This document addresses the use of implantable transvenous and subcutaneous cardioverter-defibrillator devices 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:
Implantable transvenous cardioverter-defibrillator (ICD) therapy 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 (A through J):
Implantable transvenous cardioverter-defibrillator (ICD) therapy is considered medically necessary for individuals with a confirmed Brugada syndrome diagnosis when EITHER of the following criteria is met (A or B):
Subcutaneous cardioverter-defibrillator (S-ICD) devices are considered medically necessary for the following at-risk individuals when the medically necessary criteria above for implantable transvenous cardioverter-defibrillator (ICD) therapy have been met:
*The FDA interprets pediatrics as individuals who are 21 years of age or younger (that is, from birth through the 21st year of life, up to but not including the 22nd birthday).
SPECIAL NOTE REGARDING USE OF ICD THERAPY IN CHILDREN:
The use of ICD therapy in children has not been studied for many conditions as thoroughly as in adults, and there have been no randomized controlled trials of ICD therapy in children. As such, the potential risks and evidence of benefit from ICD therapy in children is not as well described in the medical literature. Studies have shown higher inappropriate shock rates and lead failure (Berul, 2008) and reduced quality of life (Sears, 2011) in children who have received an ICD. Prior to ICD implantation in a child, the informed consent discussion that the treating provider conducts with the family/guardian should include documentation of a thorough discussion of the probability of a life threatening event, based on the underlying condition, as well as the potential benefits and harms of the ICD and the family's/guardian's understanding of the information provided.
Note: For use of combined ICD/Biventricular pacing (CRT-ICD) devices, in cases of NYHA Class IV heart failure and for other indications, see CG-SURG-63 Cardiac Resynchronization Therapy (CRT), with or without an Implantable Cardioverter Defibrillator (CRT/ICD) for the Treatment of Heart Failure.
Investigational and Not Medically Necessary:
The use of an implantable transvenous cardioverter-defibrillator is considered investigational and not medically necessary when the criteria above are not met andfor any other indications.
The use of a subcutaneous ICD (S-ICD) is considered investigational and not medically necessary for all indications when the above criteria are not met.
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=1232). 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 MADIT trial included 196 subjects in NYHA functional Class I, II, or III HF with prior MI; an LVEF < or = 0.35; a documented episode of asymptomatic unsustained VT; and inducible, non-suppressible ventricular tachyarrhythmia on EPS. Trial participants were randomly assigned to receive an ICD (n=95) or conventional medical therapy (n=101). A two-sided sequential design was used for data analysis with death from any cause as the end point.
The MADIT II trial included 1232 subjects of either sex who were more than 21 years of age (there was no upper age limit) who were eligible for the study if they had had an MI 1 month or more before entry, as documented by the finding of an abnormal Q wave on electrocardiography, elevated cardiac-enzyme levels on laboratory testing during hospitalization for suspected MI, a fixed defect on thallium scanning, or localized akinesis on ventriculography with evidence of obstructive CAD on angiography, and an LVEF of 0.30 or less within 3 months before entry, as assessed by angiography, radionuclide scanning, or echocardiography. 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 (Goldenberg, 2010; Moss, 1996; Moss, 2002).
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 [HR], - 0.65; 95% confidence interval [CI], -0.40 to 1.06; p=0.08). The mortality rate at 2 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: 3 in the ICD group and 14 in the standard therapy group (HR, -0.20; 95% CI, -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 2 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 an 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=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 2521 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 for further information), there was a reduction in the mortality hazard ratio for ICD therapy, compared to the control (HR, 0.79; 97.5% CI, 0.60-1.04). For individuals with NIDCM (see Definitions section), there was a reduction in the mortality hazard ratio for ICD therapy, compared to the control (HR, 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 (HR, 1.04; 95% 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; HR, 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; HR, 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:
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 (CHD) 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 a 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 IDCM or NIDCM 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 2012, the term "Guideline-directed medical therapy" (GDMT) was adopted by the writing groups for the major specialty medical societies, (such as found in Tracy, 2012 and Yancy, 2013). Regarding the timeframe generally considered by consensus as adequate to determine if optimal medical therapy, (that is, GDMT) has been effective, prior to ICD placement is 3 to 6 months. In 2013, a report of the American College of Cardiology Foundation (ACCF) Appropriate Use Criteria Task Force, Heart Rhythm Society (HRS), American Heart Association (AHA), American Society of Echocardiography (ASE), Heart Failure Society of America (HFSA), Society for Cardiovascular Angiography and Interventions (SCAI), Society of Cardiovascular Computed Tomography (SCCT), and Society for Cardiovascular Magnetic Resonance (SCMR) was issued, in which the following is noted regarding the timeframe for GDMT:
Patients who are going to receive substantial benefit from medical treatment alone usually show some clinical improvement during the first 3 to 6 months. Medical therapy is also assumed to include adequate rate control for tachyarrhythmias, including atrial fibrillation. Therefore, it is recommended that GDMT be provided for at least 3 months before planned reassessment of LV function to consider device implantation. If LV function improves to the point where primary prevention indications no longer apply, then device implantation is not indicated (Russo, 2013).
