Michael W. Rich MD
Cardiovascular diseases are the leading cause of death and major disability in both men and women in the United States, and the prevalence of cardiovascular disease increases progressively with age (Figure 19-1). Persons older than 65 account for 65% of all cardiovascular hospitalizations, and cardiovascular disease is also the most common primary diagnosis on admission to a nursing home. Older persons undergo a disproportionate number of cardiovascular procedures, and >80% of all deaths attributable to cardiovascular disease occur in the 13% of the population older than 65. The prevalence of cardiovascular disease is similar in men and women after age 65, and women account for slightly more than 50% of all cardiovascular deaths.
The rising prevalence of cardiovascular disease with advancing age may be attributed to the cumulative effects of normal aging processes and cardiovascular risk factors.
Normal aging is associated with extensive changes throughout the cardiovascular system that influence the epidemiology, clinical features, response to therapy, and prognosis of cardiovascular disorders in older adults. Table 19-1 summarizes the principal clinically relevant effects of normal cardiovascular aging. These changes markedly reduce cardiovascular reserve, leading to a progressive decline in peak cardiac performance, and predispose older adults to increased risk for cardiovascular complications and adverse outcomes in the presence of superimposed cardiac (eg, myocardial infarction [MI]) or noncardiac (eg, pneumonia, major surgery) conditions or procedures. Moreover, parallel age-related changes in other organ systems may further impair cardiovascular reserve or attenuate the benefit of therapeutic interventions. Finally, prevalent comorbid conditions and geriatric syndromes, polypharmacy, and an array of psychosocial, behavioral, and financial constraints may also impact presentation, compliance with prescribed treatment, and overall prognosis of older patients with cardiovascular disease.
Increasing age is the most powerful risk factor for cardiovascular disease in the United States. Other major risk factors for cardiovascular disease include hypertension, diabetes, dyslipidemia, smoking, physical inactivity, and obesity. Because the absolute number of incident cardiovascular events attributable to each of these risk factors (ie, population-attributable risk) tends to increase with age, the absolute benefit derived from treating specific risk factors is often greater in older adults. As a result, advanced age per se is rarely a contraindication to risk factor modification. In addition, because the total risk burden reflects the cumulative effects of risk factors as well as their duration and severity, and because older adults are more likely to have multiple risk factors of prolonged duration, the greatest potential benefit from aggressive risk factor modification occurs in high-risk older adults with multiple risk factors.
ACUTE MYOCARDIAL INFARCTION
ESSENTIALS OF DIAGNOSIS
Of the estimated 1.1 million recognized acute MIs occurring in the United States each year, 62% occur in persons 65 years of age or older and 37% occur in persons 75 years of age or older. In addition, case fatality rates increase markedly with age; 85% of all MI deaths occur in persons older than 65 and 60% occur in persons older than 75. Although the incidence of MI is higher in men than in women at all ages, the total number of MIs is similar in older men and women, reflecting the fact that the proportion of women in the surviving
population increases with age. The prevalence of silent or clinically unrecognized MI increases with age and may account for 25–30% of all MIs in the elderly. The long-term prognosis after clinically unrecognized MI is similar to that of recognized MI in older adults.
Figure 19-1. Prevalence of cardiovascular diseases in Americans.
Despite the high prevalence of coronary artery disease (CAD) and acute MI in industrialized countries, these disorders are potentially preventable through early and aggressive management of hypertension, dyslipidemia, and diabetes, combined with lifelong adherence to a pattern of behavior modification, including regular physical exercise; maintenance of desirable body weight; a diet rich in fruits, vegetables, and whole-grain products but low in cholesterol and saturated fats (including trans-saturated fats); and avoidance of tobacco products.
Table 19-1. Major effects of aging on the cardiovascular system.
Aspirin, clopidogrel, β-blockers, angiotensin-converting enzyme inhibitors, and hepatic hydroxymethylglutaric coenzyme A (HMG CoA) reductase inhibitors (statins) have been shown to improve prognosis after acute MI. In addition, cardiac rehabilitation programs also reduce mortality and rehospitalizations after acute MI.
The proportion of MI patients who have chest pain declines with age; < 50% of MI patients older than 80 complain of chest pain. Likewise, diaphoresis occurs less frequently in older patients with acute MI. Conversely, dyspnea, or acute shortness of breath, is often the presenting manifestation of acute MI in the elderly and is the most common initial symptom in persons older than 80. The prevalence of atypical symptoms, (eg, gastrointestinal disturbances, fatigue, dizziness, syncope, confusion, stroke) also increases with age, and up to 20% of patients older than 85 with acute MI have neurological complaints.
Physical findings associated with acute MI are nonspecific but may include an S3 or S4 gallop, new murmur of mitral regurgitation, or signs of pulmonary or systemic venous congestion, such as fine pulmonary rales or elevated jugular venous pressure. In patients with right ventricular infarction, Kussmaul's sign may be present.
Classical electrocardiographic features of acute MI include ST-segment elevation of at least 1–2 mm in 2 or more contiguous leads corresponding to the anatomical distribution of the involved coronary artery (eg, leads II, III, AVF), with subsequent evolution of inverted T waves and pathological Q waves. However, the initial electrocardiogram (ECG) is often nondiagnostic in older adults because of preexisting conduction system disease (eg, left bundle branch block), presence of a ventricular pacemaker, prior MI or left ventricular (LV) hypertrophy, metabolic abnormalities or drug effects (eg, hypokalemia, digoxin), and the high prevalence of non-ST-elevation MI.
Atypical symptoms and physical findings, coupled with the high prevalence of nondiagnostic ECGs, often lead to delayed presentation and delayed recognition of
acute MI. This increases the risk of complications and reduces the window of opportunity for effective intervention. Physicians should maintain a high index of suspicion for acute MI in all older patients with a wide range of unexplained cardiovascular, pulmonary, gastrointestinal, or neurological symptoms.
Definitive diagnosis of acute MI requires documentation of an abnormal pattern of cardiac biomarkers. Troponins I and T have become the gold standard for diagnosis because of their greater sensitivity and specificity compared with the creatine kinase-MB (CK-MB) isoenzyme. Serial measures of biomarkers that exceed the normal range and exhibit a typical rise-and-fall pattern in a patient with clinical or electrocardiographic features of cardiac ischemia are diagnostic of acute MI. In the absence of recurrent ischemia, CK-MB levels peak at ~24 h after MI onset and return to normal within 48–72 h. Troponin levels usually peak at 24–72 h and may remain elevated for up to 2 weeks, especially in patients with large MIs.
The differential diagnosis of acute MI in the elderly includes other cardiovascular conditions as well as pulmonary, gastrointestinal, musculoskeletal, and neurological disorders. Major cardiovascular conditions that should be considered include unstable angina, aortic dissection, pericarditis, and acute pulmonary edema resulting from cardiomyopathy, valvular heart disease, or arrhythmia. Pulmonary disorders include pneumonia, pulmonary embolus, pleurisy, and pleural effusion. Gastrointestinal disorders include esophagitis or esophageal spasm, gastroesophageal reflux, peptic ulcer disease, cholelithiasis, and pancreatitis. Musculoskeletal disorders include muscular strains, costochondritis, injuries involving the cervical or thoracic spine, disorders of the shoulder joint, and chest wall trauma. Neurological conditions include stroke or transient ischemic attack, radiculopathy, and altered sensorium or delirium resulting from impaired cerebral blood flow or other causes. Psychogenic conditions, including anxiety reactions and hyperventilation syndrome, may also mimic the symptoms of acute MI.
Major complications of acute MI include heart failure (HF), hypotension, conduction disturbances (eg, bundle branch block), atrial fibrillation, myocardial rupture, and cardiogenic shock. Each of these complications is associated with worse prognosis and occurs 2–4 times more frequently in older patients. Although low-grade ventricular arrhythmias (eg, frequent ventricular premature beats) occur more frequently in older patients, the incidence of primary ventricular fibrillation is lower.
Table 19-2 lists the major therapeutic options for acute MI. Management of ST-elevation MI and non-ST-elevation MI differs with respect to the use of early reperfusion therapy but is otherwise similar.
Maintenance of adequate arterial oxygenation and relief of chest discomfort are important goals. Supplemental oxygen should be provided to maintain a minimum arterial oxygen saturation of 90%. Intravenous morphine should be administered in 2- to 4-mg boluses as needed for relief of chest pain, monitoring closely for signs of respiratory depression, bradycardia, hypotension, and impaired sensorium. Sublingual nitroglycerin should be administered acutely for the treatment of ischemic chest pain or dyspnea. Patients with persistent chest pain or signs of pulmonary congestion should receive topical nitroglycerin or an intravenous nitroglycerin infusion, titrated to control symptoms while avoiding excessive blood pressure (BP) reduction (ie, systolic BP <90 mm Hg, change in systolic BP from baseline >20 mm Hg, or signs of hypoperfusion, such as impaired mental status). In patients with signs of right ventricular infarction
(acute inferior MI with elevated jugular venous pressure, Kussmaul's sign, or ST elevation in right precordial leads), nitroglycerin may precipitate severe hypotension and should be given cautiously or avoided.
