29: Heart Failure & Heart Rhythm Disorders

Incidence and prevalence of heart failure (HF) increase exponentially with age, reflecting the increasing prevalence of hypertension and coronary heart disease (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 years. 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 higher proportion of women among older adults.

HF is currently the most common cause of hospitalization in the Medicare age group; more than 70% of the nearly 1 million annual hospitalizations for HF involve persons older than age 65 years. HF is also a major source of chronic disability in older adults, 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 64% 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 & Signs

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 older adults 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 older adults (see Chapter 7, “Atypical Presentations of Illness in Older Adults”).

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 diminished cognition. Depending on the cause of HF, additional findings may include severe 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 older adults are often nonspecific or atypical.

Special Tests

Chest radiography—

The chest x-ray can assess for presence of pulmonary edema or cardiomegaly and rule out other causes of dyspnea (pneumonia, pneumothorax). Of note, up to 40% of HF patients with elevated pulmonary capillary wedge pressure have no radiographic evidence of congestion.

Electrocardiography—

An electrocardiogram (ECG) may reveal dysrhythmias, left ventricular (LV) hypertrophy, left atrial enlargement, or signs of ischemia or infarction. Low voltage suggests infiltrative cardiomyopathy or pericardial effusion.

Echocardiography—

Echocardiography is usually the preferred test for evaluating LV function. Echocardiography provides information about atrial and ventricular chamber size and wall thickness, valve function, LV diastolic function, and pericardial disorders. Less common alternatives to echocardiography include radionuclide angiography and magnetic resonance imaging in certain circumstances.

Stress test—

A stress test should be considered if severe CHD is suspected.

Cardiac catheterization—

Cardiac catheterization is not recommended in the routine diagnostic evaluation of patients with HF, but should be considered if there is suspicion for severe CHD. Cardiac catheterization is indicated prior to coronary revascularization or valve procedures.

The diagnosis of HF is straightforward in patients with severe symptoms and overt signs of congestion but may be difficult in patients with less-severe HF and atypical symptoms. Other causes of dyspnea and fatigue in older individuals include acute and chronic pulmonary disease, obstructive sleep apnea, obesity, anemia, hypothyroidism, poor physical conditioning, and depression (see Chapter 64, “Addressing Dyspnea in Older Adults,” for more in-depth discussion of work-up of dyspnea in older adults). Lower-extremity edema, in the absence of other signs of HF, may be caused by venous insufficiency, renal or hepatic disease, or medications (especially calcium channel blockers). An elevated BNP (B-type natriuretic peptide) level may be helpful in differentiating dyspnea of cardiac origin from that resulting from pulmonary or other causes. However, BNP levels increase with age, especially in women, so the specificity of elevated levels for diagnosing HF declines with age.

In addition to establishing a diagnosis of HF and determining etiology, it is 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 (pneumonia, sepsis), iatrogenesis (postoperative volume overload, blood transfusions), and adverse drug reactions (nonsteroidal antiinflammatory drugs).

Complications include progressive symptoms and functional decline, recurrent hospital admissions, supraventricular and ventricular arrhythmias (which may lead to syncope or sudden death), cognitive impairment and worsening renal function caused by hypoperfusion, and deep vein thrombosis or mural thrombus with systemic embolization.

Goals of Treatment

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 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 an interprofessional team. Management of HF in older adults is often complicated by comorbid conditions that may influence both the clinical course and treatment (Table 29–1). Thus, it is essential that HF management be individualized, with due consideration given to concomitant illnesses, prognosis, goals of care, lifestyle, and therapeutic preferences (see Chapter 3, “Goals of Care & Consideration of Prognosis,” for more on goals of care).

Interprofessional Care

HF is responsive to a team approach and interprofessional care (see Chapter 5, “The Interprofessional Team”). 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).

Systolic Heart Failure

Angiotensin-converting enzyme (ACE) inhibitors and β blockers are the cornerstone of therapy for patients with impaired LV systolic function, whether symptomatic or asymptomatic. Available evidence indicates that older patients treated with ACE inhibitors experience improved quality of life, fewer symptoms and hospitalizations, and decreased mortality. Table 29–2 lists the ACE inhibitors approved for treatment of HF in the United States. Potential adverse effects of ACE inhibitors include worsening renal function, hyperkalemia, and hypotension. Close monitoring of renal function, electrolytes, and blood pressure 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 in 5% to 10% of cases, but there is no evidence that this occurs more frequently in older adults. In patients who are unable to tolerate ACE inhibitors because of cough, ARBs (angiotensin receptor blockers) are an acceptable alternative.

