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Exercise Training and the Ischemic Patient Robert Bertelink, Paul Oh, Cardiac Rehabilitation and Secondary Prevention Program, Toronto Rehabilitation Institute Health care providers are commonly advised to proceed with caution when prescribing exercise for individuals with coronary artery disease (CAD) who are known to develop myocardial ischemia. For example, guidelines from the American College of Sports Medicine recommend that any such individual exercise at a heart rate no greater than 10 bpm–1 below the ischemic threshold (determined by –1.0mm of horizontal or down sloping ST segmental depression).1 Providers are also cautioned against exercise training individuals to the point at which patients develop signs or symptoms of angina. “Is it time to reassess these guidelines and see if providers can train our patients more aggressively so that they can realize their functional goals, optimally improve risk factors and derive prognostic benefits associated with higher fitness without any adverse effects?” Are the current guidelines appropriate for all individuals? How effectively can an ischemic patient or one who develops angina be trained following these guidelines? Is it time to reassess these guidelines and see if providers can train our patients more aggressively so that they can realize their functional goals, optimally improve risk factors and derive prognostic benefits associated with higher fitness without any adverse effects? This article touches on this important issue and we present here two case studies as illustrations of potential training models and their outcomes. Case #1 – Silent Ischemia Mr. PA is a 51-year-old man referred for cardiac rehabilitation. His past history includes posterior circulation myocardial infarction four years ago. He has a resting ejection fraction of 40%, but no symptoms of heart failure. He describes occasional chest pressure with activity. Past history includes: smoking (30 pack years), diet controlled diabetes, and elevated cholesterol. Current medications include ASA, atenolol 50 mg, OD, ramipril 5 mg, OD, atorvastatin 20 mg, OD, and nitroglycerine PRN. An exercise perfusion study demonstrated reversible changes in the apex, inferior, and lateral walls. A coronary angiogram was performed, which demonstrated occlusion of the right coronary artery and a diffuse 70% lesion in the circumflex. The left main was normal, and the left anterior descending artery had only minor disease in the mid portion. Left to right flow through collaterals was visible. A decision was made not to have any interventional procedure and to continue with medical therapy only. As part of this, he was referred for exercise rehabilitation. A cardiopulmonary assessment with direct VO2 measure ment was carried out. The results are shown in the table below. The ECG tracings showed significant ST depression at peak of exercise although the patient did not report symptoms of angina. Table: Case 1 – Initial Cardiopulmonary Assessment Baseline Peak 67 115 Blood Pressure (mmHg) 130/70 160/70 ST Depression (lead CM5) –0.5 mm –2.75 mm Heart Rate (bpm–1) Rate Pressure Product 18,400 VO2 (mL/kg/min) 18.3 (5.2 METs) Respiratory Exchange Ratio (RER) 1.24 The assessment lasted 7 minutes and was terminated when a VO2 plateau was achieved. Current Issues in Cardiac Rehabilitation and Prevention 17 Exercise Prescription Before embarking on an exercise program, we had very careful and detailed discussions about his situation. The importance of recognizing angina, modifying activity if chest pain occurred, appropriate use of nitroglycerine, medication adherence and timing of exercise in relation to type and peak action of medication (especially beta-blockers) and good communication with staff were emphasized. Long warm-up and cool-down sessions to facilitate gradual increases and decreases in heart rate and blood pressure were also incorporated into his program. These principles meshed well with the key considerations outlined in the CACR 2004 guidelines.2 The initial exercise prescription was set at 1 mile in 20 minutes, 5 times weekly, with an upper training heart rate limit of 96 bpm–1. This HR limit corresponded to a 1.0mm ST segment change on the ECG (lead CM5) and also correlated with 60% of the heart rate reserve and 75% of the peak V02. When the patient was walking at this pace his actual training heart rate averaged 88 bpm–1, which was about 10 beats below the 1.0 mm ischemic threshold that was identified by ECG; this level of activity was consistent with parameters from the ACSM Guidelines.1 His exercise prescription and training program progressed well and he did not report any symptoms. In two weeks he was walking 2 miles in 37 minutes, at one month 2.5 miles in 45 minutes, at two months 3 miles in 54 minutes, at three months 3 miles in 51 minutes, and at four months 3 miles in 49.5 minutes (all with a frequency of 5 days per week). Because he was feeling so well, his training heart rates were titrated closer to the ECG ischemic threshold and were kept between 90 and 96 bpm–1. A second cardiopulmonary test was performed at six months in order to monitor his exercise capacity and cardiac status. Table: Six Month Cardiopulmonary Assessment Baseline Peak 67 155 Blood Pressure (mmHg) 110/65 174/74 ST Depression (CM5) –0.5 mm –2.50 mm Heart Rate (bpm–1) Rate Pressure Product 26,970 VO2 (mls/kg/min) 24.6 (7.0 METs) RER 18 1.31 The assessment lasted for 8 minutes and was terminated when a VO2 plateau was achieved. This test showed a large improvement his VO2 maximum by 34% in 6 months. He