Prinzmetal's variant angina

Coronary artery disease (CAD) remains the number one cause of death and disability In men and women in the United States and all Industrialized societies. The prevalence of CAD is increasing as the population ages. The predominant presenting symptom is angina, classified as chronic sta ble, microvascular, Prinzmetal's, or unstable. Chronic stable angina Is the form most often encountered In the primary care setting. With appropriate management, long-term prognosis is good. Because anginal thresh olds vary, treatment must address individual patients needs. Patients should be counseled throughout follow-up and educated about modifying risk factors and managing routine activities. Most patients can be treated pharmacologically with single or combination therapy including long-acting nitrates, beta-blockers, and calcium channel blockers. Consultation with a cardiologist during follow-up may also be warranted.

Despite recent declines in the death rate from coronary artery disease (CAD), its importance as the number one killer in the United States and all industrialized societies is well established. About 11 million people in the United States have a history of CAD; direct and indirect costs approach $14 billion per year. CAD causes more deaths, disability, and economic loss than any other group of diseases.1

An increase in prevalence is anticipated as the population ages. Half of all deaths in persons older than age 65 are the result of CAD, and of all coronary deaths, 80% occur in patients age 65 and older. Therefore, the prevention, recognition, and management of CAD are of major significance to public health.1-3

Although CAD has no uniform presenting syndrome, the predominant manifestation is angina pectoris, a constellation of symptoms reflecting the transient inadequacy of myocardial blood flow. Angina is typically described as a sensation of squeezing, pressure, strangling, constriction, bursting, crushing, heaviness, or burning in the chest or adjacent areas. Patients sometimes describe a vague, mild numbness that may be accompanied by dyspnea. Patients usually do not consider their symptoms painful. Although the site of discomfort is usually retrosternal, radiation is common and most frequently occurs down the ulnar surface of the left arm. Radiation may also occur to the jaw and into the back between the shoulder blades. Anginal equivalents such as dyspnea, fatigue, syncope, and eructations are particularly common in the elderly. Women may experience first-effort angina but are more likely to experience discomfort at rest, during sleep, or with mental stress. Regardless of an individual's symptoms, angina typically begins gradually, lasts for a few minutes, and is relieved quickly with rest, medication, or both.1,4,5

Symptoms result from myocardial ischemia produced by an imbalance between myocardial oxygen (O2) supply and demand (see Figure 1). In the setting of CAD, angina primarily occurs when myocardial O2 demand exceeds available vascular supply secondary to atherosclerotic coronary occlusions, usually narrowing the arterial lumen by more than 70%.

The myocardial O2 demand is elevated by increases in heart rate, systolic wall tension, and contractility. Increases in these factors occur during physical activity or exercise, after a meal, during episodes of emotional excitement or mental stress, and as a result of exposure to extremes in temperature and humidity.

The severity, duration, and nature of the discomfort and precipitating factors do not correlate with the extent of an individual's CAD. Other cardiac conditions affect the balance of myocardial O2 demand and may result in anginal symptoms. They may occur alone or in the setting of CAD and include coronary vasospasm, aortic stenosis, left ventricular hypertrophy, atrial or ventricular arrhythmias, mitral valve prolapse, and coronary microvascular dysfunction.1,6,7

Clinically, the continuum of anginal syndromes encompasses chronic stable angina (CSA), microvascular angina, Prinzmetal's (variant) angina, and unstable angina. Because CAD manifested as CSA is the syndrome most commonly encountered in the outpatient setting, it will serve as the focus of the remaining discussion. For primary care providers to adequately manage patients with CSA, they must understand the clinical presentation, natural history, goals of treatment and treatment modalities, in addition to when consultation with or referral to a cardiology specialist is indicated.

Presentation

Health professionals who treat CSA patients must be skilled in differentiating chest pain syndromes. Table 1 lists common disorders whose presentation may mimic or exacerbate angina.1,4,6,7 Because CSA frequently coexists with one or more of these disorders, the practitioner must acquire competency in taking a history and performing a physical examination in patients who complain of chest pain.

