7
Ischemic Heart Disease

This chapter describes the evaluation and management of ischemic heart disease, which has evolved significantly over the past decade. In particular, several clinical trials have documented the benefits of revascularization in patients with acute ischemic syndromes as well as the efficacy of medical therapy, including lifestyle modification in patients with stable coronary disease. A fundamental premise in establishing new listing criteria for ischemic heart disease disability is the linking of anatomic or structural evidence of coronary heart disease (CHD) with both functional impairment and severe anginal symptoms. A flow diagram has been introduced that depicts five pathways to meet listings, including clinical, standard exercise testing, stress imaging, and angiographic anatomic criteria, with one pathway specific for patients with prior coronary artery bypass graft and severe CHD. Because many patients with ischemic heart disease are unable to exercise, standard stress electrocardiographic criteria for ischemia (the sole determinant of objective ischemia assessment in prior cardiovascular disability listings) have been expanded significantly to encompass nonexercise modalities (including nuclear imaging and echocardiography provoked by pharmacologic vasodilator stress) to assess the presence of severe inducible ischemia that, when combined with severe angina (Canadian Cardiovascular Society Class III or IV) would meet a cardiovascular disability listing. Additionally, the criteria by which angiographic CHD meet a listing have been specified, and severe CHD is defined by greater than or equal to 50 percent left main



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7 Ischemic Heart Disease this chapter describes the evaluation and management of ischemic heart disease, which has evolved significantly over the past decade. In particular, several clinical trials have documented the benefits of revascularization in patients with acute ischemic syndromes as well as the efficacy of medical therapy, including lifestyle modification in patients with stable coronary disease. a fundamental premise in establishing new listing criteria for ischemic heart disease disability is the linking of anatomic or structural evidence of coronary heart disease (Chd) with both functional impairment and severe anginal symptoms. a flow diagram has been introduced that depicts five pathways to meet listings, including clinical, standard exercise testing, stress imaging, and angiographic anatomic criteria, with one pathway specific for patients with prior coronary artery by- pass graft and severe Chd. because many patients with ischemic heart disease are unable to exercise, standard stress electrocar- diographic criteria for ischemia (the sole determinant of objective ischemia assessment in prior cardiovascular disability listings) have been expanded significantly to encompass nonexercise modalities (including nuclear imaging and echocardiography provoked by pharmacologic vasodilator stress) to assess the presence of se - vere inducible ischemia that, when combined with severe angina (Canadian Cardiovascular Society Class III or IV) would meet a cardiovascular disability listing. additionally, the criteria by which angiographic Chd meet a listing have been specified, and severe Chd is defined by greater than or equal to 0 percent left main 0

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0 0 CaRdIoVaSCUlaR dISabIlIty stenosis and/or greater than or equal to 0 percent proximal/mid stenoses in greater than or equal to two native arteries or bypass grafts. these updated criteria now provide a significantly enhanced and evidence-based approach for making disability determinations based on anatomic and functional criteria in patients with severe angina. DESCRIPTION Ischemia is defined as inadequate blood supply (circulation) to a lo- cal area due to blockage of the blood vessels supplying the area. Ischemic means that an organ (e.g., the heart) is not getting enough blood and oxygen. Ischemic heart disease, also called coronary heart disease (CHD) or coronary artery disease, is the term given to heart problems caused by narrowed heart (coronary) arteries that supply blood to the heart muscle. Although the narrowing can be caused by a blood clot or by constriction of the blood vessel, most often it is caused by buildup of plaque, called athero- sclerosis. When the blood flow to the heart muscle is completely blocked, the heart muscle cells die, which is termed a heart attack or myocardial infarction (MI). Most people with early (less than 50 percent narrowing) CHD do not experience symptoms or limitation of blood flow. However, as the atherosclerosis progresses, especially if left untreated, symptoms may occur. They are most likely to occur during exercise or emotional stress, when the demand for the oxygen carried by the blood increases. The discomfort experienced when the heart muscle is deprived of ad- equate oxygen is called angina pectoris. This is a clinical syndrome char- acterized by discomfort in the chest, jaw, shoulder, back, or arms that is typically aggravated by exertion or emotional stress and relieved promptly with rest or by taking nitroglycerin. Angina usually occurs in patients with CHD, but also can occur in individuals with valvular disease, hypertrophic cardiomyopathy, and uncontrolled hypertension. Infrequently, patients with normal coronary arteries may experience angina related to coronary spasm or endothelial dysfunction (Gibbons et al., 2002a). Angina is classified using the Canadian Cardiovascular Society (CCS) scheme, which grades angina or an anginal equivalent (e.g., exertional dys- pnea) based on a description of the level of activity that causes symptoms (Table 7-1). Class I is defined by angina that occurs with strenuous or rapid or prolonged exertion at work or recreation, but not with ordinary physical activity. Class I activities include chopping wood, climbing hills, cycling, aerobic ballet, ballroom (fast) or square dancing, jogging a 10-minute mile, rope skipping, skating, skiing, playing tennis or squash, and walking 5 miles per hour. Class II is defined by angina that slightly limits ordinary activity, such that angina is precipitated by walking or climbing stairs rapidly, walk-

