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Safety of exercise testing in the chest pain unit: 31-mm ST elevation in variant angina
Journal of Electrocardiology 39 (2006) 309.e1 – 309.e4 www.elsevier.com/locate/jelectrocard
Safety of exercise testing in the chest pain unit: 31-mm ST elevation in variant angina Fausan S. Tsai, MDa,4, Shahriar Heidary, MDb, Radha Sarma, MDb, Uri Elkayam, MDb a
b
Department of Medicine, University of Southern California/Los Angeles County Medical Center, Los Angeles, CA 90033, USA Division of Cardiovascular Medicine, University of Southern California/Los Angeles County Medical Center, Los Angeles, CA 90033, USA Received 1 December 2005; accepted 22 February 2006
Abstract
We discuss a patient who presented with symptoms classic for variant angina with dramatic 31-mm ST elevation secondary to exercise testing in the chest pain unit, in whom neither myocardial infarction nor severe arrhythmia resulted. Although exercise testing is deemed generally safe, it has not been studied for safety per se in patients with variant angina. Further studies are needed to determine if the magnitude of ST elevation during exercise testing carries prognostic significance. D 2006 Elsevier Inc. All rights reserved.
Keywords:
Variant angina; ST elevation; Chest pain; Exercise testing
Introduction The classic scenario of variant angina is angina at rest, occurring in a diurnal pattern, typically late at night or in early morning hours. Patients affected by variant angina can be completely symptom-free in between episodes. Although mortality from variant angina is low, coronary vasospasm can result in myocardial infarction and life-threatening arrhythmias. Serious arrhythmias and myocardial infarction were reported in 43% and 27% of patients, respectively, in a study of 30 patients with variant angina.1 In 59 patients with variant angina followed for an average of 6 years, myocardial infarction occurred in 19% and major arrhythmias in 24%.2 Severe coronary stenosis does not have to be present for myocardial infarction to occur.3 We present a patient without significant obstructive coronary artery disease who despite demonstrating dramatic ST elevation secondary to exercise testing from coronary vasospasm did not develop myocardial infarction or severe arrhythmia. Narrative VC, a 60-year-old Vietnamese male, presented to the emergency department with a 3-month history of 5 of 10 nonexertional, nonradiating substernal chest pain. He described it bas if someone is punching me in the chest.Q He 4 Corresponding author. Tel.: +1 323 226 7541; fax: +1 323 226 8076. E-mail address: [email protected] (F.S. Tsai). 0022-0736/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2006.02.012
first experienced this pain 3 months before admission, and it has occurred weekly since then. The chest pain usually awakened him from sleep around 3 am and spontaneously resolved after 10 minutes. At the time of admission, he was chest pain–free. He did not report shortness of breath, orthopnea, palpitations, nausea, diaphoresis, or syncope. He had been able to walk without chest pain or dyspnea 2 blocks to his store everyday for the past 10 years; this has not changed recently. His cardiac risk factors included dyslipidemia, for which he has been taking a lipid-lowering medication for the last 2 years, and a 20-pack-year smoking history. He did not have hypertension, diabetes mellitus, or a family history of premature coronary artery disease. In the emergency department, he presented with the following vitals: blood pressure 115/80 mm Hg, heart rate 72 bpm, respiratory rate 18, temperature 97.6 F, SaO2 98% on room air. Physical exam was unremarkable: he had a normal body weight index; there was no jugular venous distention; cardiac exam demonstrated a point of maximal impulse in the fifth intercostal space at the midclavicular line, a regular rate and rhythm, normal S1 and S2 with no murmurs, S3 or S4; lungs were clear; peripheral pulses were normal; and there was no extremity edema. Initial electrocardiogram (EKG) (Fig. 1) showed normal sinus rhythm at 60 bpm with upsloping ST segments in V2-V3 and biphasic T waves in V1-V4. The patient reported no chest pain during this EKG. Chest x-ray was normal, as were electrolytes, creatinine clearance, complete blood count, and coagulation profile.
