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Arrhythmia and Survival Outcomes Among Black Patients and White Patients With a Primary Prevention Defibrillator

Originally publishedhttps://doi.org/10.1161/CIRCULATIONAHA.123.065367Circulation. 2023;148:241–252

Abstract

BACKGROUND:

Black Americans have a higher risk of nonischemic cardiomyopathy (NICM) than White Americans. We aimed to evaluate differences in the risk of tachyarrhythmias among patients with an implantable cardioverter-defibrillator (ICD).

METHODS:

The study population comprised 3895 ICD recipients in the United States enrolled in primary prevention ICD trials. Outcome measures included ventricular tachyarrhythmia (VTA), atrial tachyarrhythmia (ATA), ICD therapies, VTA burden (using Andersen-Gill recurrent event analysis), death, and the predicted benefit of the ICD. All events were adjudicated blindly. Outcomes were compared between self-reported Black patients versus White patients with cardiomyopathy (ischemic and NICM).

RESULTS:

Black patients were more likely to be female (35% versus 22%) and younger (57±12 versus 62±12 years) with a higher frequency of comorbidities. In NICM, Black patients had a higher rate of first VTA, fast VTA, ATA, and appropriate and inappropriate ICD therapy (VTA ≥170 bpm, 32% versus 20%; VTA ≥200 bpm, 22% versus 14%; ATA, 25% versus 12%; appropriate therapy, 30% versus 20%; and inappropriate therapy, 25% versus 11%; P<0.001 for all). Multivariable analysis showed that Black patients with NICM experienced a higher risk of all types of arrhythmia or ICD therapy (VTA ≥170 bpm, hazard ratio [HR] 1.71; VTA ≥200 bpm, HR 1.58; ATA, HR 1.87; appropriate therapy, HR 1.62; inappropriate therapy, HR 1.86; P≤0.01 for all), higher burden of tachyarrhythmias or therapies (VTA, HR 1.84; appropriate therapy, HR 1.84; P<0.001 for both), and a higher risk of death (HR 1.92; P=0.014). In contrast, in ischemic cardiomyopathy, the risk of all types of tachyarrhythmia, ICD therapy, or death was similar between Black patients and White patients. Both Black patients and White patients derived a significant and similar benefit from ICD implantation.

CONCLUSIONS:

Among patients with NICM with an ICD for primary prevention, Black patients compared with White patients had a high risk and burden of VTA, ATA, and ICD therapies with a lower survival rate. Nevertheless, the overall benefit of the ICD was maintained and was similar to that of White patients.

Clinical Perspective

What Is New?

  • Black patients have a higher risk than White patients of developing nonischemic cardiomyopathy but are underrepresented in clinical trials of implantable cardioverter defibrillators.

  • This analysis represents the largest group of self-identified Black patients implanted in the United States with an implantable cardioverter defibrillators for primary prevention with adjudication of all arrhythmic events.

What Are the Clinical Implications?

  • In patients with nonischemic cardiomyopathy, self-identified Black patients compared with White patients experienced an increased incidence and burden of ventricular tachyarrhythmia, atrial tachyarrhythmia, and implantable cardioverter defibrillators therapies.

  • These differences were not observed in Black patients versus White patients with ischemic cardiomyopathy.

  • Although Black patients with nonischemic cardiomyopathy were implanted at a significantly younger age (57±12 versus 62±12 years), they experienced a 2-fold higher rate of all-cause mortality during a mean follow-up of 3 years compared with White patients.

  • These findings highlight the need for early intervention with an implantable cardioverter defibrillators, careful monitoring, and intensification of heart failure and antiarrhythmic therapies among Black patients with nonischemic cardiomyopathy.

Editorial, see p 253

In the United States, heart failure (HF) disproportionately affects Black patients, a population in whom the prevalence of the disease is higher, the cause is more often nonischemic cardiomyopathy (NICM), and the disease trajectory is more severe when compared with White patients.1–3 Those differences are less evident in patients with ischemic cardiomyopathy (ICM).4–6

There are conflicting findings when looking at outcomes of Black patients with HF. Some studies have suggested no significant differences in patient-reported health status between Black patients and White patients with HF,7,8 whereas others suggest that Black patients experience significantly worse clinical outcomes, including cardiovascular mortality and readmissions.9,10 These conflicting results are also evident when assessing the risk of ventricular tachyarrhythmia (VTA) or implantable cardioverter-defibrillator (ICD) therapies among Black patients. Several reports have shown that Black patients with HF experience increased risk of developing VTA, as well as sudden cardiac death (SCD), compared with White patients.8,9 On the other hand, several studies have reported a similar VTA risk between Black patients and White patients.7,8

Black patients are underrepresented in all major ICD randomized clinical trials, generally accounting for <20% of a study cohort, which may be contributing to inconsistent racial differences in outcomes. In addition, implantation of an ICD has been shown to be significantly less common among Black patients compared with White patients, especially for primary prevention, despite data suggesting increased risk of SCD.8,9 None of the aforementioned studies focused on NICM, which is more prevalent and has a more severe HF trajectory among Black patients compared with White patients, possibly because of associated comorbidities, such as diabetes, hypertension, or morbid obesity.11–15 Thus, ICD candidacy for primary prevention does not consider potential differences in the risk of arrhythmic events, appropriate and inappropriate device therapy, or survival among Black patients and White patients on the basis of type of cardiomyopathy.

