This document addresses the use of an implantable cardioverter-defibrillator to monitor heart rhythm and deliver an electrical shock when a life threatening ventricular arrhythmia is detected.

For information regarding other technologies for cardiac disease, see:

• MED.00055 Wearable Cardioverter Defibrillators;
• SURG.00064 Cardiac Resynchronization Therapy (CRT) with or without an Implantable Cardioverter Defibrillator (CRT/ICD) for the Treatment of Heart Failure.

Medically Necessary:

ADULT Indications:

Implantable cardioverter-defibrillator (ICD) therapy in adults is considered medically necessary for the treatment of ventricular tachyarrhythmias and for the prevention of sudden cardiac death (SCD) in individuals who are receiving optimal medical therapy and have a reasonable expectation of survival with a good functional status for more than 1 year when one of the following indications is present:

1. After evaluation to define the cause of the event and to exclude any completely reversible causes in survivors of cardiac arrest due to ventricular fibrillation (VF) or hemodynamically unstable sustained ventricular tachycardia (VT); or
2. Those with structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable; or
3. Those with syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT; or
4. Those with left ventricular ejection fraction (LVEF) less than 35% due to prior myocardial infarction (MI) who are at least 40 days post-MI and are in New York Heart Association (NYHA) functional Class II or III; or
5. Those with nonischemic dilated cardiomyopathy (NIDCM) who have an LVEF less than or equal to 35% after six months of optimum medical therapy and who are in NYHA functional Class II or III; or
6. Those with ischemic cardiomyopathy* and who have had no MI in the past 40 days and have an LVEF less than 30% after six months of optimum medical therapy and are in NYHA functional Class I; or
7. Those with nonsustained VT due to prior MI, LVEF less than 40%, and inducible VF or sustained VT at electrophysiological study; or
8. Those with long-QT syndrome who are experiencing syncope or VT while receiving beta blockers; or
9. Those with confirmed hypertrophic cardiomyopathy (HCM) with two (2) or more major risk factors for sudden cardiac death (SCD) which are:
   • Family history of HCM-related SCD in at least 1 first-degree relative;
   • At least 1 episode of unexplained syncope within the previous 12 months;
   • Nonsustained VT on ECG;
   • Abnormal blood pressure (BP) response during upright exercise testing;
   • Left ventricular (LV) wall thickness greater than or equal to 30 mm. 

*Ischemic cardiomyopathy:  Left ventricular systolic dysfunction associated with marked stenosis (at least 75% narrowing) of at least 1 of the 3 major coronary arteries, or a documented history of myocardial infarction.

Note: For use of combined ICD/Biventricular pacing (CRT-ICD) devices, in cases of NYHA Class IV heart failure and for other indications, see SURG.00064 Cardiac Resynchronization Therapy (CRT), with or without an Implantable Cardioverter Defibrillator (CRT/ICD) for the Treatment of Heart Failure.

PEDIATRIC Indications:
Implantable cardioverter-defibrillator (ICD) therapy in children is considered medically necessary for the treatment of ventricular tachyarrhythmias and for the prevention of sudden cardiac death (SCD) in individuals who are receiving optimal medical therapy and have a reasonable expectation of survival with a good functional status for more than 1 year when one of the following indications is present:

1. For survivors of cardiac arrest after evaluation to define the cause of the event and to exclude any reversible causes; or
2. For individuals with symptomatic sustained VT in association with congenital heart disease who have undergone hemodynamic and electrophysiological evaluation; (Catheter ablation or surgical repair may offer possible alternatives in carefully selected individuals) or
3. For individuals with congenital heart disease with recurrent syncope of undetermined origin in the presence of either ventricular dysfunction or inducible ventricular arrhythmias at electrophysiological study.

Investigational and Not Medically Necessary:

The use of an implantable cardioverter-defibrillator is considered investigational and not medically necessary for any other diagnosis not listed above as medically necessary under Adult Indications or Pediatric Indications.

ICDs are an important treatment option for individuals with a history of life-threatening ventricular arrhythmias. Randomized clinical trials have shown that ICD use significantly reduces mortality rates for those with coronary artery disease (CAD) and/or a prior MI who have poor ventricular function. Although ICDs for the treatment of atrial fibrillation (AF) have been used in studies, evidence on efficacy and long-term outcomes is limited, and thus, clear conclusions concerning the efficacy of this treatment modality cannot be drawn.

Available literature indicates that ICDs are now widely used for the secondary prevention of SCD, due to VF or VT. ICD implantation is the generally accepted treatment for those who have experienced an episode of VF not accompanied by an acute MI or other transient or reversible cause. Accepted guidelines prefer this treatment in individuals with sustained VT, causing syncope or hemodynamic compromise. As primary prevention, the literature shows that ICD use is superior to conventional antiarrhythmic drug therapy for those who have survived an MI and who have spontaneous, non-sustained VT, a low left ventricular ejection fraction (LVEF), and inducible VT at electrophysiological study (EPS).

Two prospective, randomized, controlled trials compared the use of ICDs to that of conventional therapy: the Multi-Center Automatic Defibrillator Implantation Trial (MADIT; n = 196) and the Multi-Center Automatic Defibrillator Implantation Trial II (MADIT II; n = 1,232). Both trials were conducted on individuals with CAD who had experienced MIs and who had reduced LVEFs. Both trials were well designed and of good quality. The observed all-cause mortality rate in the conventionally treated group was somewhat lower in MADIT II (19.8%, with average follow-up at 20 months) than in MADIT (38.6%, with average follow-up at 27 months), suggesting some differences in the baseline mortality risk between these two populations. Both trials reported that ICD treatment resulted in more statistically significant reductions in all-cause mortality (primary endpoint) than conventional therapy did. The MADIT and MADIT II trials provide consistent evidence that individuals with CAD, prior MI and reduced LVEF who meet selection criteria for either trial have significantly reduced mortality when treated with ICDs than when given conventional therapy (Moss, 1996).

The Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINITE) trial was a prospective, randomized study to test the hypothesis that an ICD will reduce the risk of SCD in individuals with non-ischemic dilated cardiomyopathy (NIDCM) and moderate-to-severe left ventricular dysfunction. Inclusion criteria were: LVEF less than 36%, the presence of ambient arrhythmias, a history of symptomatic heart failure, and the presence of NIDCM. The primary endpoint was death from any cause; the secondary endpoint was sudden death from arrhythmia. A total of 458 trial participants were enrolled: 229 were randomly assigned to receive standard medical therapy and 229 to receive standard medical therapy plus a single-chamber ICD. Results of the study included 68 deaths, 28 of which occurred in the ICD group, as compared to 40 in the standard therapy group (hazard ratio - 0.65; 95%; confidence interval - 0.40-1.06; p = 0.08). The mortality rate at two years was 14.1% in the standard therapy group (annual mortality rate, 7%) and 7.9% in the ICD group. There were 17 sudden deaths from arrhythmia: three in the ICD group and 14 in the standard therapy group (hazard ratio - 0.20; 95% confidence interval - 0.06 to 0.71; P = 0.006). The researchers noted that fewer subjects died in the ICD group than in the standard therapy group (28 vs. 40), but that the difference in survival was not significant (p = 0.08). The researchers concluded that this was still a well-supported study, based on the p value results (Schaechter, 2003).

A post-hoc analysis of the DEFINITE trial data was conducted by Kadish and colleagues (2006) which noted that study subjects with reversible causes of left ventricular dysfunction had been excluded from the DEFINITE trial. The authors noted that the time immediately after development of cardiomyopathy may be a time when the disease process and consequent remodeling are in rapid evolution which may stabilize with time (Kadish, 2006).

The Defibrillator in Acute Myocardial Infarction Trial (DINAMIT) randomized 674 adults to receive either an ICD or no ICD within 40 days of an MI (Hohnloser, et al. on behalf of the DINAMIT Investigators, 2004). All trial participants had reduced ejection fractions (LVEF less than or equal to 35%) and impaired cardiac autonomic function. The primary outcome was mortality from any cause, and the secondary outcome was death from arrhythmia. During a mean follow-up of 30 + 13 months, there was no difference in overall mortality between the two groups. Of 120 subjects who died, 62 were in the ICD group, and 58 were in the control group. There were 12 deaths due to arrhythmia in the ICD group and 29 in the control group. There were 50 deaths from nonarrhythmic causes in the ICD group, however, and 29 in the control group. The authors concluded that ICD therapy does not reduce overall mortality in high-risk candidates who have recently had an MI. Although ICD therapy was associated with a reduction in arrhythmia-related death, this was offset by an increase in nonarrhythmic-related death.

These findings were consistent with the results of another study, the VALsartan In Acute myocardial infarctioN Trial (VALIANT), which was reviewed and described in a recent article (Pouleur, 2010). The VALIANT study was a double-blind, randomized, controlled trial comparing valsartan, captopril, and their combination in high-risk individuals post-MI.  In this study, cardiac rupture was identified in 45 (0.31%) subjects enrolled in VALIANT, occurring 9.8 +/- 6.0 days after the qualifying MI. Rupture accounted for 7.6% (45/589) of all deaths occurring in the first 30 days of follow-up and 24% (33/138) of deaths in which autopsies were obtained. Compared with survivors, rupture was associated with increased age, hypertension, increased Killip class, lower estimated glomerular filtration rate, and Q wave MI, and inversely related to beta-blocker and diuretic use. The authors noted that, compared with subjects who died of other causes within 30 days of acute MI, subjects with myocardial rupture were more likely to have had an inferior MI, Q wave MI, or hypertension; also to have used oral anticoagulants or to have received thrombolytic therapy (Shamshad, 2010).

The further assessment of the VALIANT results conducted by Pouleur sought to understand the pathophysiological events that lead to sudden death after MI, based on a review of the VALIANT subjects' autopsy records, which were available in 398 cases (14% of deaths). The investigators determined that 105 subjects had clinical circumstances consistent with sudden death. On the basis of the autopsy findings, the probable cause of sudden death was evaluated to determine how these causes varied with time after MI. Of 105 deaths considered sudden on clinical grounds, autopsy suggested the following causes: 3 index MIs in the first 7 days (2.9%); 28 recurrent MIs (26.6%); 13 cardiac ruptures (12.4%); 4 pump failures (3.8%); 2 other cardiovascular causes (stroke or pulmonary embolism; 1.9%); and 1 noncardiovascular cause (1%). Fifty-four cases (51.4%) had no acute specific autopsy evidence other than the index MI and were thus presumed arrhythmic. The percentage of sudden death due to recurrent MI or rupture was highest in the first month after the index MI. By contrast, after 3 months, the percentage of presumed arrhythmic death was higher than recurrent MI or rupture (chi[2] = 23.3, P < 0.0001).  The investigators concluded that these findings may help explain the lack of benefit of ICD therapy in the early post-acute MI period, since recurrent MI or cardiac rupture seemed to account for the high proportion of sudden deaths early after acute MI in this examination of the VALIANT results which would not be beneficially impacted or prevented by placement of an ICD (Pouleur, 2010).

The Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) was conducted to test whether amiodarone therapy or an ICD will improve survival, compared to a placebo, in adults with systolic dysfunction from ischemic dilated cardiomyopathy (IDCM) or non-ischemic dilated cardiomyopathy (NIDCM) who also have NYHA class II or class III heart failure, chronic stable congestive heart failure (CHF) and reduced LVEF less than or equal to 35%. A total of 2,521 subjects were randomly assigned: 847 received placebo plus conventional heart failure therapy; 845 received amiodarone plus conventional heart failure therapy; and 829 received single-lead ICD plus conventional heart failure therapy. The results of the trial showed a significant reduction in mortality in the ICD group, compared to the placebo group: (hazard ratio compared to control = 0.77; 97.5% CI = 0.62-0.96; p = 0.007).

For individuals with IDCM (see Definitions section on pg. 6), there was a reduction in the mortality hazard ratio for ICD therapy, compared to the control (hazard ratio = 0.79; 97.5% CI = 0.60-1.04). For individuals with NIDCM (see Definitions section on pg. 6), there was a reduction in the mortality hazard ratio for ICD therapy, compared to the control (hazard ratio = 0.73; 97.5% CI = 0.50-1.07). Amiodarone therapy did not improve survival. The results of this study showed that overall mortality was lower for participants with NIDCM than for those with IDCM. The authors concluded that ICD placement is safe and effective for the treatment of ischemic and non-ischemic cardiomyopathy (Bardy, 2005).