Table 19-2. Management of acute myocardial infarction.
Recanalization of the involved coronary artery within 6–12 h of MI onset substantially reduces mortality and morbid complications. Reperfusion can be achieved either pharmacologically, through the use of fibrinolytic agents, or mechanically, through the use of percutaneous coronary angioplasty with or without intracoronary stent implantation. In general, mechanical reperfusion is more effective than fibrinolysis. Intracranial hemorrhage occurs less frequently with mechanical reperfusion, particularly in patients older than 75, in whom the risk of intracranial bleeding is 1–2% with fibrinolytic therapy. Mechanical reperfusion has been shown to benefit patients with either ST-elevation or non-ST-elevation MI. Fibrinolytic therapy is only effective in ST-elevation MI and is contraindicated for the treatment of non-ST-elevation MI. Because of limited access to catheterization facilities, intravenous fibrinolysis is the most commonly used reperfusion strategy in the United States.
Table 19-3. Properties of fibrinolytic agents.
Low-molecular-weight (LMW) heparins such as enoxaparin and dalteparin provide more stable anticoagulation than unfractionated heparin and offer the advantage of subcutaneous administration without the need to monitor activated partial thromboplastin time (aPTT). In addition, LMW heparins have been associated with improved clinical outcomes. LMW heparin therapy is indicated in all patients with non-ST-elevation MI, but the benefits in patients with ST-elevation MI are less well established.
and tirofiban reduce the risk of recurrent ischemic events and improve clinical outcomes in patients with documented MI, particularly those undergoing percutaneous coronary revascularization. In addition, the benefits of these agents are similar in younger and older patients, although the risk of bleeding is somewhat higher in the elderly; dosage adjustment may be necessary in patients with impaired renal function. Currently, the value of glycoprotein IIb/IIIa inhibitors in older patients with acute MI who are unlikely to undergo mechanical revascularization is uncertain.
Table 19-4. Criteria for fibrinolytic therapy in older adults.
Early administration of intravenous β-blockers reduces mortality, recurrent ischemic events, and both supraventricular and ventricular tachyarrhythmias in appropriately selected patients with acute MI. Intravenous β-blocker therapy should be initiated as soon as possible in all patients with suspected acute MI in the absence of contraindications (ie, heart rate < 45 bpm, systolic BP < 90–100 mm Hg, PR interval ≥240 ms or heart block >first degree, moderate or severe pulmonary congestion, or active bronchospasm).
Intravenous metoprolol and atenolol have been approved for treatment of acute MI. Metoprolol is administered as three 5-mg boluses at 2- to 5-min intervals followed by 25 mg orally every 6 h with further dosage increases as tolerated to reach a target dose of 200 mg daily. Atenolol is administered as two 5-mg boluses at an interval of 10 min followed by 25 mg twice daily, increasing to 50 mg twice daily as tolerated. Patients receiving intravenous β-blockers should be carefully observed for bradyarrhythmias, hypotension, dyspnea, and bronchospasm, and the dose and duration of therapy should be adjusted accordingly if these side effects occur. It is prudent to use lower dosages and a slower dose titration schedule in patients older than 75 and in older patients with multiple comorbidities or unstable hemodynamics.
ACE inhibitors are clearly beneficial in reducing mortality after acute MI in patients 65–74 years of age, but there is not clear evidence of benefit in patients older than 75. Data suggest that ACE inhibitors are particularly beneficial in patients with anterior ST-elevation MIs and in patients with MIs complicated by HF or significant LV systolic dysfunction (LV ejection fraction < 40%). Early initiation of ACE inhibitor therapy is recommended for all patients with anterior MI, active HF, or significant LV dysfunction in the absence of contraindications. In addition, wider use of ACE inhibitors in patients younger than 75 may be beneficial. Contraindications to ACE inhibitors in the setting of acute MI include systolic BP < 100 mm Hg, advanced renal insufficiency (serum creatinine ≥2.5–3.0 mg/dL, especially if worsening renal function is evident), hyperkalemia
(serum potassium ≥5.5 mEq/L), and known intolerance to ACE inhibitors. ACE inhibitor therapy should be initiated with captopril 6.25 mg three times a day or enalapril 2.5 mg twice daily. The dose should be gradually increased as tolerated to a maintenance dose of captopril 50 mg 3 times a day or enalapril 10 mg twice daily. Once the maintenance dose has been achieved, changing to a once-daily agent at equivalent dosage (eg, lisinopril 20–40 mg or ramipril 10 mg) is appropriate. Throughout the initiation and titration phase of ACE inhibitor therapy, BP, serum creatinine, and serum electrolytes (especially potassium) should be carefully monitored.
Nitrate preparations are effective in controlling ischemia and in treating HF in patients with acute MI.
Angiotensin receptor blockers (ARBs) appear to be somewhat less effective than ACE inhibitors for improving outcomes after acute MI. Nevertheless, for patients who are appropriate candidates for ACE inhibitor therapy but who are intolerant because of cough, ARBs may provide a suitable alternative.
Calcium channel blockers have not been shown to improve outcomes in patients with acute MI, and the use of short-acting dihydropyridines (eg, nifedipine) may be harmful.
HMG CoA reductase inhibitors (statins) decrease mortality and recurrent ischemic events after acute MI. Unless contraindicated, statin therapy should be initiated early in the course of acute MI and continued indefinitely.
Lidocaine and amiodarone are effective in the treatment of life-threatening ventricular arrhythmias in the setting of acute MI, but routine use of these agents as prophylaxis is not recommended.
Routine administration of intravenous magnesium in patients with acute MI is not efficacious.
Approximately 15–20% of patients with acute MI die before reaching the hospital, and this proportion likely increases with advancing age. Among patients with recognized MI, both short- and long-term mortality increases progressively with age. Total mortality within 1 year after MI is ~40% among persons older than 65. Factors associated with increased mortality include older age, anterior MI, clinical HF, impaired LV systolic function, atrial fibrillation, complex ventricular arrhythmias, poor functional status, diabetes mellitus, and lack of treatment with aspirin and β-blockers. Although short-term prognosis is more favorable in non-ST-elevation MI than in ST-elevation MI, mortality rates at 2 years are similar.
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ESSENTIALS OF DIAGNOSIS
Unstable angina is characterized by ischemic symptoms of increasing frequency, severity, or duration; symptoms occurring with less provocation; or symptoms of recent onset occurring with minimal exertion or at rest. Patients with unstable angina are at increased risk for progression to acute MI during short-term follow-up; therefore, aggressive treatment is warranted.
Measures effective in the primary prevention of CAD and acute MI are also efficacious in the prevention of unstable angina.
The symptoms and physical findings of unstable angina may be indistinguishable from those of acute MI, reflecting the similar pathogenesis of these disorders.
During chest pain, the ECG usually demonstrates ST-segment depression or T-wave inversion, or both, in 1 or more contiguous leads; less commonly, ST-segment elevation may be seen. Electrocardiographic changes often resolve with resolution of chest pain, so that a nondiagnostic or even normal ECG taken when the patient is free of symptoms does not exclude unstable angina. The principal feature that distinguishes unstable angina from acute MI is the lack of elevation of cardiac biomarker proteins (troponin I, troponin T, and CK-MB).
The differential diagnosis of unstable angina is similar to that of acute MI.
The principal complication of unstable angina is progression to acute MI. Unstable angina may also be associated with ventricular arrhythmias, including ventricular tachycardia, ventricular fibrillation, and sudden cardiac death as well as supraventricular arrhythmias, bradyarrhythmias, and acute HF.
The primary goals of therapy for unstable angina are to relieve symptoms and prevent progression to acute MI. Patients should be hospitalized for observation and receive prompt treatment with aspirin, nitrates, and β-blockers. In patients with persistent or severe symptoms or electrocardiographic changes, nitroglycerin should be administered intravenously. Heparin should also be administered, either intravenously (unfractionated heparin) or as subcutaneous LMW heparin. Patients with marked electrocardiographic abnormalities and those for whom percutaneous coronary revascularization is planned should also be treated with an intravenous glycoprotein IIb/IIIa inhibitor. Additional therapy for unstable angina is similar to that discussed
previously for non-ST-elevation MI. In most cases, patients with severe or recurrent symptoms or electrocardiographic abnormalities should undergo cardiac catheterization and coronary angiography followed by percutaneous or surgical revascularization based on anatomical findings. Patients who respond to medical therapy and have no further symptoms should undergo a stress test to stratify risk. Patients with severe ischemia, ischemia at low cardiac workload, or ischemia in association with reduced LV systolic function should proceed to catheterization. Those with less severe ischemia or a normal stress test may be managed conservatively.
The natural history of unstable angina is characterized by frequent progression to MI. With current therapeutic options, the short-term prognosis is favorable, and < 10% of patients hospitalized with unstable angina experience acute MI. The majority of patients with unstable angina have severe coronary atherosclerosis and are at risk for future coronary events. Aggressive treatment of coronary risk factors and implementation of other preventive measures, including aspirin, β-blockers, and ACE inhibitors, is warranted.