In this study, we aimed to assess differences in arrhythmic and survival outcomes between Black patients and White patients according to cardiomyopathy type among patients enrolled in the US landmark ICD trials, with a focus on the risk of first and recurrent VTA, device-detected atrial tachyarrhythmia (ATA), appropriate and inappropriate ICD therapy, and all-cause mortality rate. Outcomes were assessed separately in patients with NICM or ICM.

METHODS

The data that support the findings of this study are available from the corresponding author upon reasonable request.

Study Population

The study cohort consisted of 3895 US patients with an ICD or cardiac resynchronization therapy–defibrillator (CRT-D) who were enrolled in 5 primary prevention ICD studies conducted between July 1997 and January 2017. Design, study protocol, and results of each of these trials have been published previously. In brief, MADIT-II (Multicenter Automatic Defibrillator Implantation Trial II) and MADIT-Risk (MADIT-II Risk Score) enrolled a total of 1130 patients implanted with an ICD for primary prevention therapy because of ICM. The main inclusion criteria were previous myocardial infarction and a left ventricular ejection fraction (LVEF) ≤30%.16 MADIT-CRT (Multicenter Automatic Defibrillator Implantation With Cardiac Resynchronization Therapy) enrolled 1814 patients with HF (993 ICM and 821 NICM), LVEF ≤30%, QRS ≥130 milliseconds, and New York Heart Association (NYHA) functional class I or II. Patients were randomly assigned in a 3:2 ratio to receive CRT-D (n=1083) or an ICD alone (n=731).17 MADIT-RIT (Multicenter Automatic Defibrillator Implantation Trial–Reduce Inappropriate Therapy) enrolled 1465 patients (838 ICM and 627 NICM) and all patients met guideline criteria to receive an ICD or CRT-D for primary prevention.18 RAID (Ranolazine Implantable Cardioverter-Defibrillator Trial) enrolled 1012 high-risk patients with an ICD (primary prevention, n=669; secondary prevention, n=343) who were randomized to treatment with ranolazine or placebo. Treatment with ranolazine did not affect the VTA risk or the all-cause mortality risk significantly. For the current study, we included primary prevention RAID participants only (n=669).19

For the primary analysis, the total study cohort was stratified by NICM and ICM. Outcomes in each type of heart disease cohort were compared between self-identified Black patients and White patients. All categorizations are on the basis of self-identification at the time of enrollment. Patients could identify themselves as more than one race or ethnicity. No patients identified themselves as Black and White at the same time. All Black patients and White patients were unique patients. The study design and population are summarized in Figure S1. Information on main inclusion criteria, interventions, years of enrollment, and frequency of Black patients per year and study are summarized in Tables S1 and S2.

Each study was approved by the institutional review boards at the respective enrolling sites before participation. All patients provided informed consent before enrollment into the respective trials.

Definitions and End Points

In all trials, ICM was defined by a documented (Q-wave or enzyme-positive) previous myocardial infarction >90 days before enrollment or ≥1 previous coronary artery bypass graft surgeries or percutaneous coronary interventions (balloon or stent angioplasty) >90 days before enrollment. NICM was defined by an abnormality of the myocardium capable of producing HF that does not meet the criteria for ICM. Detailed definition is found in Table 1 of Appendix S1.

In all MADIT trials and in RAID, device interrogations were reviewed and adjudicated blindly by an independent committee of at least 2 experienced electrophysiologists and cardiologists using identical definitions. Details of device programming and VTA definitions are provided in Table 3 of Appendix S1. In all studies, ICD programming was similar for Black patients and White patients.

First Arrhythmic Event End Points

The primary end point of the current study was the first occurrence of VTA, defined as ICD-recorded, treated, or monitored sustained ventricular tachycardia ≥170 bpm or ventricular fibrillation (VF). Secondary end points included fast VTA ≥200 bpm, any ATA event (atrial fibrillation or flutter [AF] or supraventricular tachycardia [SVT]), appropriate ICD therapy, and inappropriate ICD therapy.

Arrhythmic Burden End Points

Additional analysis was performed to assess the burden of all types of arrhythmia listed previously (in a recurrent event analysis). Arrhythmic burden was defined as the total number of events per patient during follow-up. Analysis included all patients but was limited to 10 events per patient (censored at 10 events) to lessen the effect of participants with large counts of arrhythmic occurrences.

Arrhythmias were defined by the adjudication committee on the basis of combined evaluation of frequency, QRS morphology, and regularity of the rhythm. A VTA event was defined as lasting >30 seconds or if therapy was administered and terminated the arrhythmia (including polymorphic ventricular tachycardia). Detection zone was ≥145 bpm in all studies. Arrhythmia events detected by the ICD and CRT-D devices were categorized as ATA if they included the occurrence of AF or other supraventricular tachyarrhythmias. Regular SVT included regular atrial tachycardias, such as atrioventricular reentry tachycardia, and atrial tachycardia with 1:1 conduction. All devices in the current study were at least dual-chamber devices (1 electrode in the right atrium and 1 in the right ventricle). Inappropriate therapies attributable to nonarrhythmic causes (eg, lead malfunction, device undersensing) were excluded.

