Frequency of Sudden Cardiac Death and Profiles of Risk

Myerburg, Robert J.; Interian, Alberto; Mitrani, Raul M; Kessler, Kenneth M.; Castellanos, Agustín

doi:10.1016/s0002-9149(97)00477-3

Cited by 378 publications

(196 citation statements)

References 66 publications

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“…In the Deutsche Diabetes Dialyse Studie, patients with a hemoglobin A1c level of 8% or greater had a twofold increased risk for sudden death compared with those with a hemoglobin A1c level less than 6%; however, it remains to be determined whether tighter glycemic control reduces the risk for SCD in clinical trials (20). The finding that IHD was associated with SCD is also consistent with previous reports and is probably due to the fact that IHD provides a substrate for arrhythmias (7,21,22). Peripheral vascular disease was a significant predictor of SCD and may reflect underlying generalized atherosclerosis.…”

Section: Discussionsupporting

confidence: 82%

Predictors of Sudden Cardiac Death

Shastri

Tangri

Tighiouart

et al. 2012

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives There are few data on risk factors for sudden cardiac death (SCD) in patients undergoing hemodialysis (HD). The study objective was to identify predictors associated with various causes of death in the Hemodialysis (HEMO) Study and to develop a prediction model for SCD using a competing risk approach.Design, setting, participants, & measurements In this analysis of 1745 HEMO participants, all-cause mortality was classified as SCD, non-SCD, and noncardiac death. Predictors for each cause of death were evaluated using cause-specific Cox proportional hazards models, and a competing risk approach was used to calculate absolute risk predictions for SCD.Results During a median follow-up of 2.5 years, 808 patients died. Rates of SCD, non-SCD, and noncardiac death were 22%, 17%, and 61%, respectively. Predictors of various causes of death differ somewhat in HD patients. Age, diabetes, peripheral vascular disease, ischemic heart disease, serum creatinine, and alkaline phosphatase were independent predictors of SCD. The 3-year C-statistic for SCD was 0.75 (95% confidence interval, 0.70-0.79), and calibration was good (x 2 =1.1; P=0.89). At years 3 and 5 of follow-up, the standard Cox model overestimated the risk for SCD as compared with the competing risk approach on the relative scale by 25% and 46%, respectively, and on the absolute scale by 2% and 6%, respectively.Conclusions Predictors of various causes of death differ in HD patients. The proposed prediction model for SCD accounts for competing causes of death. External validation of this model is required.

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Section: Discussionsupporting

confidence: 82%

Predictors of Sudden Cardiac Death

Shastri

Tangri

Tighiouart

et al. 2012

Clinical Journal of the American Society of Nephrology

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“…17,18 The importance of understanding the potential role of endothelial dysfunction in SCD is underscored by the observations that SCD is the first and terminal manifestation of coronary artery disease in more than 50% of all cases and that more than two thirds of the victims had no documented coronary artery disease before death. 19 These events are likely to be dependent on the vascular wall properties and components of the plaque, its vulnerability, and its interaction with the circulation. The endothelium regulates all these activities in the plaque as well as the thrombogenicity and the vulnerability of the circulation.…”

Section: Acute Coronary Syndrome and Sudden Deathmentioning

confidence: 99%

Endothelial Function

2005

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“…Most cases of SCD are attributed to an ischemic event, superimposed on underlying coronary atherosclerosis, which triggers a fatal ventricular arrhythmia. A significant fraction of the victims are middle-aged and otherwise may appear in good health (44). Generalized failure may trace its origin to a variety of clinical disorders as well as to aging.…”

Section: Commentsmentioning

confidence: 99%

Air pollution and daily mortality: a hypothesis concerning the role of impaired homeostasis.

Frank

Tankersley

2002

Environ Health Perspect

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Perhaps the most compelling evidence for an effect of low levels of airborne particulate matter (PM) on health comes from timeseries regression analyses that link daily fluctuations in PM and mortality. The evidence is descriptive; the studies were retrospective, so variables could not be manipulated to test specific hypotheses. The approach, although powerful statistically, has rested on several premises: a) that a limited number of fixed outdoor monitors of air quality, a circumstance universal to these analyses, provided reliable estimates of exposure of the population-at-risk; and that adequate adjustments were made for both b) potential confounders, such as collinear air pollutants and changes in weather, and for c) cyclic factors that might modify mortality rate, such as day of the week and seasonal trends. Daily and seasonal changes in weather may affect mortality rate both directly and indirectly, the latter by influencing the physicochemical properties and ground-level concentrations of PM and of air pollution in general. The soundness of these underlying premises remains a matter of debate.Is the association causal? Descriptive epidemiologic studies alone generally are viewed as insufficient to establish causation, especially if the estimated effect is small. They may, however, be used to infer causation. To justify the inference, a number of criteria should be met (1-3). Perhaps the most elusive of these criteria has been a biologic explanation or mechanism for the association (4). Indeed, weak biologic plausibility has been cited by Vedal (5) as "the single largest stumbling block to accepting the association as causal" (p. 558). Our objective (accepting the weight of the evidence as supporting a casual association) is to propose an explanatory hypothesis that, in accordance with Popperian principal, is refutable. We first briefly review salient features of the time-series evidence and their implications.First, the association has been found among communities and nations that differed in their principal sources and composition of air pollution, including PM, as well as in climate. This would imply that no specific attribute of air pollution is an essential proximate cause of death and that an undefined number of such attributes may qualify as sufficient causes. Other forms of environmental stress, including meteorologic variables, may also qualify as sufficient causes (6-8).Second, the association appears independent of population size and density. It has involved chiefly elderly persons with one or more chronic diseases, usually of the heart, blood vessels, or lungs. This would imply that failing health, attributable to aging or illness, largely defines the population at risk. As a corollary, the rest of the population is probably not at risk, especially at current levels of air pollution. And because the rate of physiologic decline can vary markedly among individuals, chronologic age is not a reliable index of vulnerability. However, one must be cautious regarding attributed causes of death. Death ...

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Frequency of Sudden Cardiac Death and Profiles of Risk

Cited by 378 publications

References 66 publications

Predictors of Sudden Cardiac Death

Predictors of Sudden Cardiac Death

Endothelial Function

Air pollution and daily mortality: a hypothesis concerning the role of impaired homeostasis.

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