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CHRONIC CORONARY HEART DISEASE
ESSENTIALS OF DIAGNOSIS
CHD is the leading cause of death in the United States in both men and women. Although the incidence and prevalence of CHD are both higher in men than in women, the rates for women increase progressively after menopause, and the greater longevity of women compared with men results in a slight predominance of women in the total number of CHD cases. The prevalence of CHD increases progressively with age, affecting 16.1% of women and 18.6% of men older than 75.
Primary prevention of CHD may be achieved through lifelong avoidance of tobacco products, participation in regular physical exercise, maintenance of desirable body weight, consumption of a diet rich in fruits, vegetables, and whole-grain foods, and limited consumption of foods high in saturated fats and cholesterol. Early identification and aggressive treatment of hypertension, dyslipidemia, and diabetes are essential as well.
The most common symptom of chronic CHD is central chest discomfort, often described as pressure, tightness, or heaviness, typically brought on by physical exertion or emotional stress and relieved by rest or nitroglycerin. However, many older adults with CHD, including those with prior MI or unstable angina, manifest atypical symptoms, such as dyspnea, fatigue, weakness, dizziness, or abdominal discomfort, whereas others, particularly diabetics, are entirely asymptomatic, in part because of the high prevalence of physical inactivity at older age. Thus, despite the high prevalence of CHD in the elderly, a substantial proportion of patients do not experience typical angina pectoris, and the physician must maintain a high index of suspicion for CHD in older persons with atypical symptoms or multiple risk factors.
The physical findings of chronic CHD are nonspecific but may include an S3 or S4 gallop, a murmur of mitral regurgitation, a laterally displaced or dyskinetic apical impulse (especially in patients with prior MI), or signs of HF (eg, pulmonary rales, elevated jugular venous pressure, peripheral edema).
radionuclide imaging. These tests provide 80–90% sensitivity and specificity for diagnosing CHD, although the predictive accuracy of the test is dependent on the pretest likelihood that the patient has the disease. In general, it is preferable to perform an exercise test if the patient is capable of doing so. However, because many elderly patients are limited by arthritis, neurological conditions, or poor physical conditioning, it is often necessary to perform a pharmacological stress test in older patients (eg, dobutamine echo, adenosine sestamibi).
The differential diagnosis of chest pain includes cardiac, vascular, gastrointestinal, pulmonary, neurological, musculoskeletal, and psychogenic causes. In patients with recent onset or progression of symptoms suggestive of ischemia, the possibility of unstable angina or acute MI must be considered.
The major complications of chronic CHD are progression to an acute coronary event (MI, unstable angina), development of HF because of the cumulative effects of myocardial injury or infarction (ischemic cardiomyopathy), and development of conduction abnormalities or arrhythmias, including ventricular tachycardia and ventricular fibrillation. Sudden cardiac death is the initial manifestation of CHD in up to 20% of cases.
The goals of therapy for chronic CHD are to control symptoms and prevent major complications. Optimal treatment involves lifestyle modifications, attention to risk factors, pharmacological interventions, and, in selected patients, percutaneous or surgical revascularization.
Patients with CHD, regardless of age, should be strongly advised to discontinue the use of all tobacco products. Gradual weight reduction through a program of diet and regular exercise should be encouraged in overweight patients (body mass index >25–30 kg/m2). Patients with CHD should eat a balanced diet rich in fruits, vegetables, and whole grains while limiting intake of saturated fats (including partially hydrogenated oils) and cholesterol. Patients should also engage in a total of at least 20–30 min of moderate intensity physical activity on most days of the week unless limited by active cardiovascular symptoms or other medical conditions. Walking, stationary cycling, and swimming are suitable exercise modalities for most older adults. When beginning an exercise program, patients should be instructed to start at a slow and comfortable pace, gradually increasing the duration of exercise over a period of weeks. The addition of flexibility and strengthening exercises is also beneficial to overall health. Patients who have suffered an MI or who have had coronary bypass surgery should be strongly encouraged to participate in a formal cardiac rehabilitation program. Such programs have been associated with reduced mortality, improved exercise tolerance and quality of life, and enhanced mood and sense of well-being.
Smoking should be discouraged. Antihypertensive therapy should be titrated to maintain a resting BP < 140/90 mm Hg (< 130/80 mm Hg in diabetics and patients with HF or renal insufficiency). The lipid profile should be monitored and the low-density lipoprotein (LDL) cholesterol level reduced to < 100 mg/dL through dietary modifications and, if necessary, lipid-lowering agents. Diabetes should be controlled through diet and medications to achieve a hemoglobin A1C level of < 7 g/dL. Obesity and physical inactivity should be addressed through lifestyle modifications.
angina. As a result of drying of the oral mucosa, nitroglycerin spray may be more effective than tablets in older patients. Older patients may also be more likely to experience orthostatic hypotension with nitroglycerin; they should be advised to take the medication in a sitting or reclining position. Long-term nitrates are effective antianginal agents but have not been shown to improve clinical outcomes. In addition, tolerance to nitrates develops rapidly, requiring a daily 6- to 8-h nitrate-free interval. Several oral and transdermal nitrate preparations are available for chronic use.
Percutaneous coronary revascularization and coronary artery bypass surgery are highly effective in improving symptoms and quality of life in older patients with CHD; >50% of all revascularization procedures in the United States are now performed in patients older than 65. On the other hand, both coronary angioplasty and bypass surgery are associated with increased mortality and major complications in the very elderly, especially patients older than 80; thus, careful selection of candidates for revascularization procedures is paramount. In general, percutaneous coronary revascularization is associated with lower mortality and major morbidity (including stroke, delirium) as well as much more rapid recovery compared with coronary bypass surgery in elderly patients. However, the need for repeat revascularization procedures is higher after angioplasty, and long-term outcomes are similar. Thus, both procedures represent suitable options for older patients with severe symptomatic CHD, and the choice of procedure should be based on anatomical considerations, prevalent comorbidities, and patient preferences. Up to 50% of elderly patients undergoing coronary bypass surgery may experience a decline in cognitive function in the perioperative period. Although these cognitive deficits are transient in many patients, a significant proportion may exhibit persistent cognitive impairment during long-term follow-up.
The prognosis of chronic CHD is highly variable. Although some patients remain minimally symptomatic or asymptomatic for decades, others experience marked disability despite multiple therapeutic interventions. Still others succumb to the disease after suffering a large MI or fatal arrhythmia. Factors that adversely influence prognosis include older age, male gender, more severe CHD, more severe HF or LV systolic dysfunction (lower ejection fraction), more severe symptoms or functional limitations, presence of diabetes or atrial fibrillation, and presence of significant ventricular arrhythmias.
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VALVULAR HEART DISEASE
ESSENTIALS OF DIAGNOSIS
Aortic stenosis (AS) increases in prevalence with age and affects 15–20% of men and women older than 80. Approximately 2–3% of persons older than 75 experience AS of sufficient severity to warrant consideration for aortic valve replacement. AS is the second most common indication for major cardiac surgery in the elderly (after coronary bypass surgery).
There are no known interventions for prevention of AS in the elderly; however, statins may slow the rate of progression.
The classic triad of symptoms associated with severe AS includes exertional angina, dizziness or syncope, and dyspnea or orthopnea. However, AS in the elderly is often occult until it reaches an advanced stage because sedentary older persons may experience few symptoms or may attribute their symptoms to another disease or to old age.
Significant AS is almost invariably associated with a ≥grade II systolic ejection murmur that is usually harsh and best heard in the right second intercostal space with radiation to the carotid arteries. The murmur may be difficult to hear in obese patients and in those with increased chest diameter because of chronic lung disease, whereas in others it may be best heard at the apex. Murmurs that peak in late systole tend to be associated with more severe AS, but the intensity of the murmur often diminishes in patients with severe LV failure. Other physical findings include an LV heave, S4 gallop, and reduced intensity or absence of the A2 component of the second heart sound. Classically, the carotid upstroke is delayed in patients with severe AS, but this finding may be masked in older patients with stiff, noncompliant vessels.
echocardiographic features include a moderately or severely thickened and calcified valve with restricted opening. Doppler examination reveals increased mean and peak velocities across the valve, and the continuity equation permits estimation of the effective aortic valve area. A calculated aortic valve area of 1.1–1.5 cm2 indicates mild AS, 0.8–1.1 cm2 moderate AS, and < 0.8 cm2 severe AS.
Aortic sclerosis (ie, thickening of the aortic valve cusps without valvular stenosis) occurs more frequency with age and is a marker for increased cardiovascular morbidity and mortality. The symptoms of AS may mimic many other cardiac and noncardiac diseases, including CAD, HF, arrhythmia, and chronic lung disease. Likewise, the physical findings, ECG, and chest radiograph are often nonspecific. The physician must, therefore, maintain a high index of suspicion in patients with symptoms possibly attributable to AS in association with a systolic ejection murmur. Echocardiography and cardiac catheterization are diagnostic.