Mortality Outcomes

To account for the competing risk of death, we evaluated the following mortality outcomes: all-cause mortality and nonarrhythmic mortality (defined as death without experiencing sustained fast VTA at any time during follow-up after ICD implantation).

Social Determinants of Health and Medication Compliance

To account for the effect of potential social determinants of health on our findings, we carried out a secondary analysis in which findings were adjusted further for the Gini index. The Gini index is a socioeconomic validated index that measures the extent to which the income distribution among units within an area deviates from a perfectly equal distribution and ranges from 0 for perfectly equitable distributions to 1 where all income is concentrated in 1 individual.20 The Gini index value was obtained on the basis of zip codes of the enrolling sites and their catchment areas. In the United States, a Gini index ≥0.50 corresponds with severe income disparity and represents very low socioeconomic status.20

Medication compliance was defined as the percent of patients who reported continuing to take their medication at 1 year.

Statistical Analysis

Categorical data are summarized as frequencies and percentages (in parentheses). Continuous data are summarized as mean±SD. Baseline characteristics were compared between Black patients and White patients using the Wilcoxon rank-sum test (for continuous variables) or χ2 test (for categorical variables) in each cardiomyopathy separately.

Interaction testing using Cox regression (end point: VTA) between Black patients and cardiomyopathy type was performed. Kaplan-Meier cumulative probabilities were used to display graphically the cumulative risk in Black patients and White patients for the outcomes over time. The log-rank test was used for determination of statistical significance.

Multivariable Cox proportional hazards regression analysis was used to estimate hazard ratios (HRs) for Black patients versus White patients for the mentioned outcomes. The proportional hazard assumption was tested for all Cox models and was found to be valid. For the multivariable adjustment, relevant clinical covariates were determined on the basis of the results of a stepwise selection process and were included if statistically significant at P<0.05 (for both entry and retention) in multivariable models for either end point (VTA or death). Potential risk factor candidates are shown in Table S4. We used a dichotomized functional form of continuous variables and continuous variable. Thresholds for categorization of numeric variables were prespecified using clinically well-accepted criteria.

The following independent predictors were identified: age, sex, smoking, diastolic blood pressure, CRT-D, NYHA class, history of HF hospitalization, LVEF, and history of ATA. These predictors were included in the multivariable model. All models were further stratified by study type (MADIT-II, MADIT-RISK, MADIT-CRT, MADIT-RIT, and RAID). In addition, for the sensitivity analysis, models were further adjusted for medications (detailed in Table S6), heart rate, and body mass index, and were stratified by socioeconomic quintile on the basis of their Gini index. For the primary end point of VTA, additional competing risk modeling using Fine and Gray methodology, and using death as the competing risk for VTA, was performed to validate the consistency of our findings. Anderson Gill non–gap-time model, using a robust variance estimator for patient heterogeneity, was used to estimate the hazard ratios for recurrent VTA events, recurrent fast VTA ≥200 bpm, recurrent appropriate ICD shocks, and recurrent appropriate ICD antitachycardia pacing. Models were adjusted for covariates as noted previously. Mean cumulative event rate was presented using Ghosh-Lin curves to display mean number of recurrent events per patient as appropriate.

To assess the benefit of ICD and CRT-D versus no respective therapy in Black patients and in White patients, we carried out 2 separate additional analyses that included all patients enrolled in MADIT-II and in MADIT-CRT. In patients with a defibrillator, the predicted benefit of the defibrillator can be assessed by calculating the risk of fast VTA minus the risk of death without any previous fast VTA in life.21,22 In accordance, within each group (Black patients and White patients), we used cumulative incidence function curves to estimate the probability of first VTA as the event of interest and the probability of death without previous VTA as a competing risk. The P value is obtained from a competing risk Fine and Gray hazard model analysis.

All tests of significance were 2-tailed with P<0.05 accepted to indicate statistical significance. Analysis was carried out using SAS statistical software (version 9.4; SAS Institute).

RESULTS

Baseline Characteristics

Among all ICD recipients, 638 (16%) self-identified as Black and 3257 as White (84%). Mean age was 59±11 years and 245 (38%) were women. Black patients were more likely to have NICM compared with ICM (26% versus 11%; P<0.001), whereas White patients were more likely to have ICM compared with NICM (P<0.001). Baseline characteristics of Black patients and White patients with NICM or ICM are shown in Table 1. In both types of heart disease, self-identified Black patients compared with White patients were significantly younger (ICM 62±11 versus 66±10 years; NICM 57±12 versus 62±12 years; P<0.001 for each comparison), more likely to be female, and exhibited a higher frequency of cardiovascular comorbidities, including hypertension and diabetes (P<0.001 for all comparisons with White patients). History of previous ATA and guideline-directed medical therapies were similar between Black patients and White patients, with the exception of aldosterone antagonists, diuretics, hydralazine, and nitrates, which were prescribed at a significantly higher rate among Black patients with ICM or NICM (Table 1).