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0 ISChEmIC hEaRt dISEaSE TABLE 7-1 Canadian Cardiovascular Society Functional Classification of Angina Class Definition Limitations I No limitation of ordinary Angina may occur with chopping wood, activity. Angina occurs with climbing hills, cycling, aerobic ballet, ballroom strenuous, rapid, or prolonged (fast) or square dancing, jogging a 10-minute exertion at work or recreation. mile, rope skipping, skating, skiing, playing tennis or squash, and walking 5 miles per hour. II Slight limitation of ordinary Angina may occur with walking or climbing activity. stairs rapidly, walking uphill, walking or climbing stairs after meals; in cold or in wind; under emotional stress; only during the first few hours after awakening; or with walking more than two blocks on level ground and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions. III Marked limitation of ordinary Angina may occur with walking one or two physical activity. blocks on level ground, and climbing one flight of stairs in normal conditions and at normal pace, playing a musical instrument, performing household chores, gardening, vacuuming, walking a dog, or taking out the trash. IV Inability to perform any Angina may occur at rest. physical activity without discomfort. SOURCE: Adapted from Goldman et al., 1981. ing uphill, walking or climbing stairs after meals; in cold or in wind; under emotional stress; only during the first few hours after awakening; or with walking more than two blocks on level ground and climbing more than one flight of ordinary stairs at a normal pace and in normal conditions. Class III is defined by marked limitation of ordinary physical activity such that angina is precipitated by walking one or two blocks on level ground, climb- ing one flight of stairs in normal conditions and at normal pace, playing a musical instrument, performing household chores, gardening, vacuuming, walking a dog, or taking out the trash. Class IV is defined by inability to carry on any physical activity without discomfort; anginal syndrome may be present at rest (Campeau, 1976, 2002; Goldman et al., 1981). As many as 3 to 4 million Americans may have silent ischemia, or ischemia without pain, or a heart attack without prior warning. People with angina may also have undiagnosed episodes of silent ischemia. Furthermore, those who have had heart attacks or individuals with diabetes are at risk for developing silent ischemia.