Once CAD has been diagnosed and symptoms have been stable for several months-that is, with no increase in severity, frequency, or duration and no change in precipitating factors-a patient is considered to have CSA. Appreciating the wide variation in the levels of metabolic demand that lead to myocardial ischemia (anginal threshold) among patients and within individuals improves assessment and follow-up (see Table 2).1,8-10

Patients with variable-threshold CSA often complain of a circadian variation of angina in which discomfort is most pronounced in the morning. The probable reason is an increase in catecholamines, sympathetic activity, the cortisol pattern of secretion, and platelet aggregability on rising.1,8-10 Variable threshold angina is believed to result from dynamic coronary artery vasoconstriction superimposed on an underlying fixed obstruction. The concept of ischemic preconditioning is postulated to describe the phenomenon of first-effort (warm-up) angina.'1,11

Physical Examination and Electrocardiogram The physical and, particularly, the cardiovascular examination are often normal in persons with established CSA. Signs associated with previously identified risk factors (hypertension, hyperlipidemia, diabetes, obesity, and smoking) may be apparent, however. A third heart sound and pulmonary crackles may be auscultated during an episode of angina secondary to transient left ventricular dysfunction. The auscultatory findings of coexisting cardiac abnormalities (for example, aortic stenosis and mitral valve prolapse) may also be present. Carotid and femoral bruits are fairly common because of the strong association between peripheral vascular disease and CAD.1,4

The resting electrocardiogram (ECG), specifically the ST segment and T wave, remains normal in approximately half of patients with CSA, including those who have multivessel CAD but who have not previously had a myocardial infarction (MI). In addition, nonspecific ST segment-T-wave changes are commonly observed in the resting ECG in the general population (8.5% in men; 7.5% in women), increasing in prevalence with increasing age and in the presence of hypertension, diabetes, or smoking.

Left ventricular hypertrophy, electrolyte abnormalities, neurogenic effects, and antiarrhythmic drugs may also produce these ECG variances. In people with CSA, however, ST segment-T-wave changes may occur at rest during an episode of ischemia whether angina coexists or not. Half of the CSA population has been estimated to experience episodes of silent ischemia or MIs while performing normal daily activities whether or not they also have diabetes. Therefore, interval ECGs may reveal new ST segment-T-wave changes or Q-wave MIs that were symptomatically unrecognized.1,6

Natural History The clinical course of CSA may go on for more than 20 years; however, there is an increased risk of cardiac death by virtue of CAD presence. The prognosis is significantly correlated with three factors: the number and location of coronary stenosis (see Table 3);5 the presence and severity of ischemia as determined by stress testing; and the degree of left ventricular dysfunction determined by measurement of the ejection fraction (EF). An EF of less than 50% (normal = 60% to 65%) in the setting of CAD incurs higher risk.1,7,12-14

Patients with CSA often have single- or two-vessel CAD without involvement of the proximal left anterior descending coronary artery and preserved left ventricular function. Thus, both short- and long-term survival rates are good. The annual death rate is only 1.6% to 2.3 % in patients who are given adequate follow-up and lifestyle management.13

Treatment Goals and Modalities

Table 4 outlines the immediate therapeutic aims of the clinical management of CSA.6,7,13 The ultimate goal of treatment is to reduce the risk of MI and death.

Favorable outcomes are accomplished via comprehensive patient and family education, counseling on reducing coronary risk factors, pharmacologic intervention, treatment of comorbidities that can adversely affect the balance between myocardial 02 supply and demand, and, in some circumstances, revascularization.

Education and Counseling

The clinician should provide comprehensive education and counseling from the beginning and reinforce the information throughout follow-up. Patients and their families should be reassured about the relatively benign course of the disease and they should be advised on ways to reduce the CAD's progression and the risk of MI.

Because modifiable risk factors have an established physiologic link to the development and progression of CAD, the clinician must assist patients in developing strategies for managing those risk factors. Patients who smoke must stop. All patients must maintain sensible eating habits and weight, perform 30 minutes of physical activity a day, and keep their hypertension and diabetes well controlled.

Medications, including the appropriate use of sublingual nitroglycerin, can lead to positive outcomes. Patients should be advised about relevant aspects of work, leisure activities, and exercise (see Patient Education).

Many patients with CSA want to maintain active lifestyles; therefore, they want to know how much work or exercise is "safe." Because standard prescriptions for activity do not exist, the patient's clinical presentation and needs must be considered. The presence of CAD and CSA do not necessarily render vigorous exertion dangerous. If a strenuous activity repeatedly produces angina, however, it should be modified by performing it at a slower pace, taking breaks, lessening the work (for example, carrying several small loads rather than one large one), or eliminated altogether. Patients should not engage in a new vigorous activity that can not be stopped immediately if angina occurs (for example, scuba diving).

