Ectopic Beats and Tachyarrhythmias

The presence of supraventricular or ventricular ectopic beats, even if frequent or complex, is not an accurate marker for organic heart disease or for increased risk of cardiac mortality in the elderly (see Table 91-1). Supraventricular and ventricular arrhythmias appear to be benign in healthy elderly persons but may not be benign in patients with heart disease. Regardless of patient age, the nature and severity of underlying heart disease have much greater prognostic significance than does the arrhythmia.

Epidemiology and Pathogenesis

The incidence of supraventricular and ventricular ectopic beats and tachyarrhythmias is increased in the elderly for reasons that are not fully understood. The increased incidence may be partially accounted for by age-related increases in left atrial size and pressure, in left ventricular mass, and in catecholamine levels. Supraventricular and ventricular ectopic beats are more common and more complex among patients with structural heart disease, which dramatically increases in incidence with age.

An overload of ionized calcium (Ca⁺⁺) in senescent myocardium may play an important role in arrhythmogenesis. Under conditions that enhance cell Ca⁺⁺ loading, senescent myocardium is more likely to spontaneously release Ca⁺⁺ from the sarcoplasmic reticulum (ie, to undergo diastolic afterdepolarization). This greater likelihood for Ca⁺⁺ overload may make the senescent heart more susceptible to arrhythmias when calcium homeostasis is disturbed (eg, by use of inotropic drugs or during postischemic reflow). Furthermore, the threshold for Ca⁺⁺-dependent ventricular fibrillation is lower in the senescent heart.

Symptoms, Signs, and Diagnosis

Tachyarrhythmias may produce palpitations or, occasionally, symptoms of hemodynamic upset (eg, dizziness, syncope, heart failure). Patients often notice the onset and offset of intermittent tachyarrhythmias.

The diagnosis is suggested by characteristic symptoms and by a rapid, possibly irregular peripheral arterial pulse, which reflects ventricular activity. Examination of the jugular venous pulse, which reflects atrial and ventricular activity, may help differentiate atrial from ventricular arrhythmias. Standard 12-lead ECG confirms the diagnosis.

Treatment

Antiarrhythmics (see Table 91-2) are more likely to cause adverse effects in the elderly than in younger patients.

Serum digoxin levels for the same dose are higher in the elderly than in younger patients because of reduced renal clearance. Digitalis toxicity is relatively common among the elderly. Concurrent use of quinidine (class I) increases serum digoxin levels by about 100%; concurrent use of verapamil (class IV) or amiodarone (class III) can also increase serum digoxin levels.

Clearance of quinidine is reduced by 34% and elimination half-life is prolonged from 7.3 to 9.7 hours in persons aged 60 to 69 compared with those aged 23 to 29. Clearance of procainamide and disopyramide (class I) is also reduced with age; disopyramide should not be used in the elderly because it has anticholinergic effects on bladder and bowel function.

Because hepatic flow decreases with age, the infusion rate of lidocaine (class Ib) should be reduced to avoid central nervous system toxicity, which is common among the elderly. Similar dosage reduction is advised for most -blockers (class II) and for the calcium channel blockers (class IV) verapamil and diltiazem, partly because these drugs undergo first-pass hepatic metabolism.

How aging affects the clinical pharmacology of newer antiarrhythmic drugs (eg, class Ic drugs flecainide, encainide, and propafenone; class III drugs amiodarone and sotalol) is not well characterized. However, clearance of encainide but not flecainide is reduced in the elderly.

Supraventricular Ectopic Beats

Premature beats resulting from an abnormal electrical focus or from reentry in the atria or other supraventricular tissue.

The incidence of supraventricular ectopic beats--whether simple or complex or whether detected during rest, routine activity, or exercise--increases with age, even among persons carefully screened to exclude latent coronary artery disease (CAD). Isolated supraventricular ectopic beats have been detected by exercise ECG in 8% of apparently healthy persons aged 20 to 29 but in 76% of those aged 80 to 89. Frequent (> 100 in 24 hours) supraventricular ectopic beats have been detected during 24-hour ambulatory ECG monitoring in 26% of healthy persons aged 60 to 85 with no evidence of CAD.