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04 04 CaRdIoVaSCUlaR dISabIlIty EPIDEMIOLOGY On the basis of data from the National Health and Nutrition Examina- tion Survey (NHANES) for the period 2003 to 2006, an estimated 17.6 mil- lion Americans age 20 or older have CHD, with an overall prevalence of 7.9 percent (9.1 percent in men and 7 percent in women). The overall prevalence of MI is 3.6 percent (4.7 percent in men and 2.6 percent in women). The estimated annual incidence of MI is 935,000, which includes 610,000 new and 325,000 recurrent infarctions. The overall prevalence of angina pectoris is 4.6 percent, with age-adjusted prevalence higher in women than men. CHD accounts for more than half of all cardiovascular events in men and women under age 75. The lifetime risk of developing CHD after age 40 is 49 percent for men and 32 percent for women (Lloyd-Jones et al., 2010). CHD is the leading cause of death in both men and women. It caused one of every six U.S. deaths in 2006; CHD mortality was 425,425, and MI mortality was 141,462. Approximately every 25 seconds, an American will experience a coronary event, and approximately every minute a death will be attributed to a coronary event. Approximately every 34 seconds, an American will have an MI and 15 percent will die of it (Lloyd-Jones et al., 2010). In addition, in 2006, 1,115,000 inpatient diagnostic cardiac catheteriza- tions were performed as well as 661,000 inpatient percutaneous coronary interventions (PCIs) and 253,000 coronary artery bypass surgery (CABG) procedures. The estimated direct and indirect cost of coronary heart disease for 2010 is $177.1 billion (Lloyd-Jones et al., 2010). DIAGNOSTIC CRITERIA AND METHODS CHD can be diagnosed in several ways. Patients with documented (prior) MI or coronary artery revascularization (either with PCI or CABG) have CHD. Moreover, the presence of typical angina suggests a clinical diagnosis of CHD, but most often requires confirmation by additional diag- nostic tests, such as coronary angiography. However, this test is an invasive and relatively costly procedure associated with a low, yet definite, risk of an adverse event. Coronary angiography is most often performed follow- ing an abnormal stress test or in the setting of an acute coronary syndrome (unstable angina or heart attack) in individuals who are candidates for revascularization (either by PCI or CABG). Exercise Stress Tests Stress testing is usually performed using an exercise tolerance test (ETT) with a treadmill or, occasionally, with bicycle ergometry. The most

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0 ISChEmIC hEaRt dISEaSE commonly applied treadmill protocol is the Bruce protocol, with the modi- fied Bruce, Naughton, Balke (Balke-Ware), Wilson, Taylor, or “ramp” protocols used in some patients. Noting the specific protocol is important because protocols differ by the rate at which the workload increases. The workload achieved during a test for any given protocol can be estimated in units of metabolic equivalents of task (METs) from published nomograms (Fletcher et al., 2001; Thompson et al., 2010). Completion of the first stage of the Bruce protocol is equivalent to 5 METs. Exercise testing can be performed with electrocardiogram (ECG) moni- toring alone or combined with a cardiac imaging test: single photon emis- sion computed tomography (SPECT), positron emission tomography (PET), or with echocardiography imaging. Each modality has specific criteria for an abnormal test. An abnormal exercise ECG is defined by ST-segment dis- placement, usually an ST-segment depression greater than or equal to 1 mm, measured 0.08 seconds after the J-point, that is horizontal or downsloping (Gibbons et al., 2002b). ST-segment elevation greater than or equal to 1 mm in leads without Q waves occurs infrequently, but this is also consid- ered an abnormal response. An abnormal SPECT or PET study is defined by a perfusion defect (Klocke et al., 2003), with a defect that is the same with rest or exercise (a fixed defect) suggesting infarction. An abnormal ex- ercise echocardiogram is a wall motion abnormality (Pellikka et al., 2007). Usually, such an abnormality that develops or worsens during exercise represents ischemia, whereas a wall motion abnormality that is present at rest and unchanged (fixed) with exercise indicates infarction. The presence of either ischemia or infarction on a stress-imaging study is consistent with the diagnosis of CHD in a patient with angina symptoms. Stress test results are commonly reported in a dichotomous manner: normal or abnormal, positive or negative for ischemia, and so on. How- ever, for a positive test, the degree of severity of abnormality provides additional information. All stress-testing modalities are limited by their false-positive results (abnormal stress test result, but CHD is not present) and false-negative results (normal stress test result, but CHD is present). Due to variability in image interpretation and imaging artifacts, isolated small mild abnormalities on stress SPECT or stress echocardiogram may be false-positive results, but the more severely abnormal results are more likely to represent a true-positive test (i.e., CHD is present). Additionally, a more severely abnormal test result is associated with an increased likelihood of multivessel CHD and a worse prognosis. An abnormal test result at a low workload is one of the most reliable indications of a high likelihood of multivessel CHD (McNeer et al., 1978). Other variables associated with multivessel CHD or worse prognosis are shown in Table 7-2 (Dubach, 1988; Gibbons et al., 2002a,b; Klocke et al., 2003; McNeer, 1978; Pellikka et al., 2007). Earlier versions of the CHD