The major complications of untreated severe AS include progressive HF, ischemia, syncope, and sudden death as a result of ventricular arrhythmias or asystole. Sudden death occurs predominantly in patients with severe symptomatic AS but occasionally represents the initial manifestation of the disease.
There is no effective medical therapy for severe AS. All patients with a heart murmur resulting from AS should receive antibiotic prophylaxis for dental work and other procedures in accordance with American Heart Association (AHA) guidelines. Vasodilators, including nitrates and ACE inhibitors, should be administered with caution in patients with moderate or severe AS because of the risk of hypotension. Once symptoms develop, patients with severe AS should be referred for aortic valve replacement because the prognosis is poor in the absence of definitive therapy.
Aortic valve replacement is the procedure of choice for patients with severe symptomatic AS, and the results of valve replacement are excellent. In patients with significant CAD, coronary bypass surgery is performed concomitantly. Factors that militate against surgery include dementia, severe pulmonary disease, advanced frailty, and reluctance to undergo the procedure. In patients older than 75, most cardiac surgeons will implant a bioprosthetic valve, which has acceptable durability in this age group and obviates the need for long-term anticoagulation. Operative mortality rates for octogenarians undergoing aortic valve replacement are 4–7%; most patients report substantial improvement in symptoms and functional status after recovery.
Without surgery, median survival in elderly patients with severe symptomatic AS is 18–24 mo, and the prognosis is worse for patients with HF. After aortic valve replacement, survival is similar to that for persons of comparable age in the general population.
ESSENTIALS OF DIAGNOSIS
The prevalence of aortic insufficiency (AI) increases with age, but few cases are severe enough to warrant valve surgery.
Appropriate treatment of hypertension and dyslipidemias may reduce the risk of aortic root aneurysms and dissection. Early treatment of syphilis is effective in preventing syphilitic aortitis.
Patients with acute severe AI generally have symptoms of overt HF, those with mild or moderate chronic AI are usually asymptomatic, and those with chronic severe
AI report progressive exercise intolerance, shortness of breath, orthopnea, and fatigue. Palpitations and chest pain are less prominent features.
In patients with acute severe AI, the clinical picture is dominated by signs of LV failure, including shortness of breath and pulmonary congestion. A diastolic murmur of AI may be present. In patients with mild to moderate chronic AI, a short early diastolic decrescendo murmur is often the only physical finding. In those with chronic severe AI, the diastolic murmur becomes louder, occasionally reaching grade V or VI, and longer, often persisting throughout diastole with presystolic accentuation. The LV apical impulse is often diffuse and displaced laterally and inferiorly. An S3 gallop is often present and may be palpable. BP is characterized by a widened pulse pressure and especially by a low diastolic BP. Peripheral manifestations of severe chronic AI include bounding pulses, head bobbing, Quincke's pulses (capillary pulsations), and femoral bruits with light compression of the artery.
Acute severe AI usually manifests as severe LV failure that may not respond to conventional therapy. The differential diagnosis includes other causes of acute pulmonary edema, such as acute MI, severe hypertension, and cardiac arrhythmia. Other causes of chronic HF must be considered in the differential diagnosis of severe chronic AI.
Acute severe AI is often associated with intractable HF and death without surgical intervention. The course of chronic severe AI is insidious and gradually progressive over many years, ultimately leading to severe HF.
Acute severe AI complicated by HF requires prompt surgical intervention, usually consisting of aortic valve replacement. Medical stabilization while awaiting surgery should be directed at the underlying cause (eg, aortic dissection) and at the treatment of HF with diuretics and vasodilators. Afterload reduction with intravenous nitroprusside may result in marked clinical improvement but rarely obviates the need for surgery.
Patients with chronic AI, especially if moderate or severe, should receive antibiotic prophylaxis for dental work and other procedures. BP should be treated aggressively in accordance with current guidelines. Mild chronic AI requires no additional treatment. Patients with moderate or severe chronic AI should be treated with ACE inhibitors or other afterload-reducing agents to slow disease progression. Patients with severe chronic AI should undergo serial echocardiography at regular intervals. Criteria for aortic valve replacement include onset of HF symptoms, decline in LV ejection fraction to < 50%, or progressive LV dilatation with an end-systolic dimension >5.5 cm by echocardiography.
For patients with acute severe AI, surgical outcomes are dependent on the severity of HF and hemodynamic compromise as well as the cause of AI. In chronic AI patients, results of surgery are excellent in those with preserved LV function and minimal symptoms but are less favorable in those with markedly dilated ventricles, significantly reduced systolic function, or severe symptoms. Bioprosthetic valves are usually implanted in elderly patients requiring aortic valve replacement for severe AI.
Patients with acute severe AI complicated by HF have a high mortality rate unless aortic valve replacement is performed promptly. The short- and intermediate-term prognosis for patients with mild or moderate chronic AI is favorable because the condition often remains stable for many years. Patients with severe chronic AI
who are asymptomatic and have stable ventricular function have a good short- and intermediate-term prognosis. However, once symptoms of HF or significant LV dysfunction develop, the prognosis is poor unless aortic valve surgery is performed.
ESSENTIALS OF DIAGNOSIS
Mitral stenosis (MS) is relatively rare in the elderly, with a reported prevalence of < 1% in the United States.
Rheumatic heart disease can be prevented by prompt identification and treatment of group A β-hemolytic streptococcal infections. No interventions have been shown to prevent or slow the development of mitral valve annulus calcification.
The clinical course of MS is often insidious, and there may be an interval of several decades after an episode of acute rheumatic fever before symptoms of MS develop. Classic symptoms include exertional fatigue, a gradual decline in exercise tolerance, hemoptysis, dyspnea, and orthopnea. Not uncommonly, older patients with MS have symptoms resulting from new-onset atrial fibrillation, such as palpitations or acute HF.
Rheumatic mitral stenosis is characterized by an opening snap in early diastole followed by a mid-diastolic rumbling murmur. The murmur is low pitched, best heard at the apex or in the left lateral decubitus position, and intensified by tachycardia. There may be presystolic accentuation during sinus rhythm. Earlier occurrence of the opening snap and longer duration of the diastolic murmur are associated with more severe stenosis. All of these features may be absent in patients with MS because of mitral annular calcification. Additional findings associated with MS may include evidence for pulmonary hypertension (right ventricular heave, augmented P2) and evidence for biventricular failure (pulmonary rales, elevated jugular venous pressure, and peripheral edema).
The differential diagnosis includes other cardiac and pulmonary conditions that may produce symptoms and signs of left- or right-sided HF as well as conditions that may cause atrial fibrillation or pulmonary hypertension.
Major complications of MS include chronic progressive HF and atrial fibrillation. Atrial fibrillation resulting from MS is associated with a high rate of thromboembolic events, which may approach 20% per year in those not receiving anticoagulation.
Patients with MS should receive antibiotic prophylaxis for endocarditis in accordance with AHA guidelines. Those with atrial fibrillation should receive warfarin to maintain an international normalized ratio (INR) of 2.5–3.5 and β-blockers, diltiazem, verapamil, or digoxin, or a combination, to maintain a resting heart rate of
< 80 bpm and a peak exercise heart rate of < 115 bpm. Patients with HF should receive diuretics to relieve congestive symptoms and edema. Vasodilator therapy (eg, ACE inhibitors) has not been shown to be beneficial in the absence of LV systolic dysfunction.
Percutaneous mitral valve balloon valvotomy, open commissurotomy, and mitral valve replacement are effective treatments for severe MS in selected patients, and persons with moderate to severe symptoms unresponsive to medical management should be considered for one of these procedures. Percutaneous mitral valvotomy is the procedure of choice in patients with favorable anatomy, which includes pliable valve leaflets, absence of severe calcification, and no more than mild mitral regurgitation. Although percutaneous valvotomy has achieved excellent results in elderly patients who are suitable candidates for the procedure, most older patients are excluded because of excessive calcification of the mitral apparatus or more severe mitral regurgitation. These patients are not suitable candidates for open mitral valve commissurotomy for the same reasons; therefore, mitral valve replacement is the only option. Mitral valve replacement is associated with somewhat higher risks than aortic valve replacement, and symptomatic improvement may be less than in patients treated for aortic stenosis. In addition, patients undergoing mitral valve replacement with either a bioprosthetic or mechanical valve for MS require long-term anticoagulation with warfarin. Despite these limitations, long-term outcomes after mitral valve replacement are generally favorable.
MS runs a protracted course, and the 10-year survival rate in patients with minimal or no symptoms is >80%. Once limiting symptoms develop, the prognosis is much worse, and few patients survive 10 years. In untreated patients with severe MS, 60–70% die from progressive HF, 20–30% from systemic embolization, and 10% from pulmonary embolism.
ESSENTIALS OF DIAGNOSIS
Mitral regurgitation (MR) is the most common valvular disorder in the elderly, but in most cases surgical intervention is not required. Nonetheless, MR is the second most common reason for valve surgery in the elderly (after AS).
