Distinctive Clinical Profile of Blacks versus Whites Presenting with Sudden Cardiac Arrest

Abstract

Background

Sudden cardiac arrest (SCA) is a major contributor to mortality, but data are limited among non-whites. Identification of differences in clinical profile based on race may provide opportunities for improved SCA prevention.

Methods and Results

In the ongoing Oregon Sudden Unexpected Death Study (SUDS), individuals suffering SCA in the Portland, Oregon metropolitan area were identified prospectively. Patient demographics, arrest circumstances, and pre-SCA clinical profile were compared by race, among cases 2002 – 2012 (for clinical history, n = 126 blacks, 1262 whites). Incidence rates were calculated for cases from the burden assessment phase (2002 – 2005; n = 1077). Age-adjusted rates were two-fold higher among black men and women (175 and 90 per 100,000, respectively), compared to white men and women (84 and 40 per 100,000, respectively). Compared to whites, blacks were >6 years younger at the time of SCA and had a higher pre-arrest prevalence of diabetes (52% vs. 33%, p<0.0001), hypertension (77% vs. 65%, p=0.006), and chronic renal insufficiency (34% vs. 19%, p<0.0001). There were no racial differences in previously documented coronary artery disease or left ventricular dysfunction, but blacks had more prevalent congestive heart failure (43% vs. 34%, p=0.04), left ventricular hypertrophy (77% vs. 58%, p=0.02), and a longer QT interval (QTc) (466 ± 36 vs. 453 ± 41, p=0.03).

Conclusions

In this US Community, the burden of SCA was significantly higher in blacks compared to whites. Blacks with SCA had a higher pre-arrest prevalence of risk factors beyond established CAD, providing potential targets for race-specific prevention.

INTRODUCTION

Sudden cardiac arrest (SCA) is a major cause of mortality in the US, contributing to 300,000-350,000 sudden cardiac deaths (SCD) annually and accounting for 50% of all cardiovascular mortality.¹ However, there is little information regarding SCA in non-white racial groups. US studies published two to three decades ago estimated SCA incidence by race, and all reported a significantly higher incidence in blacks compared to whites.^2-6 However, differences by race in the clinical profile of SCA cases have not been evaluated. Also, these studies used single sources of ascertainment, which can lead to under-ascertainment or misclassification. For example, use of only the emergency medical response system as a source misses 30-40% of all SCA cases that do not undergo resuscitation.⁷ Most importantly, the majority of previous studies, especially those evaluating larger numbers of subjects, determined SCD from death certificates, now shown to have significant limitations when compared to prospective community-based ascertainment.^{7, 8} Our objective was to compare medical history among SCA cases by race using a prospective, multiple-source, population-based approach, the Oregon Sudden Unexpected Death Study (Oregon SUDS). This study, ongoing since 2002, collects detailed information on cardiac arrest circumstances and lifetime medical history.

METHODS

Study population

The Oregon SUDS is an ongoing community-based epidemiologic study that uses multiple-source ascertainment to identify cases of out of hospital cardiac arrest occurring in the Portland, Oregon metropolitan region, including Portland's Multnomah County. Methods for this study have been previously published.^{7, 9} Briefly, cases are identified prospectively through collaboration with the region's two-tiered Emergency Medical Services (EMS) system, the state Medical Examiner's office, and the region's 16 hospitals.

For the period Feb. 1, 2002 – Jan. 31, 2005 (“burden assessment period”), all patients with an out of hospital cardiac arrest in Multnomah County were prospectively identified for potential inclusion in Oregon SUDS, including: all cases with EMS response regardless of outcome; cases without EMS response who were found deceased and reported directly to the Medical Examiner; and a small proportion who suffered SCA in hospital emergency rooms. To identify cases missed during prospective reporting, we performed periodic retrospective review of electronic EMS records using pre-selected keywords, as well as periodic reviews of all non-traumatic sudden deaths identified by the Medical Examiner, with the goal of identifying all potential cases of out of hospital SCA in the county. Cases included deceased subjects as well as survivors of SCA. Data from the burden assessment phase of Oregon SUDS were used to calculate incidence rates. Since February 1, 2005, case ascertainment has been limited to the subset of cases with a blood sample collected during attempted resuscitation by EMS or following survival from SCA, or with a tissue sample collected during autopsy. Collection of data regarding arrest circumstances, outcomes, and pre-arrest medical history remained consistent throughout the Oregon SUDS study period.