Patients with supraventricular ectopic beats, even when frequent, are usually asymptomatic and rarely require treatment. However, they may have a propensity for sustained supraventricular tachyarrhythmia. Supraventricular ectopic beats do not appear to be associated with an increased risk of coronary events, including sudden cardiac death.

Atrial (Supraventricular) Tachycardias

(Narrow QRS Tachycardias)

Incidence increases with age. Nonsustained supraventricular tachycardia has been detected by exercise ECG in < 1% of apparently healthy persons aged 20 to 29 but in 10% of those aged 80 to 89. Risk of developing a spontaneous supraventricular tachyarrhythmia was 2% in the younger group and 10% in the older group; however, the tachycardia was not associated with an increased risk of coronary events.

Paroxysmal supraventricular tachycardia: A regular narrow QRS complex at 150 to 200 beats/minute is characteristic. Short asymptomatic episodes of paroxysmal supraventricular tachycardia have been reported in 13% of elderly patients with no evidence of heart disease.

This tachycardia is usually due to a reentrant mechanism. It can often be terminated by vagal maneuvers (eg, Valsalva's maneuver, gagging, carotid sinus massage). Note: Because an arterial embolus can be precipitated, carotid sinus massage should not be performed on elderly patients until significant carotid stenosis (defined by a readily audible bruit) has been excluded by physical examination.

If vagal maneuvers are unsuccessful and the patient does not have hypotension, verapamil 5 to 10 mg IV should be given slowly over a period of 2.5 to 5 minutes. Alternatively, adenosine IV, which has a rapid onset of action and low risk of hypotension, can be used. Adenosine is very effective and has the same low incidence of adverse effects in patients > 70 as in those < 70. If paroxysmal supraventricular tachycardia precipitates hypotension, cerebral ischemic symptoms, angina pectoris, or heart failure, immediate cardioversion is indicated, starting at 25 to 50 joules.

Digoxin, -blockers, or calcium channel blockers, given once daily, are similarly effective in preventing recurrences of this tachycardia.

Atrial tachycardia with block: A rapid atrial rate with a slower ventricular rate due to atrioventricular (AV) block is characteristic. Digitalis toxicity is the most common cause. Treatment consists of withholding digoxin and correcting hypokalemia.

Multifocal atrial tachycardia: P-wave morphology, the PR interval, and cycle length vary from beat to beat. This tachycardia is common among elderly patients with chronic obstructive pulmonary disease. Treatment is directed at correcting the underlying pulmonary disorder; verapamil is usually effective as short-term therapy.

Accelerated junctional rhythm: A heart rate of 70 to 130 beats/ minute is characteristic; the P wave is usually inverted and may precede, follow, or fall within the QRS complex. Among the elderly, digitalis toxicity and acute inferior myocardial infarction (MI) are the most common causes. Although this tachycardia is not usually a cause of hemodynamic impairment, it can cause heart failure. Sudden regularization of the ventricular rate in an elderly patient receiving digoxin for chronic atrial fibrillation suggests this diagnosis. Treatment is directed at the underlying disorder.

Atrial flutter: Rapid, regular atrial activity between 250 and 350 beats/minute with sawtooth flutter waves (best seen in leads II, III, and aVF) is characteristic. Ventricular response is often regular at 75 beats/minute (4:1 AV block), 150 beats/minute (2:1 AV block), or, less commonly, 100 beats/minute (3:1 AV block). Atrial flutter usually indicates the presence of organic heart disease. Among the elderly, common causes are CAD and chronic obstructive pulmonary disease. Palpitations usually occur when the ventricular rate is > 120 beats/minute; patients may be asymptomatic when the rate is slower. Diagnosis is suggested by a regular tachycardia at a ventricular rate close to 150 beats/minute. The diagnosis is confirmed if carotid sinus massage (and probably other vagal maneuvers as well; see warning, above) abruptly slows the ventricular response and causes the emergence of sawtooth flutter waves at about 300/minute on an ECG. Digoxin is the drug of choice for hemodynamically stable patients. For unstable patients, low-level DC cardioversion (25 to 50 joules) almost always converts flutter to sinus rhythm.