β Blockers reduce mortality and hospitalizations in patients with HF and reduced LV systolic function. These agents are recommended for all patients with stable HF in the absence of contraindications. Major contraindications include resting heart rate <45 beats/min, systolic blood pressure (BP) <90–100 mm Hg, markedly prolonged PR interval or heart block greater than first degree, active bronchospasm, and decompensated HF. β Blockers approved for the treatment of HF in the United States include sustained-release metoprolol succinate and carvedilol. The starting dosage for metoprolol is 25 mg once daily; for carvedilol, it is 3.125 mg twice daily. The dose should be increased gradually 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. However, some may experience a transient increase in symptoms, and a small minority may require discontinuation 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 mortality. The benefits of digoxin in octogenarians are similar to those in younger patients. Digoxin is recommended for 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 daily is usually sufficient; patients with reduced renal function may require lower dosages. Serum digoxin levels of 0.5–1.0 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. Because of the risk of potential side effects of digoxin—including bradycardia, heart block, supraventricular and ventricular arrhythmias, gastrointestinal disturbances, and central nervous system disorders (especially visual changes)—the risks and benefits of using digoxin in the individual older patient should be weighed carefully. Hypokalemia, hypomagnesemia, and hypercalcemia increase the risk of digoxin toxicity, and numerous medications, including quinidine, amiodarone, dronedarone, 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 essential for relieving congestion and edema and for maintaining an euvolemic state. Some patients with mild HF may respond to a thiazide diuretic, but most will require a more potent loop diuretic. 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 pounds 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. Serial monitoring of electrolytes is warranted, and supplements should be prescribed as needed. Overdiuresis may result in hypotension, fatigue, and worsening renal function.

Spironolactone reduces mortality by up to 30% in patients with advanced systolic HF. The dose of spironolactone is 12.5–25 mg 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. Eplerenone, a selective aldosterone antagonist, has demonstrated benefit in patients with post-myocardial infarction (MI) LV dysfunction already taking an ACE inhibitor and β-blocker, and in patients with New York Heart Association (NYHA) Class II symptoms and LV ejection fraction ≤35%. Gynecomastia is less common with eplerenone than with spironolactone; other adverse effects are similar.

Figure 29–1 summarizes current pharmacotherapy of systolic HF. All patients with LV systolic dysfunction should receive an ACE inhibitor or ARB and β-blocker unless contraindicated. Diuretics should be prescribed and the dosage adjusted to maintain euvolemia. In patients unable to tolerate an ACE inhibitor or ARB, the combination of hydralazine and nitrates provides an alternative. Although this combination has not been studied extensively in older adults, it has demonstrated morbidity and mortality benefits in younger patients with systolic HF. The most common side effects are headache and dizziness. Digoxin can be added to the regimen of patients with persistent symptoms despite other therapeutic measures, and aldosterone blockade should be prescribed for patients with moderate-to-severe HF symptoms unless contraindicated.

Device therapy—

Patients with systolic HF are at increased risk for sudden cardiac death (SCD) from malignant ventricular arrhythmias. Implantable cardioverter-defibrillators (ICDs) are efficacious in reducing SCD in high-risk patients with systolic dysfunction. However, the benefit of ICDs in reducing all-cause mortality appears to decline with age, in part because older patients are at increased risk for death from other causes, both cardiac and noncardiac. In addition, older adults are more likely to have procedure-related complications, and may be more likely to receive inappropriate shocks (eg, for atrial fibrillation), which can significantly worsen quality of life. Therefore, the decision to pursue ICD therapy in older adults must be individualized.

Heart Failure with Preserved Ejection Fraction

The prevalence of heart failure with preserved ejection fraction (HFPEF) increases with age, especially among women. HFPEF is often associated with hypertension, chronic kidney disease, diabetes, concentric LV hypertrophy, vascular stiffness, and LV diastolic dysfunction. Primary therapy entails aggressive management of hypertension and CHD. BP should be treated in accordance with current guidelines, 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 for atrial fibrillation (AF), and AF is a common precipitant of acute HF. In such cases, restoration and maintenance of sinus rhythm may be desirable. In patients with persistent AF, the ventricular rate should be controlled with β blockers, calcium channel blockers (diltiazem or verapamil), or digoxin.

Medical therapy for HFPEF focuses on treating hypertension, restricting sodium, and optimizing volume status. Diuretics are indicated to relieve congestion and volume overload. Overdiuresis should be avoided, as patients with HFPEF may be preload-dependent and insufficient LV preload may reduce cardiac output. Although ACE inhibitors, ARBs, β blockers, and aldosterone antagonists improve outcomes in systolic HF, there is currently no evidence of benefit in patients with HFPEF.

Advanced Heart Failure

Some HF patients have persistent severe symptoms and an unacceptable quality of life despite maximum medical therapy. Additional options for these patients may include cardiac resynchronization or surgical approaches.