This study was approved by the institutional review boards of Cedars-Sinai Medical Center, Oregon Health and Science University, and all participating hospital systems.

Definition and adjudication of sudden cardiac arrest

All identified potential cases of SCA were then subjected to detailed adjudication for determination of SCA. All existing records were obtained for each case, including the EMS pre-hospital care report, the patient's complete medical records from the region's hospitals (including records from the index SCA event and pre-SCA clinical history), death certificates from Oregon state vital statistics records, and the Medical Examiner report and autopsy if available. Based on this detailed information, three physicians performed in-house adjudication for determination of SCA, which was defined as a sudden, unexpected pulseless condition of likely cardiac origin;¹ unwitnessed cases were required to have been seen in normal health within 24 hours of arrest. All cases deemed to have a non-cardiac etiology for cardiac arrest were excluded, such as trauma, drug overdose, and chronic terminal illness (e.g., on home oxygen, or malignancy not in remission). Approximately one-quarter of initially identified cases did not meet pre-specified criteria and were excluded during the adjudication process. A comparison of the method of case ascertainment and adjudication used in Oregon SUDS with SCD determined by death certificates during the first year of the study (353 cases) revealed that the Oregon SUDS method was significantly more specific and complete.⁷

Patient demographics and medical history

Definition of race

Race data for individual cases were obtained from death certificates, the Medical Examiner report, medical records, and the EMS pre-hospital care report, and were available for 96% of all SCA cases age ≥18 in Multnomah County from 2002-2012, and for >99% of cases with medical records prior to arrest. US Census data were used for the race/ethnic composition of the community.¹⁰ Race was categorized as white, black, Hispanic, Asian and Other. “Hispanic” included any individual reporting Hispanic ethnicity, regardless of race. “Other” included American Indian/Alaska Native and Hawaiian/Pacific Islander.

Medical history

Circumstances of the cardiac arrest event were obtained from the EMS pre-hospital care report and characterized using the Utstein template.¹¹ To determine the outcome of arrest for each patient, we review the EMS report and/or Medical Examiner report and all available hospital records, and search Oregon death certificate records for all cases. If vital status still remains uncertain, we also search the national Social Security Death Index. Individuals are only placed in an “unknown” survival category following this extensive search.

From the patient's complete medical records, documented coronary artery disease was defined as ≥50% stenosis on a pre-arrest angiogram or a documented history of myocardial infarction (MI) or revascularization. Body mass index was the height (cm) divided by the weight (kg) squared, with obesity defined as BMI ≥30. Diabetes was defined as a chart history of diabetes or use of insulin or oral hypoglycemic agents; chronic renal insufficiency by a chart history of renal failure or hemodialysis; and hypertension and congestive heart failure by chart history. Medication use prior to arrest was noted in the medical record closest to the date of arrest.

For the subset of cases with pre-arrest or peri-arrest angiograms, we obtained information regarding quantitative stenosis of coronary arteries. For the subset with pre-arrest ECGs available, heart rate and QRS were obtained from the computer-read values on the 12-lead ECG; the QT interval was manually read using digital on-screen software (Datinf Measure: DataInf GmbH; Tübingen, Germany). LVH by ECG was diagnosed if Sokolow-Lyon criteria (S V1 + R V5 or V6 ≥ 35 mm)¹² or Cornell voltage criteria (S in V3 + R in aVL > 28 mm in men and 20 mm in women) were met. For the subset of patients with echocardiograms, we obtained ejection fraction, and considered left ventricular hypertrophy (LVH) present if left ventricular mass indexed to body surface area was >115 g/m² in men or >95 g/m² in women.¹³

For the subset of SCA cases with autopsy (16.2% of total cases, including cases that occurred outside of Multnomah County to maximize sample size), we examined the following data from the Medical Examiner's autopsy report: evidence of recent or old infarction; coronary evaluation and quantification of stenosis; heart weight; and cardiac conditions, including hypertrophic cardiomyopathy, arrhythmic right ventricular dysplasia, aortic stenosis, myocarditis, congenital heart disease, and coronary anomalies. Consistent with our case definition, any suspected SCA case was excluded if there was a non-arrhythmic cause of death (e.g., cardiac tamponade, pulmonary embolism) or if toxicology findings revealed illicit drug use.