For patients with pure atrial flutter, the risk of thromboembolism is probably low. However, patients who have mixed atrial flutter and fibrillation or who also have valvular heart disease or reduced left ventricular function should be evaluated with transesophageal echocardiography because their risk of thromboembolism may be increased. Treatment with warfarin may be warranted.

Atrial fibrillation: A lack of organized atrial activity and totally irregular timing of the QRS complexes are characteristic. Atrial fibrillation, unlike other supraventricular tachyarrhythmias, is much more likely to be chronic than acute. Atrial fibrillation occurs in 1 to 2% of elderly persons with no evidence of heart disease, accounting for about 12% of atrial fibrillation cases. Risk doubles with each decade of age. In one study, the biennial incidence of atrial fibrillation was 6.2 per 1000 men and 3.8 per 1000 women aged 55 to 64 and 75.9 per 1000 men and 62.8 per 1000 women aged 85 to 94. Hypertension, CAD, mitral valve disease, and heart failure are the most common predisposing disorders for elderly as well as middle-aged patients. Less common causes include thyrotoxicosis, sick sinus syndrome, and amyloidosis.

Atrial fibrillation usually indicates the presence of organic heart disease, but the risk of cardiovascular morbidity and mortality is substantially increased for elderly persons with atrial fibrillation even if they do not have organic heart disease. After adjustment for coexisting cardiovascular disorders, mortality risk is increased by 1.5 to 1.9. Risk is increased primarily because atrial fibrillation increases the risk of thromboembolic stroke by 4 or 5 times. In patients with atrial fibrillation, thrombi form in the atria or atrial appendages. Stroke attributable to atrial fibrillation has been reported in 1.5% of patients in their 50s but in 23.5% of those in their 80s.

Acute or paroxysmal atrial fibrillation usually produces disagreeable palpitations or chest discomfort because of the dramatic increase in heart rate and the irregular rhythm. Heart failure may result. However, chronic atrial fibrillation is often well tolerated, especially if the ventricular response is < 100 beats/minute.

About one third of elderly patients with atrial fibrillation have a controlled ventricular response (because of associated AV nodal disease) and require no specific therapy. For other patients, initial therapy is the same as that for younger patients: Digoxin, diltiazem, verapamil, or propranolol is given IV to slow the ventricular response to 60 to 100 beats/minute. These drugs, given orally and sometimes in combination, are also used for long-term control of the ventricular rate. Digoxin and verapamil are contraindicated in patients with the Wolff-Parkinson-White syndrome, which is rare among the elderly.

Before electrical cardioversion is performed in patients with chronic atrial fibrillation, the cause and duration of atrial fibrillation, atrial size, and the risks of anticoagulants should be considered. Because elderly persons with chronic (including lone) atrial fibrillation have a high risk of thromboembolic events, use of anticoagulants before conversion should be strongly considered. For most elderly patients, an early attempt at cardioversion (generally after a few weeks of warfarin) is probably warranted; warfarin should be continued for 4 weeks after successful cardioversion. A proposed alternative is use of transesophageal echocardiography to rule out preexisting left atrial thrombi; if no thrombi are present, cardioversion can be performed immediately, without anticoagulant prophylaxis. Immediate cardioversion may also be considered if atrial fibrillation has been present for <= 48 hours. However, these approaches are controversial, because atrial dysfunction occurs for several days after cardioversion, increasing the risk of de novo atrial thrombi.