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:
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).
In 2011, the American College of Cardiology (ACCF) and the AHA published guidelines for the diagnosis and treatment of HCM which, "Represent a consensus of expert opinion after a thorough review of the available current scientific evidence and are intended to improve patient care." The recommendations for ICD within this guideline align with the current criteria in this document. The following summary is excerpted from the guideline:
The decision to recommend and pursue ICD placement is a complex process that can be oversimplified. The individuality of each patient and family circumstance, including level of anxiety, life situation, and views on death, and individual assessment of the relative weight of potential benefits compared with potential risks must be processed for each patient. The low positive predictive value of any of the SCD risk factors and the variability in the strength of data also introduce a degree of ambiguity to the SCD risk assessment and dramatically limit the applicability of counting the number of risk factors as the primary risk assessment methodology. Based on the weight of evidence, plausibility, and consensus judgment reflecting clinical experience, it is recognized that patients with massive hypertrophy, a family history of HCM-related SCD, or recent unexplained syncope would probably benefit from ICD placement. Apart from these, it was believed that a combination of conventional risk factors and other risk modifiers provided the optimal identification of the subset of patients with HCM with sufficient risk of SCD to warrant strong consideration of ICD placement (Gersh, 2011).
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 6-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% CI) 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 6-year SD-free survival rate of 95% (CI, 91% to 99%). The corresponding 6-year estimates (with 95% CI) 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 6-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:
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.
In 2014, the HRS/ACC/AHA published an expert consensus statement on the use of ICD therapy in those who are not included or not well represented in clinical trials. This document provided expert opinion about when ICD is considered "Recommended" or "May be useful" for a variety of clinical indications. Although this document relied on consensus opinion, as opposed to evidence based science, its recommendations largely align with the current criteria within this document and reflect the consensus of physicians in the practice community (Kusumoto, 2014).
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.
In 2013, the Agency for Healthcare Research and Quality (AHRQ) issued a technology report entitled, Assessment on Implantable Defibrillators and the Evidence for Primary Prevention of Sudden Cardiac Death (Uhlig, 2013). Key questions examined ICD versus no ICD, ICD with antitachycardia pacing (ATP) versus ICD alone, or ICD with CRT versus ICD alone, and differences among subgroups. The report also examined early and late adverse events and inappropriate shocks after ICD implantation and differences among subgroups; and also eligibility criteria and evaluation methods for trial subjects included in comparative studies and the risk of SCD. Analyses failed to show statistically significant differences for all-cause mortality or SCD across subgroups by age, sex, and other individual characteristics; however, there may be an indication that ICDs are more effective in subjects with more distant coronary revascularization, compared with recent surgery. Studies of subjects with recent MIs (within 31 or 40 days) had no reduction in all-cause mortality, in contrast with studies in individuals with more distant MIs. Due to discordant findings among studies, there is insufficient evidence from four randomized controlled trials (RCT) regarding the relative effect on all-cause mortality among individuals who receive cardiac resynchronization therapy with ICD devices (CRT-D), compared to those who receive ICD alone. Heart failure (HF) outcomes and related quality of life measures were not reviewed. Regarding eligibility criteria for ICD placement, comparative studies included individuals with ischemic or nonischemic dilated cardiomyopathy, and LVEF ≤ 35% in all but one study. Eligibility criteria regarding HF class were variable. The trials of CRT-D used QRS interval data for eligibility; most other trials did not. Most of the RCTs of ICD tested all subjects for nonsustained VT, but with different diagnostic tools. Only one RCT reported performing electrophysiology testing (EPS) in all subjects. Only 4 of the 13 RCTs explicitly tested for coronary stenosis, mostly with coronary angiography or exercise testing. Most of the included studies excluded older adults over 70 to 80 years. SCD occurred in 4 to 13% of control subjects during the 2 to 5 years after randomization. Limitations of the reviewed evidence base in some RCTs was noted to include lack of blinding of outcome assessors of arrhythmia outcomes or SCD, high attrition rates (>20%), or differential rates of attrition or crossover between study groups, and differences in the control treatments or in the rates of concomitant use of beta blockers between the study groups.