Cardiac resynchronization therapy—

In patients with severe HF symptoms despite optimal medical therapy, left ventricular ejection fraction (LVEF) ≤35%, and prolonged QRS duration on ECG, biventricular pacing or “cardiac resynchronization” may improve symptoms and cardiac hemodynamics. Although few patients older than age 75 years were enrolled in clinical trials testing cardiac resynchronization therapy (CRT), several small observational studies have demonstrated improvements in quality of life and exercise tolerance in patients ≥75–80 years of age. Therefore, CRT may be a reasonable therapeutic option in selected older adults with severe HF symptoms (ie NYHA class III or IV).

Surgical management

Left ventricular assist devices—

Left ventricular assist devices (LVADs) are surgically implanted heart pumps that provide support to the LV to increase cardiac output and reduce congestion in patients with advanced systolic HF. Implantable LVADs are approved as “bridge to transplant” (BTT) or “destination therapy” (DT; permanent use without plans for transplantation) in individuals with advanced HF who are not candidates for a cardiac transplantation; as such, these devices are increasingly being used in older adults.

Randomized trials have demonstrated improved quality of life and survival in patients with refractory HF receiving LVADs as compared with medical management alone, including continuous intravenous inotropic therapy. However, there is considerable morbidity and mortality with LVAD therapy, especially in DT patients who tend to be older than BTT patients. The 1- and 2-year survival rates for participants in the HeartMate II DT trial were 68% and 58%, respectively, but more recent registry data following FDA approval show 1-year survival rates exceeding 70%. Most deaths occur in the first few months after implantation, with the most common modes of death being stroke, multiorgan failure, and HF. Older age increases the risk of complications, but age alone is not an exclusion criterion for LVAD therapy. In a retrospective single-center study, hospital length of stay, survival, adverse events, and quality of life were similar in patients younger or older than age 70 years who received an LVAD. Multidimensional preoperative assessment is performed to enhance patient selection and outcomes. This assessment should be combined with individualized decision making focused on goals, risks, and benefits to determine the best approach to care for each patient. With improved patient selection and technologic advances, perioperative morbidity and mortality will likely decline.

Heart transplantation—

Heart transplantation provides definitive therapy for end-stage HF but is only available for a tiny fraction of patients because of a lack of donor availability. The annual number of heart transplants in the United States has plateaued at approximately 2200. Although there is not a firm age “cutoff” for transplantation, candidacy is based on the overall clinical picture, making it very uncommon in individuals older than age 70 years. Most centers consider advanced age a relative contraindication for transplantation. Other contraindications include severe pulmonary hypertension, active infection or malignancy, severe chronic lung disease, significant renal impairment, severe peripheral vascular disease or carotid disease, severe psychiatric disease, primary liver disease with coagulopathy, and diabetes with end-organ dysfunction.

Although older heart transplant recipients (age >60 years) are at increased risk for posttransplantation morbidity and death, survivors report better quality of life, psychological adjustment, and adherence than younger patients. Thus, heart transplantation may be considered in highly selected patients 65–75 years of age with advanced HF.

End-of-Life Care

In light of the exceptionally poor prognosis associated with established HF (worse than for most forms of cancer, see “Prognosis” below), 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 a durable power-of-attorney. In patients with end-stage HF and persistent severe symptoms despite optimal medical therapy, referral for palliative care or hospice should be considered.

The prognosis for older patients with HF is poor, with 5-year survival rates of 20% to 40% in patients older than age 65 years and 2-year survival rates of 40% to 50% in those older than age 85 years. The long-term prognosis is similar in patients with either systolic HF or HFPEF. Factors associated with a worse prognosis include older age, male gender, more severe symptoms, lower LVEF, ischemic etiology, AF, diabetes, hyponatremia, renal insufficiency, anemia, and ventricular arrhythmias. Among patients with systolic HF, approximately 50% of deaths attributable to HF occur suddenly as a result of arrhythmia, while the remainder are attributable to progressive HF. In contrast, mortality in patients with HFPEF is often unrelated to HF and may occur as a complication of other acute illness (eg, pneumonia, hip fracture) or associated comorbid conditions (eg, dementia).

American Heart Association (excellent source of materials for both practitioners and patients). www.americanheart.org

Heart Failure Society of America (source materials for physicians and patients). www.hfsa.org

Bradyarrhythmias

General Principles in Older Adults

Bradycardias in older adults are mainly caused by degenerative changes affecting impulse formation and conduction. Sinus node dysfunction includes sinus bradycardia, sinus pauses, chronotropic incompetence (inability to increase heart rate according to activity needs), and tachybrady syndrome (atrial fibrillation or atrial flutter alternating with sinus bradycardia). Pacemaker implantation is the only effective treatment for symptomatic bradycardia without reversible cause.