309.e2
F.S. Tsai et al. / Journal of Electrocardiology 39 (2006) 309.e1 – 309.e4
Fig. 1. Baseline.
Fig. 2. After progressive ST elevation with exercise to 28 mm, ST elevation peaked at 31 mm at 2 minutes during recovery.
F.S. Tsai et al. / Journal of Electrocardiology 39 (2006) 309.e1 – 309.e4
Laboratory tests were abnormal only for dyslipidemia: cholesterol 201 mg/dL, triglycerides 111 mg/dL, highdensity lipoprotein 47 mg/dL, low-density lipoprotein 132 mg/dL. Serial troponin-I values were negative every 6 hours for a total of 3. The patient was then admitted to the chest pain unit (a 23-hour observation unit for low cardiac risk patients), where he underwent standard Bruce protocol exercise testing. At 1 minute, ST elevations emerged in leads II, III, aVF, and V2-V4 (all of which did not have diagnostic Q waves); he was chest pain–free. Loose leads or artifact was suspected by the emergency department resident and technician; hence, the patient was allowed to continue. At 3 minutes, ST elevation persisted, and at this time, he began to experience chest discomfort. He continued to exercise up to 6 minutes, when his chest pain intensified to 5 of 10, which was similar to the pain he presented with, and EKG showed progressive elevation of the ST segment up to 28 mm. The patient was told to stop exercising, and during the recovery period, ST segment elevation peaked at 31 mm at 2 minutes (Fig. 2). The patient’s chest pain resolved with rest. Troponin-I rose slightly after exercise testing from b0.1 to 0.4 ng/mL but was within the reference range (0.0 to 1.2 ng/mL) according to our laboratory.
309.e3
Because of the magnitude of the ST segment elevation and the patient’s chest pain, coronary angiography was performed later the same day. It showed normal left main, circumflex, and right coronary artery, and a 90% lesion in the middle segment of the left anterior descending artery was noted. LV gram showed mild anterolateral hypokinesis and normal systolic function. With administration of intracoronary nitroglycerin (200 Ag), the left anterior descending lesion reduced to 30%; no thrombus was seen. The diagnosis of variant angina was confirmed. The patient reported no chest pain during the procedure, and subsequent troponin-I values were negative. The patient was started on isosorbide mononitrate (120 mg daily), amlodipine (10 mg daily), aspirin (81 mg daily), benazepril (5 mg daily), and atorvastatin (80 mg daily), with no recurrences of chest pain during hospitalization. Exercise testing using the Bruce protocol was repeated 3 days after the above medical regimen was started. The patient was able to exercise for 9 minutes with no changes of the ST segment and no chest pain (Fig. 3). He was discharged on the above regimen, and smoking cessation was advised. At 10 months follow-up, the patient is chest pain–free on the above medication regimen but has resumed smoking.
Fig. 3. On medical therapy, the patient exercised for 9 minutes up to the fourth stage with no ST elevation or chest pain.