It was also noted that knowledge gaps currently exist for familial or inherited conditions, as well as less common cardiomyopathies including, but not limited to, long-QT syndrome (LQTS), Brugada syndrome (BrS), catecholaminergic polymorphic VT (CPVT), hypertrophic cardiomyopathy (HCM), arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C), cardiac sarcoidosis, and left ventricle noncompaction. These disease states are less prevalent than IDCM and NIDCM and were, in large part, implicitly or explicitly excluded from the studies in this review. The investigators concluded that:
There is a high strength of evidence that ICD therapy for primary prevention of SCD, versus no ICD therapy, shows benefit with regard to mortality and SCD in selected patients with reduced LVEF and ischemic or nonischemic cardiomyopathy. There is low strength of evidence that the risk of all-cause mortality is similar for patients who receive CRT-Ds versus ICD alone for primary prevention. A high strength of evidence shows overall early in-hospital adverse event rates of approximately 3% and serious adverse event rates of approximately 1%. Low strength of evidence shows variable late adverse events. Moderate strength of evidence shows inappropriate shocks are experienced by 3 to 21% of patients over 1 and 5 years of follow-up (AHRQ, 2013).
Regarding ICD therapy in less prevalent cardiac conditions, such as BrS, the 2008 ACC/AHA/HRS Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities provide a Class IIa recommendation for, "ICD implantation as reasonable for patients with Brugada syndrome (BrS) who have had syncope" and for, "ICD implantation as reasonable for patients with BrS who have documented VT that has not resulted in cardiac arrest" (Level of Evidence: C). The following is provided as the basis for these recommendations:
Primary electrical conditions, (in reference to genetic syndromes that predispose to sustained VT or VF, such as BrS), typically exist in the absence of any underlying structural heart disease and predispose to cardiac arrest. Although controversy still exists with regard to risk factors for SCD in these conditions, there is consensus that those with prior cardiac arrest or syncope are at very high risk for recurrent arrhythmic events. On the basis of the absence of any clear or consistent survival benefit of pharmacological therapy for individuals with these genetic arrhythmia syndromes, the ICD is the preferred therapy for those with prior episodes of sustained VT or VF and may also be considered for primary prevention for some with a very strong family history of early mortality… Individuals with syncope and the ECG pattern of spontaneous STsegment elevation (associated with BrS) have a 6-fold higher risk of cardiac arrest than those without syncope and the spontaneous ECG pattern (Epstein, 2008).
A recent review article regarding the indications for ICD in BrS summarized the evidence as follows:
A multi-variable analysis identified a history of syncope and inducibility of sustained ventricular arrhythmias during an EP study as predictors of future sudden death or VF. Accordingly, some approaches [to risk stratification] favored the use of the combination of the clinical characteristics, history of syncope, and findings of EP study for the risk stratification in this patient population. High-risk patients, who present with syncope and/or have inducible ventricular arrhythmia during an EPS study, are recommended a prophylactic implantation of an ICD for the prevention of sudden death (Shimizu, 2013).
The findings (above) align with results of a large prospective study conducted at 5 medical centers in Italy for the purpose of determining risk for SCD in individuals with BrS (type 1 ECG pattern) but who had not experienced a prior cardiac arrest. A total of 320 subjects (258 males, median age 43 years) with type 1 ECG pattern BrS were enrolled. None of the trial participants had experienced a previous cardiac arrest. Study subjects consisted of 54% with a spontaneous and 46% a drug-induced type 1 ECG pattern. One-third had syncope, two-thirds were asymptomatic. A total of 245 subjects underwent electrophysiologic study (EPS) and 110 received an ICD. During follow-up (at median length 40 months [IQ 20-67]), 17 subjects had major arrhythmic events (MAE); 14 were resuscitated from VF and 3 experienced SCD. The investigators noted that both a spontaneous type 1 ECG pattern BrS and syncope significantly increased the risk for SCD (2.6 and 3.0% event rate per year vs. 0.4 and 0.8%). MAE occurred in 14% of subjects with positive EPS, but in no subjects with negative EPS and in 5.3% of subjects without EPS. On the basis of the data, the authors concluded that a multi-parametric approach (including syncope, family history of SD, and positive EPS) helps to identify populations with type 1 BrS who are at highest risk for SCD (Delise, 2011).