In elderly patients with nonrheumatic atrial fibrillation, warfarin has been reported to reduce stroke risk by 68%, with virtually no increase in major bleeding. Aspirin 325 mg daily has reduced stroke risk by 36%, although only in patients <= 75. Nevertheless, because the risk of major bleeding from anticoagulant use is higher for elderly than for younger patients, the decision to use anticoagulants should be made case by case, considering factors such as patient compliance, risk of falling, and coexistence of other major disorders.

Chemical cardioversion using quinidine or other class I drugs may be considered for elderly patients with atrial fibrillation, although some analyses suggest that patients receiving long-term quinidine therapy have an increased mortality rate, presumably due to proarrhythmia. Alternatively, sotalol or amiodarone (class III), which may have a lower risk of proarrhythmia, can be used.

Whether restoration with attempted maintenance of sinus rhythm reduces long-term morbidity and mortality rates in the elderly more effectively than simple rate control of atrial fibrillation plus anticoagulation is under study.

Ventricular Ectopic Beats

Premature beats resulting from abnormal electrical foci in the ventricles.

Incidence of ventricular ectopic beats--whether simple or complex or detected during rest, routine activity, or exercise--increases with age, even among persons carefully screened to exclude latent CAD. Isolated ventricular ectopic beats have been detected by exercise ECG in 11% of apparently healthy persons aged 20 to 29 but in 57% of those aged 80 to 89. With 24-hour ambulatory ECG monitoring, isolated ventricular ectopic beats have been detected in 80% of healthy persons aged 60 to 85 who had no evidence of CAD; frequent (> 100 in 24 hours) ventricular ectopic beats have been detected in 17%. Ventricular ectopic beats were detected by resting ECG in 8% of randomly selected patients > 70.

Unless extremely frequent, isolated ventricular ectopic beats usually produce no symptoms. Symptomatic ventricular ectopic beats commonly are perceived as missed beats. This perception is probably related to the augmented stroke volume of the following sinus beats rather than to the ventricular ectopic beats themselves.

The presence of ventricular ectopic beats, whether isolated or frequent and complex, does not appear to increase the long-term risk of cardiovascular mortality in healthy elderly persons. In contrast, even isolated ventricular ectopic beats increase the risk in patients with documented CAD. However, treating patients with CAD and isolated ventricular ectopic beats has not been shown to reduce the long-term risk of mortality.

The risk of adverse reactions to antiarrhythmic drugs is generally higher in the elderly. These drugs should be used only when the ventricular ectopic beats cause ventricular tachycardia or intractable palpitations. The drugs should be started in low doses, which are gradually increased until the density of ventricular ectopic beats is reduced by 75% and ventricular tachycardia is eliminated.

Flecainide and encainide (class Ic) have been shown to increase the mortality rate for patients with asymptomatic or mildly symptomatic frequent ventricular ectopic beats after acute MI. Because of the increased mortality risk observed with class Ic drugs, they should not be given to elderly patients with heart disease unless other drugs are ineffective. -Blockers are probably the initial drugs of choice, especially for elderly patients with CAD. If patients are unresponsive to or intolerant of -blockers, amiodarone or sotalol (a -blocker with class III effects) may be used. Using low-dose combination therapy with various drugs may minimize the risks of adverse effects from a single drug. Treatment should also be directed at controlling underlying or exacerbating factors (eg, electrolyte disturbances, hypoxia, heart failure).

Ventricular Tachycardia

Usually, a regular tachycardia with broad QRS complexes and a ventricular rate of 100 to 200 beats/minute.

With 24-hour ambulatory ECG monitoring, ventricular tachycardia has been detected in 4% of women and 10% of men aged 65 to 100. Asymptomatic runs of exercise-induced ventricular tachycardia (<= 6 beats) have been reported in nearly 4% of apparently healthy persons >= 65--25 times the prevalence in younger persons.

In the elderly, severe myocardial ischemia, acute MI, digitalis toxicity, and heart failure are common precipitating disorders.

Ventricular tachycardia is associated with increased left ventricular mass and a higher incidence of left ventricular dysfunction and heart failure. Even when patients with known CAD are excluded, the incidence of abnormal left ventricular function is higher in patients with ventricular tachycardia. Some data suggest that unsustained exercise-induced ventricular tachycardia is not associated with angina, MI, syncope, or cardiac death in apparently healthy elderly persons.