Table 1. Baseline Characteristics of the Study Cohort, by Cardiomyopathy Type

Clinical characteristicsIschemicP valueNonischemicP value
White patients (n=2276)Black patients (n=290)White patients (n=981)Black patients (n=348)
Age, yrs66±1062±11<0.00162±1257±12<0.001
Female sex326 (14)90 (31)<0.001380 (39)155 (45)0.058
Hispanic ethnicity66 (3)6 (2)0.4534 (3)1 (0)0.002
Gini index0.49±0.050.52±0.06<0.0010.50±0.050.51±0.05<0.001
Gini index ≥0.5*639 (35)116 (53)<0.001262 (35)164 (58)<0.001
BMI, kg/m229±629±60.4230±732±8<0.001
Systolic BP, mm Hg123±18125±200.021122±17123±190.031
Diastolic BP, mm Hg71±1175±11<0.00172±1175±12<0.001
Heart rate, bpm70±1272±12<0.00171±1275±13<0.001
Ejection fraction, %26±625±70.02225±723±80.021
Ejection fraction ≤25%1189 (52)165 (57)0.14576 (59)244 (70)<0.001
CRT-D643 (28)60 (21)<0.001592 (60)156 (45)<0.001
LBBB536 (32)44 (25)0.047540 (69)97 (45)<0.001
QRS138±31131±330.019158±22149±24<0.001
NYHA ≥III1699 (75)247 (87)<0.001929 (96)330 (96)0.78
Hypertension1526 (67)247 (85)<0.001585 (60)283 (82)<0.001
Atrial arrhythmia450 (20)51 (18)0.34189 (20)63 (19)0.63
Diabetes806 (36)131 (45)<0.001211 (22)132 (38)<0.001
Current cigarette use342 (15)47 (17)0.45112 (12)43 (14)0.37
Previous CABG1271 (56)105 (36)<0.0016 (1)3 (1)0.76
Aldosterone antagonists374 (22)64 (28)0.039338 (34)150 (43)<0.001
Amiodarone129 (6)9 (3)0.06938 (4)19 (5)0.21
ACE inhibitor or ARB1618 (71)215 (74)0.26720 (73)235 (68)0.037
Aspirin1774 (78)215 (74)0.16558 (57)189 (54)0.41
β-blocker1946 (86)251 (87)0.58924 (94)334 (96)0.20
Digitalis639 (28)79 (27)0.78241 (25)105 (30)0.041
Diuretic1428 (63)215 (74)<0.001638 (65)285 (82)<0.001
Statins1738 (76)203 (70)0.019489 (50)160 (46)0.22
Hydralazine50 (2)24 (10)<0.00131 (2)44 (14)<0.001
Nitrates601 (23)75 (32)<0.00188 (6)46 (15)<0.001

Values are mean±SD or n (%). ACE indicates angiotensin-converting enzyme; ARB, angiotensin II receptor blocker; BMI, body mass index; BP, blood pressure; CABG, coronary artery bypass grafting; CRT-D, cardiac resynchronization therapy with a defibrillator; LBBB, left bundle branch block; and NYHA, New York Heart Association.

* In the United States, a Gini index >0.50 corresponds with severe income disparity and represents very low socioeconomic status.

† Atrial arrhythmia requiring medical treatment with ablation or medication.

Medication compliance at 1 year did not differ significantly between Black patients or White patients with ICM. In contrast, among patients with NICM, the compliance rate was significantly lower in Black patients compared with White patients for the following medications: aldosterone antagonists, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, β-blockers, diuretics, and statins. The reported rates for the remaining medications (ie, hydralazine, nitrates, aspirin, amiodarone, and digitalis) were similar (Table S5).

The Gini index (inversely related to socioeconomic status) was significantly higher for Black patients when compared with White patients for both cardiomyopathies (Table 1). A Gini index ≥0.5 (corresponding with severe income disparity) was significantly more prevalent in Black patients than in White patients (ICM: 53% versus 35%; NICM: 58% versus 35%; P<0.001).

Type of Cardiomyopathy

Analysis in the total population model showed a statistically significant interaction in the association of Black patients compared with White patients with the risk of the primary end point by the type of cardiomyopathy (ICM/NICM Pinteraction=0.0083). Therefore, outcomes herein are reported separately for patients with NICM or ICM.

Patients With NICM

First Event End Points

At 3 years, the Kaplan-Meier cumulative probability of a first VTA (defined as ventricular tachycardia ≥170 bpm or VF) was significantly higher among Black patients than White patients (34% versus 20%, respectively; P<0.001 for the overall difference during follow-up; Figure 1A). Fast VTA (defined as ventricular tachycardia ≥200 bpm or VF) occurred at a significantly higher rate among Black patients when compared with White patients (fast VTA: 24% versus 15%; Figure 1B), as well as appropriate ICD therapy (30% versus 20%, respectively; P<0.001) and inappropriate ICD therapy (25% versus 11%, respectively; P<0.001; Figure S2A and S2B, respectively). The cumulative rate of first appropriate antitachycardia pacing and the cumulative rate of first appropriate shock were also higher in Black patients compared with White patients (antitachycardia pacing: 26% versus 16%; shock: 16% versus 11%, respectively; P<0.01; Figure S3A and S3B).