Regarding ARVD/C, the 2012 focused update (Tracy, 2012) to the 2008 ACCF/AHA/HRS Guidelines for Device-based Therapy of Cardiac Rhythm Abnormalities (Epstein, 2008) continued to inform that:
It is evident that there is not yet clear consensus on the specific risk factors that identify those patients with ARVD/C in whom the probability of SCD is sufficiently high to warrant an ICD for primary prevention. In the future, the results of large prospective registries with rigorous enrollment criteria for patients with ARVD/C in whom ICDs have been placed for primary prevention will give insights into the optimal risk stratification techniques for primary prevention. In the meantime, individualized decisions for primary prevention of SCD must be based on experience, judgment, and the available data. In considering this decision, the clinician should be mindful that in patients with ARVD/C, the ICD has proved safe and reliable in sensing and terminating sustained ventricular arrhythmias, however, SCD is rare in the available clinical series, whereas appropriate ICD shocks are common (Tracy, 2012).
On September 28, 2012 the U.S. Food and Drug Administration (FDA) granted clearance for the first subcutaneous ICD device, the S-ICD® System, (developed by Cameron Health® , Inc., now owned by Boston Scientific Corp., San Clemente, CA). According to the FDA press release:
The S-ICD System is cleared to provide an electric shock to the heart (defibrillation) when the individual's heart is beating at a dangerous level or abnormally fast (ventricular tachyarrhythmias). It is approved only for individuals who do not require a pacemaker or pacing therapy.
This press release went on to say: "The S-ICD System provides an alternative for treating patients with life-threatening heart arrhythmias for whom the routine ICD placement procedure is not ideal," said Christy Foreman, director of the Office of Device Evaluation at FDA's Center for Devices and Radiological Health. "Some patients with anatomy that makes it challenging to place one of the implantable defibrillators currently on the market may especially benefit from this device."
The approved indications for use from the FDA (2012) are as follows:
The S-ICD System is intended to provide defibrillation therapy for the treatment of life threatening ventricular tachyarrhythmias in patients who do not have symptomatic bradycardia, incessant ventricular tachycardia, or spontaneous, frequently recurring ventricular tachycardia that is reliably terminated with anti-tachycardia pacing.
The FDA based its approval on data from a study of 321 subjects in which 304 trial participants were successfully implanted with the S-ICD System which was successful at converting all detected abnormal heart rhythms during a 6 month study period. As part of the approval, the FDA is requiring the manufacturer to conduct a postmarket study to assess the long-term safety and performance of the device and to assess differences in effectiveness across genders. The study will follow 1616 subjects for 5 years and has an estimated completion date of June 2018. At the present time, there is insufficient published data regarding the safety, efficacy and long-term outcomes from use of the S-ICD System, and further study is needed to confirm its usefulness as an alternative to conventional transvenous ICD devices (Bardy, 2010; Gold, 2012; Jarman, 2012; Köbe, 2012). Another technology report issued by AHRQ in 2012 commented on the potential future capability of the S-ICD device to reduce complication rates related to lead failure, but it also noted the substantial limitations of a device that does not utilize leads and lacks the ability to pace cardiac rhythms. The report concluded that longer term outcomes data is needed before the S-ICD device could be considered comparable to conventional ICD devices (ECRI, 2012). Although the evidence is evolving that demonstrates the safety/efficacy of the S-ICD System, particularly for certain limited populations with inadequate vascular access for an ICD device, to date, trial results are inadequate to support the widespread use of the S-ICD System for all the guideline-directed indications for ICD therapy (Saxon, 2013; Weiss, 2013).
On March 13, 2015 the EMBLEM™ S-ICD System (Boston Scientific Corp., St. Paul, MN) obtained pre-market clearance from the FDA for indications very similar to the original S-ICD System for individuals who are at risk for SCD but who do not also require a pacemaker or pacing therapy. The FDA required that a post-approval study be conducted by the manufacturer. This prospective cohort study (of 1616 subjects from approximately 50 investigational centers [including up to 150 in the US]) is underway with 5-year results expected on September 27, 2017. On August 9, 2016 the FDA cleared the Emblem MRI S-ICD System, which allows individuals with this subcutaneous device to safely undergo magnetic resonance (MR) imaging. The FDA has also allowed for MR conditional labeling for all previously implanted Emblem S-ICD Systems. According to the manufacturer, the company is also actively pursuing MRI compatibility for their currently approved implanted cardiac defibrillation and cardiac resynchronization therapy systems via the global ENABLE MRI study.
