HIV Infection and the Risk of World Health Organization-Defined Sudden Cardiac Death.
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ABSTRACT:
SUBMITTER: Freiberg MS
PROVIDER: S-EPMC8649505 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND:Conventional definitions of sudden cardiac death (SCD) presume cardiac cause. We studied the World Health Organization-defined SCDs autopsied in the POST SCD study (Postmortem Systematic Investigation of SCD) to determine whether premortem characteristics could identify autopsy-defined sudden arrhythmic death (SAD) among presumed SCDs. METHODS:Between January 2, 2011, and January 4, 2016, we prospectively identified all 615 World Health Organization-defined SCDs (144 witnessed) 18 to 90 years in San Francisco County for medical record review and autopsy via medical examiner surveillance. Autopsy-defined SADs had no extracardiac or acute heart failure cause of death. We used 2 nested sets of premortem predictors-an emergency medical system set and a comprehensive set adding medical record data-to develop Least Absolute Selection and Shrinkage Operator models of SAD among witnessed and unwitnessed cohorts. RESULTS:Of 615 presumed SCDs, 348 (57%) were autopsy-defined SAD. For witnessed cases, the emergency medical system model (area under the receiver operator curve 0.75 [0.67-0.82]) included presenting rhythm of ventricular tachycardia/fibrillation and pulseless electrical activity, while the comprehensive (area under the receiver operator curve 0.78 [0.70-0.84]) added depression. If only ventricular tachycardia/fibrillation witnessed cases (n=48) were classified as SAD, sensitivity was 0.46 (0.36-0.57), and specificity was 0.90 (0.79-0.97). For unwitnessed cases, the emergency medical system model (area under the receiver operator curve 0.68 [0.64-0.73]) included black race, male sex, age, and time since last seen normal, while the comprehensive (area under the receiver operator curve 0.75 [0.71-0.79]) added use of β-blockers, antidepressants, QT-prolonging drugs, opiates, illicit drugs, and dyslipidemia. If only unwitnessed cases <1 hour (n=59) were classified as SAD, sensitivity was 0.18 (0.13-0.22) and specificity was 0.95 (0.90-0.97). CONCLUSIONS:Our models identify premortem characteristics that can better specify autopsy-defined SAD among presumed SCDs and suggest the World Health Organization definition can be improved by restricting witnessed SCDs to ventricular tachycardia/fibrillation or nonpulseless electrical activity rhythms and unwitnessed cases to <1 hour since last normal, at the cost of sensitivity.
| S-EPMC6738572 | biostudies-literature
Project description:Arrhythmic sudden cardiac death (SCD) may be caused by ventricular tachycardia/fibrillation or pulseless electric activity/asystole. Effective risk stratification to identify patients at risk of arrhythmic SCD is essential for targeting our healthcare and research resources to tackle this important public health issue. Although our understanding of SCD because of pulseless electric activity/asystole is growing, the overwhelming majority of research in risk stratification has focused on SCD-ventricular tachycardia/ventricular fibrillation. This review focuses on existing and novel risk stratification tools for SCD-ventricular tachycardia/ventricular fibrillation. For patients with left ventricular dysfunction or myocardial infarction, advances in imaging, measures of cardiac autonomic function, and measures of repolarization have shown considerable promise in refining risk. Yet the majority of SCD-ventricular tachycardia/ventricular fibrillation occurs in patients without known cardiac disease. Biomarkers and novel imaging techniques may provide further risk stratification in the general population beyond traditional risk stratification for coronary artery disease alone. Despite these advances, significant challenges in risk stratification remain that must be overcome before a meaningful impact on SCD can be realized.
| S-EPMC4466101 | biostudies-literature
Project description:PurposeCardiovascular health (CVH) status is associated with several cardiovascular outcomes; however, correlations between changes in CVH status and risk of sudden cardiac death (SCD) are unknown. We aimed to evaluate associations between changes in CVH status and risk of SCD and all-cause death in older adults.Materials and methodsWe used data from the Korea National Health Insurance Service-Senior cohort database (2005-2012). Six metrics from the American Heart Association (smoking, body mass index, physical activity, blood pressure, total cholesterol, and fasting blood glucose) were used to calculate CVH scores. Changes in CVH status between two health checkups were categorized as low to low, low to high, high to low, and high to high.ResultsWe included 105200 patients whose CVH status for an initial and follow-up health checkup (2-year interval) was available. During a median of 5.2 years of follow-up after a second health checkup, 688 SCDs occurred. Compared to patients with a persistent low CVH status, those with a consistently high CVH status had a reduced risk of SCD [adjusted hazard ratio (HR), 0.69; 95% confidence interval (CI), 0.56-0.86] and all-cause death (adjusted HR, 0.74; 95% CI, 0.69-0.78). The risk of all-cause death followed similar trends. However, an inconsistent linear relationship was observed for changes in CVH status and the risk of SCD, but not of all-cause death.ConclusionMaintaining a high CVH status was associated with future risks of SCD and all-cause death among an older adult population.