In 2009, another study of ICD use as primary prevention of SCD early after acute MI was published. This study was a randomized, prospective, open-label, investigator-initiated, multicenter trial that registered 62,944 unselected participants with MI. Of this total, 898 subjects were enrolled 5 to 31 days after the event if they met certain clinical criteria (a LVEF less than or equal to 40% with a heart rate of 90 or more beats per minute on the first available electrocardiogram or non-sustained VT greater than or equal to 150 beats per minute during Holter monitoring or both criteria). Of the 898 subjects enrolled, 445 were randomly assigned to treatment with an ICD and 453 were treated with medical therapy alone. During a mean follow-up of 37 months, 233 subjects died: 116 in the ICD group and 117 in the control group. Overall mortality was not reduced in the ICD group (hazard ratio, 1.04; 95% confidence interval [CI], 0.81 to 1.35; P = 0.78). There were fewer incidence of SCD in the ICD group than in the control group (27 vs. 60; hazard ratio, 0.55; 95% CI, 0.31 to 1.00; P = 0.049), but the number of non-sudden cardiac deaths was higher (68 vs. 39; hazard ratio, 1.92; 95% CI, 1.29 to 2.84; P = 0.001). Hazard ratios were similar among the three groups of trial participants categorized according to the enrollment criteria they met. Prophylactic ICD therapy did not reduce overall mortality among those with acute MI and clinical features that placed them at increased risk (Steinbeck, 2009).

In 2006, the American College of Cardiology (ACC), in conjunction with the American Heart Association (AHA), the European Society of Cardiology (ESC), the European Heart Rhythm Association (EHRA), and the Heart Rhythm Society (HRS) published Practice Guidelines for the Management of Patients with Ventricular Arrhythmias and the Prevention of SCD (Zipes, 2006).  The guidelines, which were based on published evidence, expert opinion, and medical consensus, provide recommendations for use of ICDs, in addition to other recommendations related to diagnostics and medical/surgical treatment options for a variety of cardiac conditions. In 2008, the ACC/AHA/HRS published updated Guideline Recommendations for Device-Based Therapy of Cardiac Rhythm Abnormalities (Epstein, 2008). These guidelines update the prior 2002 ACC/AHA/NASPE Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices (Gregoratos, et al., 2002). The ACC/AHA/HRS guidelines have been updated due to the expanding body of knowledge and experience related to the treatment of bradyarrhythmias and tachyarrhythmias, as well as the significant advances in the technology of device-based therapy for these conditions.  These guidelines are intended to add to the information in the former 2002 ACC/AHA/NASPE guidelines, as well as the 2006 ACC/AHA/ESC Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of SCD. This updated 2008 guidance document reviews available clinical trial data in detail and also provides specific guideline recommendations for use of ICD devices in adults and also in the pediatric population, which have been incorporated into the medical necessity criteria in this document. 

According to this ACC/AHA/HRS guideline document (Epstein, 2008):

The indications for ICD implantation in young patients and those with congenital heart disease have evolved over the past 15 years based on data derived primarily from adult randomized clinical trials. Similar to adults, ICD indications have evolved from the secondary prevention of SCD to the treatment of patients with sustained ventricular arrhythmias to the current use of ICDs for primary prevention in patients with an increased risk of SCD. However, in contrast to adults, there are minimal prospective data regarding ICD survival benefit, because fewer than 1% of all ICDs are implanted in pediatric or congenital heart disease patients. Considerations, such as the cumulative lifetime risk of SCD in high-risk patients and the need for decades of antiarrhythmic therapy, make the ICD an important treatment option for young patients. Prospective identification and treatment of young patients at risk for sudden death is crucial because compared with adults, a very low percentage of children undergoing resuscitation survive to hospital discharge…Because of concern about drug-induced proarrhythmia and myocardial depression, an ICD (with or without cardiac resynchronization therapy [CRT]) may be preferable to antiarrhythmic drugs in young patients with dilated cardiomyopathy (DCM) or other causes of impaired ventricular function who experience syncope or sustained ventricular arrhythmias…The role of ICDs in primary prevention for children with genetic channelopathies, cardiomyopathies, and congenital heart defects should be defined more precisely and is an area in need of further research (Epstein, 2008).

In 2009, the ACC/AHA published a focused update to the 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults which gave a Class IIa recommendation for ICD placement in individuals with IDCM who are at least 40 days post-MI, have an LVEF of 30% or less, are in NYHA functional class I on chronic optimal medical therapy, and have reasonable expectation of survival with a good functional status for more than 1 year (Hunt, 2009). This was based, in part, on the findings of the SCD-HeFT trial previously described (Bardy, 2005) and has been incorporated into the medical necessity criteria for adult indications.

The decision to place an ICD in an individual with ischemic or non-ischemic cardiomyopathy is based, in part, on the measured LVEF. This measurement is subject to change over time based on medical interventions. The placement of an ICD should be reserved for individuals who have received an adequate trial of optimal medical management (Al-Khatib, 2011).

In 2003, a clinical expert consensus document on hypertrophic cardiomyopathy (HCM) was published by the American College of Cardiology (ACC) and the European Society of Cardiology (ESC), a report of the ACC Foundation Task Force and the ESC Committee for Practice Guidelines (Maron, 2003). The purpose of this document was to clarify the issues relevant to HCM, which is described as a complex and relatively common genetic disorder that is a common cause of SCD in young people, such as athletes, but also causes SCD in some afflicted individuals of all ages.  This paper provides the major risk factors for SCD considered to be useful in risk stratification of individuals with HCM who are considered at high risk for SCD.  The major risk factors are:

• Cardiac arrest (ventricular fibrillation);
• Spontaneous sustained ventricular tachycardia;
• Family history of premature sudden death;
• Unexplained syncope;
• LV thickness greater than or equal to 30 mm;
• Abnormal exercise blood pressure;
• Nonsustained ventricular tachycardia (Holter).

This consensus document further states:

Although the available data on the stratification of SCD risk are substantial and a large measure of understanding has been achieved, it is important to underscore that precise identification of all individual high-risk patients by clinical risk markers is not completely resolved…When the risk level for SCD is judged by contemporary criteria to be unacceptably high and deserving of intervention, the ICD is the most effective and reliable treatment option available, harboring the potential for absolute protection and altering the natural history of this disease in some patients…The ICD is strongly warranted for secondary prevention of SCD in those patients with prior cardiac arrest or sustained and spontaneously occurring VT. The presence of multiple clinical risk factors conveys increasing risk for SCD of sufficient magnitude to justify aggressive prophylactic treatment with an ICD for primary prevention of SCD. (Maron, 2003).