Statistical analysis

Clinical characteristics by race

Figure 1 shows the flow chart for subject inclusion in analyses. For comparisons of clinical history, cases age ≥18 from Multnomah County from Feb. 1, 2002 – Jan. 31, 2012 were included if white or black race, with pre-arrest medical history available from physician records. Circumstances and outcomes of arrest were evaluated among cases age ≥18 from Multnomah County from Feb. 1, 2002 – Jan. 31, 2012 if white or black race, with resuscitation attempted by EMS personnel. All comparisons in whites vs. blacks used independent samples t-tests and chi-square tests. Multiple logistic regression was used to test whether survival to hospital discharge was associated with race, adjusting for covariates.

Figure 1.

Flow chart. Oregon Sudden Unexpected Death Study cases included in analysis. *Incidence calculations included cases 2002 – 2005 (burden assessment phase), all ages, including cases without resuscitation attempt and cases without complete pre-arrest medical history. †Arrest circumstances analyses included cases 2002 – 2012, age ≥18, subset with resuscitation attempted. ‡Clinical history analyses included cases 2002 – 2012, age ≥18, subset with pre-arrest medical records available

Calculation of SCA incidence rates

Age-specific and age-adjusted incidence rates were calculated for whites and blacks using data from the burden assessment period of Oregon SUDS in Multnomah County (Feb. 1, 2002 to Jan. 31, 2005; n = 106 blacks cases and 971 white cases, including all ages) (Figure 1). For age-specific rates, the number of cases in each age category comprised the numerator (age <1 year, 1-4 years, 5-9 years, then by five-year categories to age ≥85 years), and race- and age-specific US Census 2003 intercensal population estimates for Multnomah County comprised the denominator; 95% confidence intervals (CIs) for age-specific rates were calculated assuming rates were the approximate mean of a Poisson distribution.¹⁴ Age-adjusted rates were estimated using direct standardization with the US Census 2000 standard population as the adjustment weight,¹⁵ and 95% CIs were estimated according to the gamma distribution method.¹⁶

RESULTS

Overall distribution of race

A total of 2144 cases of SCD (36% women) were identified in Multnomah County, Oregon from February 1, 2002 through January 31, 2012. Race was available for 2069 (96.5% of total cases): 1745 (84.9%) were white, 179 (8.4%) were black, and 145 (7.0%) were other races. All subsequent comparisons were limited to whites and blacks, given the small numbers in the other groups (Figure 1).

Incidence rates of SCA by race, 2002 - 2005

Figure 2 shows age-specific incidence rates by race. Differences were apparent in both men and women across the age spectrum, with rates among blacks higher than among whites in all age categories. Age-adjusted incidence of SCA was two-fold higher in black men (175 per 100,000, 95% CI 101 – 291) compared to white men (84 per 100,000, 95% CI 73 – 97). While absolute rates were lower in women, a two-fold higher rate was also observed comparing black women (90 per 100,000, 95% CI 48 – 150) to white women (40 per 100,000, 95% CI 33 – 48).

Figure 2.

Age-specific incidence of SCA in men and women, by race, in Oregon SUDS 2002-2005.

Circumstances and outcomes of arrest by race

All cases age ≥18 with resuscitation attempted were included in analyses of the circumstances and outcomes of SCA (Table 1). A similar proportion of both black and white cases had resuscitation attempted: 130 (76%) of 171 black cases and 1288 (75%) of 1730 white cases. Blacks were younger at the time of SCA than whites (61.0 ± 16.2 vs. 67.2 ± 15.6, p<0.0001), and significantly more were younger than age 65 (58% vs. 43%, p=0.002).

Table 1.

