treatment strategy for angina requires an understanding of an individual patient's symptoms and history.
Angina pectoris—chest discomfort caused by myocardial ischemia (insufficient oxygen)—affects approximately 10 million Americans, with 500,000 new cases reported each year. Angina pectoris, or simply angina, can occur in the absence of other coronary diseases; however, approximately 58% of patients suffering from coronary heart disease experience angina. 1
Prevalence increases with age; women are disproportionately affected (femaleto-male ratio of 1.7:1). 2 Symptoms include sensations of discomfort, burning, dull aches, and squeezing or “heaviness” of the chest. Pain may radiate to the shoulders, arms, neck, throat, jaw, or back. Patients often mistake angina for heartburn. 3
Myocardial ischemia develops when blood flow is inadequate to meet myocardial demand. This results in myocardial cells switching from aerobic to anaerobic metabolism, leading to impaired cardiac function. 2 Numerous factors can induce angina (eg, abnormal constriction of vessels, abnormal heart rate, microvascular disease, structural abnormalities of arteries), but the most common is atherosclerosis—the narrowing and constricting of arteries resulting from cholesterol plaque and other deposits that build up over a period of years. It takes approximately 10 years of atherosclerosis progression before symptoms appear (when vessel narrowing exceeds 50%). 4
Risk factors associated with angina include family history of coronary heart disease, hypertension, diabetes, smoking, alcohol consumption, obesity, hypercholesterolemia, metabolic syndrome, and low levels of high-density lipoprotein cholesterol. 2,5 Elevated C-reactive protein is an important risk factor for women. 6
Several types of angina exist, but 2 account for the majority of cases:
• Stable angina: Pain onset is predictable and present only during physical exertion or extreme emotional distress. Stable angina is generally relieved by resting for several minutes.
• Unstable angina: Occurs more frequently, lasts longer, and may occur while resting or after a few minutes of moderate activity. Unstable angina may signal a pending heart attack. 5,6
Patient assessment must differentiate angina from noncoronary causes of chest pain, such as pulmonary disease, gastrointestinal disorders, chest wall trauma, and infections. Coronary angiography remains the gold standard in diagnosing coronary artery obstructions. 6
Treatment’s 3 primary interrelated goals are to limit the number and severity of attacks; protect against future and potentially more lethal ischemic syndromes, such as sudden death and myocardial infarction; and lower the risk for atherosclerosis progression. 6
Treatment strategies, consisting of pharmacotherapy, surgical interventions, and lifestyle changes, differ for each variant of angina. Combination treatments are more effective than any single intervention. 7
Traditional anti-ischemia therapy relies on 3 drug classes: nitrates, beta-blockers, and calcium channel blockers (Table 1). Pharmacologic agents are effective in managing symptoms, but are not disease modifying, ie, they do not alter the risk for heart attack or sudden death. 5 Lifestyle changes are disease modifying, however. It is important to note that antiplatelet agents may be prescribed for patients with other forms of coronary disease, but are contraindicated for patients with unstable angina. 4 Sublingual nitroglycerin has been the mainstay for treating stable angina for those with a maximum of 1 episode per week. It is used for acute episodes, or prophylactically prior to physical activity.
For those experiencing more frequent episodes, a long-acting nitrate or betablocker is added. Beta-blockers reduce myocardial oxygen demand and decrease heart rate and myocardial contractility. Long-term nitrates are not recommended; patients quickly develop a tolerance, and new evidence suggests long-term use increases risk for and severity of heart attacks. 8 Patients taking sublingual nitroglycerin do not build up a tolerance.
Calcium channel blockers are used for patients who cannot take beta-blockers or for patients in whom both nitroglycerin and beta-blockers are ineffective. Calcium channel blockers dilate arteries, lower blood pressure, and decrease the force of the heart’s contractions. 7 Shortacting dihydropyridine calcium channel blockers are avoided; they increase risk for adverse cardiac events. 8
Beta-blockers are considered first-line agents and are more effective in reducing angina’s frequency than calcium channel blockers.
Ranolazine, a piperazine derivative, is the newest anti-ischemic agent (approved by the FDA in 2002), and when combined with traditional anti-ischemia agents, often results in more positive outcomes, such as higher levels of exercise tolerance. Unlike beta-blockers, ranolazine does not alter heart rate or blood pressure. 9
Refractory angina—angina that cannot be controlled with available treatment options—affects up to 900,000 Americans. Ranolazine combined with enhanced external counterpulsation has emerged as an effective treatment option. 9 Although allopurinol is not FDA approved for ischemia, studies suggest that it, too, may be useful in treating refractory angina. 9
Patients need to understand treatment options, treatment risks and benefits, and the importance of healthy lifestyles (Table 2). Research demonstrates that angina patients can benefit if pharmacists provide more information on the importance of lifestyle factors and the purpose of medications, and their potential adverse effects. 10
Angina is not a contemporary disorder; atherosclerotic lesions have been identified in 3500-year-old Egyptian mummies. 6 Unlike in ancient Egypt, however, cardiovascular disease is now the leading cause of death in the United States. What your patients need to know is that it is preventable. PT
Dr. Zanni is a psychologist and health systems consultant based in Alexandria, Virginia.
1. Lloyd-Jones DM, Hong Y, Labarthe D, et al; American Heart Association Strategic Planning Task Force and Statistics Committee. Defining and setting national goals for cardiovascular health promotion and disease reduction: the American Heart Association’s strategic Impact Goal through 2020 and beyond. Circulation. 2010;121:586-613.
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3. WebMD Heart disease health center, heart disease and angina (chest pain). www.webmd.com/heart-disease/guide/heart-disease-angina. Accessed October 20, 2011.
4. Haber M. Angina pectoris in emergency medicine. http://emedicine.medscape.com/article/761889-overview. Accessed October 21, 2011.
5. Kones R. Recent advances in the management of chronic stable angina II: anti-ischemic therapy, options for refractory angina, risk factor reduction, and revascularization. Vasc Health Risk Manag. 2010;6:749-774.
6. Kones R. Recent advances in the management of chronic stable angina I: approach to the patient, diagnosis, pathophysiology, risk stratification, and gender disparities. Vasc Health Risk Manag. 2010;6:635-656.
7. Aroesty J, Kannam J. Patient information: angina treatment - medical therapy. www.uptodate.com/contents/patient-information-angina-treatment-medical-therapy. Accessed October 21, 2011.
8. Sun L, Ferreira JC, Mochly-Rosen D. ALDH2 activator inhibits increased
myocardial infarction injury by nitroglycerin tolerance. Sci Transl Med. 2011;3(107):107ra111.
9. Manchanda A, Aggarwal A, Aggarwal N, Soran O. Management of refractory angina pectoris. Cardiol J. 2011;18:343-351.
10. Haugbølle LS, Sørensen EW, Gundersen B, et al. Basing pharmacy counselling on the perspective of the angina pectoris patient. Pharm World Sci. 2002;24:71-78.
11. Tobin KJ. Stable angina pectoris: what does the current clinical evidence tell us? J Am Osteopath Assoc. 2010;110:364-370.
12. Mayo Clinic. Angina treatment: stents, drugs, lifestyle changes -what’s best? www.mayoclinic.com/health/angina-treatment/HB00091. Accessed October 20, 2011.