Prevention

Currently there are no known measures to prevent age-related sinus node dysfunction or conduction system disease.

Clinical Findings

Symptoms & Signs

Patients with sinus node dysfunction may have symptoms associated with bradycardia or tachycardia. The most common presentation of sinus bradycardia is fatigue. Patients with chronotropic incompetence may have no symptoms at rest but develop fatigue or shortness of breath with exercise. Sinus pauses may result in dizziness or syncope. In patients with tachybrady syndrome, the tachyarrhythmias may cause palpitations. Termination of the tachycardia may be associated with a prolonged pause and symptoms of dizziness or syncope.

Older patients often have delayed conduction in the atrioventricular (AV) node (first-degree AV block or Mobitz type I second-degree AV block), which is usually asymptomatic and benign. Mobitz type II AV block (infranodal block) is frequently asymptomatic, but associated with a high risk of progression to complete AV block. Complete heart block (CHB) can present with symptoms of fatigue, shortness of breath, or syncope. In older patients with CHB, stable escape rhythm, and minimal symptoms, the systolic BP is usually elevated.

Carotid hypersensitivity is a common cause of unexplained falls in older patients. Gentle carotid sinus massage, after careful auscultation to rule out bruits, may elicit sinus pauses of greater than 3 seconds in patients with carotid hypersensitivity. Pauses less than 3 seconds during carotid sinus massage are not considered abnormal.

Special Tests

Electrocardiography—

Twelve-lead ECGs and rhythm strips may reveal sinus bradycardia, sinus pauses, AV-nodal conduction delay, or His-Purkinje system disease (left or right bundle-branch block, fascicular block).

Ambulatory monitoring—

Documentation of a rhythm abnormality associated with symptoms is essential for determining therapy. Twenty-four- or 48-hour monitors are useful in patients with frequent symptoms, whereas 30-day monitors are preferable in those with less-frequent symptoms. In patients with rare but potentially serious symptoms (eg, syncope), an implantable loop recorder should be considered. In a study of patients 61–81 years of age with recurrent unexplained syncope, an implantable loop recorder established a diagnosis in 43% of cases, compared with conventional methods which were diagnostic in 6% of cases.

Other cardiac tests—

Treadmill exercise testing can be useful in patients with suspected chronotropic incompetence. Exertional shortness of breath or fatigue associated with an inadequate increase in heart rate confirms the diagnosis. Exercise testing can also elicit Mobitz type II AV block or CHB in patients with advanced His-Purkinje system disease. Electrophysiology studies are not usually helpful in establishing an etiology for bradyarrhythmias, but markedly prolonged conduction from His bundle activation to ventricular depolarization (≥100 milliseconds) is an indication for pacemaker placement with or without symptoms.

Differential Diagnosis

The symptoms of bradycardia are nonspecific and may be a result of a variety of other causes, both cardiac (HF, coronary artery disease, valvular heart disease) and noncardiac (chronic lung disease, anemia, hypothyroidism, deconditioning). Light-headedness or syncope may be caused by hypotension, autonomic dysfunction (eg, as a result of diabetes or parkinsonism), pulmonary embolism, or neurologic events. Many medications can cause symptoms that mimic those of bradycardia. Polypharmacy, decreased renal function, and systemic absorption of topical medications (eg, β-blocker eye drops) must all be considered as potential etiologies of bradycardia.

Complications

Bradyarrhythmias may result in falls or syncope with potential for serious injuries, for example, hip fracture or intracranial hemorrhage, especially in patients receiving anticoagulation. Rarely, profound sinus arrest or CHB without an escape rhythm may be fatal.

Treatment

Management of bradycardia begins with identification of potentially aggravating factors. Medications that can cause bradycardia should be discontinued, if feasible. Patients should be asked about herbal preparations that may cause bradycardia (eg, motherwort and valerian root). Evaluation and treatment for thyroid, lung, or other heart disease should be undertaken if indicated.

In patients with symptomatic bradycardia not from correctable causes, permanent pacemaker implantation is the only effective therapy. Pacemakers are also indicated in Mobitz type II block or CHB. Asymptomatic sinus bradycardia, first-degree AV block, and Mobitz type I second-degree AV block are not indications for pacemaker implantation.

Prognosis

Pacemaker implantation does not affect survival but does reduce symptoms and improve quality of life in patients with symptomatic bradyarrhythmias. Patients with tachybrady syndrome have worse prognosis as a consequence of thromboembolism and other complications from atrial tachyarrhythmias.

General Principles in Older Adults

The prevalence of AF increases with age. Currently, there are approximately 3 million people in the United States with AF, and this number is projected to double by the year 2050, with 50% of affected individuals being older than the age of 80 years. AF is more common in men than in women at all ages. Atrial flutter (AFL) is closely related to AF, and patients frequently will have both arrhythmias at different times.