309.e4
F.S. Tsai et al. / Journal of Electrocardiology 39 (2006) 309.e1 – 309.e4
Discussion Patients with variant angina will not always be symptomatic when they arrive at the hospital or clinic seeking attention, and there may not be electrocardiographic evidence of ST segment changes. Therefore, exercise testing, which can provoke ST segment changes during or immediately afterward, can aid with diagnosis. Generally, ST elevation is not a common electrocardiographic abnormality seen on exercise testing. In a study of 6040 patients without myocardial infarction being evaluated for coronary disease, ST segment elevation induced by exercise was seen only 8%.4 In contrast, the incidence of exercise-induced ST-segment elevation in patients with variant angina is 18% to 30%.5-7 It is important to note that diurnal variation plays a significant role in variant angina. Of 13 patients with variant angina, exercise-induced ST segment elevation was seen in all patients when performed in the early morning, but only in 2 patients when performed in the afternoon.8 Thus, performing the exercise test at certain times of the day may influence the frequency at which one sees ST segment changes. Absolute indications for stopping exercise testing include N 1 mm ST elevation in leads without diagnostic Q waves, other than V1 or aVR; N 10 mm Hg drop in systolic blood pressure with other evidence of ischemia; moderate to severe angina; increasing ataxia, dizziness, or near-syncope; signs of poor perfusion; sustained ventricular tachycardia; technical inability to monitor the patient; and if the patient wishes to stop.9 If these guidelines are adhered to, exercise testing is deemed safe, with a rate of myocardial infarction and death around 1 per 2500 tests.10 In determining the safety of exercise testing in patients with variant angina who present to the chest pain unit, it should be kept in mind that this patient population is not a large one, and this topic has not been particularly investigated. Presence of ST segment elevation in patients with variant angina does not always correlate with poor performance on exercise testing. In a study of 16 patients, 8 patients developed exercise-induced ST elevation, but only those with significant coronary artery disease demonstrated poor exercise capacity and hemodynamic response.1 Another study reported no statistically significant difference in incidence of ventricular arrhythmias between those who demonstrated ST segment changes and those who did not.5 No adverse events were reported as a result of exercise testing, even in the setting of acute ST segment elevation, in 82 patients with variant angina studied by Waters et al,5 91 patients studied by Castello et al,11 and 138 patients studied by Maseri et al.7 However, these studies did not measure postexercise cardiac enzymes. In one study that allowed patients to continue maximal exercise testing, despite
ST elevation, until the onset of exhaustion, angina pectoris, or ventricular arrhythmia, 4 of 6 patients developed severe ventricular arrhythmias.12 The greatest reported magnitude of exercise-induced ST elevation was 10 mm.1,5,12 Further collaboration between the emergency and cardiology departments is necessary to review the exercise testing guidelines, so as not to overlook ST elevation as a possible finding in routine exercise testing in the chest pain unit. In our patient, exercise testing should have been terminated as soon as 1 mm or higher ST elevation was seen. Fortunately, despite a dramatic 31 mm ST elevation from severe coronary vasospasm, neither myocardial infarction nor ventricular arrhythmia resulted. Further studies are needed to determine if the magnitude of exercise-induced ST elevation in patients with variant angina correlates with incidence of myocardial infarction and severe arrhythmias, and if it carries prognostic significance.
References 1. Kerin NZ, Rubenfire M, Naini M, et al. Prinzmetal’s variant angina: electrocardiographic and angiographic correlations. J Electrocardiol 1982;15:365. 2. Bott-Silverman C, Heupler FA. Natural history of pure coronary artery spasm in patients treated medically. JACC 1983;2:200. 3. Waters DD, Szlachcic J, Miller D, Theroux P. Clinical characteristics of patients with variant angina complicated by myocardial infarction or death within 1 month. Am J Cardiol 1982;49:658. 4. Longhurst JC, Kraus WL. Exercise-induced ST elevation in patients without myocardial infarction. Circulation 1979;3(60):616. 5. Waters DD, Szlachcic J, Bourassa MG, et al. Exercise testing in patients with variant angina: results, correlation with clinical and angiographic features and prognostic significance. Circulation 1982;65:265. 6. Chaitman BR, Waters DD, Theroux P, Hanson JS. S-T segment elevation and coronary spasm in response to exercise. Am J Cardiol 1981;47:1350. 7. Maseri A, Severi S, De Nes M, et al. bVariant Q angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia. Am J Cardiol 1978;42:1019. 8. Yasue H, Omote S, Takizawa A, et al. Circadian variation of exercise capacity in patients with Prinzmetal’s variant angina: role of exerciseinduced coronary arterial spasm. Circulation 1979;59:938. 9. Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). 2002. American College of Cardiology website. Available at: www.acc.org/clinical/guidelines/ exercise/dirIndex.htm. 10. Stuart RJ, Ellestad MH. National survey of exercise stress testing facilities. Chest 1980;1(77):94. 11. Castello R, Alegria E, Merino A, et al. The value of exercise testing in patients with coronary artery spasm. Am Heart J 1990;119:259. 12. Detry JMR, Mengeot P, Rousseau MF, et al. Maximal exercise testing in patients with spontaneous angina pectoris associated with transient ST segment elevation. Br Heart J 1975;37:897.