Ventricular tachycardia may produce no symptoms, especially in persons without organic heart disease and with short runs (< 10 beats). More commonly, palpitations occur. Among patients with organic heart disease, significant hemodynamic upset, including hypotension and syncope, is common, particularly when the arrhythmia is sustained for > 30 seconds.

Ventricular tachycardia is strongly suggested by the presence of AV dissociation, fusion beats, and QRS duration of > 0.14 seconds or a QRS axis between 190 and 1180°. However, it is often difficult to distinguish from paroxysmal supraventricular tachycardia when the QRS complex is widened.

Regardless of age, patients with ventricular tachycardia that is sustained or that produces hypotension or syncope must be treated immediately. If ventricular tachycardia is well tolerated hemodynamically, a rapid IV infusion (bolus) of lidocaine 50 to 75 mg (eg, 1 mg/kg) may be given initially, followed by 50 mg 2 minutes later. If the arrhythmia recurs, a full loading dose of 5 mg/kg may be required, followed by an infusion at 1 to 4 mg/minute. Patients who have recurrent ventricular tachycardia or who do not respond to lidocaine may be treated with IV procainamide or -blockers. Data, largely from studies of younger patients, suggest that bretylium is the most effective drug for acute therapy in patients who do not respond to lidocaine.

One approach to symptomatic patients with primary recurrent ventricular tachycardia is intracardiac programmed electrophysiologic stimulation: The tachycardia is induced and the prophylactic efficacy of various antiarrhythmic drugs is then assessed in a specialized catheterization laboratory. Using this procedure to select antiarrhythmic therapy may result in a lower rate of symptomatic ventricular tachyarrhythmia than does an empiric approach and may markedly reduce the 1- to 2-year mortality rate. A less invasive and less expensive approach is ambulatory ECG monitoring, with or without exercise testing. In one study, this approach predicted antiarrhythmic drug efficacy more frequently than intracardiac programmed electrophysiologic stimulation and had a similar success rate for preventing recurrences of arrhythmia.

If therapy chosen by programmed electrophysiologic stimulation or ECG monitoring is ineffective, an automatic implantable cardioverter-defibrillator (AICD) or endocardial resection guided by intraoperative mapping may be appropriate. Almost two thirds of the patients who receive an AICD are > 65. Although age alone should not determine whether an AICD is used, the devices are not indicated for patients who have a life expectancy of < 6 months with treatment. The life expectancy of candidates for AICD implantation is determined primarily by the extent of heart disease and the severity of left ventricular dysfunction. The prevention of sudden cardiac death by AICD implantation appears to be unaffected by patient age. The use of a transvenous rather than an epicardial technique for AICD implantation has markedly reduced morbidity and mortality rates.

The benefits of AICDs compared with those of antiarrhythmic drugs (particularly amiodarone) for certain patients are unclear. Some data suggest that for elderly patients with life-threatening ventricular tachyarrhythmias, the mortality rate is lower with AICDs than with amiodarone or sotalol. For patients with heart disease and asymptomatic high-density ventricular ectopic activity, whether amiodarone reduces the mortality rate relative to conventional therapy for the underlying heart disease (without antiarrhythmics) is unclear, and the role of AICDs is controversial. Most studies have excluded patients > 75, although age has not been shown to affect study results.

Long-term prophylaxis is not required for ventricular tachycardia that was precipitated by an acute event (eg, MI, digitalis toxicity), because the tachycardia rarely recurs. However, aggressive prophylaxis is required for primary sustained ventricular tachycardia (without an obvious precipitant), because the tachycardia recurs within 1 year in about 35% of patients and mortality risk is increased. A 1-year mortality rate of 29% has been reported for patients (mean age, 68.5) who had an out-of-hospital cardiac arrest caused by a primary arrhythmia.