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0 0 CaRdIoVaSCUlaR dISabIlIty TABLE 7-2 Other Variables Associated with Multivessel CHD or Worse Prognosis ETT SPECT Echocardiogram Magnitude ST-segment Number of perfusion defects High WMI score depression Number of leads ST-segment High SSS Decrease in LVEF depression Duration ST-segment depression High SRS Number of segments in recovery period with WMA Angina (especially if limiting TID n/a symptom) Decrease in systolic BP below n/a WMA involving baseline multiple coronary artery territories Chronotropic incompetence Defects involving multiple Rest LVEF < 35 percent coronary artery territories Abnormal heart rate recovery Rest LVEF at < 35 percent Increase in ESV scorea High-risk Duke treadmill T 201 lung uptake n/a aThe Duke treadmill score can be calculated as follows: Duration (minutes Bruce protocol) – 5 X magnitude ST-segment deflection (mm) – angina index. NOTE: BP = blood pressure; CHD = coronary heart disease; ESV = end systolic volume; ETT = exercise tolerance test; LVEF = left ventricular ejection fraction; SPECT = single-photon emission computerized tomography; SRS = summed reversibility score; SSS = summed stress score; TID = transient ischemic dilatation; WMA = wall motion abnormality; WMI = wall motion index. SOURCES: Dubach et al., 1988; Gibbons et al., 2002a,b; Klocke et al., 2003; McNeer, 1978; Pellikka et al., 2007. listings included detailed descriptions of interpretation of the exercise ECG. However, most reports in patient records do not provide these descriptors, but rather they simply categorize the exercise ECG as being normal or ab- normal, positive or negative. Exercise duration is included in most reports. Similarly, for the stress-imaging procedures, the results can be character- ized most accurately by applying the 17-segment model advocated by the American Heart Association (AHA) (Cerqueira et al., 2002). This model can be used to develop a summed stress score or summed reversibility score for SPECT imaging and a wall motion index score for echocardiography. These scoring systems have been validated as accurate tools for prognostic purposes. However, this information is not usually included in reports. Instead, the anatomical location of the defects (reflecting coronary artery distribution) and exercise duration are most often included in exercise imaging reports.

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0 ISChEmIC hEaRt dISEaSE Nuclear and echocardiographic imaging can localize the site of ische- mia, although the correlation with angiographic CHD is not perfect. The assignment of coronary artery territories by imaging to anatomical CHD at angiography is as follows: anterior/anteroseptal—left anterior descend- ing artery; inferior/inferoseptal—right coronary artery; lateral—circumflex artery (Cerqueira et al., 2002). Involvement of the lateral territory may be further specified as anterolateral or inferolateral. The artery supplying the apex is variable. For this reason, defects involving the apex alone are not assigned to a coronary artery territory. In addition to multiple coronary ar- tery territories, other markers shown by imaging usually represent extensive ischemia. For nuclear imaging this marker is transient ischemic dilatation, or poststress dilatation of the left ventricle. For echocardiography these markers include a decrease in left ventricular ejection fraction (LVEF) or an increase in end systolic volume between rest and exercise. In contrast to the imaging modalities, the exercise ECG cannot local- ize the site of ischemia. Thus, for application of the exercise ECG, there cannot be a requirement for involvement of greater than or equal to two coronary artery territories (for further discussion, refer to the following paragraph, as well as to item 3 in the section on concluding concepts and Recommendation 7-3). Nonetheless, studies have shown that the develop- ment of ischemic ECG changes at a low workload is associated with a high likelihood of multivessel CHD (McNeer, 1978). Another variable that can be measured during exercise testing and that occurs less commonly than ECG changes, but also reflects multivessel CHD and a poor prognosis, is a decrease in systolic blood pressure at peak exercise greater than or equal to 10 mm Hg below the baseline blood pressure (Dubach et al., 1988). To facilitate application of the listings in a uniform manner across the stress-testing modalities, a claimant will meet a listing if exercise capacity is limited (less than or equal to 5 METs), combined with objective evidence of CHD. Given the poor specificity of single mild abnormalities on SPECT or echocardiographic imaging, the presence of defects involving less than or equal to two coronary artery territories is required to increase the like- lihood that the claimant has CHD before being granted disability. This requirement for involvement of less than or equal to two-vessel CHD is analogous to the coronary angiogram criteria. The criteria to meet a listing through the use of an exercise stress test (standard treadmill test, nuclear SPECT or PET, echocardiography) include exercise duration less than or equal to 5 METs and objective evidence for significant ischemia defined in Table 7-3. Pharmacologic (Nuclear and Echocardiography) Stress Tests Pharmacologic stress testing using SPECT, PET, or echocardiographic imaging is reserved for patients who are either unable to perform dynamic

