13
Arrhythmias

The previous arrhythmia listing should be revised to focus on arrhythmias (i.e., tachycardias and bradycardias) rather than on their symptoms (i.e., syncope and near syncope), which can be caused not only by arrhythmias but also by other etiologies. This chapter recommends that the listing be met if recurrent episodes of tachycardia or bradycardia cause syncope, near syncope, or other debilitating symptoms that very seriously limit the ability of the claimant to independently initiate, sustain, or complete activities of daily living or instrumental activities of daily living.

DESCRIPTION

An arrhythmia is an abnormal change in the regular beat of the heart and may include irregular heartbeats, skipped beats, rapid heartbeats (tachycardia), or slow heartbeats (bradycardia) (Libby et al., 2008). Arrhythmias are characterized by the location of their origin in the heart and the symptoms the patient experiences when the arrhythmia occurs. Arrhythmias originating in the upper chambers of the heart (the atria) are called atrial or supraventricular arrhythmias. Arrhythmias originating in the lower chambers of the heart (the ventricles) are called ventricular arrhythmias. Atrial and ventricular arrhythmias can occur in individuals with or without other cardiac disorders (Zipes et al., 2006). Bradycardia may be due to abnormalities of initiation of the heart beat or of transmission of electrical impulses within the heart. The latter are called conduction disturbances. In general, ventricular arrhythmias that are associated with structural heart



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13 Arrhythmias the previous arrhythmia listing should be revised to focus on arrhythmias (i.e., tachycardias and bradycardias) rather than on their symptoms (i.e., syncope and near syncope), which can be caused not only by arrhythmias but also by other etiologies. this chapter recommends that the listing be met if recurrent episodes of tachycardia or bradycardia cause syncope, near syncope, or other debilitating symptoms that very seriously limit the ability of the claimant to independently initiate, sustain, or complete activities of daily living or instrumental activities of daily living. DESCRIPTION An arrhythmia is an abnormal change in the regular beat of the heart and may include irregular heartbeats, skipped beats, rapid heartbeats (tachycardia), or slow heartbeats (bradycardia) (Libby et al., 2008). Ar- rhythmias are characterized by the location of their origin in the heart and the symptoms the patient experiences when the arrhythmia occurs. Arrhyth- mias originating in the upper chambers of the heart (the atria) are called atrial or supraventricular arrhythmias. Arrhythmias originating in the lower chambers of the heart (the ventricles) are called ventricular arrhythmias. Atrial and ventricular arrhythmias can occur in individuals with or without other cardiac disorders (Zipes et al., 2006). Bradycardia may be due to abnormalities of initiation of the heart beat or of transmission of electrical impulses within the heart. The latter are called conduction disturbances. In general, ventricular arrhythmias that are associated with structural heart 

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00 00 CaRdIoVaSCUlaR dISabIlIty diseases and genetic disorders can lead to the most serious and potentially life-threatening and disabling conditions. Arrhythmias may manifest in a variety of ways, and some patients with arrhythmias are asymptomatic. Others may experience palpitations (pounding sensations in the chest), chest discomfort, dyspnea, syncope, or near syncope (Libby et al., 2008). Syncope, sometimes called “faint- ing,” is defined as a sudden loss of consciousness and postural tone with spontaneous recovery. Near syncope is a period of altered consciousness. Since syncope is complete loss of consciousness, it is not merely a feeling of light-headedness, momentary weakness, or dizziness. Cardiac syncope is due to inadequate blood flow to the brain from any cardiac cause, such as obstruction of flow or disturbance in rhythm or conduction resulting in inadequate cardiac output (Grubb and Olshansky, 1998). Determin- ing the cause of syncope can be difficult, as there are several cardiac and noncardiac disturbances that may lead to loss of consciousness (Grubb and Olshansky, 1998). Cardiac syncope may be caused by bradycardia, tachycardia, valve disease, or myocardial disease leading to hypotension. Cardiac syncope may also be due to nonarrhythmic causes, such as vasovagal syncope (mediated by discharge of the vagus nerve) that is purely vasodepressor (hypotensive) with no cardioinhibitory (bradycardic) component, an extremely rare con- dition. Noncardiac causes of loss of consciousness include epilepsy and pseudoseizures from psychiatric disease (Grubb and Olshansky, 1998). Since syncope is a symptom and not a disease, it is important to identify accurately its underlying cause. Due to the multiple causes of syncope, it is important to recognize that only syncope in association with arrhythmias is discussed here. Types of Arrhythmias Bradycardia is defined as a heart rate of less than 60 beats per minute and requires treatment if accompanied by symptoms, which may include fatigue, lethargy, nausea, shortness of breath, mental confusion, dizziness, and near syncope or syncope (Grubb and Olshansky, 1998). A diagnosis of bradycardia in the absence of symptoms is rarely an indication for treat- ment, for example, the implantation of a pacemaker. Symptoms drive the need for intervention. Tachycardias, sometimes called tachyarrhythmias, may be supraven- tricular or ventricular in origin. Supraventricular arrhythmias may be often highly symptomatic but are rarely life threatening (Wood et al., 2010). Examples include atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT) in association with the Wolff- Parkinson-White syndrome, atrial flutter, and atrial fibrillation. The latter