Circumstances and outcome of arrest among black and white SCA cases in Multnomah County age ≥18 with resuscitation attempted by EMS, Oregon SUDS 2002 - 2012

	Black (n = 130)	White (n = 1288)	P-value
Male	82 (63%)	843 (65%)	0.59
Age (years)	61.0 ± 16.2	67.2 ± 15.6	<0.0001
Age <65	75 (58%)	557 (43%)	0.002
Witnessed arrest*
By bystander	76 (59%)	784 (61%)	0.84
By EMS	10 (8%)	87 (7%)
Not witnessed	43 (33%)	408 (32%)
Arrest location
Home	88 (68%)	868 (68%)	0.94
Public	22 (17%)	205 (16%)
ED/Outpatient/Care Center	19 (15%)	181 (14%)
Other	1 (1%)	32 (2%)
Response time (minutes)	6.4 ± 2.5	6.7 ± 3.2	0.29
Initial rhythm
VF/VT	48 (37%)	550 (43%)	0.39
PEA	43 (33%)	345 (27%)
Asystole	32 (25%)	306 (24%)
Other	7 (5%)	87 (7%)
Return of spontaneous circulation	41 (32%)	500 (39%)	0.09
Survival to hospital discharge	10 (8%)	162 (13%)	0.12

PEA: pulseless electrical activity; VF/VT: ventricular fibrillation/ventricular tachycardia

Apart from the age difference, no other significant differences were noted in the circumstances of cardiac arrest, including the proportion of witnessed arrests, arrest location, bystander CPR, response time, and initial arrhythmia (Table 1; p≥0.29). Outcomes were slightly worse among blacks, but differences were not significant (return of spontaneous circulation (ROSC) in the field was 39% in whites and 32% in blacks, p=0.09; survival to hospital discharge (STHD) was 13% in whites and 8% in blacks, p=0.12). In sensitivity analyses, we examined the association of race with ROSC and STHD assuming that (a) all unknowns did have ROSC / did survive, or (b) all did not, and results were consistent with the findings excluding the unknowns. Because of the large age difference, we repeated comparisons adjusting for age, and results were consistent. Furthermore, in a multivariable model adjusted for age, sex, initial arrhythmia (VF/VT vs. other), witnessed (yes/no), location (home vs. elsewhere), and EMS response time, there was no significant difference in survival by race (odds ratio 0.64, 95% CI 0.31 – 1.3, p=0.22).

Clinical profile prior to arrest by race

Among incident cases of SCA in Multnomah County 2002 - 2012, 1262 of 1730 whites (73.0%) and 126 of 171 blacks (73.7%) had physician records available to ascertain medical history prior to arrest. The majority of both black and white cases had their last medical encounter, ECG, and echocardiogram within two years of the date of arrest, and there were no significant differences in the time elapsed (p≥0.58). In this subset (Table 2), the age difference between whites and blacks was similar to that in the resuscitated subset (61.2 ± 15.8 years in blacks, 68.1 ± 15.6 years in whites, p<0.0001). Diabetes was significantly more prevalent among blacks than among whites (52% vs. 33%; p<0.0001). Hypertension was also more common among black than white cases of SCA (77% vs. 65%, p=0.006), as was chronic renal insufficiency (34% vs. 19%, p<0.0001). Other clinical comparisons revealed no black-white differences (obesity, hyperlipidemia, peripheral vascular disease, cerebrovascular disease, current smoking, COPD, liver disease, depression, and dementia: p≥0.13).

Table 2.

Clinical history prior to SCA among black and white SCA cases age ≥18, Oregon SUDS 2002 – 2012

	Black (n = 126)	White (n = 1262)	p-value
Male	71 (56%)	808 (64%)	0.09
Age (years)	61.2 ± 15.8	68.3 ± 15.6	<0.0001
Age <65	74 (59%)	526 (42%)	0.0002
Body mass index (kg/m2)	31.0 ± 11.3	29.4 ± 8.4	0.18
Obesity	36 (37%)	311 (37%)	0.96
Diabetes	66 (52%)	410 (33%)	<0.0001
Hypertension	97 (77%)	814 (65%)	0.006
Hyperlipidemia	52 (41%)	564 (45%)	0.43
Peripheral vascular disease	15 (12%)	167 (13%)	0.66
Cerebrovascular disease	27 (21%)	203 (16%)	0.13
Current smoking	40 (44%)	333 (39%)	0.36
Chronic renal insufficiency	43 (34%)	241 (19%)	<0.0001
Chronic obstructive pulmonary disease	26 (21%)	283 (23%)	0.63
Liver disease	4 (3%)	28 (2%)	0.50
Depression	21 (17%)	208 (17%)	0.98
Dementia	10 (8%)	124 (10%)	0.48

All comorbidities as defined in text. Due to missing data, sample sizes were smaller for body mass index and obesity: white n=840, black n=98; and current smoking: white n=834, black n=90.