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0 0 CaRdIoVaSCUlaR dISabIlIty TABLE 7-3 Criteria to Meet a Listing Through the Use of an Exercise Stress Test Exercise Workload Less Than or Equal to 5 METs Plus at Least One of the Following Criteria: Criterion Modality Ischemic ECG Standard treadmill Decrease in systolic BP ≥ 10 mm Hg below Standard treadmill baseline Fixed/reversible perfusion defects ≥ 2 coronary Nuclear imaging (SPECT or PET) territories Transient ischemic dilation Nuclear imaging (SPECT or PET) Fixed/reversible regional wall motion abnormality Echocardiography ≥ 2 coronary territories Decrease in LVEF between rest and exercise Echocardiography Increase in ESV between rest and exercise NOTE: BP = blood pressure; ECG = electrocardiogram; ESV = end systolic volume; LVEF = left ventricular ejection fraction; METs = metabolic equivalents of task; PET = positron emission tomography; SPECT = single-photon emission computerized tomography. exercise or unable to achieve at least 85 percent of the age-predicted maxi- mal heart rate with exercise, which is the effort level required to achieve adequate sensitivity to detect coronary artery stenosis capable of causing angina (Klocke et al., 2003; Pellikka et al., 2007). Pharmacologic stress does not consistently cause angina or ECG changes of ischemia, so only the imaging results are diagnostic. Pharmacologic agents are administered intravenously in place of dynamic exercise stress, and the resulting perfu- sion or wall motion response is compared with the resting state and is interpreted using the same criteria for perfusion defects and wall motion abnormalities listed above for dynamic exercise. The most frequently used pharmacologic stress agents for SPECT and PET are the vasodilators dipyridamole, adenosine, and regadenoson, which increase blood flow through the coronary arteries, but only modestly in- crease heart rate in most patients. Many patients experience chest discomfort during the administration of these agents, which should not be interpreted as angina. The agents create differences in blood flow between coronary arteries that have high-grade blockages and normal arteries, which result in perfusion defects that can be detected using radioactive imaging. The most frequently used pharmacologic agent in stress echocardiog- raphy is dobutamine, a positive inotropic agent that increases the force or energy of muscular contractions and increases heart rate and blood pressure. Dobutamine is administered intravenously in increasing doses until the patient reaches 85 percent of the maximal age-predicted heart rate. Atropine may also be required in some patients. If the patient does

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0 ISChEmIC hEaRt dISEaSE not achieve 85 percent of the heart rate response, the resulting images may underestimate the presence of CHD. The positive inotropic effect and increases in heart rate and blood pressure may cause angina and result in abnormal wall motion at peak stress in portions of the heart muscle sup- plied by coronary arteries with high-grade blockages. Dobutamine may also be used for SPECT imaging. Coronary CT Angiography Coronary computed tomography (CT) angiography is an imaging tech- nique during which an iodinated contrast dye is injected through a periph- eral vein and images of the coronary arteries are taken using a CT system. It provides images of the coronary arteries similar to those obtained using coronary angiography, during which the dye is injected directly into the coronary arteries using an arterial catheter. It is most useful in patients with an intermediate risk of coronary heart disease. In patients with extensive calcium deposits or prior coronary artery stents, detection of stenosis is dif- ficult (Budoff et al., 2006). Tremendous progress has been made in changing this technique, but lack of standardization and unresolved technical issues do not allow it to be used in place of coronary angiography as a basis for determining disability (Mark et al., 2010; Miller et al., 2008). TREATMENT Comprehensive management of angina and stable CHD entails multiple therapeutic approaches, including the following: • Identification and treatment of associated diseases that can precipi- tate or worsen angina and ischemia; • Cardiac risk factor identification and intervention; • Application of pharmacological and nonpharmacological interven- tions for secondary prevention; • Pharmacological and symptomatic management of angina and ischemia; and • Myocardial revascularization with PCI or CABG surgery, when indicated. A multidimensional management approach integrates all of these con- siderations, often simultaneously, in each patient. Among pharmacothera- pies, three drug classes have been demonstrated to reduce mortality and morbidity in patients with stable CHD and preserved left ventricular (LV) function: aspirin, angiotensin-converting enzyme (ACE) inhibition, and effective lipid lowering. Beta-blockers have been shown to reduce mortal-