Patients should be encouraged to maintain sexual activity to a familiar and desired extent. This subject is a frequent source of anxiety for patients and their partners. The prophylactic use of sublingual nitroglycerin frequently provides short-term protection (for less than 30 minutes) for patients who engage in usual and desired activities (including sex), especially if previous experience suggests that the person may have an anginal response. Table 5 provides general guidelines for activity prescription.1,6,8

Stress test results can help the clinician determine appropriate activity and exercise, and so can participation in a structured cardiac rehabilitation program, if available. The clinician should remind the patient that he should not fear an occasional angina episode because an individual's anginal threshold can be learned only by trial and error. An episode of angina that is quickly relieved with rest or sublingual nitroglycerin is not life-threatening.

Patients and families should be instructed how to recognize and report a change in anginal symptoms. Because the most significant factor in survival and morbidity in the setting of an acute MI is the timeliness of reperfusion therapy, the clinician must reinforce MI signs and symptoms and outline strategies for appropriate action.15

Pharmacologic Intervention

Three classes of medications-nitrates, beta-adrenergic blockers, and calcium channel blockers-are used alone or in combination as clinical presentation and response dictate. These agents increase myocardial O2 supply, limit myocardial O2 demand, or both, allowing the patient with CSA to perform at a higher activity level, thus raising his or her anginal threshold.1,2,7 All of these agents provide equally effective angina prophylaxis and improvement in exercise. Consequently, the choice may be individualized, taking into consideration the coexistence of other diseases as outlined in Table 6.7

In many instances, sublingual nitroglycerin is the only antianginal agent required. If episodes occur more than two or three times per week, however, add a beta-- blocker or a calcium channel blocker. Table 7 provides an algorithm for prescribing antianginal medications.1,2,7

Other Pharmacologic Agents

All patients with established CAD should take 75 to 325 mg of aspirin daily unless contraindicated. This form of therapy has convincingly been shown to decrease mortality and morbidity in patients with CSA. The use of appropriate lipid-lowering agents in the secondary prevention of CAD, when indicated, positively affects the rate of coronary events.1,16,17

The role of estrogen-replacement therapy (ERT) and antioxidants in the primary and secondary prevention of CAD continues to receive attention.18 For ERT, each patient's risk-benefit ratio should be evaluated. The National Cholesterol Education Program has tentatively endorsed ERT in selected postmenopausal women within this category.19 The American College of Physicians guidelines suggest that ERT may be useful in women who are at high risk for developing CAD and for secondary prevention in women who have CAD but who are not at high risk for breast cancer.20 The use of combined estrogen/progestin therapy has not demonstrated significant benefit as a strategy to prevent recurrent coronary events in postmenopausal women.21

Antioxidants remain a promising but unproven means of decreasing the risks of cardiovascular disease. Trials are ongoing in both men and women to evaluate antioxidant use in the primary and secondary prevention of CAD.22,23

Management of Comorbidities

Crucial to the management of CSA is the identification and treatment of conditions that can increase myocardial 02 or reduce O2 delivery. Among such conditions that may aggravate a previously stable anginal pattern are anemias, occult thyrotoxicosis, fever, infections, tachycardias, hypoglycemia, and marked weight gain.

Patients should avoid amphetamines, cocaine, and drugs that stimulate the sympathetic nervous system. Patients frequently voice concern about how much caffeine is safe. Moderate consumption (four to five cups per day) of caffeinated coffee or the equivalent has not been shown to significantly increase the risk of coronary events or arrhythmia frequency. 1,6,24

Revascularization

Catheter-based interventions and coronary bypass graft surgery are generally not indicated in the management of CSA. To address patients' questions and concerns, primary care providers should understand when these procedures may be appropriate (see Table 8).

Providers should discuss these options with older adults. Retrospective studies indicate that rates of survival after coronary bypass and catheter-based procedures may not differ significantly from those noted in randomized trials of younger cohorts. Therefore, the clinician should discuss these procedures with older patients who might benefit from them.

Consulting a Cardiologist: When to Refer?