Cardiac history

Blacks were as likely as whites to have had a clinically-recognized history of coronary artery disease and myocardial infarction (Table 3). Whites were somewhat more likely to have had a coronary artery revascularization prior to cardiac arrest, while blacks had a higher prevalence of pre-arrest congestive heart failure (43% vs. 34%, p=0.04). In the subset of patients with a pre- or peri-arrest angiogram (18% of subjects), blacks were slightly but non-significantly less likely to have findings of significant coronary artery disease (≥50% stenosis in ≥1 coronary artery, p=0.10). Among the 50% of subjects with pre-arrest ECGs (Table 3), the Bazett's heart-rate corrected QT interval was significantly longer among blacks (QTc 466 ± 36 vs. 453 ± 41 ms, p=0.03), and LVH by ECG criteria was more common among blacks (24% vs. 13%, p=0.008). Heart rate and QRS duration were similar by race. Finally, in the 33% of subjects with a pre-arrest echocardiogram (Table 3), LVH by echocardiographic criteria was highly prevalent, and significantly more common among blacks compared to whites (77% vs. 58%, p=0.02), and left ventricular size was significantly greater (p=0.02). No racial differences in ejection fraction were observed.

Table 3.

Cardiac history among white and black SCA cases in Multnomah County age ≥18, Oregon SUDS 2002 – 2012

	Black (n = 126)	White (n = 1262)	p-value
Documented pre-arrest coronary artery disease	47 (37%)	509 (40%)	0.51
History of myocardial infarction	39 (31%)	394 (31%)	0.95
History of revascularization	16 (13%)	261 (21%)	0.03
Congestive heart failure	54 (43%)	422 (34%)	0.04
Atrial fibrillation / flutter	23 (19%)	285 (23%)	0.30
Angiogram findings
≥1 coronary artery with ≥50% stenosis	20 (74%)	197 (86%)	0.10
	n = 27	n = 229
ECG Parameters
Heart rate (bpm, mean ± SD)	82.0 ± 18.9	79.0 ± 18.8	0.18
	n = 77	n = 612
QTc (Bazett's, ms, mean ± SD)	466 ± 36	453 ± 41	0.03
	n = 51	n = 387
QRS duration (ms, mean ± SD)	104 ± 28	102 ± 25	0.62
	n = 77	n = 615
LVH by ECG*	19 (24%)	81 (13%)	0.008
	n = 78	n = 616
Echo Parameters
Ejection Fraction	n = 56	n = 414
EF ≥55%	19 (34%)	166 (40%)	0.38
EF 36-54%	15 (27%)	123 (30%)
EF ≤35%	22 (39%)	125 (30%)
Left ventricular hypertrophy	34 (77%)	170 (58%)	0.02
	n = 44	n = 291
Left ventricular size (LVIDD†, mm, mean ± SD)	55.1 ± 9.9	51.4 ± 10.5	0.02
	n = 49	n = 324

^*LVH by ECG: Left ventricular hypertrophy by Sokolow-Lyon or Cornell voltage criteria.

^†LVIDD: Left ventricular internal diameter end diastole.

Angiograms, ECGs, and echocardiograms were not available in all subjects. Sample sizes for variables derived from these tests are indicated in the table.

Medication use by race

Use of medications to treat cardiovascular risk factors was common among both white and black patients who went on to have SCA (Table 4). Among patients with diabetes, there was no racial difference in the proportion taking anti-diabetic medications (p=0.39); among patients with hypertension, there was no racial difference in the proportion taking ACE inhibitors, angiotensin receptor blockers, calcium channel blockers, diuretics, or beta-blockers (p≥0.13); and among patients with hyperlipidemia, there was no difference in the proportion taking lipid lowering drugs (p=0.85). Finally, among all patients, white patients were somewhat more likely than blacks to be taking anti-coagulants (18% vs. 10%, p=0.04); there were no other significant differences by race in the proportion of patients taking beta-blockers, statins, lipid lowering drugs, or anti-anginal drugs (p≥0.28).

Table 4.