Safety of exercise testing in the chest pain unit: 31-mm ST elevation in variant angina Fausan S. Tsai, MDa,4, Shahriar Heidary, MDb, Radha Sarma, MDb, Uri Elkayam, MDb a
b
Department of Medicine, University of Southern California/Los Angeles County Medical Center, Los Angeles, CA 90033, USA Division of Cardiovascular Medicine, University of Southern California/Los Angeles County Medical Center, Los Angeles, CA 90033, USA Received 1 December 2005; accepted 22 February 2006
Abstract
We discuss a patient who presented with symptoms classic for variant angina with dramatic 31-mm ST elevation secondary to exercise testing in the chest pain unit, in whom neither myocardial infarction nor severe arrhythmia resulted. Although exercise testing is deemed generally safe, it has not been studied for safety per se in patients with variant angina. Further studies are needed to determine if the magnitude of ST elevation during exercise testing carries prognostic significance. D 2006 Elsevier Inc. All rights reserved.
Keywords:
Variant angina; ST elevation; Chest pain; Exercise testing
Introduction The classic scenario of variant angina is angina at rest, occurring in a diurnal pattern, typically late at night or in early morning hours. Patients affected by variant angina can be completely symptom-free in between episodes. Although mortality from variant angina is low, coronary vasospasm can result in myocardial infarction and life-threatening arrhythmias. Serious arrhythmias and myocardial infarction were reported in 43% and 27% of patients, respectively, in a study of 30 patients with variant angina.1 In 59 patients with variant angina followed for an average of 6 years, myocardial infarction occurred in 19% and major arrhythmias in 24%.2 Severe coronary stenosis does not have to be present for myocardial infarction to occur.3 We present a patient without significant obstructive coronary artery disease who despite demonstrating dramatic ST elevation secondary to exercise testing from coronary vasospasm did not develop myocardial infarction or severe arrhythmia. Narrative VC, a 60-year-old Vietnamese male, presented to the emergency department with a 3-month history of 5 of 10 nonexertional, nonradiating substernal chest pain. He described it bas if someone is punching me in the chest.Q He 4 Corresponding author. Tel.: +1 323 226 7541; fax: +1 323 226 8076. E-mail address: [email protected] (F.S. Tsai). 0022-0736/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2006.02.012
first experienced this pain 3 months before admission, and it has occurred weekly since then. The chest pain usually awakened him from sleep around 3 am and spontaneously resolved after 10 minutes. At the time of admission, he was chest pain–free. He did not report shortness of breath, orthopnea, palpitations, nausea, diaphoresis, or syncope. He had been able to walk without chest pain or dyspnea 2 blocks to his store everyday for the past 10 years; this has not changed recently. His cardiac risk factors included dyslipidemia, for which he has been taking a lipid-lowering medication for the last 2 years, and a 20-pack-year smoking history. He did not have hypertension, diabetes mellitus, or a family history of premature coronary artery disease. In the emergency department, he presented with the following vitals: blood pressure 115/80 mm Hg, heart rate 72 bpm, respiratory rate 18, temperature 97.6 F, SaO2 98% on room air. Physical exam was unremarkable: he had a normal body weight index; there was no jugular venous distention; cardiac exam demonstrated a point of maximal impulse in the fifth intercostal space at the midclavicular line, a regular rate and rhythm, normal S1 and S2 with no murmurs, S3 or S4; lungs were clear; peripheral pulses were normal; and there was no extremity edema. Initial electrocardiogram (EKG) (Fig. 1) showed normal sinus rhythm at 60 bpm with upsloping ST segments in V2-V3 and biphasic T waves in V1-V4. The patient reported no chest pain during this EKG. Chest x-ray was normal, as were electrolytes, creatinine clearance, complete blood count, and coagulation profile.
309.e2
F.S. Tsai et al. / Journal of Electrocardiology 39 (2006) 309.e1 – 309.e4
Fig. 1. Baseline.
Fig. 2. After progressive ST elevation with exercise to 28 mm, ST elevation peaked at 31 mm at 2 minutes during recovery.