still demonstrated ST segmental depression of –2.50 mm at the peak of exercise, but it now occurred at a higher Rate Pressure Product (RPP), i.e., –2.75 mm at a RPP of 18,400 on the initial test compared with –2.5 mm at a RPP of 26,970 6 months after exercise training. This case illustrates a positive outcome with training following standard guidelines for exercise rehabilitation in a man with silent ischemia. Could the patient have further improved his fitness, exercise capacity and ischemic threshold by exercising at a higher intensity, i.e. one that actually brought on a degree of ischemia? This is explored in the next case. Case #2 – Ischemia Mr. RC is a 53-year-old man referred for cardiac rehabilitation. His past history includes anterior wall infarction 6 years ago followed by PCI with stent to his LAD. The patient was left with mild to moderate left ventricular dysfunction. Recently, the patient began to experience exertional chest discomfort again (when climbing stairs). He under went exercise testing which was positive for symptoms and suggestive of inferior wall ischemia. A subsequent catheterization demonstrated an occluded RCA (new lesion) not amenable to angioplasty with minimal restenosis in the stented portion of his LAD and minor irregularities in the circumflex. Medications included metoprolol 50 mg bid, ramipril 10 mg OD, ASA 325 mg, rosuvastatin 40 mg OD, and nitroglycerine PRN. The patient was referred for cardiac rehabilitation. How do we proceed with exercise training in this patient with prior anterior MI, LV dysfunction and now exercise induced chest pain? Initial exercise test data are shown in the table. Current Issues in Cardiac Rehabilitation and Prevention Initial Cardiopulmonary Assessment Baseline Peak 46 111 Blood Pressure (mmHg) 120/70 170/85 ST Depression (CM5) –0.1mm –1.4mm Heart Rate (bpm–1) Rate Pressure Product 18,870 VO2 (mL/kg/min) 28.8 (8.2 METs) RER At week eleven, his prescription was progressed to include 100 m of jogging every 300 m and at week fifteen, to alternate 100 m of jogging with 100 m of walking. On each increase in exercise intensity, the patient reported an initial increase in frequency of chest tightness, gradually decreasing as time progressed. By week fifteen, his exercising heart rates were reported to be in the 110-120 bpm–1 range and he wasn’t experiencing any angina. He was monitored closely with periodic telemetry sessions and stress tests. At the end of one year the patient underwent a final cardiopulmonary assessment with the following results. One-Year Cardiopulmonary Assessment 1.32 The patient developed chest tightness in the 10th minute of exercise (on a 100 kpm/min incremental bicycle protocol; corresponding to about one minute into stage 3 of a Bruce protocol). The pain was rated at 2/10, and occurred at a heart rate of 102 bpm–1 and VO2 of 23.8 mL/kg/min. The tightness cleared after one minute of recovery. The test was terminated when a VO2 plateau was achieved. Exercise Prescription Despite his cardiac status, this man was quite active, walking 3.5 miles 2 to 3 times per week, sometimes with chest discomfort. His goal was to become much more active to meet the needs of his work and home life. His initial exercise prescription was therefore set at 3 miles in 45 minutes, 5 times weekly, with an upper training heart rate limit of 102 bpm–1. This corresponded with a -0.65 mm ST segmental change on the ECG (lead CM5), 63% of VO2 peak, and the level of exertion at which the patient first began to experience his symptoms. When the patient was walking at the prescribed pace, his heart rate was found to be approximately 90 bpm–1 and he experienced chest tightness on a regular basis. The patient was advised to lengthen his cardiovascular warm-up and to continue exercising as long as the chest tightness remained “mild” (pain rating 2/10 or less). After exercising at this level for 2-3 weeks, the patient reported a reduced frequency of chest tightness. After three weeks, his prescription was increased to 4 miles walking in 60 minutes without discomfort. The patient remained mostly symptom free. At week seven, his prescription was increased to include 100 m of jogging every 700 m at a pace of 12 minutes per mile. The patient reported a recurrence of chest tightness with the increased intensity (pain rating 2/10) for the first 2-3 weeks at the higher intensity, followed by a decrease in frequency over the next 2 weeks. Baseline Peak 57 130 Blood Pressure (mmHg) 110/70 180/60 ST Depression (CM5) –0.2 mm –2.0 mm** Heart Rate (bpm) Rate Pressure Product 23,400 VO2 (mL/kg/min) 41.8 (11.9 METs) RER 1.25 On this test, the patient developed chest tightness in the 9th minute of exercise on a treadmill using a Bruce protocol (pain rating 2/10, at heart rate of 120 bpm–1 and VO2 of 34.3 mL/kg/min). This threshold was at a much higher intensity than the baseline test. The tightness cleared after 4 minutes of recovery. The test was terminated due to increasing ST segmental depression and thus underestimated his true maximal fitness. The patient was able to improve his VO2 peak by 45% in one year. He was also able to push back his anginal threshold and thus engage in a higher level of activity, which was the main reason the patient wished to participate in a cardiac rehabilitation program. This case illustrates a successful outcome associated with training at or slightly above the ischemic threshold. Had the patient been trained more intensely, could his anginal threshold have been pushed back even further or his ST segmental changes improved? These situations happen in real life every day. People