In 2015, 2-year results from a pooled analysis of the IDE study and the EFFORTLESS Registry were published. The Evaluation oF Factors ImpacTing CLinical Outcome and Cost EffectiveneSS of the S-ICD (EFFORTLESS S-ICD) Registry is an ongoing, observational, non-randomized, standard-of-care evaluation designed to demonstrate the early, mid- and long-term clinical effectiveness of the S-ICD System for adults with ventricular tachyarrhythmias. This manufacturer sponsored registry is being conducted at 50 centers outside the US, where the S-ICD device has been available since 2009. Trial subjects will be followed for up to 60 months (NCT01085435). The S-ICD® System Clinical Investigation (IDE) study, which was also sponsored by Boston Scientific Corp., is an ongoing, prospective, non-randomized, multicenter clinical study without a control group, which is being conducted in the United States, Europe, and New Zealand. The IDE study included 314 adults who were successfully implanted with the S-ICD device for a standard indication for an ICD, who neither required pacing nor had documented pace-terminable ventricular tachycardia. The primary safety end point was the 180-day complication-free rate, compared with a pre-specified performance goal of 79%. The primary effectiveness end point was the induced ventricular fibrillation conversion rate, compared with a pre-specified performance goal of 88%, with success defined as 2 consecutive ventricular fibrillation conversions of 4 attempts. Detection and conversion of spontaneous episodes were evaluated over a mean duration of 11 months. The 180-day system complication-free rate was 99%, and sensitivity analysis of the acute ventricular fibrillation conversion rate was > 90% in the entire cohort. There were 38 discrete spontaneous episodes of ventricular tachycardia/ventricular fibrillation recorded in 21 subjects (6.7%), all of which successfully converted. Thus far, a total of 41 subjects (13.1%) have received an inappropriate shock (NCT01064076; Weiss, 2013).
The 2-year pooled results of the IDE study and EFFORTLESS Registry included 882 subjects who underwent implantation of the S-ICD and were followed for 651 ± 345 days. Spontaneous ventricular tachyarrhythmia (VT)/ventricular fibrillation (VF) events (n=111) were treated in 59 subjects; 100 (90.1%) events were terminated with 1 shock, and 109 events (98.2%) were terminated within the 5 available shocks. The estimated 3-year inappropriate shock rate was 13.1%. Estimated 3-year, all-cause mortality was 4.7% (95% confidence Interval [CI]: 0.9% to 8.5%), with 26 deaths (2.9%). Device-related complications occurred in 11.1% at 3 years. There were no electrode failures, and no S-ICD–related endocarditis or bacteremia occurred. Three devices (0.3%) were replaced for right ventricular pacing. The 6-month complication rate decreased by quartile of enrollment (Q1: 8.9%; Q4: 5.5%), and there was a trend toward a reduction in inappropriate shocks (Q1: 6.9%; Q4: 4.5%). The authors concluded that the S-ICD system demonstrated high efficacy for VT/VF. Complications and inappropriate shock rates were reduced consistently with strategic programming and as operator experience increased (Burke, 2015). The S-ICD device has shown comparable efficacy to transvenous ICDs in terminating ventricular arrhythmias in the IDE trial (Burke, 2015) and the EFFORTLESS S-ICD Registry (Weiss, 2013). The outcomes data from these trials, reported thus far, is considered sufficient to demonstrate the safety and efficacy of the S-ICD devices for a limited subset of individuals who do not have a pacing requirement.
At this time, the data on the use of ICD therapy in children is limited to observational studies, case series or extrapolation from prospective trials in adults. In 2008, Berul reported results of a multicenter retrospective case series taken from an ICD registry of pediatric subjects and subjects with CHD. The median age of this study population was 16 years, although some adults were included up to the age of 54 years. Registry data from a total of 443 subjects were included over a 12 year study period. The most common diagnoses were tetralogy of Fallot and HCM. ICD implantation was performed for primary prevention in 52% of study participants and for secondary prevention in 48%. Over a 2 year period of follow-up, appropriate shocks occurred in 26% of test subjects and inappropriate shocks occurred in 21%, which were mainly attributable to lead failure (14%), sinus or atrial tachycardias (9%), and/or oversensing (4%). Overall, appropriate shocks were observed in 66 of 290 (23%) pediatric subjects (age < 18 years) and in 39 of 119 (33%) adult subjects (over age 18 years) in this cohort (p<0.05, chi-square test). There were no differences seen in subgroup testing among different diagnostic categories (primary electrical diseases vs. congenital heart disease vs. cardiomyopathies) for either pediatric or adult test subjects. Among the study cohort, there was a total of 18 deaths (4% all-cause mortality) during follow-up, of which only 4 (1%) were known to be SCD or documented fatal arrhythmia. The non-sudden deaths were attributed to progressive congestive heart failure, pulmonary embolism, cerebrovascular accident, or unknown (non-sudden) etiology. A total of 16 study participants (3.6%) underwent orthotopic heart transplant at some point following their ICD implantation. They did not receive a new ICD system during or following transplant, and 3 of these 16 individuals subsequently died after transplantation. The authors' conclusions from this series, as well as that of other similar pediatric studies, suggest potential benefit to ICD therapy in children, particularly in those implanted for secondary prevention, where high rates of appropriate shocks were reported in the Berul study (32%), compared with primary prevention subjects (18%; p<0.001) (Berul, 2008; Gradaus, 2004; Silka, 1993). Additional observational retrospective data analysis studies have provided further evidence of clinical benefit from ICD therapy in selected pediatric subgroups at risk for SCD, such as HCM, DCM, and CHD (Kaski, 2007; Pahl, 2012; Von Bergen, 2011).