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0 0 CaRdIoVaSCUlaR dISabIlIty ity in patients with prior MI (CAPRICORN Investigators, 2001). Other therapies such as nitrates, beta-blockers, calcium channel blockers, and ranolazine have been shown to improve angina and exercise performance and to reduce ischemia, but have not been proven to reduce mortality in patients with stable CHD. Clinical practice guidelines for the diagnosis and treatment of chronic stable angina (Fraker et al., 2007; Gibbons et al., 2002a), unstable angina/ non-ST-segment elevation myocardial infarction (Anderson et al., 2007), and ST-segment elevation myocardial infarction (Antman et al., 2004; Kushner et al., 2009), have been jointly published by AHA and the Ameri- can College of Cardiology (ACC). These guidelines detail the indications and timing of medical therapy (including lifestyle modification) and revas- cularization with PCI and/or CABG (Eagle et al., 2004) and provide guid- ance for secondary prevention that includes risk factor reduction (Smith et al., 2006). Although revascularization has specific indications, treatment with medical therapy, lifestyle modification, and risk factor reduction is recommended across the spectrum of CHD in both stable and unstable patients and following a coronary event or revascularization. Recent Advances The most recent advance in medical therapy consists of the intro- duction of ranolazine (Chaitman, 2006; Chaitman et al., 2004; Morrow et al., 2007). Nonpharmacologic treatments include spinal cord stimula- tion (Taylor et al., 2009) and enhanced external counterpulsation (EECP) (Akhtar et al., 2006; Michaels et al., 2004; Soran et al., 2006) for the treatment of angina and ischemia. Advances in revascularization include development of drug-eluting stents (Novack et al., 2009), the introduction of percutaneous support devices in patients undergoing PCI (Goldstein et al., 1998), and increased use of off-pump techniques, as well as minimal access and robotic procedures in patients undergoing CABG (Poston et al., 2008; Sabik et al., 2002). Interest and experience also have been growing in the performance of hybrid revascularization procedures (Stahl et al., 2002) using a collaborative approach between interventional cardiologists and cardiothoracic surgeons. Ranolazine is the newest antianginal agent approved by the Food and Drug Administration and the first new drug class for angina since calcium channel blockers (CCBs) were introduced 30 years ago. Ranolazine acts by reducing intracellular calcium overload in ischemic myocytes by inhibiting late inward sodium current entry. The net effect of reduced late inward sodium current is a reduction in LV wall tension and myocardial oxygen demand, thereby reducing angina and ischemia. Ranolazine increases exer- cise tolerance in patients with stable angina, reduces episodes of recurrent