Prevention

In older adults, AF most commonly occurs in the setting of hypertension, coronary artery disease (CAD), valvular abnormalities, or HF. AF also occurs frequently in older patients with systemic illnesses, such as pneumonia, and following cardiac or noncardiac surgery. Hyperthyroidism (including subclinical hyperthyroidism), acute or chronic lung disease, sleep-disordered breathing, pulmonary embolism, and pericardial disease are additional precipitants of AF. Prevention and appropriate treatment of these conditions can reduce incident AF.

Clinical Findings

Symptoms & Signs

Symptoms associated with AF are highly variable. Palpitations caused by rapid ventricular rates are common, as are shortness of breath, fatigue, and dizziness. Many patients are asymptomatic or mildly symptomatic. Acute HF caused by tachycardia and loss of atrial contraction is a common presentation of AF in older patients, especially those with impaired diastolic function. Some patients have no cardiac symptoms but present with thromboembolic events, such as a transient ischemic attack or stroke. Rarely, asymptomatic patients with AF and rapid ventricular rates present with HF symptoms as a result of tachycardia-mediated cardiomyopathy.

The cardinal physical finding of AF is an irregularly irregular rhythm. AF can be very rapid, with ventricular rates of 130–180 beats/min In older patients with conduction disease, ventricular rates can be normal or even slow. AFL is often regular as a result of more organized atrial activity that conducts to the ventricle with 2:1, 3:1, or 4:1 AV block. An irregular rhythm caused by variable block is also common, and may be indistinguishable from AF based on physical examination alone. Signs of volume retention and HF may be seen in patients with diastolic or systolic ventricular dysfunction in whom the loss of atrial contraction diminishes cardiac output.

Special Tests

Electrocardiography—

The ECG is diagnostic in patients with ongoing AF or AFL. AF is characterized by lack of organized atrial activity and irregular QRS intervals. AFL is more organized, and the most common finding is a “sawtooth” pattern best seen in the inferior leads (II, III, and aVF).

Echocardiography—

Echocardiography is useful to assess underlying cardiac disease and chamber dimensions, and to rule out tachycardia-mediated cardiomyopathy. Increasing left atrial size is associated with greater risk for recurrent arrhythmias. Severe valvular disease, systolic dysfunction, and pulmonary hypertension are associated with reduced likelihood of restoring and maintaining sinus rhythm.

Cardiac catheterization—

Cardiac catheterization is not routinely indicated in evaluation of AF, but may be considered for assessment of CAD, cardiomyopathy, or valvular abnormalities.

Other tests—

Serum electrolytes and thyroid function tests should be measured in all patients with newly diagnosed AF or AFL. In patients with a permanent pacemaker or ICD, device interrogation can provide information about rate control and overall AF burden.

Differential Diagnosis

AF and AFL must be distinguished from other types of supraventricular arrhythmias. Frequent premature atrial complexes, paroxysmal atrial tachycardia, and multifocal atrial tachycardia (MAT) may present with similar symptoms and physical findings to those seen with AF or AFL, but in most cases the 12-lead ECG is sufficient to establish the correct diagnosis. Occasionally, vagal maneuvers or administration of adenosine may be necessary to distinguish AFL from other supraventricular arrhythmias. AF or AFL may also present as a wide complex tachycardia that may be difficult to distinguish from ventricular tachycardia.

Complications

AF and AFL are not immediately life-threatening but can result in significant complications if not properly treated. The most devastating complication is stroke. Stroke can occur in the presence or absence of AF; indeed, in 1 major study more than 60% of patients were in sinus rhythm at the time of stroke. Risk factors for stroke, as indicated by the CHADS₂ score, include congestive HF, hypertension, age 75 years or older, diabetes, and prior stroke or transient ischemic attack (TIA). CHADS₂ assigns 2 points for stroke and 1 point for each of the other risk factors. Patients with no risk factors have an annual stroke risk of less than 3%, whereas those with all 5 risk factors have an annual stroke risk of greater than 18%. A recent update of the CHADS₂ scoring system (CHA₂DS₂-VASc) assigns 2 points for age 75 years or older, 1 point for age 65–74 years, 1 point for vascular disease (coronary, aortic, or peripheral arterial disease), and 1 point for female sex. A CHADS₂ or CHA₂DS₂-VASc score of ≥2 is associated with an annual stroke risk of at least 4%. In addition to stroke and TIA, thromboembolic events attributable to AF can affect circulation to the bowel, kidney, other organs, or limbs.

In patients with chronic AF and rapid ventricular rates, tachycardia-mediated cardiomyopathy can occur. HF and SCD may result from the cardiomyopathy. In older patients with LV hypertrophy and diastolic dysfunction, myocardial ischemia and non–ST-elevation MI can occur as a result of oxygen supply–demand mismatch.