Therapies directed at preventing the various disorders that cause acute or chronic MR may reduce the prevalence of this condition.
The clinical findings of MR are dependent on acuity and severity. Mild acute MR is usually well tolerated, but acute MR of moderate severity (eg, complicating acute MI) may be associated with dyspnea and signs of pulmonary edema. Acute severe MR (eg, from papillary muscle rupture) is almost always associated with acute pulmonary edema and respiratory failure and may result in rapid hemodynamic deterioration and death. Chronic mild or moderate MR is usually asymptomatic, and chronic severe MR is often well tolerated as long as LV function is preserved. Once LV dysfunction develops, patients with severe chronic MR typically experience symptoms and signs of left-sided HF, including exertional dyspnea, orthopnea, an S3 gallop, and pulmonary rales. As the disease progresses, signs of right-sided HF, including elevated jugular venous pressure and peripheral edema, may ensue.
Physical findings associated with acute, severe MR, in addition to signs of HF, include a harsh early systolic murmur best heard at the apex. In patients with severe HF, the murmur may be difficult to appreciate, and the absence of a systolic murmur does not preclude acute severe MR. An S3 gallop and signs of pulmonary hypertension may be present. Chronic MR is characterized by an apical holosystolic murmur radiating to the axilla, back, or across the precordium. In patients with mitral valve prolapse, a mid-systolic click may be heard, followed by the MR murmur. In patients with severe chronic MR, the apical impulse is usually laterally displaced, and an S3 gallop may be present.
unremarkable unless the MR is due to an acute coronary ischemic event. In chronic severe MR the ECG reveals left atrial enlargement or atrial fibrillation; in advanced stages there may be evidence of right ventricular hypertrophy.
The differential diagnosis of MR includes numerous other conditions that may result in the clinical findings of left- or right-sided HF. Often, multiple such conditions coexist in elderly patients, and it may be difficult to determine the extent to which the patient's symptoms are due to MR or other causes.
Acute severe MR is almost always associated with pulmonary congestion and may be complicated by respiratory failure, hemodynamic decompensation, and death resulting from cardiogenic shock. Complications of chronic severe MR include progressive LV failure eventually leading to death, pulmonary hypertension, and atrial fibrillation.
Treatment of chronic MR should be directed at the primary cause when feasible. BP control should be optimized and antibiotic prophylaxis administered before dental work and other procedures, except in patients with mild MR in the absence of structural abnormalities of the mitral valve (including mitral valve prolapse). Mild chronic MR usually requires no specific therapy, but patients with moderate or severe chronic MR should be treated with ACE inhibitors for afterload reduction. Patients intolerant to ACE inhibitors should receive ARBs or the combination of nitrates and hydralazine. Atrial fibrillation should be treated with rate-controlling agents and anticoagulation with warfarin. HF should be managed with diuretics, ACE inhibitors, β-blockers, and digoxin as appropriate.
Acute severe MR complicated by pulmonary edema or hemodynamic instability requires urgent surgical intervention. Placement of an intra-aortic balloon pump may help stabilize the patient before surgery. Other measures include diuresis, vasodilator therapy to reduce afterload as tolerated, and endotracheal intubation if needed for respiratory failure.
Surgical options for the treatment of severe MR include mitral valve repair and mitral valve replacement. Whenever feasible, mitral valve repair is preferred because it preserves the integrity of the mitral valve apparatus and obviates the need for long-term anticoagulation (unless atrial fibrillation is present). Valve surgery is indicated in patients with acute MR complicated by significant HF and in those with severe chronic MR associated with moderate or severe symptoms, ejection fraction >30%, and LV end-systolic dimension < 5.5 cm by echocardiography.
Elderly patients with severe LV dysfunction or markedly dilated left ventricles respond poorly to surgery and should be managed medically. Results of surgery for ischemic MR also tend to be less favorable than for nonischemic MR. Other factors that influence surgical outcomes include older age, prevalent comorbidities, and symptom severity. Although mitral valve surgery in elderly patients is associated with significant morbidity and mortality, long-term outcomes are favorable, with symptomatic improvement in the majority of patients.
The prognosis of nonoperated acute severe MR complicated by pulmonary edema is poor; the majority of patients die within hours to days. The prognosis for mild to moderate chronic MR is good. The clinical course of severe chronic MR is highly variable, but patients should be monitored closely with serial echocardiograms because the development of significant symptoms or progressive LV dilatation or dysfunction is a
harbinger of poor outcome and mandates prompt consideration of surgical intervention.
Asimakopoulos G et al: Aortic valve replacement in patients 80 years of age and older: survival and cause of death based on 1100 cases: collective results from the UK Heart Valve Registry. Circulation 1997;96:3403. [PMID: 9396434]
Bellamy MF et al: Association of cholesterol levels, hydroxymethylglutaryl coenzyme-A reductase inhibitor treatment, and progression of aortic stenosis in the community. J Am Coll Cardiol 2002;40:1723. [PMID: 12446053]
Bonow RO et al: Guidelines for the management of patients with valvular heart disease: executive summary. Circulation 1998;98:1949. [PMID: 9799219]
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Krasuski RA et al: Comparison of results of percutaneous balloon mitral commissurotomy in patients ≥65 years with those in patients aged < 65 years. Am J Cardiol 2001;88:994. [PMID: 11703995]
Otto CM et al: Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly. N Engl J Med 1999;341:142. [PMID: 10403851]
ESSENTIALS OF DIAGNOSIS
Incidence and prevalence of HF increase exponentially with age, reflecting the increasing prevalence of hypertension and CHD at older age and the marked reduction in cardiovascular reserve that accompanies normative aging. There is a 4-fold increase in the incidence of HF between ages 65 and 85. Although the incidence of HF is higher in men than in women at all ages, women comprise slightly more than half of prevalent HF cases because of the increased proportion of women among older adults.
HF is currently the most common cause of hospitalization in the Medicare age group; 77% of the nearly 1 million annual hospitalizations for HF involve persons older than 65. HF is also a major source of chronic disability in the elderly and is the most costly Medicare diagnosis-related group.
Primary prevention of HF is feasible through aggressive treatment of the major conditions that cause HF (ie, hypertension and CHD). Antihypertensive therapy reduces the risk of incident HF by as much as 50% in older adults. The greatest benefit is seen in octogenarians with systolic hypertension. Similarly, treatment of other coronary risk factors may prevent or delay the onset of CHD, thus reducing the risk of HF.
Symptoms include exertional shortness of breath, effort intolerance, fatigue, cough, orthopnea, paroxysmal nocturnal dyspnea, and swelling of the feet and ankles. However, exertional symptoms are less prominent in the elderly in part because of reduced physical activity. Conversely, altered sensorium, irritability, lethargy, anorexia, abdominal discomfort, and gastrointestinal disturbances are more common symptoms of HF in the elderly.
Signs of HF include tachycardia, tachypnea, an S3 or S4 gallop, pulmonary rales, elevated jugular venous pressure, hepatojugular reflux, hepatomegaly, and dependent edema. In severe HF, the pulse pressure may be narrowed, and there may be signs of impaired tissue perfusion, such as cool skin, central or peripheral cyanosis, and diminished cognition. Depending on the cause of HF, additional findings may include marked hypertension (especially systolic hypertension), a dyskinetic apical impulse, a murmur of aortic or mitral origin, or peripheral signs of endocarditis. As with symptoms, the signs of HF in the elderly are often nonspecific or atypical.
Although certain features are more common in patients with systolic HF (prior MI, S3 gallop), whereas others suggest diastolic HF (marked hypertension, S4 gallop), there is considerable overlap. Therefore, it is essential to assess LV function in all patients with a new HF diagnosis.
The diagnosis of HF is usually straightforward in patients with severe symptoms and a chest radiograph demonstrating pulmonary edema but may be more difficult in patients with mild to moderate HF and atypical symptoms. Other causes of dyspnea and fatigue in older individuals include acute and chronic pulmonary disease (chronic obstructive lung disease, restrictive lung disease, pneumonia, pulmonary emboli), obstructive sleep apnea, obesity, anemia, hypothyroidism, poor physical conditioning, and depression. Lower extremity edema, in the absence of other signs of HF, may be due to venous insufficiency, renal or hepatic disease, or medications (especially calcium channel blockers). An elevated brain natriuretic peptide (BNP) level may be helpful in differentiating dyspnea of cardiac origin from that resulting from pulmonary or other causes, but the role of BNP in the diagnosis of HF in elderly patients remains to be established.
In addition to establishing a diagnosis of HF and determining cause, it is also important to identify factors that may contribute to worsening HF symptoms. Common precipitants of HF exacerbations in older adults include nonadherence to dietary restrictions or medications, myocardial ischemia or infarction, uncontrolled hypertension, arrhythmias (especially atrial fibrillation or flutter), anemia, systemic illness (eg, pneumonia, sepsis), iatrogenesis (eg, postoperative volume overload, blood transfusions), and adverse drug reactions (eg, NSAIDs).