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 ISChEmIC hEaRt dISEaSE ischemia, and provides additional antianginal benefit in patients who are already on intensive antianginal therapy with beta-blockers and CCBs. While multiple nonspecific side effects of ranolazine have been reported, the drug is well tolerated in clinical practice. The most common side ef- fects are dizziness (6.2 percent), headache (5.5 percent), constipation (4.5 percent), and nausea (4.4 percent), which are more commonly observed at the 1,000 mg twice a day dose. Mean QT prolongation noted in clinical trials ranges from 6 to 8 milliseconds; the clinical relevance of the modest QT prolongation that occurs in a dose-related manner is unclear, but there has been no increased risk of a serious proarrhythmic effect (torsades de pointes) or sudden cardiac death reported in a large, placebo-controlled trial of more than 6,500 patients (MERLIN Trial) (Morrow et al., 2007). EECP is an alternative treatment for patients with refractory angina. It is generally administered as 35 sequential treatments (1 hour daily; 5 days per week) over 7 weeks. EECP was shown to increase the time to ST-seg- ment depression during exercise testing, reduce angina, and improve health- related quality of life for at least 1 year in a randomized, double-blind study of patients with chronic stable angina (Soran et al., 2006). EECP does not reduce ischemia on myocardial perfusion imaging, and the mechanisms underlying its effects are poorly understood. Side Effects of Treatments Nitroglycerin and nitrates can cause vasodilation-induced headache, a decrease in blood pressure, and, more rarely, severe hypotension with bra- dycardia. The vasodilation by nitroglycerin may be markedly exaggerated and prolonged in the presence of the phosphodiesterase inhibitors sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis), so these agents should not be used concurrently with nitrates. Most of the adverse effects of beta-blockers occur as a consequence of the known properties of these drugs and include cardiac effects (e.g., severe sinus bradycardia, sinus arrest, reduced LV contractility), bronchoconstric- tion, fatigue, mental depression, nightmares, gastrointestinal upset, sexual dysfunction, intensification of insulin-induced hypoglycemia, and cutaneous reactions. Lethargy, weakness, and fatigue may be caused by reduced car- diac output or may arise from a direct effect on the central nervous system. Bronchoconstriction results from blockade of beta2 receptors in the tracheo- bronchial tree. As a consequence, reversible obstructive lung disease (e.g., asthma) may be considered as relative contraindications to beta-blockers, even to beta1-selective agents (Egred et al., 2005). Calcium channel blockers are potent vasodilators, which may lead to dizziness, hypotension, and reflex tachycardia—particularly with some di- hydropyridines. Peripheral edema can occur, usually with the dihydropyri-

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  CaRdIoVaSCUlaR dISabIlIty Ischemic Hear t Disease and CCS III, IV Angina 1 Listing requires both diagnosis and functional Ischemic Hear t Disease limitation Listing ( Documentation by prior M I or revascularization, requires only Dx or by stress test or by angiography) severe + anatomy and on regimen of prescribed treatment prior CABG FUNCTION OR OR OR 3 separate No exercise or No exercise or Ischemic response on Ischemic ischemic episodes pharmacologic pharmacologic exercise test at response on requiring stress test workload ≤ 5 METs 2 stress test stress unplanned ≥ 50 % stenosis imagin g test 3 hospitalization and ≥ 50 % stenosis left main ar tery revascularization left main ar tery or ≥ 70 % within 12 months or ≥ 70 % Listing proximal/ mid proximal/ mid stenosis in ≥ 2 stenosis in ≥ 2 native ar teries native ar teries Listing (non-bypassed) + LVEF < 5 0 % and/ or bypass graf ts + Prior CABG Listing Listing FIGURE 7-1 Coronary heart disease listings. NOTE: CABG = coronary artery bypass graft; CCS = Canadian Cardiovascular Society; Dx = diagnosis; LVEF = left igure 7-1.ejection fraction; METs = metabolic F ventricular eps equivalents of task; MI = myocardial infarction. 1 Defined in report: Canadian Cardiovascular Society Class III or IV. 2 Defined in report: See Recommendation 7-2. 3 Defined in report: See Recommendation 7-2. waves or fall in systolic blood pressure greater than or equal to 10 mm Hg below resting systolic blood pressure at a workload of less than or equal to 5 metabolic equivalents of task; OR 3. Stress-imaging test: Ischemic response with either exercise or pharmacologic vasodilator stress indicated by greater than or equal to two reversible and/or fixed regional myocardial per- fusion defects during nuclear testing and transient ischemic dilation or resting left ventricular ejection fraction (LVEF) less than 50 percent, OR greater than or equal to two reversible and/or fixed regional wall motion abnormalities and either a fall in LVEF OR resting LVEF less than 50 percent;