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0 aRRhythmIaS is the most common arrhythmia in older populations, since its prevalence increases with age (Fuster et al., 2006; Go et al., 2001; Miyasaka et al., 2006). Atrial fibrillation is especially important because its consequences cause significant morbidity and mortality. All the aforementioned arrhyth- mias are treatable with drug or catheter ablation therapy; success rates are dependent on the particular arrhythmia. Catheter ablation involves the placement of wires (catheters) into the heart (or sometimes on its surface) through which energy is delivered that destroys the origin of the targeted arrhythmia, or interrupts the circuit supporting the arrhythmia. Ablation is considered a first-line therapy for AVNRT, AVRT, and atrial flutter. Indeed, when patients are given the choice between drug therapy and ablation, they most commonly choose the latter, because ablation has demonstrated suc- cess rates of 95 percent or more. Since AVNRT, AVRT, and atrial flutter are usually curable by this technique, they are rarely disabling. Ventricular arrhythmias may occur in isolation or in association with structural heart disease and genetic abnormalities. Like supraventricular arrhythmias, ventricular arrhythmias that occur in the setting of a structur- ally normal heart and in the absence of genetic disease are generally not life threatening although they may be debilitating. Most are treatable by drug therapy, and many are curable with catheter ablation. The most common ventricular arrhythmias requiring treatment are those that occur in associa- tion with coronary artery disease. They are responsible for cardiac arrest and sudden cardiac death, which are not chronic conditions (although car- diac arrest may result in a chronic cardiovascular or other condition). EPIDEMIOLOGY Supraventricular arrhythmias other than atrial fibrillation and atrial flutter are most common in the young. The incidence of atrial fibrillation increases with age, approximately doubling with each decade of life, and is an independent risk factor for death. In U.S. Air Force recruits the incidence is 0.04 percent, and by age 75 years it is 11.6 percent (Cairns and Connolly, 1991). The Anticoagulation and Risk Factors in Atrial Fibrillation Study predicted that the number of patients with atrial fibrillation in the United States is likely to increase 2.5-fold in the next 50 years as a consequence of the aging of the population, from approximately 2.3 million in the early 2000s to 5.6 million by the year 2050 (Go et al., 2001). A more recent study projected the number of persons with atrial fibrillation in the United States might exceed 10 million by 2050 (Miyasaka et al., 2006). Based on data from the Resuscitation Outcomes Consortium, 295,000 out-of-hospital cardiac arrests occur annually in the United States (Lloyd- Jones et al., 2009). Approximately 60 percent of sudden cardiac deaths are treated by emergency medical services, and 31 percent of out-of-hospital