Complications of HF include progressive symptoms and functional decline, recurrent hospital admissions as a result of acute exacerbations, supraventricular and ventricular arrhythmias, which may lead to syncope or sudden death, and, less frequently, deep vein thrombosis or mural thrombus formation with systemic embolization.
The goals of HF therapy are to alleviate symptoms, improve functional capacity and quality of life, reduce hospitalizations, and maximize functional survival. Optimal management of the older HF patient involves identification and treatment of the underlying cause and precipitating factors, implementation of an effective pharmacotherapeutic regimen, and coordination of care through the use of a multidisciplinary team. Management of HF in the elderly is often complicated by the presence of comorbid conditions that may influence both the clinical course and treatment (Table 19-5). Thus, it is essential that HF management be individualized, with due consideration given to concomitant illnesses,
prognosis, expectations, lifestyle, and therapeutic preferences.
Table 19-5. Impact of common comorbidities in older patients with heart failure.
Despite major advances in HF therapy, hospital readmission rates remain high; noncompliance, social factors, and inadequate follow-up are major contributors to early readmission. A multidisciplinary approach to HF management is designed to address the medical, behavioral, psychosocial, and economic aspects of care through a coordinated delivery system that provides comprehensive patient education, fosters provider adherence to evidence-based guidelines for HF treatment, and ensures effective follow-up through telephone contacts, home health visits, and office appointments. Common features of successful interventions include a nurse coordinator, intensive patient education and promotion of self-management skills (eg, daily weights), and close follow-up (especially after hospital discharge). Multidisciplinary HF care is recommended for older patients with moderate or severe chronic HF, especially those at increased risk for adverse outcomes because of comorbidities, social isolation, depression, or a history of recurrent hospitalizations.
Current HF guidelines focus on systolic HF and acknowledge that optimal management of patients with diastolic HF is unknown. It is thus important to distinguish patients with predominantly systolic HF (LV ejection fraction < 45%) from those with predominantly diastolic HF (LV ejection fraction ≥45%) because pharmacotherapy of the former is largely evidence based, whereas treatment of the latter remains empiric.
ACE inhibitors are the cornerstone of therapy for patients with impaired LV systolic function, whether symptomatic or asymptomatic, and available evidence indicates that older patients treated with ACE inhibitors experience improved quality of life, fewer symptoms and hospitalizations, and decreased mortality. ACE inhibitors approved for treatment of HF in the United States are listed in Table 19-6, along with recommended initial and maintenance dosages. Potential adverse effects of ACE inhibitors include worsening renal function, hyperkalemia, and hypotension. Therefore, close monitoring of renal function, electrolytes, and BP is warranted during initiation and titration of ACE inhibitor therapy. Cough occurs in up to 20% of patients receiving ACE inhibitors and may be severe enough to require discontinuation of therapy in 5–10% of cases, but there is no evidence that this occurs more frequently in the elderly. In patients who are unable to tolerate ACE inhibitors because of cough, ARBs are an acceptable alternative. However, they have not been shown to be equivalent to ACE inhibitors and should not be considered a first-line therapy for HF. The combination of hydralazine and isosorbide dinitrate is an additional option in patients unable to take ACE inhibitors or ARBs.
Table 19-6. Angiotensin-converting enzyme inhibitors for systolic heart failurea.
β-Blockers have been shown to reduce mortality and hospitalizations in patients with moderate to severe HF. These agents are recommended for all patients with stable HF in the absence of contraindications. Major contraindications to β-blockers include resting heart rate < 45 bpm, systolic BP < 90–100 mm Hg, markedly prolonged PR interval or heart block >first degree, active bronchospasm, and decompensated HF. β-Blockers approved for the treatment of HF in the United States include metoprolol and carvedilol. The starting dosage for metoprolol is 12.5 mg twice daily, and for carvedilol 3.125 mg twice daily. The dose should be increased gradually, at no less than 2-week intervals, to achieve daily dosages of 100–200 mg for metoprolol and 50 mg for carvedilol. With proper patient selection and dose titration, most HF patients tolerate β-blockers without difficulty. However, some may experience a transient increase in symptoms, and a small minority may require discontinuation of therapy because of severe side effects.
Digoxin is a mild inotropic agent that improves symptoms and reduces hospitalizations in patients with moderate HF but has no effect on total mortality. The benefits of digoxin in octogenarians are similar to those in younger patients. Digoxin is recommended in HF patients who remain symptomatic despite other therapy. The volume of distribution and renal clearance of digoxin are reduced in older patients. As a result, a digoxin dosage of 0.125 mg once daily is usually sufficient; patients with reduced renal function may require lower dosages. Serum digoxin levels of 0.5–1.1 ng/mL are therapeutic. Higher levels provide no additional benefit but increase the risk of toxicity. Routine monitoring of serum digoxin levels is not recommended, but
a level should be obtained whenever toxicity is suspected. Side effects associated with digoxin include bradycardia, heart block, supraventricular and ventricular arrhythmias, gastrointestinal disturbances, and central nervous system disorders (especially visual changes). Hypokalemia, hypomagnesemia, and hypercalcemia increase the risk of digoxin toxicity, and a variety of medications, including quinidine, amiodarone, and verapamil, are associated with an increase in serum digoxin levels.
Diuretics, with the exception of spironolactone and eplerenone, have not been shown to improve clinical outcomes in HF patients, but they are nonetheless essential for relieving congestion and edema and for maintaining a euvolemic state. Some patients with mild HF may respond to a thiazide diuretic, but most will require a more potent loop diuretic, such as furosemide. Patients should be instructed to restrict dietary sodium intake to no more than 2 g/day, and the diuretic dosage should be adjusted to maintain euvolemia, as reflected by daily-recorded weights that are within 2 lb of the patient's predetermined dry weight. Patients with more severe HF or refractory volume overload may benefit from the addition of metolazone 2.5–10 mg daily. Diuretics are commonly associated with potassium and magnesium loss, and older patients are at increased risk for diuretic-induced electrolyte disturbances. Therefore, serial monitoring of electrolytes is warranted, and supplements should be prescribed as needed. Overdiuresis may also result in hypotension, fatigue, and worsening renal function.
Spironolactone has been shown to reduce mortality by up to 30% in patients with advanced HF resulting from severe LV systolic dysfunction. The dose of spironolactone is 12.5–25 mg once daily. Spironolactone is contraindicated in patients with serum creatinine >2.5 mg/dL or serum potassium >5.0 mEq/L, and serum electrolytes and renal function should be assessed within 1–2 weeks after initiating therapy. Up to 10% of patients treated with spironolactone experience painful gynecomastia requiring discontinuation of therapy.
Current pharmacotherapy of systolic HF is summarized in Figure 19-2. All patients with LV systolic dysfunction should receive an ACE inhibitor, and all symptomatic patients should receive a β-blocker unless contraindicated. Diuretics should be prescribed and the dosage adjusted to maintain euvolemia. Digoxin should be added to the regimen of patients with persistent symptoms despite other therapeutic measures, and spironolactone should also be prescribed for patients with advanced HF symptoms unless contraindicated.
Figure 19-2. Pharmacological treatement of systolic heart failure
Because the majority of older patients with diastolic HF have hypertension or CHD, primary therapy for diastolic HF entails aggressive management of these conditions. Thus, BP should be maintained at levels no higher than 130–140/80–90 mm Hg, and CHD should be controlled with medications and percutaneous or surgical revascularization if appropriate. Older patients with impaired LV diastolic filling are at increased risk of atrial fibrillation, and this arrhythmia is a common precipitant of acute HF. In such cases, restoration and maintenance of sinus rhythm is desirable. In patients with persistent or chronic atrial fibrillation, the ventricular response should be well controlled with β-blockers, calcium channel blockers (diltiazem or verapamil), or digoxin.
In patients with symptomatic diastolic HF, judicious use of diuretics is indicated to relieve congestion and correct volume overload. However, overdiuresis should be avoided because patients with diastolic HF are preload dependent, and insufficient LV preload reduces
cardiac output. Additional agents that may be helpful in improving symptoms and exercise tolerance in older patients with diastolic HF include ACE inhibitors, ARBs, β-blockers, calcium channel blockers, nitrates, and digoxin.
The prognosis for older patients with HF is poor, with 5-year survival rates of 20–25% in patients older than 65 and 2-year survival rates of 40–50% in those older than 85. Patients with diastolic HF have a more favorable short-term prognosis than those with systolic HF, but the long-term prognosis is similar. Other factors associated with a worse prognosis include older age, male gender, more severe symptoms, lower LV ejection fraction, ischemic cause, atrial fibrillation, diabetes, and high-grade ventricular arrhythmias. Approximately 50% of HF deaths occur suddenly as a result of ventricular fibrillation or asystole, whereas the remaining 50% are attributable to progressive HF.
In light of the exceptionally poor prognosis associated with established HF (worse than for most forms of cancer), end-of-life issues should be addressed in all HF patients. Information should be provided about the clinical course and prognosis, and patients should be encouraged to express their preferences for end-of-life care and should assign durable power-of-attorney. In patients with end-stage HF and persistent severe symptoms despite optimal medical therapy, referral for hospice care should be considered.