Figure 1.

Figure 1. Cumulative probability of VTA in NICM. Three-year Kaplan-Meier cumulative probability for (A) sustained ventricular tachyarrhythmia (VTA) and (B) fast VTA ≥200 bpm in Black patients and White patients with nonischemic cardiomyopathy (NICM). Numbers outside the parentheses represent the size of the risk group at different points in time of follow-up (ie, the number of participants who have not yet had the event of interest, died, or were lost to follow-up); numbers inside the parentheses represent the cumulative event rate as calculated by the Kaplan-Meier estimator at each given time point among patients who are at still at risk of experiencing the end point.

The rate of first ATA, AF, and SVT were also significantly higher in Black patients compared with White patients (ATA 25% versus 12%, AF 9% versus 4%, SVT 21% versus 8%, respectively; P<0.001; Figure 2A and 2C).

Figure 2.

Figure 2. Cumulative probability of ATA, AF, and SVT in NICM. Three-year Kaplan-Meier cumulative probability of (A) atrial tachyarrhythmia (ATA), (B) atrial fibrillation (AF), and (C) supraventricular tachycardia (SVT) in Black patients and White patients with nonischemic cardiomyopathy (NICM). Numbers outside the parentheses represent the size of the risk group at different points in time of follow-up (ie, the number of participants who have not yet had the event of interest, died, or were lost to follow-up); numbers inside the parentheses represent the cumulative event rate as calculated by the Kaplan-Meier estimator at each given time point among patients who are at still at risk of experiencing the end point.

Consistent with the univariate findings, multivariable Cox modeling (Figure 3) adjusted for age, sex, smoking, diastolic blood pressure, LVEF, CRT-D, NYHA class, HF hospitalization, and history of ATA also showed that, compared with White patients with NICM, Black patients experienced a significantly higher risk of first VTA events/therapies, including 71% higher risk of sustained VTA, 72% increased risk of fast VTA (≥200 bpm), and 69% increased risk of a first appropriate ICD therapy (P<0.01 for all). Results were consistent replacing dichotomized with continuous variables (including LVEF and systolic blood pressure).

Figure 3.

Figure 3. Risk for first arrhythmic event, first ICD therapy, and death in NICM

. Multivariable Cox regression evaluating the association of Black versus White race with the development of arrhythmic end points, implantable cardioverter defibrillator (ICD) therapy, and death in patients with nonischemic cardiomyopathy (NICM). Models were adjusted for age, sex, smoking, diastolic blood pressure, left ventricular ejection fraction, cardiac resynchronization therapy–defibrillator, New York Heart Association class, history of heart failure hospitalization, and history of atrial tachyarrhythmia. Models were adjusted further for study type by stratification. SVT indicates supraventricular tachycardia; and VTA, ventricular tachyarrhythmia.

In addition, competing risk analysis, using death as the competing risk for VTA, demonstrated consistent findings (Black patients versus White patients: HR, 1.60 [95% CI, 1.17–2.18]; P<0.01 for the VTA ≥170 bpm end point). Multivariable results were also consistent for ATA end points. Thus, compared with White patients, Black patients experienced a significant 107% increased risk for any ATA, 71% increased risk for AF, 134% increased risk for SVT, and 156% increased risk for inappropriate therapy associated with ATA (Figure 3).

Recurrent Events End Points

Assessment of VTA burden showed similar findings. During follow-up, a total of 2581 VTA events occurred in 275 study patients with at least 1 event. At 3 years, the mean cumulative number of all types of arrhythmias or therapies was higher in Black patients than White patients (VTA, mean 1.0 versus 0.55 events per patient; fast VTA, mean 0.43 versus 0.24 events per patient; appropriate therapy, mean 0.43 versus 0.24 events per patient; inappropriate therapy, mean 0.43 versus 0.24 events per patient; P<0.001; Figure 4A and 4B and Figure S4A and S4B).

Figure 4.

Figure 4. The burden of ventricular tachyarrhythmia in NICM. Mean cumulative rate for recurrent events per patient stratified by study group for (A) ventricular tachyarrhythmia (VTA) and (B) fast VTA ≥200 bpm in Black patients and White patients with nonischemic cardiomyopathy (NICM). Numbers outside the parentheses represent the size of the risk group at different points in time of follow-up (ie, the number of participants who have not yet had the event of interest, died, or were lost to follow-up); the numbers inside the parentheses represent the cumulative mean event rate at designated points in time. This mean cumulative function incorporates all recurrent events over the follow-up time.

Multivariable analysis (Figure S5) confirmed these findings and showed that, compared with White patients, Black patients exhibited a higher risk of high VTA burden (HR 1.84), fast VTA (HR 1.28), ATA (HR 2.59), appropriate therapies (HR 1.84), and inappropriate therapies (HR 2.90; P<0.001 for all).