The identification of risk factors for SCD in HCM was the subject of a study previously published in 2000 (Elliott, et al.) that sought to identify individuals with HCM at high risk of sudden death (SD).  This study used a referral center registry to investigate a smaller number of generally accepted noninvasive risk markers studied in 368 subjects (14 to 65 years old, 239 males) with HCM.  Five risk variables were noted as follows: (1) nonsustained ventricular tachycardia (NSVT), (2) syncope, (3) exercise blood pressure response (BPR), (4) family history of sudden death (FHSD), and (5) left ventricular wall thickness (LVWT).   During follow-up (3.6 +/- 2.5 years [range 2 days to 9.6 years]), 36 individuals (9.8%) died, 22 of them suddenly. Two study subjects received heart transplants. The six-year SD-free survival rate was 91% (95% confidence interval [CI] 87% to 95%). In the Cox model, there was a significant pair-wise interaction between FHSD and syncope (p = 0.01), and these were subsequently considered together. The multivariate SD risk ratios (with 95% CIs) were 1.8 for BPR (0.7 to 4.4) (p = 0.22); 5.3 for FHSD and syncope (1.9 to 14.9) (p = 0.002); 1.9 for NSVT (0.7 to 5.0) (p = 0.18) and 2.9 for LVWT (1.1 to 7.1) (p = 0.03). Subjects with no risk factors (n = 203) had an estimated six-year SD-free survival rate of 95% (CI 91% to 99%). The corresponding six-year estimates (with 95% CIs) for one (n = 122), two (n = 36), and three (n = 7) risk factors were 93% (87% to 99%), 82% (67% to 96%), and 36% (0% to 75%), respectively. Study subjects with two or more risk factors had a lower six-year SD survival rate (95% CI) compared with those with one or no risk factors (72% [56% to 88%] vs. 94% [91% to 98%]) (p = 0.0001).  The authors concluded that this study demonstrates that individuals with multiple risk factors have a substantially increased risk of SD sufficient to warrant consideration for prophylactic therapy.

In 2010, Maron published another paper on strategies for risk stratification and prevention of SCD in HCM in which the current knowledge was summarized, and the following indicators were listed as major risk factors for SCD in HCM:

• Family history of at least one HCM-related SCD (defined as SCD in at least 1 first-degree relative);
• At least one episode of unexplained recent syncope (defined as 1 or more episodes of unexplained loss of consciousness within the previous 12 months);
• Massive left ventricular (LV) hypertrophy (thickness greater than or equal to 30 mm);
• Nonsustained VT on ambulatory 24-hour (Holter) ECG (defined as a run of 3 or more consecutive ventricular beats at a rate of at least 120 beats/minute, lasting less than 30 seconds);
• Hypotensive or attenuated blood pressure response to exercise (defined as failure of blood pressure to rise, or as a fall in blood pressure).  (Elliott, 2000; Maron, 2010)

The above five major risk factors are compiled from the findings of both Elliott (2000) and Maron (2010) and have been incorporated into the indications for ICD therapy in HCM considered medically necessary in this document.

The Centers for Medicare and Medicaid Services (CMS) expanded its national coverage determination policy (January 27, 2005), to include individuals with IDCM and NIDCM, subject to additional policy limitations and requirements regarding data collection.  This expanded policy is based on the results of published trial data, as described above.

Description of Relevant Disease
SCD (also called sudden arrest) is defined as unexpected death, resulting from an abrupt loss of heart function (cardiac arrest). All known heart diseases can lead to cardiac arrest and SCD. Most of the cardiac arrests that lead to SCD occur when the electrical impulses in the diseased heart become rapid (ventricular tachycardia - VT) or chaotic (ventricular fibrillation - VF) or both. This irregular rhythm causes the heart to suddenly stop beating. Some cardiac arrests are due to extreme slowing of the heart (bradycardia). Brain death and permanent death start to occur in just four to six minutes after someone experiences cardiac arrest.  Cardiac arrest is reversible in most victims if it is treated within a few minutes with an electrical shock to the heart to restore a normal heartbeat (defibrillation). Cardiovascular mortality as a consequence of VF or VT continues to be a major health problem, despite advances in the overall management of cardiovascular disease.  SCD kills approximately 400,000 people per year, with survival rates for cardiac arrest less than 5% in most industrialized countries. If the cardiac arrest was due to VT or VF, survivors are at risk for another arrest, especially if they have underlying heart disease.

Description of Implantable Defibrillators (ICD)
Defibrillation is a process in which an electronic device gives an electric shock to the heart.  This helps re-establish normal contraction rhythms in a heart having dangerous arrhythmia or in cardiac arrest. A surgically implanted ICD is a device used in individuals at high risk for SCD due to arrhythmia, usually due to sustained VT. The device is connected to leads positioned inside the heart or on its surface.  These leads are used to deliver electrical shocks, sense the cardiac rhythm and sometimes pace the heart, as needed. The various leads are connected to a pulse generator, which is implanted in a pouch beneath the skin of the chest or abdomen. The ICD is designed to continuously monitor an individual's heart rate, recognize VF or VT, and deliver an electric shock to terminate these arrhythmias, in order to reduce the risk of SCD.  Multiple ICD devices have been approved by the U.S. Food and Drug Administration (FDA) through the premarket approval (PMA) process, subject to FDA-approved labeling indications.

Abnormal blood pressure (BP) response during upright exercise testing:  Failure of BP to rise by more than 25 mmHg (flat) or a fall in BP more than 15 mmHg (considered to be a hypotensive response) that occurs during upright exercise stress testing.

Arrhythmia (or dysrhythmia): problems that affect the electrical system of the heart muscle, producing abnormal heart rhythms and may be classified as either atrial or ventricular, depending on which part of the heart they originate from.

Atrial Fibrillation:  A condition in which the atrium (the heart's two upper chambers) produce uncoordinated electrical signals.

Cardiomyopathy: A disease in which the heart muscle becomes inflamed and doesn't work as well as it should; there are three main types of cardiomyopathy:

• Dilated - This is the most common form, in which the heart cavity is enlarged and stretched (cardiac dilation). The heart is weak and doesn't pump normally, and most individuals develop congestive heart failure. Abnormal heart rhythms and disturbances in the heart's electrical conduction may also occur.