There remains limited data on the clinical utility of ICD in children for many conditions which would commonly be treated with ICD in adults. Based on specialty society input and opinions from the practice community, it was determined that ICD therapy should be made available to children based on the currently accepted adult indications for ICD, subject to the expert evaluations and treatment discretion of the treating physician in collaboration with the child's parents or legal guardians (Alexander, 2004; Berul, 2008; Decker, 2009; Dimitrow, 2010; Epstein, 2008; Gersh, 2011; Monserrat, 2003; Silka, 1993).
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 4 to 6 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 transvenous 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 that are implanted via a transvenous approach and 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. These conventional transvenous ICD devices differ from the new subcutaneous device which is implanted under the skin along the bottom of the rib cage and breast bone. Because the lead is placed under the skin, rather than through a vein into the heart (that is, the transvenous approach), a physician can implant the device without accessing the individual's blood vessels or heart and without the need for fluoroscopic guidance. This new subcutaneous ICD device, the S-ICD® System, (Cameron Health® , Inc., San Clemente, CA), obtained clearance from the FDA on September 28, 2012.
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.
Brugada syndrome (BrS): An autosomal-dominant inherited arrhythmic disorder characterized by ST elevations with successive negative T waves in the right precordial leads without structural cardiac abnormalities. Individuals with BrS are at risk for sudden cardiac death (SCD) due to ventricular fibrillation (VF). Mutations in the SCN5A gene represent the most common genotype responsible for BrS but mutations in additional genes have also been associated with BrS and risk for SCD.
Cardiomyopathy (CM): A disease in which the heart muscle becomes inflamed affecting cardiac function. There are multiple types of CM, (with the three main types being dilated, hypertrophic, and restrictive [see below]):
Congestive Heart Failure (CHF), also referred to as Heart Failure (HF): 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).
According to the 2012 European Society of Cardiology, American College of Cardiology Foundation, American Heart Association, and the World Heart Federation (ESC/ACCF/AHA/WHF) Expert Consensus Document: Third Universal Definition of Myocardial Infarction, the following definitions are provided for acute evolving MI and prior MI:
Acute MI is defined as – Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin [cTn]) with at least one value above the 99th percentile upper reference limit (URL) and with at least one of the following:
Prior MI is defined as – Any one of the following:
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:
Non-sustained/Sustained Ventricular Tachycardia: Ventricular tachycardia is considered non-sustained (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).
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).
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."
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 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 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.
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:
|00534||Anesthesia for transvenous insertion or replacement of pacing cardioverter-defibrillator|
|33202||Insertion of epicardial electrode(s); open incision (eg, thoracotomy, median sternotomy, subxiphoid approach) [when specified as ICD]|
|33203||Insertion of epicardial electrode(s); endoscopic approach (eg, thoracoscopy, pericardioscopy) [when specified as ICD]|
|33216||Insertion of a single transvenous electrode, permanent pacemaker or implantable defibrillator [when specified as ICD]|
|33217||Insertion of 2 transvenous electrodes, permanent pacemaker or implantable defibrillator [when specified as ICD]|
|33240||Insertion of implantable defibrillator pulse generator only; with existing single lead|