F.S. Tsai et al. / Journal of Electrocardiology 39 (2006) 309.e1 – 309.e4
Laboratory tests were abnormal only for dyslipidemia: cholesterol 201 mg/dL, triglycerides 111 mg/dL, highdensity lipoprotein 47 mg/dL, low-density lipoprotein 132 mg/dL. Serial troponin-I values were negative every 6 hours for a total of 3. The patient was then admitted to the chest pain unit (a 23-hour observation unit for low cardiac risk patients), where he underwent standard Bruce protocol exercise testing. At 1 minute, ST elevations emerged in leads II, III, aVF, and V2-V4 (all of which did not have diagnostic Q waves); he was chest pain–free. Loose leads or artifact was suspected by the emergency department resident and technician; hence, the patient was allowed to continue. At 3 minutes, ST elevation persisted, and at this time, he began to experience chest discomfort. He continued to exercise up to 6 minutes, when his chest pain intensified to 5 of 10, which was similar to the pain he presented with, and EKG showed progressive elevation of the ST segment up to 28 mm. The patient was told to stop exercising, and during the recovery period, ST segment elevation peaked at 31 mm at 2 minutes (Fig. 2). The patient’s chest pain resolved with rest. Troponin-I rose slightly after exercise testing from b0.1 to 0.4 ng/mL but was within the reference range (0.0 to 1.2 ng/mL) according to our laboratory.
309.e3
Because of the magnitude of the ST segment elevation and the patient’s chest pain, coronary angiography was performed later the same day. It showed normal left main, circumflex, and right coronary artery, and a 90% lesion in the middle segment of the left anterior descending artery was noted. LV gram showed mild anterolateral hypokinesis and normal systolic function. With administration of intracoronary nitroglycerin (200 Ag), the left anterior descending lesion reduced to 30%; no thrombus was seen. The diagnosis of variant angina was confirmed. The patient reported no chest pain during the procedure, and subsequent troponin-I values were negative. The patient was started on isosorbide mononitrate (120 mg daily), amlodipine (10 mg daily), aspirin (81 mg daily), benazepril (5 mg daily), and atorvastatin (80 mg daily), with no recurrences of chest pain during hospitalization. Exercise testing using the Bruce protocol was repeated 3 days after the above medical regimen was started. The patient was able to exercise for 9 minutes with no changes of the ST segment and no chest pain (Fig. 3). He was discharged on the above regimen, and smoking cessation was advised. At 10 months follow-up, the patient is chest pain–free on the above medication regimen but has resumed smoking.
Fig. 3. On medical therapy, the patient exercised for 9 minutes up to the fourth stage with no ST elevation or chest pain.
309.e4
F.S. Tsai et al. / Journal of Electrocardiology 39 (2006) 309.e1 – 309.e4
Discussion Patients with variant angina will not always be symptomatic when they arrive at the hospital or clinic seeking attention, and there may not be electrocardiographic evidence of ST segment changes. Therefore, exercise testing, which can provoke ST segment changes during or immediately afterward, can aid with diagnosis. Generally, ST elevation is not a common electrocardiographic abnormality seen on exercise testing. In a study of 6040 patients without myocardial infarction being evaluated for coronary disease, ST segment elevation induced by exercise was seen only 8%.4 In contrast, the incidence of exercise-induced ST-segment elevation in patients with variant angina is 18% to 30%.5-7 It is important to note that diurnal variation plays a significant role in variant angina. Of 13 patients with variant angina, exercise-induced ST segment elevation was seen in all patients when performed in the early morning, but only in 2 patients when performed in the afternoon.8 Thus, performing the exercise test at certain times of the day may influence the frequency at which one sees ST segment changes. Absolute indications for stopping exercise testing include N 1 mm ST elevation in leads without diagnostic Q waves, other than V1 or aVR; N 10 mm Hg drop in systolic blood pressure with other evidence of ischemia; moderate to severe angina; increasing ataxia, dizziness, or near-syncope; signs of poor perfusion; sustained ventricular