• Hypertrophic - In this condition, the muscle mass of the left ventricle enlarges or "hypertrophies." In one form of the disease, the wall between the two pumping chambers becomes enlarged and obstructs the blood flow from the left ventricle. In the other form of the disease, non-obstructive hypertrophic cardiomyopathy, the enlarged muscle doesn't obstruct blood flow.

• Restrictive - This is the least common type in the United States.  The myocardium (heart muscle) of the ventricles becomes excessively "rigid," making it more difficult for the ventricles to fill with blood between heartbeats.  This type of cardiomyopathy is usually due to another disease process.

Ischemic Cardiomyopathy (IDCM): Left ventricular systolic dysfunction (or disease of the heart muscle) associated with at least 75 percent narrowing of at least one of the three major coronary arteries (marked stenosis) or a documented history of myocardial infarction.

Nonischemic Cardiomyopathy (NIDCM): Left ventricular systolic dysfunction (or disease of the heart muscle) that is not associated with Coronary Artery Disease (CAD) or narrowing of the coronary arteries. There are a few different types of NIDCM but all involve thickening (abnormal enlargement) of the walls of the heart and progressive weakening of the pumping efficiency of the heart. 

Congestive heart failure (CHF) or heart failure:  This is a condition in which the heart can't pump enough blood to the body's other organs.  The "failing" heart keeps working but not as efficiently as it should. As blood flow out of the heart slows, blood returning to the heart through the veins backs up, causing congestion in the tissues.

Coronary Artery Disease (CAD): Heart problems caused by narrowed heart arteries.  When arteries are narrowed, less blood and oxygen reaches the heart which can ultimately lead to a heart attack (myocardial infarction - MI).

Defibrillation: A process in which an electronic device (a defibrillator) gives the heart an electric shock, helping to re-establish normal contraction rhythms in a heart that is not properly beating.  This may be done using an external device or by a device implanted in the body.

Ejection Fraction (EF) or Left Ventricular Ejection Fraction (LVEF):  The percentage of blood ejected from the left ventricle with each heartbeat. Normal readings would be in the 58-70% range and lower values would indicate ventricular dysfunction.

Electrophysiology Studies (EPS): These studies evaluate the electrophysiological properties of the heart, such as automaticity, conduction, and whether the condition is refractory to management with medications. Additional capabilities of this testing include: ability to initiate and terminate tachycardia to map activation sequences and to evaluate individuals for various forms of therapy and to judge response to therapy.

Myocardial Infarction (MI): This is the medical term for "heart attack."  An MI occurs when the blood supply to part of the heart muscle (the myocardium) is severely reduced or blocked (stenosed).

New York Heart Association (NYHA) Definitions:

The NYHA classification of heart failure is a 4-tier system that categorizes based on subjective impression of the degree of functional compromise.  The four NYHA functional classes are as follows:

• Class I - individuals with cardiac disease but without resulting limitation of physical activity; ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain; symptoms only occur on severe exertion;
• Class II - individuals with cardiac disease resulting in slight limitation of physical activity; they are comfortable at rest; ordinary physical activity, (e.g., moderate physical exertion, such as carrying shopping bags up several flights of stairs) results in fatigue, palpitation, dyspnea, or anginal pain;
• Class III - individuals with cardiac disease resulting in marked limitation of physical activity; they are comfortable at rest; less than ordinary activity causes fatigue, palpitation, dyspnea or anginal pain;
• Class IV - individuals with cardiac disease resulting in inability to carry on any physical activity without discomfort; symptoms of heart failure or the anginal syndrome may be present even at rest; if any physical activity is undertaken, discomfort is increased.

QRS Complex: The portion of an electrocardiogram (EKG) reading, which represents the spread of the electrical impulse through the ventricles.

Sudden Cardiac Death (SCD also called sudden death):  Death resulting from an abrupt loss of heart function (cardiac arrest).

Ventricular tachyarrhythmias: This medical term refers to a rapid heartbeat that may be regular or irregular and arises from the ventricle or pumping chamber of the heart.  Two common tachyarrhythmias are ventricular tachycardia and ventricular fibrillation.

Ventricular Fibrillation (Vfib or VF): This is a condition in which the heart's electrical activity becomes disordered, resulting in the heart's lower (pumping) chambers contract in a rapid, unsynchronized fashion, (i.e., the ventricles "flutter" rather than beat), and the heart pumps little or no blood.

Ventricular Tachycardia (Vtach or VT): This is a fast regular heart rate (usually of 100 or more beats per minute) that starts in the lower chambers (ventricles) and may result from serious heart disease that usually requires prompt treatment.

Sustained/Non-sustained Ventricular Tachycardia: VT is considered nonsustained (NSVT) when 3 or more consecutive ventricular beats occur at a rate of at least 120 beats/minute which lasts less than 30 seconds.  If the rhythm lasts more than 30 seconds, it is known as a sustained ventricular tachycardia (even if it terminates on its own, [that is, without medical intervention] after 30 seconds).

Syncope: An episode where the individual experiences loss of consciousness lasting at least several seconds.  If the person only experiences extreme dizziness but with no actual loss of consciousness, this is termed "Pre-Syncope."

The following codes for treatments and procedures applicable to this document are included below for informational purposes.  Inclusion or exclusion of a procedure, diagnosis or device code(s) does not constitute or imply member coverage or provider reimbursement policy. Please refer to the member's contract benefits in effect at the time of service to determine coverage or non-coverage or these services at it applies to an individual member.

 When services may be Medically Necessary when criteria are met:

When services are Investigational and Not Medically Necessary:
For the procedure codes listed above specified as ICD when criteria are not met, or when the code describes a procedure indicated in the Position Statement section as investigational and not medically necessary.