Subgroup Analysis

Interaction-term analysis showed that the increased risk of VTA among Black patients versus White patients with NICM was consistent regardless of age, sex, NYHA Class, the presence or absence of diabetes, the presence or absence of hypertension, and an ICD versus CRT-D device (Table 7 of Appendix S1).

Risk of Death

Although Black patients were significantly younger (57±12 versus 62±12 years), they experienced a 2-fold higher rate of all-cause mortality at 3 years compared with White patients (12% versus 6%; P<0.001 for the overall comparison during follow-up; Figure 5). Cox proportional hazards regression analysis confirmed these findings after multivariable adjustment (HR, 1.92 [95% CI, 1.16–3.16]; P=0.011; Figure 3).

Figure 5.

Figure 5. Cumulative probability of all-cause mortality in NICM. Three-year Kaplan-Meier cumulative probability of all-cause mortality in Black patients and White patients with nonischemic cardiomyopathy (NICM). Numbers outside the parentheses represent the size of the risk group at different points in time of follow-up (ie, the number of participants who have not yet had the event of interest, died, or were lost to follow-up); numbers inside the parentheses represent the cumulative event rate as calculated by the Kaplan-Meier estimator at each given time point among patients who are at still at risk of experiencing the end point.

Sensitivity Analysis

Further analysis adjusting for the original variables (as in Figure 3) and for additional potential differences between Black patients and White patients, including medications at baseline (β-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, aldosterone antagonists, diuretics, hydralazine, nitrates, statin, aspirin, amiodarone, or digitalis), body mass index, heart rate at baseline, and Gini index, demonstrated consistent findings (Table S6). Of note, a Gini index ≥0.5 was associated with an increased risk of death in patients with NICM (HR, 1.71 [95% CI, 1.04–2.83]; P=0.036). However, there was no statistically significant interaction between the Gini index and the association of NICM in Black patients versus White patients with increased risk of VTA and death (both Pinteraction>0.10), suggesting that the increased risk of arrhythmic and mortality outcomes among Black patients with NICM was maintained regardless of socioeconomic status.

Patients With Ischemic Cardiomyopathy

At 3 years, the Kaplan-Meier cumulative probability of a first VTA was similar among Black patients and White patients (22% versus 23%, respectively; P=0.55 for the overall difference during follow-up; Figure S6). The cumulative rate of first episode of fast VTA (19% versus 14%; P=0.15), appropriate ICD therapy (25% versus 23%; P=0.53), and inappropriate therapy (12% versus 11%; P=0.28) did not differ significantly between Black patients and White patients (Figure S6B through S6D).

Assessment of VTA burden showed similar findings. At 3 years, the mean cumulative number of all types of arrhythmias or therapies did not differ significantly between Black patients and White patients (Figure S7A through S7D).

The cumulative rate of all-cause mortality was also similar between Black patients and White patients despite Black patients being implanted at a younger age (15% versus 16%; P=0.42; Figure S8).

ICD and CRT-D Benefit in Black Patients and White Patients

The MADIT-II (total n=1232 patients, 747 [60%] allocated to ICD and 485 [40%] allocated to no ICD) and MADIT-CRT (total n=1820 patients, 1015 [56%] allocated to CRT-D and 805 [44%] allocated to ICD) analyses showed that the benefit of ICD or CRT-D therapy for the primary end point of the 2 trials is similar in Black patients and in White patients (MADIT-II: all-cause mortality HR for ICD versus no ICD, Black patients HR 0.69, White patients HR 0.64, interaction=0.90; MADIT-CRT: all-cause mortality or heart failure event HR for CRT-D versus ICD only, Black patients HR 0.79, White patients HR 0.67, Pinteraction=0.64).

DISCUSSION

Our study using a combined database of patients with ICM or NICM enrolled in MADIT trials and the recent RAID trial addresses differences in the risk of arrhythmic events and survival between Black patients and White patients with an ICD for primary prevention. Our findings show that in patients with NICM, self-identified Black patients compared with White patients have many differences, including a significantly younger age at presentation and higher burden of comorbidities; a significantly higher incidence and burden of VTA and ATA events; increased incidence and burden of appropriate and inappropriate ICD therapies; and lower survival rates despite receiving an ICD at a significantly younger age. In contrast, in patients with ICM, the risk of tachyarrhythmias and ICD therapies did not differ significantly between Black patients and White patients. Our findings highlight the important differences between Black patients and White patients with NICM, suggesting a need for more intensive arrhythmia monitoring and management, as well as potentially earlier consideration for more advanced HF therapies, in Black patients because of increased likelihood for device therapy, adverse arrhythmic events, and death after prophylactic ICD implantation.