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ARRHYTHMIAS & CONDUCTION DISTURBANCES
SICK SINUS SYNDROME
ESSENTIALS OF DIAGNOSIS
Increasing age is associated with diffuse degenerative changes in the sinus node and atrial conduction system. The number of sinus node pacemaker cells declines with age, so that by age 75 only ~10% of the cells remain functional. In addition, conduction of the electrical impulse from the sinus node to the atrial tissues may be impaired (sinus exit block), and conduction within the atria and through the AV node is often delayed. These abnormalities in sinoatrial function, often referred to as sick sinus syndrome, predispose elderly individuals to both bradyarrhythmias (eg, inappropriate sinus bradycardia, sinus pauses, sinus arrest) and supraventricular tachyarrhythmias (atrial fibrillation,
atrial flutter, atrial tachycardia). Many patients with sinoatrial dysfunction manifest both tachy- and bradyarrhythmias, a condition referred to as tachy-brady syndrome. In the United States, sinus node dysfunction is the most common indication for permanent pacemaker implantation, accounting for approximately 50% of all pacemaker procedures.
There are currently no known measures effective in preventing age-related sinoatrial dysfunction.
Patients with sick sinus syndrome may have symptoms resulting from bradycardia, tachycardia, or both. Patients with this disorder often have an asymptomatic resting sinus bradycardia, but there may be failure to increase the heart rate in response to exertion (chronotropic incompetence), resulting in exercise intolerance, shortness of breath, or, less commonly, anginal chest discomfort. Excessive sinus bradycardia may be associated with fatigue or light-headedness in addition to effort intolerance. Sinus pauses more than several seconds in duration often result in severe light-headedness or syncope without premonitory symptoms. Supraventricular tachyarrhythmias may be asymptomatic or result in palpitations, dyspnea, angina, dizziness, or syncope. Not uncommonly, termination of supraventricular arrhythmias is associated with prolonged sinus pauses, resulting in dizziness or syncope.
Physical findings may include bradycardia, tachycardia, or an irregular rhythm. In the absence of symptoms, BP is usually normal or elevated. Gentle carotid sinus massage may elicit an abnormal bradycardic response (sinus pause >3 s) or reproduce the patient's symptoms of dizziness or syncope. Other physical findings are nonspecific.
The symptoms of sick sinus syndrome are nonspecific and may be due to a wide range of other cardiac or noncardiac causes, including CHD, HF, ventricular arrhythmias, aortic stenosis, pulmonary disorders (pulmonary embolus, chronic lung disease), autonomic dysfunction (vagal reactions, carotid hypersensitivity syndrome, postural hypotension, postprandial hypotension), hypothyroidism, hyperthyroidism, obesity, deconditioning, pulmonary hypertension, anemia, and anxiety reactions. In addition, bradycardia and orthostatic symptoms may be due to several commonly used medications, including β-blockers (including ophthalmological agents), diltiazem, verapamil, amiodarone and other antiarrhythmic agents, clonidine, other antihypertensive medications, and donepezil.
Bradyarrhythmias may be associated with falls and syncope, which may result in significant injury. Acute atrial fibrillation or atrial flutter with rapid ventricular response is a common precipitant of HF or acute pulmonary edema and may also be associated with non-ST-elevation MI. Patients with tachy-brady syndrome are at increased risk for thromboembolic events, including stroke. Rarely, profound bradycardia or sinus arrest may be fatal.
Management begins with identification and treatment of other possible causes or aggravating factors. Potentially offending medications, such as β-blockers, should be discontinued if feasible. Electrolyte abnormalities should be corrected. Thyroid function should be assessed and appropriate therapy implemented if hypothyroidism or hyperthyroidism is detected. Additional evaluation for ischemia, valve disease, pulmonary disease, or other potential causes should be undertaken on a case-by-case basis.
Patients with documented symptoms attributable to bradyarrhythmias not resulting from other treatable causes should undergo permanent pacemaker implementation. Pacemaker therapy is effective in alleviating symptoms mediated by bradycardia and improves quality of life in patients with effort intolerance or fatigue related to chronic bradycardia or chronotropic incompetence. A rate-responsive dual-chamber pacing device (ie, capable of pacing both the atria and the ventricles as well as increasing the pacing rate during exercise) is
preferable in patients with sinus rhythm. Such devices have been associated with improved quality of life and reduced atrial fibrillation compared with single-lead ventricular pacing.
Supraventricular tachyarrhythmias occurring in the context of tachy-brady syndrome should be managed with rate controlling agents (eg, digoxin, β-blockers, diltiazem, verapamil), anticoagulation (warfarin preferred), and antiarrhythmic agents as needed to maintain sinus rhythm. Many of the agents used to treat supraventricular tachyarrhythmias may exacerbate the associated bradyarrhythmias, necessitating pacemaker implantation.
Most patients with appropriately treated sick sinus syndrome are able to maintain good quality of life in the absence of other major cardiac or noncardiac conditions. The prognosis is worse in patients with tachy-brady syndrome who experience thromboembolic complications, especially stroke.
ATRIAL FIBRILLATION & ATRIAL FLUTTER
ESSENTIALS OF DIAGNOSIS
The prevalence of atrial fibrillation increases from < 1% in persons younger than 40 to >10% in persons older than 80. The median age of patients with atrial fibrillation is 75. Atrial fibrillation is more common in men than in women at all ages, but the proportion of women increases with age.
Prompt identification and treatment of conditions that predispose to atrial fibrillation (eg, hyperthyroidism, electrolyte disorders) may prevent arrhythmia. Perioperative treatment of cardiac surgical patients with amiodarone or β-blockers reduces the risk of postoperative atrial fibrillation and shortens length of hospital stay. β-Blockers also reduce the risk of postoperative atrial fibrillation in older adults undergoing major noncardiac surgery, especially chest, abdominal, or vascular procedures. Dual-chamber pacing reduces the risk of atrial fibrillation in patients with sick sinus syndrome.
New-onset atrial fibrillation or flutter is often associated with a rapid ventricular rate, resulting in palpitations, shortness of breath, and, in some cases, chest pain, dizziness, or syncope. However, many patients are asymptomatic or minimally symptomatic, and the rhythm disturbance may be detected as an incidental finding on physical examination. Still other patients have acute pulmonary edema or a thromboembolic event, such as transient ischemic attack or stroke.
The cardinal physical finding of atrial fibrillation is an irregularly irregular rhythm. In untreated older patients, ventricular rates of 130–180 bpm are common, but rates as low as 50–70 bpm may also be seen. In atrial flutter, the rhythm is often regular, and the rate is typically either 150 bpm (2:1 block) or 75 bpm (4:1 block). However, an irregular rhythm resulting from variable AV block is also common, and it may not be possible to distinguish atrial fibrillation from atrial flutter on the basis of physical examination alone. Other physical findings are nonspecific but may include signs of HF, a mitral or aortic valvular murmur, evidence for chronic lung disease or pulmonary hypertension, or, less commonly, manifestations of hyperthyroidism.
Atrial fibrillation and flutter must be distinguished from other supraventricular and ventricular tachyarrhythmias. Multifocal atrial tachycardia (MAT) is an irregularly irregular tachyarrhythmia that most commonly occurs in patients with severe chronic lung disease. The ECG demonstrates prominent P waves of varying morphology. Atrial flutter at a rate of 150 bpm may be difficult to distinguish from other supraventricular rhythms, including sinus tachycardia and paroxysmal supraventricular tachycardia (PSVT). Carotid sinus massage or intravenous adenosine 6–12 mg is often helpful in differentiating these rhythm disorders. Occasionally, wide-complex supraventricular arrhythmias may be difficult to distinguish from ventricular tachycardia. The latter condition does not respond to adenosine but may respond to lidocaine.
The most important complication of atrial fibrillation or atrial flutter is systemic embolization, which may result in stroke, MI, ischemia or infarction of abdominal viscera, or impaired circulation to the extremities. The proportion of strokes attributable to atrial fibrillation increases with age, from < 2% in persons younger than 60 to >20% in those older than 80. Risk factors for stroke in older patients with atrial fibrillation include HF, hypertension, diabetes, and a prior thromboembolic event. The risk of embolization is lower in patients with “pure” atrial flutter, but most patients with atrial flutter also have atrial fibrillation. Other complications of atrial fibrillation and flutter include HF, non-ST-elevation MI, and syncope; these clinical events most often occur at the onset of atrial fibrillation or flutter with rapid ventricular response.
Management of atrial fibrillation and flutter involves identification and treatment of the underlying cause and precipitating factors when feasible, controlling the ventricular rate, restoring and maintaining normal sinus rhythm, and reducing the risk of thromboembolic events.
Effective control of the ventricular rate is a primary goal of therapy during both the acute and chronic phases of management. Optimal rate control is defined as a resting heart rate of 60–80 bpm and a heart rate of 90–115 bpm during moderate exercise. β-Blockers, diltiazem, verapamil, and digoxin slow conduction through the AV node, thus slowing the ventricular response rate. Although digoxin is widely used for this indication, it is less effective than other agents and is relatively ineffective in controlling the ventricular rate during exertion. In some patients with persistent symptomatic tachycardia despite aggressive pharmacological intervention, AV nodal ablation with placement of a permanent ventricular pacemaker is an effective alternative for controlling rate and reducing symptoms.