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 ISChEmIC hEaRt dISEaSE Ischemic Heart Disease and CCS III–IV Angina 1 Yes Clinical Criterion: Listing 3 hospitalizations for revascularization within 12 months? No Standard ETT Without Yes Yes Imaging Criteria: Ischemic response at workload ≤ 5 METs (≤ 3 min ETT available? Bruce protocol)?2 Listing No No No listing Stress (Exercise or Ischemic response? 3 Yes Yes Nuclear Yes Pharmacologic) Imaging Criteria: study? Listing Imaging study available? No No No listing No Yes Yes Listing Ischemic response?4 Echocardiography study? No No listing Catheterization Criteria: Yes Prior Yes Y es Listing ≤ 50% stenosis ungrafted Catheterization available? CABG? left main or ≤ 70% stenosis proximal/mid ≤ 2 (without grafts) native vessels or bypass grafts? No ≤ 50% stenosis left main or No Yes Yes ≤ 70% proximal/mid LVEF < 50% stenosis ≤ 2 coronary Listing arteries? No No No listing No listing No listing FIGURE 7-2 Coronary heart disease listings: Ischemic heart disease ladder flow diagram. NOTE: CABG = coronary artery bypass graft; CCS = Canadian Cardiovascular Society; ETT = exercise tolerance test; LVEF = left ventricular ejection fraction; Figure 7-2 new METs = metabolic equivalents of task. 1 Defined: Canadian Cardiovascular Society Class III or IV. 2 Defined in report: See Recommendation 7-2. 3 Defined in report: See Recommendation 7-2. 4 Defined in report: See Recommendation 7-2.

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4 4 CaRdIoVaSCUlaR dISabIlIty OR 4. Among patients who have not had prior CABG, severe coro- nary heart disease with either 50 percent stenosis in the left main artery or greater than or equal to 70 percent stenosis in the proximal or midportion of greater than or equal to two major coronary arteries and a LVEF less than 50 percent. RECOMMENDATION 7-3. The committee recommends that patients with prior coronary artery bypass graft and either severe disease in native coronary arteries that have not been bypassed (greater than or equal to 50 percent stenosis in the left main artery or greater than or equal to 70 percent stenosis in the proximal or midportion of greater than or equal to two major native coronary arteries) and/or greater than or equal to 70 percent stenosis in greater than or equal to two bypass grafts and with Canadian Cardiovascular Society Class III or IV angina (or angina-equivalent symptoms) meet a listing. RECOMMENDATION 7-4. The committee recommends that children who are disabled prior to interventions are considered as disabled until 6 months following surgery and then reevaluated. The table of pharmacologic interventions for ischemia in adults cannot be applied to children as necessarily appropriate therapies. REFERENCES Abbott, J., and N. Berry. 1991. Return to work during the year following first myocardial infarction. british Journal of Clinical Psychology 30(Pt 3):268–270. Akhtar, M., G. F. Wu, Z. M. Du, Z. S. Zheng, and A. D. Michaels. 2006. Effect of external counterpulsation on plasma nitric oxide and endothelin-1 levels. american Journal of Cardiology 98(1):28–30. Al-Mallah, M. H., I. M. Tleyjeh, A. A. Abdel-Latif, and W. D. Weaver. 2006. Angiotensin- converting enzyme inhibitors in coronary artery disease and preserved left ventricular systolic function: A systematic review and meta-analysis of randomized controlled trials. Journal of the american College of Cardiology 47(8):1576–1583. Anderson, J. L., C. D. Adams, E. M. Antman, C. R. Bridges, R. M. Califf, D. E. Casey Jr., W. E. Chavey II, F. M. Fesmire, J. S. Hochman, T. N. Levin, A. M. Lincoff, E. D. Peterson, P. Theroux, N. K. Wenger, R. S. Wright, S. C. Smith Jr., A. K. Jacobs, J. L. Halperin, S. A. Hunt, H. M. Krumholz, F. G. Kushner, B. W. Lytle, R. Nishimura, J. P. Ornato, R. L. Page, and B. Riegel. 2007. ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation

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