Treatment

Goals of Treatment

Management of patients with new-onset AF or AFL should begin with identification of possible precipitating causes (see above). The primary objectives of treatment include prevention of stroke and other thromboembolic events, controlling the ventricular rate, and alleviating symptoms.

Antithrombotic Therapy

The risks of thromboembolic events are not significantly different between AF and AFL, or between paroxysmal and persistent forms of AF. Stroke risk should be assessed using the CHADS₂ or CHA₂DS₂-VASc score. If the score is 2 or higher, long-term anticoagulation with warfarin or one of the newer agents is recommended. Note that under the CHA₂DS₂-VASc system, all men age 75 years or older and all women age 65 years or older are candidates for systemic anticoagulation, even in the absence of other risk factors. Furthermore because stroke risk increases progressively with age, older patients derive the greatest absolute benefit from anticoagulation.

The annual risk of serious bleeding on warfarin is estimated at 3%, and there is no evidence that older patients have higher incidences of significant bleeding as long as the dose is carefully adjusted to maintain the international normalized ratio (INR) between 2.0 and 3.0. (Exception: Patients with mechanical prosthetic valves require an INR from 2.5–3.5.) Foods high in vitamin K (eg, green leafy vegetables), antibiotics, and amiodarone can all affect INR levels. Older patients should be cautioned against concomitant use of warfarin and nonsteroidal antiinflammatory drugs because of increased risk of gastrointestinal bleeding. Patients with CAD are often treated with warfarin, aspirin, and another antiplatelet agent (eg, clopidogrel). To minimize the risk of bleeding, unnecessary agents should be discontinued when clinically appropriate (eg, clopidogrel 3–12 months after percutaneous coronary intervention).

Recently, 3 new anticoagulants became available with therapeutic effects comparable to warfarin. Rivaroxaban, apixaban (factor Xa inhibitors) and dabigatran (a direct thrombin inhibitor) have been shown to be as effective as warfarin in preventing thromboembolic events in patients with AF, without an increase in major bleeding and with reduced risk of intracranial hemorrhage (ICH). All have the advantage of a fixed-dose regimen without the need for INR monitoring. However, there are no available measures to acutely reverse the effects of these agents in patients with significant bleeding. In older patients with decreased creatinine clearance, lower doses are recommended, and the drugs are contraindicated in patients with creatinine clearances <15 mL/min. In addition, postmarketing data have raised concern that the risk of serious or life-threatening bleeding may be increased in patients older than 80 years of age who are receiving dabigatran.

In patients with absolute contraindications to warfarin and other anticoagulants, such as history of bleeding requiring blood transfusions or ICH, daily aspirin is reasonable. Combination therapy with clopidogrel and aspirin is more effective than aspirin alone in reducing stroke risk, but the risk of bleeding is similar to that of warfarin.

Rate Control

Effective control of ventricular rate during AF and AFL is a primary goal in both acute and chronic phases of management. Optimal rate control is traditionally defined as a resting heart rate (in AF) of 60–80 beats/min and a heart rate of 90–115 beats/min with activity. However, “lenient” rate control, defined as a resting heart rate of <110 beats/min, is associated with similar quality-of-life scores as stricter rate control. β Blockers are the drugs of choice in patients with CAD or reduced systolic function. Calcium channel blockers are not recommended in patients with depressed LV systolic function. Digoxin slows ventricular conduction through its effect on the parasympathetic nervous system but has limited efficacy in patients with high sympathetic tone, such as during physical exertion, in the immediate postoperative period, or in the setting of infection. In relatively sedentary patients, low-dose digoxin may provide adequate rate control, alone or in combination with β blockers or calcium channel blockers. In patients refractory to pharmacologic rate control, radiofrequency ablation of the AV node with permanent pacemaker implantation is an effective method of rate control and is associated with improved quality of life.

Rhythm Control

Restoration and maintenance of sinus rhythm is often necessary to alleviate symptoms. Rhythm control has not been shown to reduce mortality or strokes, and it does not circumvent the need for long-term anticoagulation in patients at high risk for thromboembolic events. Rhythm control is more difficult to achieve in patients with prolonged AF duration, depressed systolic function, severe diastolic dysfunction, or larger atrial size.

