A reduction in physical activity is common in the aged, especially those with CHD. Comorbidities such as chronic lung disease, peripheral vascular disease, and osteoarthritis make the performance of meaningful physical activity difficult. As a result, activity-related manifestations of CHD may not be apparent until the disease is significantly advanced. This may account for the relatively high number of acute ischemic presentations in this population.

Elderly patients commonly experience chest discomfort as a manifestation of CHD. It is usually described as a tightness or pressure, and may radiate to the neck, jaw, or arm. However, atypical symptoms of myocardial ischemia such as fatigue, dyspnea, or worsening heart failure may occur. These symptoms likely result from an ischemia-induced exaggerated increase in LV end-diastolic pressure in an already noncompliant LV, increasing pulmonary capillary wedge pressure that leads to pulmonary edema and symptoms of shortness of breath. Even neurologic symptoms such as syncope and confusion may be observed as manifestations of occult CHD. Atypical symptoms must be addressed as aggressively as typical angina; studies performed in large community settings have shown similar 3-year cardiac-related death rates.

Silent ischemia is at least twice as common as clinically evident CHD at an elderly age. The etiology is unclear but may be related to the development of a collateral circulation that would reduce the effective extent of ischemic burden with minimal physical activity. Other possibilities include mental status changes that may not allow proper memory or communication, autonomic dysfunction, or tolerance to pain due to endogenous endomorphins.

Manifestations of CHD in the elderly have a vast array of potential presentations. Given the later, and more often acute presentations of elderly patients with symptomatic CHD, early diagnosis allows for a wide assortment of therapeutic options. CHD in the elderly presents as several clinical syndromes (see Table 26.1). A heightened awareness should be maintained for atypical symptoms
of myocardial ischemia. Alternate diagnoses of chest pain should be considered (see Table 26.2).

Angina is a syndrome typically characterized by chest discomfort that may be associated with jaw, neck, shoulder, back, or arm pain. This pain is typically brought on, or exacerbated by, exertion or emotional stress and is relieved by rest or nitroglycerin. Stable angina is said to be present if there is no substantial worsening of these symptoms, there is a predictable pattern of onset with exertion, and it lasts a short time (<10 to 15 minutes).

Angina results from significant narrowing of the coronary arteries, commonly the result of coronary atherosclerosis. Coronary disease is manifest by the development of atherosclerotic plaques. An injury to the endothelium by chemical, mechanical, or inflammatory events incites the process of atherosclerosis. Low-density lipoprotein cholesterol (LDL-C) diffuses into the area of the injured coronary endothelium and is then oxidized. This process initiates a cascade of events leading to a marked inflammatory reaction, which results in endothelial dysfunction. As a result of this inflammatory state, growth factors, cytokines, and chemotactic factors are released. This leads to the development of an atherosclerotic plaque, which is composed of a lipid core surrounded by smooth muscle cells and fibrous tissue. The plaque morphology that commonly causes stable angina consists of a small lipid core and is covered by a thick fibrous cap. Conversely, the plaque structure that typically leads to unstable angina is more vulnerable and dangerous, as it contains a large thrombogenic lipid core surrounded by a thin fibrous cap. Digestive enzymes, known as matrix
metalloproteinases, are released around the plaque edge, leading to plaque rupture and the development of acute coronary syndromes.

An estimated 3.6 million elderly patients have symptomatic CHD. The extent and severity of coronary disease increases with aging. The incidence of CHD is greater in younger middle-aged men than women; this disparity begins to diminish with aging, and after age 80, the incidence of CHD in men and women is comparable.

The gradual progression of a stable coronary atherosclerotic lesion to approximately 70% of its luminal diameter (90% reduction in cross-sectional surface area) results in a significant decrease in coronary perfusion pressure across the stenotic area and commonly produces symptoms of myocardial ischemia. In the elderly, however, there is a greater likelihood of subcritical coronary artery stenoses (≤70% stenosis) that span a significant length of the vessel. As a result of the dissipation of blood flow energy across a long stenotic segment, the poststenotic segment does not receive an adequate blood supply, causing symptoms.

Risk factors for the development of CHD include age, sex, family history, dyslipidemia, hypertension, diabetes mellitus, cigarette smoking, renal insufficiency, obesity, and a sedentary lifestyle. The presence of peripheral vascular disease increases the likelihood of concomitant CHD.

The initial management of elderly CHD patients should follow the mnemonic:³

A, Aspirin and antianginal therapy

B, β-Blockers and blood pressure

C, Cigarette smoking and cholesterol

D, Diet and diabetes

E, Education and exercise

These initial considerations should be included when treating patients with angina. As stated earlier, conditions that may exacerbate or provoke symptoms of angina should be managed. This may reduce the need for the intensification of medical treatment, if anginal symptoms resolve and the patient is not high-risk.