with CAD will participate in activities until they get pain or even more commonly, while they are experiencing silent ischemia. Previous teaching would have excluded individuals with exertional ST-depression (_> 1 mm) without symptoms Current Issues in Cardiac Rehabilitation and Prevention 19 or those recovering from a large MI from vigorous exercise training.3 Concerns were raised about deleterious effects on the myocardium, increasing risk of cardiac arrest, or worsening LV function post anterior MI associated with exercise.4-6 More recent studies, however, have demonstrated typical positive outcomes associated with exercise training under ischemic conditions.7-8 Perhaps in the controlled environment provided by cardiac rehabilitation, carefully selected and monitored individuals can be pushed a little harder and receive greater benefits. This topic should be explored in future studies. References: 1.ACSM’s Guidelines for Exercise Testing and Prescription. Seventh Edition, p. 180. 2.Canadian Guidelines for Cardiac Rehabilitation and Cardiovascular Disease Prevention. Enhancing the Science, Refining the Art. Canadian Association of Cardiac Rehabilitation, Winnipeg, 2004. p. 262. 3.Myers J, Froelicher VF. Predicting outcome in cardiac rehabilitation. J Am Coll Cardiol 1990;15:983-985. 4.Hess OM, Schneider J, Nonogi H, et al. Myocardial structure in patients with exercise-induced ischemia. Circulation 1988;77:967977. 5.Hoberg E, Schuler G, Kunze B, et al. Silent myocardial ischemia as a potential link between lack of pre-monitoring symptoms and increased risk of cardiac arrest during physical stress. Am J Cardiol 1990;65:583589. 6.Jugdutt BI, Michorowski BL, Kappagoda CT. Exercise training after anterior Q wave myocardial infarction: importance of regional left ventricular function and topography. J Am Coll Cardiol 1988;12:362372. 7.Mark DB, Hlatky MA, Califf RM et al. Painless exercise ST deviation on the treadmill: long-term prognosis. J Am Coll Cardiol 1989;14:885892. 8.Schuler G, Shlierf G, Wirth A, et al. Low fat diet and regular supervised physical exercise in patients with symptomatic coronary artery disease: reduction of stress-induced myocardial ischemia. Circulation 1988;77:172-181. References and Reviews Lea Carlyle, BKin, RCPT(C), Faculty of Physical Education and Recreation, University of Alberta John Lester, BSc, Exercise Specialist, Northern Alberta Cardiac Rehabilitation Program, Edmonton, Alberta REVIEWS Percutaneous Coronary Intervention versus Conservative Therapy in Non-acute Coronary Artery Disease: A Meta-Analysis Katritsis DG, Ioannidis JPA. Circulation 2005; 111:2906-12. Although percutaneous coronary intervention (PCI) has been shown to improve symptoms of ischemic heart disease (IHD) compared with conservative medical treatment, there is limited evidence on the effect of PCI on the risk of death, myocardial infarction (MI), and future revascularization. This meta-analysis report results from 11 studies in 2950 patients (1476 received PCI, and 1474 received conservative treatment) with angiographically documented coronary stenoses in non-acute settings. The results of this metaanalysis revealed that PCI does not decrease mortality or the risk of MI during follow-up of patients with chronic stable coronary artery disease (CAD). However, PCI was found to be advantageous early after an MI. The authors note several limitations of the meta-analysis, but conclude that many percutaneous interventions performed in patients with stable CAD may not be warranted since PCI was not found to provide long-term benefits in hard clinical outcomes compared to conservative medical treatment. 20 Long-Term Outcomes of Coronary Artery Bypass Grafting versus Stent Implantation Hannan EL, et al. N Engl J Med 2005;352:2174-83. This observational study sought to determine whether longterm mortality differed significantly among 37,212 patients who underwent coronary artery bypass grafting and 22,102 patients who underwent stenting. The endpoints included revascularization (coronary artery bypass grafting [CABG] or percutaneous coronary intervention [PCI]) or death at any time before the completion of the 3-year follow-up. The authors found that the risk-adjusted rates of survival were significantly higher among patients who received CABG than among those who received a stent. This was evident in CABG patients with two-vessel disease with non-proximal left anterior descending (LAD) artery involvement (adjusted hazard ratio [HR] = 0.76) and in CABG patients with three-vessel disease with involvement of the proximal LAD (adjusted HR = 0.64). Revascularization rates were found to be considerably higher after stenting than after CABG (7.8% vs. 0.3% for subsequent CABG and 27.3% vs. 4.6 % for subsequent stenting). The results of this study show that CABG is associated with higher adjusted rates of long-term survival than stenting in patients with two or more diseased coronary arteries. However, the authors note that many factors need to be taken into consideration when choosing an intervention for patients with ischemic heart disease. Current Issues in Cardiac Rehabilitation and Prevention Copyright © 2006 Canadian Association of Cardiac Rehabilitation. All rights reserved The materials contained in the publication are the views/findings of the author(s) and do not represent the views/findings of CACR. The information is of a general nature and should not be used for any purpose other than to provide readers with current knowledge in the area. For more information please contact: Executive Director CACR 1390 Taylor Avenue Winnipeg, MB R3M 3V8 Canada