|33230||Insertion of implantable defibrillator pulse generator only; with existing dual leads|
|33231||Insertion of implantable defibrillator pulse generator only; with existing multiple leads|
|33249||Insertion or replacement of permanent implantable defibrillator system with transvenous lead(s), single or dual chamber|
|33270||Insertion or replacement of permanent subcutaneous implantable defibrillator system, with subcutaneous electrode, including defibrillation threshold evaluation, induction of arrhythmia, evaluation of sensing for arrhythmia termination, and programming or reprogramming of sensing or therapeutic parameters, when performed|
|33271||Insertion of subcutaneous implantable defibrillator electrode|
|93640||Electrophysiologic evaluation of single or dual chamber pacing cardioverter-defibrillator leads including defibrillation threshold evaluation (induction of arrhythmia, evaluation of sensing and pacing for arrhythmia termination) at time of initial implantation or replacement;|
|93641||Electrophysiologic evaluation of single or dual chamber pacing cardioverter-defibrillator leads including defibrillation threshold evaluation (induction of arrhythmia, evaluation of sensing and pacing for arrhythmia termination) at time of initial implantation or replacement; with testing of single or dual chamber pacing cardioverter-defibrillator pulse generator|
|C1721||Cardioverter-defibrillator, dual chamber (implantable)|
|C1722||Cardioverter-defibrillator, single chamber (implantable)|
|C1777||Lead, cardioverter-defibrillator, endocardial single coil (implantable)|
|C1882||Cardioverter-defibrillator, other than single or dual chamber (implantable)|
|C1895||Lead, cardioverter-defibrillator, endocardial dual coil (implantable)|
|C1896||Lead, cardioverter-defibrillator, other than endocardial single or dual coil (implantable)|
|G0448||Insertion or replacement of a permanent pacing cardioverter-defibrillator system with transvenous lead(s), single or dual chamber with insertion of pacing electrode, cardiac venous system, for left ventricular pacing|
|02H40KZ-02H44KZ||Insertion of defibrillator lead into coronary vein [by approach; includes codes 02H40KZ, 02H43KZ, 02H44KZ]|
|02H60KZ-02H74KZ||Insertion of defibrillator lead into atrium [right or left, by approach; includes codes 02H60KZ, 02H63KZ, 02H64KZ, 02H70KZ, 02H73KZ, 02H74KZ]|
|02HK0KZ-02HL4KZ||Insertion of defibrillator lead into ventricle [right or left, by approach; includes codes 02HK0KZ, 02HK3KZ, 02HK4KZ, 02HL0KZ, 02HL3KZ, 02HL4KZ]|
|02HN0KZ-02HN4KZ||Insertion of defibrillator lead into pericardium [by approach; includes codes 02HN0KZ, 02HN3KZ, 02HN4KZ]|
|0JH608Z-0JH838Z||Insertion of defibrillator generator into subcutaneous tissue and fascia [chest or abdomen, by approach; includes codes 0JH608Z, 0JH638Z, 0JH808Z, 0JH838Z]|
|All diagnoses including, but not limited to, the following:|
|I21.01-I21.A9||Acute myocardial infarction|
|I22.0-I22.9||Subsequent ST elevation (STEMI) and non-ST elevation (NSTEMI) myocardial infarction|
|I24.0-I24.9||Other acute ischemic heart disease|
|I25.10- I25.119||Atherosclerotic heart disease of native coronary artery|
|I25.2||Old myocardial infarction|
|I25.810-I25.9||Other forms of chronic ischemic heart disease|
|I45.81||Long QT syndrome|
|I47.0||Re-entry ventricular arrhythmia|
|I49.01- I49.02||Ventricular fibrillation, ventricular flutter|
|Q24.8||Other specified congenital malformations of heart [Brugada syndrome]|
|Q24.9||Congenital malformation of heart, unspecified (congenital disease of heart)|
|R55||Syncope and collapse|
|Z86.74||Personal history of sudden cardiac arrest|
When services are Investigational and Not Medically Necessary:
For the procedure codes listed above when criteria are not met, or when the code describes a procedure indicated in the Position Statement section as investigational and not medically necessary.
Peer Reviewed Publications:
Government Agency; Medical Society; and Other Authoritative Publications:
|Websites for Additional Information|
EMBLEM S-ICD System
The use of specific product names is illustrative only. It is not intended to be a recommendation of one product over another, and is not intended to represent a complete listing of all products available.