Determining whether consultation with a cardiologist is indicated depends on factors such as the care provider's expertise, available resources, the patient's clinical presentation, and even the status of the therapeutic relationship. If a stable anginal pattern changes while the patient is taking adequate doses of antianginal medications, the clinician should consider treatable causes and reassess the extent of CAD, then discuss treatment strategies in collaboration with a cardiologist. Some patients believe that their cardiac disease, whatever its severity, can be adequately managed only by a specialist. Providers should not fear the patient's request for a second opinion. Either the care they have provided will be validated or the patient will receive the necessary care.25

Patients whose CSA is managed appropriately may continue to lead active, productive lives and retain a relatively good prognosis. Because primary care providers are the most likely practitioners to care for this growing population, they are in a pivotal position to make a positive impact on patients' quality of life and longterm outcome.

REFERENCES

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3. 1997 Heart and Stroke Statistical Update. Dallas, Tex: American Heart Association; 1996:2-3.

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5. Douglas PS: Coronary artery disease in women. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine, 5th edition. Philadelphia, Pa.: WB. Saunders, Co.; 1997:1704-714. 6. Garoll AH: Chronic coronary heart disease. In: Garoll AH, May LA, Mulley AG, eds: Primary Care Medicine. Philadelphia, Pa.: J.B. Lippincott Co.; 1995:165-78.

7. Thandani U, Chohan A: Chronic stable angina pectoris: Strategies for effective drug therapy. Postgrad Med 1995;98(6):175-88. 8. Pepine CJ: Circadian variations in myocardial ischemia: Implications for management. JAMA 1991;265(3):386-90.

9. Effat MA: Pathophysiology of ischemic heart disease: An overview. AACN Clin Issues 1995;6(3):369-74.

10. Smith MA, Johnson DG: Evaluation and management of coronary artery disease: Guidelines for the primary care nurse practitioner. Nurs Prac Forum 1991;2(1):19-26.

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12. Gustein DE, Fuster V: Management of stable coronary artery disease. Am Fam Physician 1997;56(1):99-106.

13. O'Rourke RA: Cost-effective management of chronic stable angina. Clin

Cardiol 1996;19:497-501.

14. Alderman EL, Bourassa MG, Cohen LS, et al.: Ten-year follow-up of survival and myocardial infarction in the randomized Coronary Artery Surgery Study. Circulation 1990;82(5):1629-46. 15. Dracup K, Moser D: Beyond sociodemographics: Factors influencing the decision to seek treatment for symptoms of acute myocardial infarction. Heart Lung 1997;26(4):253-62.

16. Juul-Moller S, Edvardsson N, Jahnmatz B, et al.: Double-blind trial of aspirin in primary prevention of myocardial infarction in patients with stable chronic angina pectoris. Lancet 1992;340:1421-25. 17 Grundy SM: Cholesterol management in patients with heart disease. Postgrad Med 1997;102(2):81-90.

18. Sullivan JM, Swaag V, Hughes JP, et al.: Estrogen replacement and coronary artery disease: Effect on survival in postmenopausal women. Arch Intern Med 1990;150(12):2557-62.

19. Expert panel on detection, evaluation and treatment of high blood cholesterol in adults: Summary of the second report of the National Cholesterol Education Program (NCEP). (adult treatment panel II). JAMA 1993; 269(23):3015-23.

20. American College of Physicians: Guidelines for counseling postmenopausal women about preventive hormone therapy. Ann Intern Med 1992;117(12):1038-41.

21. Hulley S, Gradey D, Bush T, et al.: Randomized trial of estrogen plus progestin for secondary prevention of coronary heart disease in postmenopausal women. JAMA 1998;280(7):605-13.

22. Hennekens CH, GasianoM, Manson JE, Buring JE: Antioxidant vitamincardiovascular disease hypothesis is still promising, but still unproven: The need for randomized trials. AmJ Clin Nutr 1995;62(suppl):1277S-13805. 23. Hennekens CH: Antioxidant vitamins and cardiovascular disease: Current perspectives and future directions. Eur Heart J 1997;18(2):177-79. 24. Lynn AL, Kissinger JF: Coronary precautions: Should caffeine be restricted after myocardial infarction? Heart Lung 1992;21(4):365-71. 25. Chosy JJ: Referrals. In: Alpert JS, ed: Cardiology for the Primary Care Physician. St. Louis, Mo.: Mosby, Inc.; 1996:7-10.

ABOUT THE AUTHOR

Sally Beattie, RN, CS, GNP, MS, is an advanced practice nurse in

cardiology, in Columbia, Mo.

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