Lifestyle modifications include cigarette smoking cessation, dietary modification, education, and exercise.⁴ The cessation of cigarette smoking should always be encouraged, as the elderly receive a similar benefit as younger individuals. Cigarette use declines with age, with 15% of men and 11.5% of women older than 65 years continuing to smoke cigarettes. Patients with symptoms of CHD are most likely to quit. The use of transdermal nicotine replacement patches (14 to 22 mg daily, then taper after 6 weeks) and bupropion (150 mg oral twice daily) should be considered as part of a smoking cessation strategy. For this to be successful, a structured approach should be implemented. Oftentimes, the utilization of allied health professionals to implement and carry out these measures with patients should be strongly considered.

Greater than one third of patients older than 65 years perform no leisure time physical activity. Patients must be counseled on the importance of weight control and exercise. Exercise has been associated with a reduction in blood pressure and insulin resistance in addition to an increase in high-density lipoprotein cholesterol (HDL-C). Moderate exercise has proven efficacious in reducing cardiovascular events. Studies have shown that the exercise trainability of elderly patients is similar to that of younger patients, and that the elderly derive significant benefit from exercise rehabilitation. A gradual and steady increase in physical activity is strongly suggested over short bursts of vigorous physical activity, which increases the likelihood of sudden cardiac death. Exercise-based cardiac rehabilitation should be recommended to all elderly patients with CHD. Walking 30 minutes most days of the week is reasonable.

The importance of patient education in the elderly cannot be overemphasized. Dietary education as it pertains to comorbid disease states (hyperlipidemia, diabetes, hypertension, heart failure) must be given during office visits. The maximal gain that patients receive from diagnostic and therapeutic technology is dependent on their understanding of their disease. Educating the patient about their disease, if necessary by health educators or the use of professionally prepared material, is of great importance. The presence of a spouse, significant other, or family member during the office visit is important in that they may help facilitate the interview and help better clarify matters to both the clinician and the patient.

The initiation of cardiovascular medications must be closely monitored, as elderly patients are more prone to side effects such as bradycardia, conduction abnormalities, hypotension, hepatic or renal toxicity, and possible mental status changes. Medications have to be started at lower doses and gradually titrated to prevent adverse effects. Aspirin is recommended in all elderly patients (75 to 325 mg daily) with CHD regardless of symptoms, provided that no contraindications exist (Evidence Level A).⁵ Therapeutic classes of medications considered in this section focus on angiotensin-converting enzyme inhibitors (ACE-I), lipid-lowering agents, β-blockers, calcium-channel blockers, and nitrates.

ACE inhibitor therapy has been shown to reduce mortality in the secondary prevention of CHD (Evidence Level A).
The Heart Outcomes Prevention Evaluation (HOPE) trial (n = 9,297; mean age 66 ± 7 years; 55% ≥65 years) and the European Trial on Reduction of Cardiac Events with Perindopril in Stable Coronary Artery Disease (EUROPA) (n = 12,218; mean age 60 ± 9 years; 31% >65 years) showed a significant reduction in death, MI, and stroke in patients treated with ACE inhibitor therapy.⁶,⁷ However, recent results from the Prevention of Events with Angiotensin Converting Enzyme Inhibition (PEACE) trial (n = 8,290; mean age 64 ± 8 years; 11% ≥75 years) demonstrated no additional reduction in the composite endpoint (cardiovascular death, MI, or coronary revascularization) in patients with preserved left ventricular function and intensive medical therapy who received trandolapril over placebo.⁸ There is much controversy regarding the possible improved efficacy of “tissue-specific” ACE inhibitor (ramipril 2.5 to 20 mg PO daily or divided twice daily dosing; perindopril 4 to 8 mg PO daily; trandolapril 2 to 4 mg PO daily) over other ACE inhibitor preparations (lisinopril 20 to 40 mg PO daily; enalapril 10 to 40 mg PO daily; fosinopril 20 to 40 mg PO daily; benazepril 20 to 40 mg PO daily). There have been no studies specifically comparing ACE inhibitor types. Barring significant renal insufficiency, ACE inhibitor therapy should be considered in all patients with CHD, especially those with diabetes mellitus.