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0 0 CaRdIoVaSCUlaR dISabIlIty cardiac arrest patients receive bystander cardiopulmonary resuscitation. Most unexpected cardiac deaths are thought to be secondary to a ventricu- lar arrhythmia, and about 80 percent of out-of-hospital cardiac arrests oc- cur in private or residential settings. The incidence of nonfatal ventricular arrhythmias is not well defined, although in practice they are not uncom- mon. The incidence of arrhythmias due to congenital disease is highly de- pendent on the particular genetic mutation. The long QT syndrome occurs in about 1 in 3,000 individuals, but the risk is highly dependent on the individual patient’s history and location of the genetic mutation (Libby et al., 2008). DIAGNOSTIC CRITERIA AND METHODS Minimal required documentation for diagnosing arrhythmias includes either an electrocardiogram (ECG) recording, for example from an ambula- tory (Holter) monitor or from an emergency medical service unit dispatched to a cardiac arrest victim, or a 12-lead ECG. Such tracings define the origin of the arrhythmia (supraventricular or ventricular), enable risk stratifica- tion, and direct therapy. Some arrhythmias may be recorded during exercise testing, and in this case the test can be used to diagnose the arrhythmia, determine functional status independent of the arrhythmia, and sometimes determine appropriate therapy. TREATMENT Patients with arrhythmias can either be observed closely, or treated with drugs, catheter ablation, a pacemaker, an implantable cardioverter de- fibrillator (ICD), or a combination. ICDs are devices that can stimulate the heart as a pacemaker to treat bradycardia (and heart failure), or terminate ventricular tachyarrhythmias with either shocks or special pacing tech- niques (Epstein et al., 2008). The appropriate choice of therapy will depend on the particular arrhythmia, consequences of the arrhythmia (symptoms and blood pressure, for example), patient preference, and sometimes job requirements. Depending on the arrhythmia, efficacy of treatment is vari- able. Ventricular arrhythmias may be treated by drug therapy, catheter ablation, and ICDs, the latter being the mainstay of therapy when they oc- cur in patients with structural heart disease (e.g., coronary artery disease, cardiomyopathy, genetic heart diseases). Advances in Treatment Few new antiarrhythmic drugs have been approved by the Food and Drug Administration in the past decade. The major advances in arrhythmia

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0 aRRhythmIaS treatment have been in device and catheter-based therapies. Pacemakers have become reliable and effective treatments for bradycardia. ICDs can be implanted either in patients who have been resuscitated from a life- threatening ventricular arrhythmia or in patients at high risk for a life- threatening ventricular arrhythmia. The efficacy of catheter ablation de- pends on the targeted arrhythmia and the type of energy source that is used. The field of ablation is rapidly advancing with new technologies becoming available each year. Effects of Treatment No medical treatment is devoid of risk. Drugs may cause toxic reac- tions, some of which can be permanent, including organ toxicity. Some antiarrhythmic drugs can even cause cardiac arrest in susceptible indi- viduals. Catheter ablation offers the possibility of curing some arrhyth- mias, but carries risks, including injury to blood vessels leading to the heart, damage to the heart itself, and sometimes the need for a pace- maker. As noted, pacemakers are remarkably effective for the treatment of bradycardia, and the only therapy available other than withdrawing bradycardia-causing drugs. Similarly, ICDs are extremely effective in re- suscitating cardiac arrest, and in some instances can use pacing techniques to terminate ventricular arrhythmias without resorting to shock therapy. ICDs, however, do not prevent arrhythmias and thus may not prevent syncope. Furthermore, shocks are painful. Finally, all implantable devices carry the risks of complications related to implantation itself (i.e., an invasive procedure) and to infection and malfunction. Any of these com- plications may be life threatening. DISABILITY There are no generally accepted criteria to determine disability from arrhythmia. The origin of the arrhythmia, associated symptoms, and the environment of a particular occupation establish an individual’s disability status. Syncope may or may not be disabling depending on its etiology, frequency, and unique factors specific to an individual. Similarly, the same arrhythmia may be disabling for one person and not for another depending on associated symptoms. In short, the consequences, severity, and frequency of symptoms due to arrhythmia are what determine disability. The presence of comorbid depression and anxiety in patients may contribute to the disabling effects of arrhythmias. For example, patients experiencing anxiety due to the unpredictable nature of the associated symptoms of their arrhythmias, such as episodes of syncope, may avoid engaging in usual activities.