Medication use prior to arrest among white and black SCA cases in Multnomah County age ≥18, Oregon SUDS 2002 – 2012^*

	Black (n = 115)	White (n = 1138)	p-value
Among all patients
Beta blockers	58 (50%)	514 (45%)	0.28
Statins	38 (33%)	382 (34%)	0.91
Lipid lowering drugs	38 (33%)	401 (35%)	0.64
Anti-anginal drugs	27 (23%)	231 (20%)	0.42
Anti-coagulants	12 (10%)	205 (18%)	0.04
Among diabetics	n = 63	n = 386
Anti-diabetic use	45 (71%)	295 (76%)	0.39
Among hypertensives	n = 94	n = 774
ACE inhibitors	45 (48%)	378 (49%)	0.86
ARBs	10 (11%)	62 (8%)	0.38
Calcium channel blockers	28 (30%)	176 (23%)	0.13
Diuretics	54 (57%)	436 (56%)	0.84
Beta blockers	51 (54%)	417 (54%)	0.94
Among hyperlipidemics	n = 39	n = 447
Lipid lowering drugs	27 (69%)	303 (68%)	0.85

^*Table excludes 135 subjects with medical records who were missing information regarding medication use.

Autopsy findings by race

Autopsies were available for 15.7% of black cases (n = 30) and 16.2% of white cases (n = 365) in Oregon SUDS (Table 5). Findings of fresh MI were not significantly different in blacks and whites (13% vs. 20%; p=0.38), though blacks were somewhat less likely to have an old infarct identified at autopsy (7% vs. 22%, p=0.05). Blacks were also less likely than whites to have significant (≥50%) coronary artery stenosis in at least one coronary artery (55% vs. 79%, p=0.009). Blacks were more likely to have hypertrophic cardiomyopathy (HCM: 13% vs. 5%, p=0.07). There were no racial differences in the following conditions, which all had a prevalence of <3%: aortic stenosis, ARVD, congenital heart disease, coronary anomalies, and myocarditis. No differences were observed in mean heart weight or wall thickness.

Table 5.

Autopsy findings among white and black SCA cases age ≥18, Oregon SUDS 2002 – 2012^*

	Black (n = 30)	White (n = 365)	P-value
Age (years)	41.8 ± 11.0	46.5 ± 12.0	0.04
Male	22 (73%)	285 (78%)	0.55
Fresh MI at autopsy	4 (13%)	73 (20%)	0.38
Old infarct at autopsy	2 (7%)	80 (22%)	0.05
≥1 coronary artery with ≥50% stenosis	12 (55%)	232 (79%)	0.009
Hypertrophic cardiomyopathy	4 (13%)	19 (5%)	0.07

^*For the autopsy subset, subjects with arrest occurring outside of Multnomah County were also included. Autopsies were available for 16.2% of total white cases and 15.7% of total black cases.

DISCUSSION

In this community-based study, age-adjusted annual incidence of SCA among black men and women (175 and 90 per 100,000, respectively) was more than twice the incidence observed in white men and women (84 and 40 per 100,000, respectively). Blacks experienced SCA more than six years younger than whites, and had a higher prevalence of specific cardiovascular risk factors, including a history of diabetes and hypertension, as well as chronic renal insufficiency. There were no racial differences in the burden of previously-documented coronary disease overall or in the subset with coronary angiogram. However, blacks were more likely than whites to have several non-coronary cardiac findings: left ventricular hypertrophy by ECG and echocardiogram, prolonged QTc interval, and congestive heart failure. Among these community-dwelling patients who suffered SCD, differences in preventive medications did not appear to explain racial disparities in SCD rates. In the subset of cases with autopsy, blacks had less significant coronary stenosis and less evidence of old infarct, but a somewhat higher proportion had HCM. Despite the racial differences in incidence and comorbidities that we report, we found no racial differences in the circumstances or outcomes of SCA.