In patients who present with AF and rapid ventricular rate who are hemodynamically unstable, immediate electrical cardioversion is indicated. In stable patients, rate control with β blockers or calcium channel blockers should be initiated. In patients who remain symptomatic, electrical cardioversion may be performed with a low risk of thromboembolic events if the duration of AF is less than 48 hours or if the patient has been on warfarin with therapeutic INRs for at least 3 consecutive weeks. If the duration of AF is unknown, if the patient is not on long-term anticoagulation, or if recent INRs have been subtherapeutic, a transesophageal echocardiogram should be performed to rule out the presence of left atrial thrombus before cardioversion. Anticoagulation must be continued for a minimum of 1 month after cardioversion because of continuing risk of thrombus formation from atrial stunning after cardioversion. In patients with risk factors for stroke, anticoagulation should be continued indefinitely. Elective cardioversion with the new anticoagulants has not been well studied. Preliminary data suggest that continuous use of dabigatran for a minimum of 3 weeks before cardioversion is not associated with increased risk of stroke relative to warfarin.

Cardioversion may be performed either pharmacologically or electrically. Direct current cardioversion is more effective and safer than pharmacologic cardioversion. The only intravenous agent approved by the FDA for conversion of AF is ibutilide, but there is a risk of inducing prolonged QT interval and torsades de pointes ventricular tachycardia, especially in patients with HF. Although widely used, intravenous amiodarone is no more effective than placebo in the acute conversion of AF to sinus rhythm.

Long-term maintenance of sinus rhythm usually requires an oral antiarrhythmic agent. Quinidine and procainamide are rarely used because of limited efficacy and multiple side effects. Disopyramide is relatively contraindicated in older adults as a result of prominent anticholinergic side effects. Flecainide and propafenone are relatively effective for maintaining sinus rhythm but should not be used in patients with structural heart disease. Sotalol and dofetilide are renally cleared and can prolong the QT interval; consequently, these agents must be used cautiously, especially in older women (who tend to have longer QT intervals at baseline) with decreased creatinine clearance. Amiodarone is commonly used because of its effectiveness and relative lack of short-term side effects. However, thyroid, liver, neurologic, and lung toxicity may occur during long-term use, and routine monitoring of these organ systems is essential. Dronedarone is an agent similar to amiodarone without long-term organ toxicities, but rare cases of acute liver failure have been reported. Dronedarone is contraindicated in patients with active HF or persistent AF.

Radiofrequency ablation for typical “sawtooth” AFL is commonly performed with high success and low complication rates. Ablation of AF, which mainly involves electrical isolation of the pulmonary veins from the left atrium, has become a frequently performed and relatively effective procedure. The success rate, defined as freedom from recurrence of AF at 1 year, is approximately 70% for paroxysmal AF, but much lower for persistent or permanent AF. Major complications, including stroke, pulmonary hemorrhage, deep venous thrombosis, pulmonary embolism, cardiac perforation or tamponade, esophageal perforation, and death, occur in 3% to 5% of cases. AF ablation has not been shown to reduce stroke risk, so it does not obviate the need for long-term anticoagulation in high-risk patients. Few studies have specifically examined the efficacy and safety of AF ablation in older patients, but limited retrospective data suggest that in selected octogenarians outcomes are similar to those in younger patients, although postprocedure hospitalization times are longer. A surgical approach for treatment of AF, the Cox-Maze procedure, has a success rate of greater than 90% for curing AF, and has been shown to reduce strokes. In patients with a history of AF who require valvular or bypass surgery, concomitant Coz-Maze procedure should be considered.

Prognosis

Untreated AF is associated with increased mortality mainly as a consequence of strokes and tachycardia-induced cardiomyopathy with resultant HF and increased risk of sudden death. With appropriate treatment, the long-term prognosis of AF and AFL is excellent, and survival rates are similar in patients managed with rate control or rhythm control. Hemodynamic instability or severe symptoms attributable to AF are associated with significant morbidity and high costs from recurrent hospitalizations, procedures, and antiarrhythmic medications.

General Principles in Older Adults

The prevalence of ventricular arrhythmias increases with age as a result of age-related changes in the ventricular myocardium coupled with the increasing prevalence of cardiac disease. Ventricular arrhythmias range from isolated ventricular ectopic beats or nonsustained ventricular tachycardia (NSVT), both of which are benign in patients with structurally normal hearts, to ventricular tachycardia and fibrillation, which may cause syncope or SCD.

Prevention

Because most serious ventricular arrhythmias are related to underlying cardiac disease, prevention and early treatment of MIs and other conditions that may cause cardiomyopathy, such as hypertension and diabetes, are crucial. Early detection of cardiomyopathy is important to prevent lethal ventricular arrhythmias.

Clinical Findings

Symptoms & Signs

Isolated premature ventricular complexes (PVCs) are usually asymptomatic. Occasionally patients may feel “skipped” heart beats or palpitations. NSVT is defined as 3 or more consecutive PVCs at a rate in excess of 100 per minute and lasting less than 30 seconds. NSVT is often asymptomatic but can cause palpitations, transient light-headedness, or syncope. Ventricular tachycardia (VT) may cause palpitations, light-headedness or syncope. Ventricular fibrillation (VF) is associated with hemodynamic collapse and results in syncope or SCD if not immediately treated.