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04 04 CaRdIoVaSCUlaR dISabIlIty When ventricular arrhythmias are recurrent and cause syncope, espe- cially if they are unresponsive to drug or other treatment, disability may be warranted. Furthermore, having an ICD may be a contraindication for working in certain professions in which sudden, unexpected loss of con- sciousness could cause injury or death to either the patient or others. For example, having an ICD implanted precludes certification for a Depart- ment of Transportation commercial motor vehicle license (Blumenthal et al., 2002, 2007). Although it may sometimes be difficult to determine the cause of an arrhythmia, identification of the etiology of the arrhythmia is essential to properly treating the symptomatic patient. Disability of patients impaired as a consequence of arrhythmia may be based on either the arrhythmia diagnosis itself, or on its underlying cause. For example, a patient who has survived myocardial infarction, which itself may or may not be disabling, could be disabled on the basis of an arrhythmia if the latter is recurrent, or uncontrolled or unresponsive to therapy. The Social Security Administration (SSA) currently reviews applicants’ disability claims for arrhythmias based on specific diagnostic and clinical criteria. These criteria were most recently updated in 2006. A relatively low number of cardiovascular allowances are made using the current arrhyth- mias impairment code. Generally, listing-level decisions have been fairly stable with a slight increase in allowances across the past decade. The set of disability criteria at the listing-level (see Box 13-1) evaluates claimants for disability with recurrent arrhythmias with uncontrolled and recurrent episodes of cardiac syncope or near syncope documented by a resting or ambulatory (Holter) ECG or other appropriate medically acceptable tests. The claimant’s syncope or near syncope must either be unresponsive to BOX 13-1 Current Listing for Recurrent Arrhythmias 4.05 Recurrent arrhythmias, not related to reversible causes, such as electrolyte  abnormalities or digitalis glycoside or antiarrhythmic drug toxicity, resulting in un- controlled (see 4.00A3f), recurrent (see 4.00A3c) episodes of cardiac syncope or  near syncope (see 4.00F3b), despite prescribed treatment (see 4.00B3 if there is  no prescribed treatment), and documented by resting or ambulatory (Holter) elec- trocardiography, or by other appropriate medically acceptable testing, coincident  with the occurrence of syncope or near syncope (see 4.00F3c).  SOURCE: SSA, 2008.

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0 aRRhythmIaS treatment (claimants not receiving ongoing treatment may be required to undergo a consultative examination paid for by SSA or be found disabled if there is another impairment or impairments that combine with the arrhyth- mia to equal the severity of a listing). The claimant’s arrhythmia cannot be attributed to reversible causes, such as electrolyte abnormalities or digitalis glycoside or antiarrhythmic drug toxicity, as arrhythmias due to reversible causes are likely to respond to treatment. CONCLUSIONS AND RECOMMENDATION After review of the most recent medical literature and related American College of Cardiology/American Heart Association treatment and prac- tice guidelines, the committee determined the arrhythmias listing should be revised to allow claimants to meet the listing with objective diagnosis of recurrent (as defined by SSA) episodes of tachycardia or bradycardia, that cause cardiac syncope, near syncope, or other debilitating symptoms, confirmed by ECG or other appropriate medically acceptable testing. A documented arrhythmia should be coincident with the occurrence of symp- toms that very seriously limit the patient’s ability to independently initiate, sustain, or complete activities of daily living or instrumental activities of daily living. Furthermore, the arrhythmia and symptoms must occur despite prescribed treatment. As with the current listing, claimants’ medical records should show the arrhythmia is not related to a reversible cause. RECOMMENDATION 13-1. Revise listing 4.05 to define arrhythmias as recurrent episodes of tachycardia or bradycardia documented by electrocardiography or other appropriate medically acceptable testing; that cause cardiac syncope, near syncope, or other debilitating symp- toms; are not due to a reversible cause; do not respond to prescribed treatment; and very seriously limit the ability to independently initiate, sustain, or complete activities of daily living or instrumental activities of daily living. REFERENCES Blumenthal, R., J. Braunstein, H. Connolly, A. E. Epstein, B. J. Gersh, and E. H. Wittles. 2002. Cardiovascular advisory Panel guidelines for the medical examination of commercial motor vehicle drivers. McLean, VA: U.S. Department of Transportation, Federal Motor Carrier Safety Administration. Blumenthal, R. S., A. E. Epstein, and R. E. Kerber. 2007. Cardiovascular disease and com- mercial motor vehicle driver safety (expedited review). McLean, VA: Department of Transportation: Federal Motor Carrier Safety Administration.