Future ICD-10 coding (effective 10/01/2013)
A draft of ICD-10 Coding related to this document, as it might look today, is available for reference and comments at: Appendix 1: Future ICD-10 coding

Peer Reviewed Publications:

1. Al-Khatib SM, Hellkamp A, Curtis J, et al. Non-evidence-based ICD implantations in the United States. JAMA. 2011; 305(1):43-49.
2. Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter–defibrillator for congestive heart failure (SCD-HeFT Trial). N Engl J Med. 2005; 352(3):225-237.
3. Boehmer JP. Device therapy for heart failure. Am J Cardiol. 2003; 91(6A):53D-59D.
4. Bristow MR, Saxon LA, Boehmer J, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med. 2004; 350(21):2140-2150.
5. Bunch TJ, Hohnloser SH, Gersh BJ. Mechanisms of sudden cardiac death in myocardial infarction survivors: insights from the randomized trials of implantable cardioverter-defibrillators. Circulation. 2007; 115(18):2451-2457.
6. Buxton AE, Lee KL, Hafley GE, et al. for the MUSTT Investigators. Limitations of ejection fraction for prediction of sudden death risk in patients with coronary artery disease: lessons from the MUSTT study. J Am Coll Cardiol. 2007; 50(12):1150-1157.
7. Buxton AE, Sweeney MO, Wathen MS, et al. QRS duration does not predict occurrence of ventricular tachyarrhythmias in patients with implanted cardioverter-defibrillators. J Am Coll Cardiol. 2005; 46(2):310-316.
8. Buxton AE, Lee KL, Fisher JD, et al. A randomized study of the prevention of sudden death in patients with coronary artery disease. N Engl J Med. 1999; 341(25):1882-1890.
9. Carbucicchio C, Santamaria M, Trevisi N, et al. Catheter ablation for the treatment of electrical storm in patients with implantable cardioverter-defibrillators: short- and long-term outcomes in a prospective single-center study. Circulation. 2008; 117(4):462-469. Epub 2008 Jan 2.
10. Cha YM, Gersh BJ, Maron BJ, et al. Electrophysiologic manifestations of ventricular tachyarrhythmias provoking appropriate defibrillator interventions in high-risk patients with hypertrophic cardiomyopathy. Cardiovasc Electrophysiol. 2007; 18(5):483-487. Comment in: J Cardiovasc Electrophysiol. 2007; 18(5):488-489.
11. Chow AW, Lane RE, Cowie MR. New pacing technologies for heart failure. BMJ. 2003; 326(7398):1073-1077.
12. Christiaans I, van Engelen K, van Langen IM, et al.  Risk stratification for sudden cardiac death in hypertrophic cardiomyopathy:  systematic review of clinical risk markers. Europace. 2010; 12(3):313-321.
13. Coats AJ. MADIT II, the Multi-center Autonomic Defibrillator Implantation Trial II stopped early for mortality reduction, has ICD therapy earned its evidence-based credentials? Int J Cardiol. 2002; 82(1):1-5.
14. Cook JR, Rizo-Paton C, et al. Effect of surgical revascularization in patients with coronary artery disease and ventricular tachycardia or fibrillation in the antiarrhythmias versus implantable defibrillation registry. Am Heart J. 2002; 143(5):821-826.
15. Cooper JM, Katcher MS, Orlov MV. Current concepts: implantable devices for the treatment of atrial fibrillation. N Eng J Med. 2002; 346(26):2062-2028.
16. David Investigators. dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator: the dual chamber and VVI implantable defibrillator (DAVID) trial. JAMA. 2002; 288(24):3115.
17. Day JD, Doshi RN, Belott P, et al. Inductionless or limited shock testing is possible in most patients with implantable cardioverter-defibrillators/cardiac resynchronization therapy defibrillators: results of the multicenter ASSURE Study (Arrhythmia Single Shock Defibrillation Threshold Testing Versus Upper Limit of Vulnerability: Risk Reduction Evaluation With Implantable Cardioverter-Defibrillator Implantations). Circulation. 2007; 115(18):2382-2389. Epub 2007 Apr 30. Comment in: Circulation. 2007; 115(18):2370-2372.
18. Desai AS, Fang JC, Maisel WH, et al. Implantable defibrillators for the prevention of mortality in patients with nonischemic cardiomyopathy: a meta-analysis of randomized controlled trials. JAMA. 2004; 292(23):2874-2879.
19. Ellenbogen KA, Levine JH, Berger RD, et al. Are implantable cardioverter defibrillator shocks a surrogate for sudden cardiac death in patients with nonischemic cardiomyopathy? Circulation. 2006; 113(6):776-782.
20. Elliott PM, Poloniecki J, Dickie S, et al.  Sudden death in hypertrophic cardiomyopathy: identification of high risk patients. J Am Coll Cardiol. 2000; 36(7):2212-2218.
21. Engelstein ED. Prevention and management of chronic heart failure with electrical therapy. Am J Cardiol. 2003; 91(9):62. 
22. Exner DV, Klen GJ, Prytowsky EN. Primary prevention of sudden cardiac death with implantable defibrillator therapy in patients with cardiac disease: can we afford to do it? (Can We Afford Not To?). Circulation. 2001; 104(13):1564-1570.
23. Ezekowitz JA, Armstrong PW, McAlister FA. Implantable cardioverter-defibrillators in primary and secondary prevention: A systemic review of randomized, controlled trials. Ann Intern Med. 2003; 138(6):445-452.
24. Ezekowitz JA, Rowe BH, Dryden DM, et al.  Systematic review:  cardioverter defibrillators for adults with left ventricular systolic dysfunction.  Ann Intern Med. 2007; 147:251-262.
25. Fisher JD, Buxton AE, Lee KL, et al. Designation and distribution of events in the Multicenter UnSustained Tachycardia Trial (MUSTT). Am J Cardiol. 2007; 100(1):76-83. 
26. Goldenberg I, Moss AJ, Hall, J, et al. Causes and consequences of heart failure after prophylactic implantation of a defibrillator in the multicenter automatic defibrillator implantation trial II. Circulation. 2006; 113(24):2810-2817.
27. Goldenberg I, Vyas AK, Hall WJ, et al. Risk stratification for primary implantation of a cardioverter-defibrillator in patients with ischemic left ventricular dysfunction. J Am Coll Cardiol. 2008; 51(3):288-296.
28. Greenberg H, Case RB, Moss AJ, et al. and MADIT-II Investigators. Analysis of mortality events in the Multicenter Automatic Defibrillator Implantation Trial (MADIT-II). J Am Coll Cardiol. 2004; 43(8):1459-1465.
29. Heidenreich PA, Keefe B, McDonald KM, et al. Overview of randomized trials of antiarrhythmic drugs and devices for the prevention of sudden cardiac death. Am Heart J. 2002; 144(3):422-430.
30. Hlatky MA. Evidence-based use of cardiac procedures and devices. N Engl J Med. 2004; 350(21):2126-2128.