Physical findings associated with PVCs include an intermittently irregular heart beat during auscultation that may be associated with lack of peripheral pulse. NSVT and VT are associated with rapid pulse and, in some cases, hypotension. VF is associated with lack of pulse or BP.

Special Tests

Electrocardiography—

In patients with isolated PVCs, the ECG shows wide-complex beats of ventricular origin. VT manifests as consecutive wide-complex beats, which, if sustained, are usually regular. Torsades de pointes is a polymorphic VT with waxing and waning QRS amplitude that occurs in the setting of prolonged QT interval. VF is a chaotic rhythm without discreet QRS complexes. Baseline ECGs should be examined for prior MI or prolonged QT interval (eg, caused by medications or electrolyte abnormalities). A PVC burden of >25% of total heart beats may be associated with progression to cardiomyopathy.

Echocardiography, stress testing, and cardiac catheterization—

These tests provide information about the presence and severity of underlying cardiac disease and the potential for serious ventricular arrhythmias. LVEF and the presence of severe ischemia are the main determinants of prognosis. Acute coronary ischemia may cause sustained VT or VF, for which emergent cardiac catheterization is indicated.

Electrophysiology study—

The main role of an electrophysiology study (EPS) is for risk stratification of SCD in patients with structural heart disease and NSVT. In asymptomatic patients with CAD, an LVEF of 36% to 40%, and NSVT, induction of sustained VT during an EPS is associated with increased risk of SCD. In patients with syncope of unclear etiology, known CAD or a focal wall motion abnormality, and LVEF ≥40%, EPS may be considered to assess the possibility of ventricular arrhythmia as the cause of syncope. EPS is not useful for SCD risk stratification in patients with nonischemic cardiomyopathy.

Differential Diagnosis

Wide-complex beats may be ventricular or supraventricular in origin. An isolated wide-complex beat preceded by a P wave suggests supraventricular origin with aberrant conduction. Wide-complex tachycardia with AV dissociation is ventricular in origin. Other diagnostic criteria for VT are the presence of fusion or capture beats (sudden narrow QRS among wide-complex beats) and left bundle-branch block morphology with right axis deviation. In older patients, baseline conduction abnormalities are common. Comparison of tachycardia morphology with baseline sinus beats may help differentiate supraventricular tachycardia with aberrancy from VT.

Complications

The most important complication of ventricular arrhythmias is SCD, which often occurs without premonitory symptoms. Ventricular arrhythmias may also be associated with syncope, falls, chest pain, dyspnea, or acute HF.

Treatment

Isolated PVCs generally do not require therapy. In highly symptomatic patients, β blockers are the agents of choice. Rarely, in patients with disabling symptoms unresponsive to β blockers, antiarrhythmic drugs are used. Radiofrequency ablation is helpful for reducing ectopy burden if a single source of PVCs can be identified.

The presence of NSVT is an indication for further investigation. In patients with normal LVEF, treatment is the same as for isolated PVCs. In patients with CAD, LVEF of 36% to 40%, and inducible monomorphic VT during EPS, an ICD is indicated to prevent SCD. Patients with LVEFs of 35% or less, regardless of etiology, are candidates for an ICD for primary prevention of SCD. Patients with unexplained syncope in the presence of cardiomyopathy have an indication for an ICD for secondary prevention (ie, an event likely attributable to serious ventricular arrhythmias) of SCD. Ablation of sustained VT may be performed to reduce ICD shocks in patients with recurrent arrhythmias not responsive to medical therapy.

The role of ICDs in patients older than 75 to 80 years of age is controversial. Meta-analysis of existing trials and retrospective studies have concluded that in patients age 75 years or older, ICDs do not convey significant overall mortality benefit, especially in patients with renal impairment. ICD implantation in patients in their eighth or ninth decade of life carries implications that must be communicated to patients and their families. ICD shocks are frequently painful, and effective treatment of ventricular arrhythmias may alter the mode of death from sudden to a more gradual process of living longer with reduced quality of life. Device disablement in the event of terminal illness or repetitive shocks should also be discussed prior to ICD implantation.

Prognosis

The prognosis of ventricular arrhythmias is governed by the nature and severity of underlying cardiac disease. In the absence of structural heart disease or depressed LVEF, the prognosis of PVCs and NSVT is excellent. The presence of NSVT in patients with decreased systolic function is a marker for increased mortality, but there is no evidence that suppression of PVCs and NSVT improves survival. In patients with LVEF ≤35%, ICDs reduce mortality in younger patients, but the mortality benefit in older patients is unclear.

American Heart Association (excellent source of materials for both practitioners and patients). www.americanheart.org

Heart Rhythm Society (source materials for physicians and patients). www.hrsonline.org