tachycardia; technical inability to monitor the patient; and if the patient wishes to stop.9 If these guidelines are adhered to, exercise testing is deemed safe, with a rate of myocardial infarction and death around 1 per 2500 tests.10 In determining the safety of exercise testing in patients with variant angina who present to the chest pain unit, it should be kept in mind that this patient population is not a large one, and this topic has not been particularly investigated. Presence of ST segment elevation in patients with variant angina does not always correlate with poor performance on exercise testing. In a study of 16 patients, 8 patients developed exercise-induced ST elevation, but only those with significant coronary artery disease demonstrated poor exercise capacity and hemodynamic response.1 Another study reported no statistically significant difference in incidence of ventricular arrhythmias between those who demonstrated ST segment changes and those who did not.5 No adverse events were reported as a result of exercise testing, even in the setting of acute ST segment elevation, in 82 patients with variant angina studied by Waters et al,5 91 patients studied by Castello et al,11 and 138 patients studied by Maseri et al.7 However, these studies did not measure postexercise cardiac enzymes. In one study that allowed patients to continue maximal exercise testing, despite
ST elevation, until the onset of exhaustion, angina pectoris, or ventricular arrhythmia, 4 of 6 patients developed severe ventricular arrhythmias.12 The greatest reported magnitude of exercise-induced ST elevation was 10 mm.1,5,12 Further collaboration between the emergency and cardiology departments is necessary to review the exercise testing guidelines, so as not to overlook ST elevation as a possible finding in routine exercise testing in the chest pain unit. In our patient, exercise testing should have been terminated as soon as 1 mm or higher ST elevation was seen. Fortunately, despite a dramatic 31 mm ST elevation from severe coronary vasospasm, neither myocardial infarction nor ventricular arrhythmia resulted. Further studies are needed to determine if the magnitude of exercise-induced ST elevation in patients with variant angina correlates with incidence of myocardial infarction and severe arrhythmias, and if it carries prognostic significance.
References 1. Kerin NZ, Rubenfire M, Naini M, et al. Prinzmetal’s variant angina: electrocardiographic and angiographic correlations. J Electrocardiol 1982;15:365. 2. Bott-Silverman C, Heupler FA. Natural history of pure coronary artery spasm in patients treated medically. JACC 1983;2:200. 3. Waters DD, Szlachcic J, Miller D, Theroux P. Clinical characteristics of patients with variant angina complicated by myocardial infarction or death within 1 month. Am J Cardiol 1982;49:658. 4. Longhurst JC, Kraus WL. Exercise-induced ST elevation in patients without myocardial infarction. Circulation 1979;3(60):616. 5. Waters DD, Szlachcic J, Bourassa MG, et al. Exercise testing in patients with variant angina: results, correlation with clinical and angiographic features and prognostic significance. Circulation 1982;65:265. 6. Chaitman BR, Waters DD, Theroux P, Hanson JS. S-T segment elevation and coronary spasm in response to exercise. Am J Cardiol 1981;47:1350. 7. Maseri A, Severi S, De Nes M, et al. bVariant Q angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia. Am J Cardiol 1978;42:1019. 8. Yasue H, Omote S, Takizawa A, et al. Circadian variation of exercise capacity in patients with Prinzmetal’s variant angina: role of exerciseinduced coronary arterial spasm. Circulation 1979;59:938. 9. Gibbons RJ, Balady GJ, Bricker JT, et al. ACC/AHA 2002 guideline update for exercise testing: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). 2002. American College of Cardiology website. Available at: www.acc.org/clinical/guidelines/ exercise/dirIndex.htm. 10. Stuart RJ, Ellestad MH. National survey of exercise stress testing facilities. Chest 1980;1(77):94. 11. Castello R, Alegria E, Merino A, et al. The value of exercise testing in patients with coronary artery spasm. Am Heart J 1990;119:259. 12. Detry JMR, Mengeot P, Rousseau MF, et al. Maximal exercise testing in patients with spontaneous angina pectoris associated with transient ST segment elevation. Br Heart J 1975;37:897.