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0 0 CaRdIoVaSCUlaR dISabIlIty Cairns, J. A., and S. J. Connolly. 1991. Nonrheumatic atrial fibrillation. Risk of stroke and role of antithrombotic therapy. Circulation 84:469–481. Epstein, A. E., J. P. DiMarco, K. A. Ellenbogen, N. A. Estes, R. A. Freedman, L. S. Gettes, G. Gregoratos, A. M. Gillinov, S. C. Hammill, D. L. Hayes, M. A. Hlatky, L. K. Newby, R. L. Page, M. H. Schoenfeld, M. J. Silka, L. W. Stevenson, and M. O. Sweeney. 2008. Guidelines for device-based therapy of cardiac rhythm abnormalities: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Journal of the american College of Cardiology 51:e1–e62. Fuster, V., L. E. Ryden, D. S. Cannom, H. J. Crijns, A. B. Curtis, K. A. Ellenbogen, J. L. Halperin, J.-Y. Le Heuzey, G. N. Kay, J. E. Lowe, S. B. Olsson, E. N. Prystowsky, J. L. Tamargo, and S. Wann. 2006. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: A report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation). Developed in col- laboration with the European Heart Rhythm Association and the Heart Rhythm Society. Journal of the american College of Cardiology 48(4):e149–e246. Go, A. S., E. M. Hylek, K. A. Phillips, Y. Chang, L. E. Henault, J. V. Selby, and D. E. Singer. 2001. Prevalence of diagnosed atrial fibrillation in adults: National implications for rhythm management and stroke prevention: The Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. Journal of the american medical association 285(18):2370–2375. Grubb, B. P., and B. Olshansky. 1998. Syncope: mechanisms and management. 1st ed. Armonk, NY: Futura Publishing Co. Libby, P., R. O. Bonow, D. P. Zipes, and D. L. Mann. 2008. braunwald’s heart disease: a textbook of cardiovascular medicine. 8th ed. St. Louis, MO: W. B. Saunders. Lloyd-Jones, D., R. Adams, M. Carnethon, G. De Simone, T. B. Ferguson, K. Flegal, E. Ford, K. Furie, A. Go, K. Greenlund, N. Haase, S. Hailpern, M. Ho, V. Howard, B. Kissela, S. Kittner, D. Lackland, L. Lisabeth, A. Marelli, M. McDermott, J. Meigs, D. Mozaffar- ian, G. Nichol, C. O’Donnell, V. Roger, W. Rosamond, R. Sacco, P. Sorlie, R. Stafford, J. Steinberger, T. Thom, S. Wasserthiel-Smoller, N. Wong, J. Wylie-Rosett, and Y. Hong, for the American Heart Association Statistics Committee Stroke Statistics Subcommittee. 2009. Heart disease and stroke statistics—2009 update: A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 119(3):e21–e181. Miyasaka, Y., M. E. Barnes, B. J. Gersh, S. S. Cha, K. R. Bailey, W. P. Abhayaratna, J. B. Seward, and T. S. M. Tsang. 2006. Secular trends in incidence of atrial fibrillation in Olmsted County, Minnesota, 1980 to 2000, and implications on the projections for future prevalence. Circulation 114(2):119–125. SSA (Social Security Administration). 2008. listing of impairments—adult listings (Part a). disability evaluation under Social Security (blue book). http://www.socialsecurity.gov/ disability/professionals/bluebook/AdultListings.htm (accessed July 22, 2010). Wood, K. A., A. L. Stewart, B. J. Drew, M. Melvin, M. M. Scheinman, and E. S. Froelicher. 2010. Patient perception of symptoms and quality of life following ablation in patients with supraventricular tachycardia. heart & lung 39(1):12–20. Zipes, D. P., A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, R. J. Myerburg, S. G. Priori, M. A. Quinones, D. M. Roden, M. J. Silka, C. Tracy, S. C. Smith Jr., A. K. Jacobs, C. D. Adams, E. M. Antman, J. L. Anderson, S. A. Hunt, J. L. Halperin, R. Nishimura, J. P. Ornato, R. L. Page, B. Riegel, J.-J. Blanc,

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0 aRRhythmIaS A. Budaj, V. Dean, J. W. Deckers, C. Despres, K. Dickstein, J. Lekakis, K. McGregor, M. Metra, J. Morais, A. Osterspey, J. L. Tamargo, and J. L. Zamorano. 2006. ACC/AHA/ ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: A report of the American College of Cardiology/ American Heart Association Task Force and the European Society of Cardiology Com- mittee for Practice Guidelines (Writing Committee to Develop Guidelines for Manage- ment of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). Journal of the american College of Cardiology 48(5):e247–e346.

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