Differences in Outcomes Between Black Patients and White Patients With NICM

In the United States, Black patients have a higher prevalence of NICM at a younger age than the general population. The reason for this disparity is not fully understood, but potential contributing factors may include differences in the prevalence of comorbidities associated with NICM, environmental exposures, health care access, as well as potential genetic factors.11,12,23 Furthermore, Black patients with NICM frequently exhibit unique clinical presentations and imaging findings that differ from those of other populations. For example, Black patients with NICM are more likely to present with HF symptoms at an earlier age and with a higher burden of myocardial fibrosis on cardiac magnetic resonance imaging.24,25

Data on clinical outcomes suggest that Black patients with NICM have a higher risk of HF hospitalization and death compared with White patients with NICM.26–29 Differences in arrhythmic burden remain controversial because of underrepresentation of Black patients in randomized HF ICD trials.30–33 Our meta-analysis using the largest cohort of Black patients reported showed a significantly higher risk of tachyarrhythmias (VTA or ATA), ICD therapies (appropriate or inappropriate), and all-cause and nonarrhythmic death among Black patients with NICM when compared with White patients even after adjusting for age, sex, NYHA class, diabetes, hypertension, LVEF, medications, and socioeconomic status. These findings suggest a need for close arrhythmia monitoring and consideration of early intervention in Black patients with NICM regardless of baseline risk factors.

Arrhythmic Outcomes Among Black Patients and White Patients With ICM

Previous data on outcomes of Black patients in the ICM group were inconsistent. The majority of the findings from real-world data are derived from studies that did not assess outcomes by the type of cardiomyopathy and show increased risk of SCD, all-cause mortality, and tachyarrhythmia (VTA or ATA) among Black patients when compared with White patients.34–37 On the other hand, subgroup analysis in patients with ICM (n=642) enrolled in PROSE-ICD (Prospective Observational Study of Implantable Cardioverter-Defibrillators) showed similar risks for ICD therapy and all-cause mortality between Black patients and White patients.31 The landmark ICD trials MUSTT (Multicenter Unsustained Tachycardia Trial), DEFINITE (Defibrillators in Nonischemic Cardiomyopathy Treatment Evaluation), and DINAMIT (Defibrillator in Acute Myocardial Infarction Trial) included a minority of Black patients and were underpowered to conduct valid analysis. SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial) showed similar findings between Black patients and White patients, but subgroup analysis looking only at patients with ICM was not performed.30 Our data are in line with these observations and show that in patients with ICM who are implanted with an ICD in the United States, arrhythmic and mortality outcomes are similar in Black patients and White patients.

Possible Mechanisms Underlying Observed Differences in Arrhythmic Risk Between Black Patients and White Patients by Type of Cardiomyopathy

Several studies have suggested that the increased arrhythmic risk seen in Black patients may be attributed only to social determinants of health. However, the fact that these differences are dependent on type of heart disease indicate that the relationship is more complex. Results from ARIC (Atherosclerosis Risk in Communities Study), which included 3832 Black patients and 11 237 White patients, showed that income, education, and traditional risk factors explained <65% of the difference in SCD.36 Although the mechanism for differences in arrhythmic burden between Black patients and White patients remains unknown, it is likely multifactorial. Potential mechanisms include differences in baseline comorbidities, social determinants of health, environment, and possibly genetic factors that affect response to medical therapies, such as angiotensin-converting enzyme inhibitors or β-blockers.38–40 Black patients had a higher heart rate at baseline, which may be a reflection of their baseline adrenergic status and may partially explain these findings.

The Centers for Disease Control and Prevention defines health disparities as “preventable differences in the burden of disease, injury, violence, or opportunities to achieve optimal health that are experienced by socially disadvantaged populations.”41 In contrast to ICM, where VTA is mostly scar-related (which is supposed to be similar in Black patients and White patients), NICM can be precipitated by a wide variety of preventable and nonpreventable causes, consists of a heterogeneous group of cardiomyopathies, and the distribution of the specific cardiomyopathies within this group is known to be different between Black patients and White patients.42,43 Given the uncertainty and potential heterogeneous root cause of NICM in our population, it remains to be determined how the differences we identified in arrhythmic and clinical outcomes between Black patients and White patients reflect disparities.

In our study, the rate of a Gini index ≥0.5 (a marker of worse socioeconomic status) among Black patients was almost 2-fold the rate in White patients and was associated with increased risk of death in NICM (HR, 1.71 [95% CI, 1.04–2.83]; P=0.036). However, the increased risk of arrhythmic and mortality outcomes in Black patients was independent of the Gini index. In contrast, our findings of significantly lower compliance with treatment with guideline-directed medical therapies for heart failure 1 year after ICD implantation among Black patients with NICM may have partly contributed to the observed increased rates of adverse outcomes in this population.

Churchwell and colleagues44 have reported on behalf of the American Heart Association on the importance of structural racism as a fundamental driver of health disparities. Our findings in NICM, where arrhythmia risks are heterogeneous, are multifactorial, and correlate with patient care, support their advisory and highlight the crucial need for future research focusing on these disparities, aiming to narrow and eventually close the gap in health care between Black patients and White patients in the United States.