Restoration and maintenance of sinus rhythm offer the theoretical advantages of reducing stroke risk and avoiding the need for long-term anticoagulation. However, antiarrhythmic drugs used in the treatment of atrial fibrillation are only moderately effective and may be associated with significant side effects, including ventricular proarrhythmia. Patients with recent-onset atrial fibrillation or atrial flutter who remain significantly symptomatic despite optimal rate control, or who are poor candidates for long-term systemic anticoagulation, may benefit from cardioversion and antiarrhythmic therapy to maintain sinus rhythm.
Although patients with atrial fibrillation or flutter of < 48 h duration can safely undergo cardioversion with an acceptably low risk of thromboembolic complications, those with atrial fibrillation or flutter of longer duration should be anticoagulated with warfarin to maintain an INR of at least 2.0 for at least 3 weeks before attempting cardioversion. Alternatively, patients may undergo transesophageal echocardiography; if there is no evidence of atrial thrombus, cardioversion may be performed without delay. In either case, there is a risk of thromboembolic events for several weeks after cardioversion, and patients should be maintained on anticoagulation (INR ≥2.0) for a minimum of 4 weeks after cardioversion.
Cardioversion may be performed either pharmacologically or electrically. Multiple antiarrhythmic agents may restore sinus rhythm, but amiodarone is the most effective and is associated with thelowest risk of ventricular proarrhythmia. However, because of its very long half-life (1–2 mo), it may take days or even weeks of oral amiodarone loading before a therapeutic blood level isachieved. Direct current cardioversion is more
effective than drug therapy in restoring sinus rhythm but is associated with a somewhat higher risk of thromboembolic complications. Once sinus rhythm has been restored, amiodarone is the most effective agent for maintaining sinus rhythmat 1 year. Sotalol, a β-blocker, is an acceptable alternative to amiodarone, but tolerability and proarrhythmia may be problematic. One-year recurrence rates are at least 30–40%; thus, long-term anticoagulation is advisable except in patients at relatively low risk for recurrence (eg, postoperative atrial fibrillation or new-onset atrial fibrillation with spontaneous reversion to sinus rhythm within 48 h), especially if a treatable cause can be identified.
Older patients with paroxysmal or chronic atrial fibrillation benefit from long-term anticoagulation with warfarin, and stroke risk is reduced by ~66%. Because increasing age is an important risk factor for thromboembolic events, older patients derive the greatest absolute benefit from warfarin therapy. Although this benefit is tempered somewhat by increased bleeding complications, including hemorrhagic stroke, current recommendations are that all older patients with nonvalvular paroxysmal or chronic atrial fibrillation receive warfarin therapy to maintain an INR of 2.0–3.0. Patients with mitral valve disease or mechanical prosthetic valves should have INRs maintained in the range of 2.5–3.5.
Patients receiving long-term warfarin treatment should be advised to avoid cauliflower, broccoli, and other dark green, leafy vegetables because these foods are high in vitamin K and antagonize the effects of warfarin. Warfarin also interacts with numerous medications, and the INR should be monitored closely after medication changes. In addition, NSAIDs markedly increase the risk of gastrointestinal bleeding in older patients taking warfarin, and these drugs should be avoided if possible.
Older patients with prior stroke, dementia, gastrointestinal bleeding, or other conditions may be at increased risk for serious hemorrhagic complications during long-term warfarin therapy. Although substantially less effective than warfarin in reducing stroke risk, with a net reduction of ~20%, aspirin in a dose of 325 mg daily may be a suitable alternative to warfarin in selected patients.
With proper treatment, including anticoagulation, the long-term prognosis for patients with paroxysmal or chronic atrial fibrillation or flutter is relatively good, and many patients remain essentially asymptomatic for many years, even decades. Nonetheless, persons with atrial fibrillation have reduced long-term survival compared with those with sinus rhythm, and atrial fibrillation is also associated with a worse prognosis in acute MI patients as well as in those with HF or valvular heart disease.
ESSENTIALS OF DIAGNOSIS
The prevalence of ventricular arrhythmias increases with age. In the absence of underlying cardiac disease, frequent ventricular ectopic beats are not associated with increased mortality.
Early identification and treatment of risk factors for cardiovascular disease may reduce the risk of serious ventricular arrhythmias in older adults.
Isolated ventricular ectopic beats (VEBs) are usually asymptomatic, but frequent VEBs may cause palpitations. Salvos of VEBs at a rapid rate (ventricular tachycardia) may result in dizziness or syncope. Occasionally, VEBs or ventricular tachycardia may trigger ventricular fibrillation.
Physical findings associated with VEBs include an intermittently irregular rhythm and cannon A waves in the jugular venous pulse. Ventricular tachycardia is associated with a rapid pulse but may or may not be associated with hypotension or signs of tissue hypoperfusion. Ventricular fibrillation is associated with absent pulse and BP. Other findings in patients with ventricular arrhythmias reflect the presence of underlying cardiovascular disease.
wide-complex ectopic beats of ventricular origin (ie, not clearly preceded by a P wave). Ventricular tachycardia manifests as a wide-QRS tachycardia, which, when sustained, is usually regular. Torsades de pointes ventricular tachycardia usually occurs in the setting of marked QT-interval prolongation and has a polymorphic appearance with waxing and waning QRS amplitude. Ventricular fibrillation is a chaotic rhythm without well-defined QRS complexes.
Isolated wide-complex ectopic beats may be of supraventricular, junctional, or ventricular origin. The presence of a normal-appearing P wave preceding the ectopic beat suggests a supraventricular complex with aberrancy. Absent or retrograde P waves indicate a junctional or ventricular origin. Wide-complex tachycardias may be either supraventricular or ventricular. Patients with CHD or other major cardiac disorders are at increased risk for ventricular tachycardia. Other features that favor ventricular tachycardia include evidence for dissociation between atrial and ventricular activity, marked left- or right-axis deviation, QRS duration ~160 ms, and directional QRS concordance across the precordium.
The most feared complication of ventricular arrhythmias is sudden cardiac death. Ventricular tachycardia may also be associated with syncope, HF, or angina.
In most cases, isolated VEBs, even when frequent, require no specific therapy. In highly symptomatic patients, β-blockers are the agents of first choice. Rarely, other antiarrhythmic agents may be required to control severe symptoms, but there is no evidence that these agents reduce the risk of sudden death.
The treatment of patients with nonsustained ventricular tachycardia with or without symptoms is evolving. Patients with CHD and moderate or severe LV systolic dysfunction (ejection fraction ≤30%) have improved survival after implantation of an ICD. The value of ICDs in patients with nonsustained ventricular tachycardia in the absence of CHD or with CHD in the setting of preserved LV systolic function is unclear. β-Blockers reduce the risk of sudden death in patients with CHD with or without LV dysfunction and in those with nonischemic dilated cardiomyopathy. The value of other antiarrhythmic agents, including amiodarone, is unproven.
Patients with symptomatic sustained ventricular tachycardia or resuscitated sudden cardiac death outside the context of acute MI and in the absence of other treatable disorders (eg, electrolyte disturbances) should receive an ICD because these devices have been associated with substantial mortality reductions in high-risk patients. The efficacy of ICDs in preventing sudden cardiac death is similar in younger and older patients.
The prognosis of ventricular arrhythmias is governed by the presence, nature, and severity of underlying cardiac disease. In the absence of significant heart disease or LV systolic dysfunction, the prognosis for isolated VEBs and nonsustained ventricular tachycardia is excellent. Frequent VEBs in patients with CHD or reduced LV systolic function are a marker for increased mortality and sudden cardiac death, but there is no evidence that suppression of VEBs with antiarrhythmic drugs improves survival. Patients with nonsustained ventricular tachycardia associated with CHD and LV dysfunction, as well as those with symptomatic sustained ventricular tachycardia or resuscitated sudden cardiac death, are at high-risk for death within 1–2 years unless treated with an ICD.
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RELEVANT WORLD WIDE WEB SITES
American College of Cardiology: http://www.acc.org (Features access to all guidelines published by the College as well as practice management tools)
American Heart Association: http://www.americanheart.org (Excellent source of materials for both practitioners and patients)
American Heart Association: http://www.americanheart.org/profilers (Personalized web site for care providers and patients; covers CHD, heart failure, atrial fibrillation, hypertension, and dyslipidemia)
Heart Failure Online: http://www.heartfailure.org (Heart failure patient education web site with modules in English and Spanish)
Heart Failure Society of America: http://www.abouthf.org (Heart failure patient education materials)
Heart Failure Society of America: http://www.hfsa.org (Informational materials for health care providers)
Society of Geriatric Cardiology: http://www.sgcard.org (Featuring modular slide sets on selected aspects of cardiovascular disease in older adults)