|10/01/2017||Updated Coding section with 10/01/2017 ICD-10-CM diagnosis code and descriptor changes.|
|Reviewed||05/04/2017||Medical Policy & Technology Assessment Committee (MPTAC) review. Updated the formatting in the Position Statement section. The Rationale and References sections were updated.|
|Revised||05/05/2016||MPTAC review. The medically necessary criteria for ICD to treat individuals with Brugada syndrome have been revised to remove the criterion for EPS testing and to indicate that having EITHER one of the two criteria will meet medical necessity for ICD therapy. The Rationale, Coding and References sections were updated.|
|Revised||12/09/2015||MPTAC review. The MPTAC voted to approve a clarification to the S-ICD device statement to say the device is now considered medically necessary for certain at-risk individuals when criteria are met for a transvenous ICD device.|
|Revised||11/05/2015||MPTAC review. The stance for the subcutaneous device has changed to now be considered medically necessary when criteria are met. The title was changed to, "Cardioverter Defibrillators" to include the ICD and S-ICD devices. The Rationale, Coding and References sections were updated. Removed ICD-9 codes from Coding section; also removed associated post procedure SICD codes 33272, 33273, 93260, 93261, 93644.|
|Reviewed||08/06/2015||MPTAC review. The Rationale, Definitions and References were updated.|
|Revised||05/07/2015||MPTAC review. The criteria for ICD in ischemic cardiomyopathy have been clarified regarding LVEF ranges and NYHA functional classes when at least 40 days post-acute MI. The medically necessary indications for transvenous ICD have been expanded to include Brugada syndrome when criteria are met. The Rationale, Coding and References sections were updated.|
|01/01/2015||Updated Coding section with 01/01/2015 CPT changes; removed codes 0319T, 0320T, 0321T, 0322T, 0323T, 0324T, 0325T, 0326T, 0327T, 0328T deleted 12/31/2014.|
|Reviewed||08/14/2014||MPTAC review. Updated the Rationale and Reference sections.|
|Revised||02/13/2014||MPTAC review. The medically necessary criteria for ischemic and nonischemic cardiomyopathy were revised from 6 months to 3 months of prior optimal medical therapy, now referred to as, "Guideline-directed medical therapy" (GDMT). The Rationale and References were updated.|
|Revised||02/14/2013||MPTAC review. The medically necessary indications for ICD therapy were revised to apply to both adults and children. The Rationale and References were updated.|
|Revised||11/08/2012||MPTAC review. Position statements were revised to clarify use of transvenous ICD devices. A new statement was added to consider subcutaneous devices as investigational and not medically necessary. Rationale, Background and References were updated. Updated Coding section with 01/01/2013 CPT changes.|
|Reviewed||02/16/2012||MPTAC review. The Rationale and References were updated.|
|01/01/2012||Updated Coding section with 01/01/2012 CPT and HCPCS changes.|
|Revised||02/17/2011||MPTAC review. Medically necessary criterion #3 was amended to remove "VF induced at electrophysiologic study." Medically necessary criteria #5 and #6 were amended to add a requirement for "six months of optimum medical therapy." The Rationale, References and Websites updated.|
|Revised||11/18/2010||MPTAC review. Medically necessary criterion #3 was clarified and the MPTAC voted to add a new criterion to the medically necessary indications for ICD for individuals with HCM and two or more major risk factors for SCD. Final criteria for this additional indication were developed after the meeting and circulated to MPTAC for review and approval by email vote which concluded on 12/01/2010 with approval of the criteria. The Rationale, Definitions and References were updated.|
|Revised||11/19/2009||MPTAC review. Medical necessity criterion for adult indications #6 was revised to remove LV dysfunction due to prior MI who are at least 40 days post and was replaced with, "Those with ischemic cardiomyopathy and who have had no MI in the past 40 days and have an LVEF of less than 30%, and are in NYHA functional Class I" (for consistency with the 2009 updated ACC/AHA Guideline on Heart Failure in Adults, Hunt, et al; 2009). The Rationale, Definitions and References were also updated. Updated Coding section with 01/01/2010 CPT changes.|
|Revised||11/20/2008||MPTAC review. The medical necessity criteria have been revised to align with the 2008 ACC/AHA/HRS Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities. Pediatric indications considered medically necessary have now been added to the position statement section. The Rationale section and References were also updated.|
|Reviewed||11/29/2007||MPTAC review. Criteria for NIDCM were reviewed with consideration for the addition of irreversible disease to the indications considered medically necessary. However, MPTAC approved the document as written with no change to current criteria. The phrase "investigational/not medically necessary" was clarified to read "investigational and not medically necessary." Rationale and references were updated. Coding section was updated with 01/01/08 CPT/HCPCS changes; removed HCPCS G0297, G0298, G0299, G0300 deleted 12/31/2007.|
|Reviewed||03/08/2007||MPTAC review. Rationale, References, and Coding sections have been updated.|
|01/01/2007||Updated Coding section with 01/01/2007 CPT/HCPCS changes; removed CPT 33245, 33246 deleted 12/31/2006.|
|Reviewed||03/23/2006||MPTAC review. References were updated to include the recently released updated TEC Assessment Directories (2) and additional published articles.|
|11/18/2005||Added reference for Centers for Medicare and Medicaid Services (CMS) – National Coverage Determination (NCD).|
|Revised||04/28/2005||MPTAC review. Revision based on Pre-merger Anthem and Pre-merger WellPoint Harmonization.|
|Pre-Merger Organization||Last Review Date||Document Number||Title|
|09/19/2003||SURG.00033||Automatic Implantable Cardioverter-Defibrillator (AICD), Cardiac Resynchronization Therapy Defibrillator (CRT-D), Biventricular Pacemakers|
|WellPoint Health Networks, Inc||06/24/2004||9.04.03||Implantable Cardioverter-defibrillators|