Management Implications

Regardless of potential mechanisms underlying these disparities in arrhythmic outcomes among patients with NICM, our findings show that Black patients experienced both increased VTA and mortality risk compared with White patients. These findings have important implications with regard to the potential benefit of ICD in this population. The predicted benefit of ICD can be calculated as the difference in the risk for fast VTA and the risk for death without a previous fast VTA in life.22 As seen in Figure 9A and 9B of Appendix S1, this difference was similar and pronounced in both Black patients and White patients. These findings, together with the findings of the additional analysis from MADIT-II and MADIT-CRT with control groups, highlight the importance of early intervention with a prophylactic ICD or CRT-D in Black patients because of its maintained efficacy and the fact that Black patients with NICM are at increased risk of VTA. Careful follow-up and consideration of early intensification of therapies after ICD implantation are also warranted, including early consideration of ablation therapy, because of the increased burden of appropriate and inappropriate therapies in Black patients with NICM who receive an ICD. The fact that Black patients with NICM have a higher rate of arrhythmic and mortality outcomes compared with White patients, despite being implanted at a significantly younger age, suggests that social determinants of health should be evaluated and addressed to improve outcomes in this higher-risk population.

In the United States, Black patients with HF are less likely to be referred to specialists, less likely to receive ICD counseling, and less likely to have an ICD implanted when compared with White patients with HF.45–47 These factors contribute to underuse of ICDs in Black patients and ultimately to disparities in survival outcomes.

Limitations

Our study is subject to several limitations. The analysis is a post hoc and nonprespecified analysis; thus, it should be considered as hypothesis-generating. Although our models were adjusted for significant predictors, which helps reduce uncertainty when estimating the association between Black patients and the hazard of VTA or death, it is possible that the observed differences in arrhythmic and survival outcomes between Black patients and White patients were driven by differences in the frequency of comorbidities and other social determinants of health between Black patients and White patients that were not accounted for in the multivariable models.

In addition, the eligibility criteria and the exclusion of elderly patients or those with advanced diseases (such as patients with creatinine level >2.5 mg/dL) in all our trials limits the generalizability of these findings to these populations. The effect of very recent HF drugs (including angiotensin-receptor neprilysin inhibitor and sodium glucose cotransporter 2 inhibitors) on the VTA risk in ICD candidates remains unknown. In addition, the findings of this study pertain only to Black patients who are implanted with an ICD in the United States, who may be affected by disparities that may not be present in other countries.

Conclusions and Clinical Implications

Our combined data from landmark ICD trials, using uniform arrhythmia and mortality adjudication data, show that Black patients with NICM experience increased risk and burden of tachyarrhythmias and ICD therapies, as well as lower survival rates after ICD implantation, when compared with White patients. These disparities in arrhythmic and clinical outcomes suggest the need for early intervention with an ICD, careful monitoring, and intensification of HF and antiarrhythmic therapies in Black patients with NICM in the United States.

ARTICLE INFORMATION

Supplemental Material

Appendix

Figures S1–S9

Tables S1–S7

Nonstandard Abbreviations and Acronyms

AF

atrial fibrillation or flutter

ARIC

Atherosclerosis Risk in Communities Study

ATA

atrial tachyarrhythmia

CRT-D

cardiac resynchronization therapy–defibrillator

DEFINITE

Defibrillators in Nonischemic Cardiomyopathy Treatment Evaluation

DINAMIT

Defibrillator in Acute Myocardial Infarction Trial

HF

heart failure

HR

hazard ratio

ICD

implantable cardioverter-defibrillator

ICM

ischemic cardiomyopathy

LVEF

left ventricular ejection fraction

MADIT-II

Multicenter Automatic Defibrillator Implantation Trial II

MADIT-CRT

Multicenter Automatic Defibrillator Implantation With Cardiac Resynchronization Therapy

MADIT-Risk

MADIT-II Risk Score

MADIT-RIT

Multicenter Automatic Defibrillator Implantation Trial–Reduce Inappropriate Therapy

MUSTT

Multicenter Unsustained Tachycardia Trial

NICM

nonischemic cardiomyopathy

NYHA

New York Heart Association

PROSE-ICD

Prospective Observational Study of Implantable Cardioverter-Defibrillators

RAID

Ranolazine Implantable Cardioverter-Defibrillator Trial

SCD

sudden cardiac death

SCD-HeFT

Sudden Cardiac Death in Heart Failure Trial

SVT

supraventricular tachycardia

VF

ventricular fibrillation

VTA

ventricular tachyarrhythmia

Disclosures Drs Younis, Ali, Ido Goldenberg, and Aktas, and S. McNitt and B. Polonsky, have nothing to declare. Drs Kutyifa, Wazni, Zareba, and Ilan Goldenberg report receiving grants from Boston Scientific.

Footnotes

Supplemental Material is available at https://www.ahajournals.org/doi/suppl/10.1161/CIRCULATIONAHA.123.065367.

For Sources of Funding and Disclosures, see page 251.

Circulation is available at www.ahajournals.org/journal/circ

Correspondence to: Ilan Goldenberg, MD, Director, Clinical Cardiovascular Research Center, Division of Cardiology, Department of Medicine, University of Rochester Medical Center, 265 Crittenden Blvd CU 420653, Rochester, NY 14642. Email

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