31. Hodgkinson KA, Parfrey PS, Bassett AS, et al. The impact of implantable cardioverter-defibrillator therapy on survival in autosomal-dominant arrhythmogenic right ventricular cardiomyopathy (ARVD5). J Am Col Cardiol. 2005; 45(3):400-408.
32. Hohnloser SH, Kuck KH, Dorian P, et al. Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction. N Engl J Med. 2004; 351(24):2481-2488.
33. Huang DT, Sesselberg HW, McNitt S, et al. Improved survival associated with prophylactic implantable defibrillators in elderly patients with prior myocardial infarction and depressed ventricular function: a MADIT-II substudy. J Cardiovasc Electrophysiol. 2007; 18(8):833-838.
34. Kadish A, Dyer A, Daubert JP, et al. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy.N Engl J Med. 2004; 350(21):2151-2158.
35. Kadish A, Schaechter A, Subacius H, et al. Patients with recently diagnosed nonischemic cardiomyopathy benefit from implantable cardioverter-defibrillators.  J Am Coll Cardiol. 2006; 47:2477-2482.
36. Khairy P, Harris L, Landzberg MJ, et al. Implantable cardioverter-defibrillators in tetralogy of Fallot. Circulation. 2008; 117(3):363-370. Epub 2008 Jan 2.
37. Kupersmith J. The past, present, and future of the implantable cardioverter-defibrillator. Am J Med. 2002;  113(1); 82-84.
38. Kusumoto, FM, Goldschlager N. Device therapy for cardiac arrhythmias. JAMA. 2002; 287(14):1848-1852.
39. Marchlinski FE, Jessup M.  Timing the implantation of implantable cardioverter-defibrillators in patients with nonischemic cardiomyopathy.  J Am Coll Cardiol. 2006; 47(12):2483-2485.
40. Mark DB, Anstrom KJ, Sun JL, et al; Sudden Cardiac Death in Heart Failure Trial Investigators. Quality of life with defibrillator therapy or amiodarone in heart failure. N Engl J Med. 2008; 359(10):999-1008.
41. Maron BJ.  Contemporary insights and strategies for risk stratification and prevention of sudden death in hypertrophic cardiomyopathy.  Circ. 2010; 121:445-456.
42. Maron BJ, Spirito P, Shen WK, et al. Implantable cardioverter-defibrillators and prevention of sudden cardiac death in hypertrophic cardiomyopathy. JAMA. 2007; 298(4):405-412.
43. McClellan MB, Tunis SR. Medicare coverage of ICDs. N Engl J Med. 2005; 352(3):222-224.
44. Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators.  N Engl J Med. 1996; 335(26):1933-1940.
45. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002; 346(12):877-883.
46. Nagahara D, Nakata T, Hashimoto A, et al. Predicting the need for an implantable cardioverter defibrillator using cardiac metaiodobenzylguanidine activity together with plasma natriuretic peptide concentration or left ventricular function. J Nucl Med. 2008; 49(2):225-233.
47. Nanthakumar K, Dorian P, Paquette M, et al. Is inappropriate implantable defibrillator shock therapy predictable? J IntervCardiac Electrophysiol. 2003; 8(3):215-220.
48. Parkes JB, Milne AR. Implantable cardioverter-defibrillators in arrhythmias: a rapid and systematic review of effectiveness. Heart. 2002; 87(5):438-442.
49. Passman R, Subacius H, Ruo B, et al.  Implantable cardioverter defibrillators and quality of life: results from the defibrillators in nonischemic cardiomyopathy treatment evaluation study (DEFINITE). Arch Intern Med. 2007; 167(20):2226-2232.
50. Poole JE, Johnson GW, Hellkamp AS, et al. Prognostic importance of defibrillator shocks in patients with heart failure. N Engl J Med. 2008; 359(10):1009-1017.
51. Pouleur AC, Barkoudah E, Uno H, et al.  Pathogenesis of sudden unexpected death in a clinical trial of patients with myocardial infarction and left ventricular dysfunction, heart failure, or both.  Circulation. 2010; 122(6):597-602.
52. Raviele A, Bongiorni MG, Brignole M, et al. Early EPS/ICD strategy in survivors of acute myocardial infarction with severe left ventricular dysfunction on optimal beta-blocker treatment. The BEta-blocker STrategy plus ICD trial.  Europace. 2005; 7(4):327-337.
53. Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic catheter ablation for the prevention of defibrillator therapy. N Engl J Med. 2007; 357(26):2657-2665. Comment in: N Engl J Med. 2007; 357(26):2717-2719.
54. Schaechter A, Kadish AH, et al. Defibrillators in non-ischemic cardiomyopathy treatment evaluation (DEFINITE). Card Electrophysiol Rev. 2003; 7(4):457-462.
55. Scheinman MM, Keung E. The year in clinical cardiac electrophysiology.  J Am Coll Cardiol. 2007; 49(20):2061-2069.
56. Schlapfer J, Rapp F, Kappenberger L, et al. Electrophysiologically guided amiodarone therapy versus the implantable cardioverter-defibrillator for sustained ventricular tachyarrhythmias after myocardial infarction: results of long-term follow-up. J Am Coll Cardiol. 2002; 39(11):1813-1819.
57. Shamshad F, Kenchaiah S, Finn PV, et al. Fatal myocardial rupture after acute myocardial infarction complicated by heart failure, left ventricular dysfunction, or both: the VALsartan In Acute myocardial iNfarcTion Trial (VALIANT). Am Heart J. 2010; 160(1):145-151.
58. Steinbeck G, Andresen D, Seidl K, et al. Defibrillator implantation early after myocardial infarction.  N Engl J Med. 2009; 361(15):1427-1436.
59. Steinberg JS, Martins J, et al. Antiarrhythmic drug use in the implantable defibrillator arm of the antiarrhythmics versus implantable defibrillator (AVID) study. Am Heart J. 2001; 142(3):520-529.
60. Swygman C, Wang PJ, Link MS, et al. Advances in implantable cardioverter-defibrillators. Curr Op Card. 2002; 17(1):24-28.
61. Syska P, Przybylski A, Chojnowska L, et al. ICD in patients with HCM:  efficacy and complications of the therapy in long-term follow-up.  J Cardiovasc Electrophys. 2010; 21(8):883-889.
62. Varma N. Rationale and design of a prospective study of the efficacy of a remote monitoring system used in implantable cardioverter defibrillator follow-up: the Lumos-T reduces routine office device follow-up study (TRUST). Am Heart J. 2007; 154(6):1029-1034.
63. Wilber DJ, Zareba W, Hall WJ, et al. Time dependence of mortality risk and defibrillator benefit after myocardial infarction. Circulation. 2004; 109(9):1082-1084.
64. Yap SC, Roos-Hesselink JW, Hoendermis ES, et al. Outcome of implantable cardioverter defibrillators in adults with congenital heart disease: a multi-centre study. Eur Heart J. 2007; 28(15):1854-1861.

