This investigation sought to determine the characteristics of SCD in an ethnically diverse, urban community which may presage forthcoming rapid national demographic shifts in the United States in which no majority ethnicity is projected by 2042.13
Using a robust surveillance method for all consecutive SCDs fitting standard, widely accepted WHO criteria, we found a rate of WHO SCD that is comparable to recent estimates. Only 1 (0.4%) possible out-of-hospital SCD was not reported to the ME. After excluding non-cardiac and nonarrhythmic causes by ME investigation, true SAD accounted for only 57.5% of WHO SCDs. SAD varied substantially by gender and race with higher incidence in men and blacks. Among SADs undergoing autopsy, significant CAD accounted for 38.9% of cases, less than half of historical estimates, but was still associated with a 2.6-fold higher risk of SAD as compared to accidental trauma control deaths. Cardiac mass was also significantly higher in SADs as compared to controls, but linearly associated with risk for SAD among only those without CAD.
The somewhat lower rate of SAD may be due to several factors and reflect recent trends: (1) the effects of contemporary treatment of heart disease, including recent widely adopted primary prevention implantable cardioverter defibrillators (ICDs) in patients with heart failure (2) earlier recognition of sudden cardiac arrest (SCA) resulting in bystander and early resuscitation, (3) the diversity of the San Francisco population which has a significant proportion of Asian and Hispanic residents, both with lower rates of SCD as compared to Caucasians, (4) the exclusion of SCA survivors, who have been included in some studies, and (5) a concerted effort to exclude non-cardiac sudden deaths by reviewing all records to exclude cases with a known terminal illness or with obvious signs of a non-cardiac cause of death. These factors together may explain the observed lower incidence of true SAD as compared to older estimates of SCD/SCA in more homogeneous populations.
Our findings corroborate previous studies that have also demonstrated the poor specificity of the WHO definition of SCD for SAD, the most relevant phenotype from a public health standpoint and the only one prevented by ICDs. This study highlights the need for refinement of criteria for identification of SCD as true arrhythmic etiology (SAD) accounted for just over half of SCDs as defined by standard, widely accepted criteria. Despite attempts to exclude suspected and obvious non-cardiac deaths prior to autopsy, a non-cardiac cause of sudden death was found in nearly two-thirds of all autopsied WHO SCDs.
By midcentury, Caucasians are estimated to no longer represent the majority ethnic group in the United States, with rapid increases in Hispanic and Asian populations.13
As the population diversifies, investigation in diverse communities is essential to further define racial differences in disease. We demonstrate that Asians and Hispanics (combined 46% of SF population) have significantly lower rates of SCD and SAD while blacks have a greater than 3-fold higher rate as compared to Caucasians. Indeed, this may partially explain an overall WHO SCD rate (37.3/100,000) more comparable to rates recently observed in homogeneous Asian populations (Okinawa, Japan: 37/100,00017
) than predominantly Caucasian populations (Oregon, USA: 53/100,000,9
). A higher rate of SCD in blacks has been previously noted but has been reported inconsistently. While our study confirms these prior observations, further investigation is needed to determine the reason(s) for this disparity.
It has been reported that acute coronary-related events account for the majority of sudden cardiac deaths in the adult population and prior research suggests that approximately 80% of adults with SCD have severe CAD.21–26
However, in this community-based study, only one of 36 autopsied SADs had an active coronary lesion as the cause of SAD while significant CAD was found in fewer than 40% of SADs. Nevertheless, significant CAD still imparted a 2.6-fold higher risk of SCD as compared to accidental trauma deaths. These results are in notable contrast to the 80% prevalence of significant CAD found in a recent autopsy series of 71 sudden unexpected deaths in adults aged 25–64 years in Minnesota between 2001–2004.8
However, the case definition used in that study, a symptom duration up to 24 hours, may bias towards ischemic (i.e., pump failure or acute MI) rather than arrhythmic causes of death, whereas the WHO definition (symptom onset < 1 hour) may be more specific for SAD, whether ischemic or non-ischemic. In addition, as with prior reports on the prevalence of CAD in SCD,21–26
cases were uniformly Caucasian (96%) and male (86%); thus considerable differences in case demographics and definition may together account for the disparity in CAD prevalence found in sudden deaths in Minnesota vs. San Francisco. Another possibility is that we have underestimated the contribution of CAD due to the exclusion in our analysis of WHO SCDs deemed cardiac/arrhythmic without autopsy. Indeed, 40% of autopsied WHO SCD cases were determined to be arrhythmic in etiology compared to 71% of non-autopsied WHO SCD cases. This suggests that cases in which CAD was thought to be a more likely cause of SCD were less likely to undergo full autopsy. On the other hand, the fact that 60% of autopsied SCDs found non-cardiac cause suggests that many of the SCDs deemed arrhythmic without autopsy may actually have been non-cardiac had autopsy been performed.
Previous autopsy series of selected SCDs have reported inconsistent findings with regard to cardiac mass. In our population, we found a higher mean cardiac mass in SADs as compared to controls but this difference varied by the presence of significant CAD. We demonstrate a specific linear relationship between cardiac mass and increased SAD risk among those without significant CAD, but not in those with significant CAD. Cardiac mass may therefore be a useful adjunct in risk stratification for SAD in those without CAD.
Strengths and Limitations
The major strength of this study is the use of a robust surveillance method for nearly all SCDs in a diverse, urban community, incorporating comprehensive analysis including autopsy to provide data not available in prior studies based on death certificate measures of SCD. The study is limited by its retrospective design and an autopsy rate of 43% for WHO SCDs, although this is notably more than triple the respective 11.6% and 14% autopsy rates of SCDs in the recent studies of community SCDs in Oregon9
and sudden deaths in VALIANT,28
and similar to the 62% autopsy rate in the Minnesota study.8
As a retrospective study, our data are also limited by the standard practice of the medical examiner in the reviewed year. Of the 4258 deaths reported to the ME in 2007, 1420 were accepted as ME cases. In San Francisco, all out-of-hospital deaths, including deaths occurring in the emergency department, require report to the ME. Cases not accepted were typically inpatient hospital deaths, hospice deaths, and deaths for whom a primary physician was willing to sign a death certificate, usually because death was expected (e.g. metastatic cancer) or the patient was seen within 21 days of death. Thus, we may have missed a number of SCDs for which a physician signed a death certificate with assumed cardiac cause. However, we have likely captured the large majority of SCDs in 2007 as evidenced by a SCD incidence which is comparable to other recent reports.