Earlier epidemiologic reports, most conducted two to three decades ago, also noted a higher incidence of SCA among blacks compared to whites.^2-6 While our results for SCA burden are consistent with the published literature, the findings related to age, co-morbidities, and non-coronary cardiac risk factors are new and likely warrant urgent attention. SCA occurs at a significantly younger age in blacks, with a higher prevalence of clinical risk factors beyond previously-documented coronary disease. A black-white disparity in cardiovascular disease (CVD) risk factor burden and overall cardiovascular mortality is well-documented^{17,18, 19}, and based on our findings, extends to SCA occurrence in the community. Diabetes is more prevalent among blacks than whites in general,^{20, 21} as is hypertension,¹⁷ heart failure,²² chronic kidney disease,²³ and left ventricular hypertrophy.²⁴ Recent data from patients with coronary disease also suggest that the QT interval is prolonged in blacks compared to whites.²⁵ However, each of these conditions may also be specifically associated with SCA.^26-31 A combination of these risk markers may indicate high risk for SCA even in the absence of severely reduced EF. In a recent analysis among >4000 participants with heart failure and preserved EF from the I-PRESERVE trial cohort, a history of diabetes, myocardial infarction, LBBB on ECG, and higher NT-proBNP were useful in identifying patients with a ≥10% cumulative 5-year risk of SCA.³² There is additional evidence to suggest that blacks may have a higher risk specifically for SCA. In the Atherosclerosis Risk In Communities (ARIC) study with over 12 years of follow-up, incidence of SCA among blacks was two to three times higher than among whites, while race differences were smaller or absent for non-sudden cardiovascular death and non-fatal myocardial infarction.³³ Findings from the REasons for Geographic and Racial Differences in Stroke (REGARDS) study also noted a more pronounced black-white difference in fatal CHD events compared to non-fatal CHD events, though this difference became non-significant after adjustment for cardiovascular disease risk factor burden.³⁴ It is plausible that genetic variation or other yet unidentified factors may also contribute to a specific risk for SCA. Our finding that SCA occurred over six years earlier in blacks may be consistent with a genetic contribution to SCA occurrence in blacks, given existing data showing a strong genetic component in early-onset cardiovascular disease and cardiovascular outcomes.^35-38

Limitations

For incidence rate calculations, county-level census data was used for race-specific population counts. Therefore, though individual-level data on race, medical history, and demographics were available for SCA cases, individual-level analyses to further evaluate the relationship between SCA incidence, race, and comorbidities were not possible. Though the Oregon SUDS includes control subjects, we were not able to include analyses comparing black and white cases to black and white controls due to small numbers of black control subjects. Therefore, whether the identified risk factors are independently associated with SCA still requires further investigation. Analysis of outcomes was limited to whether the patient survived to hospital discharge. However, this is a standard definition used in cardiac arrest research, and the relatively small number of black survivors (n=10) limited our ability to make more detailed comparisons (e.g., functional status) in this subgroup.

The number of cases among Hispanics and Asians was relatively small necessitating a focus on blacks vs. whites. Two previous studies in the US have included SCD incidence in Hispanics,^{5, 6} both reporting somewhat lower rates than among whites, but both used death certificate data to determine SCD, which has limitations.^{7, 8} To our knowledge, no US study has reported SCA incidence among Asians. However, a review of treated out-of-hospital cardiac arrest around the globe reported the highest rate in North America (54.6 / 100,000) and the lowest in Asia (28.3 / 100,000).³⁹ Therefore, a focus on SCA among all minority groups, including non-black minority groups, is urgently needed.

Most patients with out of hospital SCA do not routinely undergo an autopsy to confirm cause of death. Based on our established protocols, we carefully reviewed circumstances of arrest as noted by EMS personnel and adjudicated every case in an attempt to rule out those in which stroke or pulmonary embolism was strongly suspected. However, we cannot exclude the possibility of some misclassification in our case population, especially with regard to stroke among black cases.

Medical records, including clinical history prior to SCA, were available for a comparable number of black and white cases (74% and 73%). Some data, such as that from ECGs and echocardiograms performed prior to arrest, were available for a smaller proportion, and were available for a somewhat larger proportion of blacks vs. whites, consistent with their higher comorbidity profile. We cannot rule out the possibility of some bias due to differential misclassification related to missing clinical data.

Our study is unique in that it included a detailed evaluation of lifetime medical history to examine racial differences in risk factors for SCA. Given low overall rates of SCA, the cases evaluated in this study represent a sizeable population, even black cases, who represented <10% of the overall study population but had a sample size of >100.

CONCLUSIONS

In this community, blacks had a significantly higher burden of SCA compared to whites, and blacks had a higher prevalence of clinical risk factors beyond previously-documented coronary disease, with the fatal event occurring at a significantly younger age. These findings are consistent with the overall trends identified for higher cardiovascular mortality in blacks. Blacks had a higher prevalence of non-coronary cardiac risk factors for SCA suggesting that use of a broader spectrum of SCA risk factors, including LVH and specific ECG parameters, may provide new opportunities to lower the significant SCA burden in blacks compared to other racial groups.