Government Agency; Medical Society; and Other Authoritative Publications:

1. American Heart Association (AHA) web site: Sudden cardiac death. 2005b. Available at: http://www.americanheart.org/presenter.jhtml?identifier=4741. Accessed on March 4, 2011.
2. Antman EM, Hand M, Armstrong PW, et al. 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction: American College of Cardiology/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the Canadian Cardiovascular Society Endorsed by the American Academy of Family Physicians 2007 Writing Group to Review New Evidence and Update the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction, Writing on Behalf of the 2004 Writing Committee. J Am Coll Cardiol. 2008; 51:210-247. Available at: http://www.guideline.gov/content.aspx?id=12192.  Accessed on March 4, 2011.
3. Blue Cross and Blue Shield Association. Use of implantable Cardioverter-Defibrillators for Prevention of Sudden Death in Patients at High Risk for Ventricular Arrhythmia. TEC Assessment, 2004; 19(19).
4. Blue Cross and Blue Shield Association.  Implantable Cardioverter Defibrillators for Primary Prevention of Sudden Death in Patients at High Risk for Ventricular Arrhythmia. TEC Assessment, 2002; 17(10).
5. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease) Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008; 52:1-142. Available at: http://content.onlinejacc.org/cgi/content/full/52/13/e1. Accessed on March 4, 2011.
6. Centers for Medicare & Medicaid Services. National Coverage Determination: Implantable Automatic Defibrillators. NCD#20.4. Effective 01/27/2005. Available at: http://www.cms.hhs.gov/mcd/viewncd.asp?ncd_id=20.4&ncd_version=3&basket=ncd%3A20%2E4%3A3%3AImplantable+Automatic+Defibrillators. Accessed on March 4, 2011.
7. Connolly SJ, Hohnloser SJ, and the DINAMIT Steering Committee and Investigators. DINAMIT: Randomized trial of prophylactic implantable defibrillator therapy versus optimal medical treatment early after myocardial infarction: The Defibrillator in Acute Myocardial Infarction Trial. American College of Cardiology Scientific Session 2004. Bethesda, MD: American College of Cardiology; 2004.
8. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 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) Developed in Collaboration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008; 51:1-62.  Available at: http://content.onlinejacc.org/cgi/content/full/51/21/e1#SEC6. Accessed on March 4, 2011.
9. Goldberger JJ, Cain ME, Kadish AH, et al. American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society Scientific Statement on Noninvasive Risk Stratification Techniques for Identifying Patients at Risk for Sudden Cardiac Death. A Scientific Statement from the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention. J Am Coll Cardiol. 2008; 52:1179-1199. Available at: http://content.onlinejacc.org/cgi/content/full/52/14/1179.  Accessed on March 4, 2011.
10. Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2009; 53:e1–90. Available at: http://content.onlinejacc.org/cgi/reprint/53/15/e1.pdf. Accessed on March 4, 2011.
11. Jessup M, Abraham WT, Casey DE, et al. writing on behalf of the 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult Writing Committee. 2009 focused update: ACCF/AHA guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2009; 53:1343– 1382. Available at: http://content.onlinejacc.org/cgi/reprint/53/15/1343.pdf. Accessed on March 4, 2011.
12. Maron BJ, McKenna WJ, Danielson GK, et al. ACC/ESC clinical expert consensus document on hypertrophic cardiomyopathy: a report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents and the European Society of Cardiology Committee for Practice Guidelines (Committee to Develop an Expert Consensus Document on Hypertrophic Cardiomyopathy). J Am Coll Cardiol. 2003; 1-27. Available at: http://content.onlinejacc.org/cgi/reprint/42/9/1687.pdf. Accessed on March 4, 2011.
13. McAlister FA, Ezekowitz J, Dryden DM, et al. Cardiac resynchronization therapy and implantable cardiac defibrillators in left ventricular systolic dysfunction. Evid Rep Technol Assess (Full Rep). 2007; (152):1-199.
14. National Institute for Health and Clinical Excellence (NICE). Implantable cardioverter defibrillators for arrhythmias: Review of Technology Appraisal 11. Technology Appraisal 95. London, UK: NICE; 2006.
15. U.S. Food and Drug Administration (FDA). Center for Devices and Radiological Health. Implantable Cardioverter Defibrillators. Available at:http://www.accessdata.fda.gov/scripts/cdrh/devicesatfda/index.cfm.  Accessed on March 4, 2011.
16. Zipes DP, Camm AJ, Borggrefe M, et al. 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 Committee for Practice Guidelines (Writing Committee to develop guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death). Circ. 2006; 114:1088-1132. Available at: http://circ.ahajournals.org/cgi/reprint/114/10/e385. Accessed on March 4, 2011.

1. U.S. Food and Drug Administration (FDA). Center for Devices and Radiological Health. FDA Preliminary Public Health Notification: Guidant Ventak Prizm 2 DR and Contak Renewal Implantable Cardioverter Defibrillators. December 28, 2005. Available at:  http://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/PublicHealthNotifications/UCM062107. Accessed on March 4, 2011.
2. National Institute for Clinical Excellence (NICE) Technology Appraisal Guidance No. 11. Guidance on the use of implantable cardioverter defibrillators for arrhythmias. London, UK. NICE; 2006. Available at: http://guidance.nice.org.uk/TA95/?c=91497. Accessed on March 4, 2011.
3. Heart failure. Available at: http://www.heartfailure.org/ Accessed on September 15, 2010.
4. What is cardiomyopathy? Cleveland Clinic web site. Available at: http://my.clevelandclinic.org/disorders/Cardiomyopathy/hic_What_is_Cardiomyopathy.aspx. Accessed on March 4, 2011.

Automatic Defibrillator
Cardioverter Defibrillator
ICD
Implantable Cardioverter-Defibrillator