Lipid-lowering agents such as hydroxyl-methylglutaryl coenzyme A reductase inhibitors (“statins”) are first-line agents in the treatment of dyslipidemia, even in those patients ≥65 years (Evidence Level A). In addition to a significant reduction in CHD mortality, treatment with statin therapy has demonstrated plaque stabilization, plaque regression, or the slowing of plaque progression. Randomized clinical trials, such as the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER) demonstrated a 15% relative risk reduction in CHD death, nonfatal MI, and stroke over placebo (5,804 patients, aged 70 to 82, mean 75 ± 3 years).⁹ Subset analysis from the elderly cohort (age range 65 to 69, n = 4,891; age range ≥70, n = 5,806) in the Heart Protection Study showed a significant reduction in the incidence of a first major coronary event, stroke, and revascularization when patients were randomized to simvastatin 40 mg over placebo over a 5-year follow-up period.¹⁰ Benefits of statin therapy, even in patients with average cholesterol levels, have been well demonstrated. Statin therapy is recommended, even for CHD patients with mild elevations in LDL-C. The most recent update of the National Cholesterol Education Program has recommended that patients with high-risk CHD be treated to achieve a goal of LDL-C ≤70 mg per dL. This recommendation is supported by the results of the Treating to New Targets (TNT) Study (n = 10,001; mean age 61 ± 8.8 years) which demonstrated a 22% relative risk reduction in the composite primary endpoint (death, nonfatal MI, resuscitation after cardiac arrest, or stroke) of atorvastatin 80 mg compared to atorvastatin 10 mg over a 4.9-year follow-up period.¹¹ In patients with CHD and an LDL-C level >100 mg per dL despite maximal statin therapy, the consideration for newer agents such as ezetimibe (10 mg PO daily) may provide additional reduction. Ezetimibe inhibits both dietary and biliary cholesterol absorption at the intestinal brush border. Although this agent has not been specifically tested in the elderly population, a 10% to 15% decrease in LDL-C is expected. If these agents are not tolerated, agents such as bile acid sequestrants (cholestyramine) (Evidence Level A), fibric acid derivatives (gemfibrozil and clofibrozil) (Evidence Level A), and niacin (Evidence Level A) should be considered for low HDL-C and elevated triglycerides.

Antianginal agents, such as β-blockers, improve survival in patients after MI and are widely used for the first-line treatment of angina in the elderly (Evidence Level A). In the treatment of stable angina, β-blockers should be titrated to achieve a heart rate range of 55 to 60 beats per minute (atenolol 25 to 100 mg PO daily; metoprolol 25 to 100 mg PO twice daily; labetolol 100 to 400 mg PO twice daily). Exercise caution in the elderly to avoid the development of heart block. Diabetes mellitus is not a contraindication to the use of β-blockers. Contraindications to the use of β-blockers include marked bradycardia, sick-sinus syndrome, and high-grade AV block. Relative contraindications include reactive airway disease, severe depression, and peripheral vascular disease.

Although their mechanisms are different, both calcium channel blocker and nitrate preparations dilate epicardial coronary arteries and reduce myocardial oxygen demand. Calcium channel blockers are as effective as β-blockers in the treatment of angina. Although β-blockers should be considered as first-line therapy, initiation of calcium channel blockers may be considered if adequate reduction in symptoms is not achieved or if contraindications exist with β-blocker use (Evidence Level B). Recent study results suggest that amlodipine (OR 0.69, CI 0.54 to 0.088; p = 0.003) favors a reduction in cardiovascular events (cardiac death, nonfatal MI, revascularization, stroke, transient ischemic attacks, and hospitalization for heart failure or angina) over enalapril (OR 0.85, CI 0.67 to 1.07; p = 0.16) compared to placebo control, especially in those patients ≥65 years (49% relative risk reduction).¹² The reduction in cardiovascular events observed with the use of amlodipine was mainly driven by a significantly greater reduction in anginal symptoms requiring hospitalization. Long-acting nitrates are generally added to β-blocker or calcium channel blocker therapy if symptoms persist (Evidence Level B). There is no survival benefit with nitrate use, but symptom improvement occurs. The major contraindications to calcium channel blocker use include overt decompensated heart failure. Evidence of bradycardia, AV block, or sinus node dysfunction should discourage the use of nondihydropyridine calcium channel blockers (verapamil and diltiazem). Nitrates should be avoided in patients with severe AS or hypertrophic obstructive cardiomyopathy.

Percutaneous coronary intervention (PCI) and coronary artery bypass graft surgery (CABG) at an elderly age has significantly increased during the last 20 years. In large retrospective national registries of coronary revascularization, octogenarians compared to patients <80 years were more likely to have chronic lung disease, chronic kidney disease, cerebrovascular disease, peripheral vascular disease, three-vessel coronary artery disease, and left main coronary artery disease. The in-hospital mortality rates are higher in octogenarians undergoing PCI (3.8%) and CABG (4.2% to 8.1%) compared to patients <80 years (1.1% and 3.0%, respectively), most likely related to comorbid illnesses.¹³,¹⁴ Randomized, multicenter clinical trials have demonstrated that invasive treatment (PCI or CABG) over medical therapy provided the most benefit in terms of improvement in quality of life and reducing angina, but few elderly patients were participants in these trials (Evidence Level A).¹⁵ The decision to pursue revascularization in elderly patients must be made on an individual basis, and after careful consideration of the patient’s overall condition. For example, those with severe functional or cognitive limitations at baseline would not be surgical candidates, given the high likelihood of overall poor postoperative recovery. Conversely, elderly patients who have a reasonable level of cognitive and functional ability with an acceptable degree of comorbidity should at least be considered for revascularization. Unfortunately, at this time, there are no prospective randomized studies that have been performed in the very elderly to make any substantive recommendations regarding the decision to pursue mechanical revascularization as it pertains to long-term outcomes.