| S-EPMC8007437 | biostudies-literature
Project description:PurposeSudden cardiac death (SCD) is an important cause of mortality in the adult population. Height has been associated with cardiac hypertrophy and an increased risk of arrhythmias but also with decreased risk of coronary heart disease, suggesting a complex association with SCD.MethodsWe examined the association of adult height with the risk of physician-adjudicated SCD in two large population-based cohorts: the Cardiovascular Health Study and the Atherosclerosis Risk in Communities study.ResultsOver an average follow-up time of 11.7 years in Cardiovascular Health Study, there were 199 (3.6%) cases of SCD among 5556 participants. In Atherosclerosis Risk in Communities study, over 12.6 years, there were 227 (1.5%) cases of SCD among 15,633 participants. In both cohorts, there was a trend toward decreased SCD with taller height. In fixed effects meta-analysis, the pooled hazard ratio per 10 cm of height was 0.84; 95% confidence interval, 0.73-0.98; P = .03. The association of increased height with lower risk of SCD was slightly attenuated after inclusion of risk factors associated with height, such as hypertension and left ventricular hypertrophy. The association appeared stronger among men than women in both cohorts.ConclusionsIn two population-based prospective cohorts of different ages, greater height was associated with lower risk of SCD.
| S-EPMC3945001 | biostudies-literature
Project description:Afferent and efferent cardiac neurotransmission via the cardiac nerves intricately modulates nearly all physiological functions of the heart (chronotropy, dromotropy, lusitropy, and inotropy). Afferent information from the heart is transmitted to higher levels of the nervous system for processing (intrinsic cardiac nervous system, extracardiac-intrathoracic ganglia, spinal cord, brain stem, and higher centers), which ultimately results in efferent cardiomotor neural impulses (via the sympathetic and parasympathetic nerves). This system forms interacting feedback loops that provide physiological stability for maintaining normal rhythm and life-sustaining circulation. This system also ensures that there is fine-tuned regulation of sympathetic-parasympathetic balance in the heart under normal and stressed states in the short (beat to beat), intermediate (minutes to hours), and long term (days to years). This important neurovisceral/autonomic nervous system also plays a major role in the pathophysiology and progression of heart disease, including heart failure and arrhythmias leading to sudden cardiac death. Transdifferentiation of neurons in heart failure, functional denervation, cardiac and extracardiac neural remodeling has also been identified and characterized during the progression of disease. Recent advances in understanding the cellular and molecular processes governing innervation and the functional control of the myocardium in health and disease provide a rational mechanistic basis for the development of neuraxial therapies for preventing sudden cardiac death and other arrhythmias. Advances in cellular, molecular, and bioengineering realms have underscored the emergence of this area as an important avenue of scientific inquiry and therapeutic intervention.
| S-EPMC4465108 | biostudies-literature
Project description:Sudden cardiac death (SCD) is a major source of mortality and is the first manifestation of heart disease for the majority of cases. Thus, there is a definite need to identify risk factors for SCD that can be modified at the population level. Exposure to traffic, measured by residential roadway proximity, has been shown to be associated with an increased risk of cardiovascular disease. Our objective was to determine whether roadway proximity was associated with an increased risk of SCD and to compare that risk with the risk of other coronary heart disease outcomes.A total of 523 cases of SCD were identified over 26 years of follow-up among 107 130 members of the prospective Nurses' Health Study. We calculated residential distance to roadways at all residential addresses from 1986 to 2012. In age- and race-adjusted models, women living within 50 m of a major roadway had an elevated risk of SCD (hazard ratio=1.56; 95% confidence interval, 1.18-2.05). The association was attenuated but still statistically significant after controlling for potential confounders and mediators (hazard ratio=1.38; 95% confidence interval, 1.04-1.82). The equivalent adjusted hazard ratios for nonfatal myocardial infarction and fatal coronary heart disease were 1.08 (95% confidence interval, 0.96-1.23) and 1.24 (95% confidence interval, 1.03-1.50), respectively.Among this sample of middle-aged and older women, roadway proximity was associated with elevated and statistically significant risks of SCD and fatal coronary heart disease, even after controlling for other cardiovascular risk factors.
| S-EPMC4382912 | biostudies-literature
Project description:BACKGROUND:This study assessed the echocardiographic predictors of sudden cardiac death (SCD) within 2 population-based cohorts. METHODS AND RESULTS:Echocardiograms were obtained on 2383 participants (1993-1995) from the ARIC study (Atherosclerosis Risk in Communities; 100% black) and 5366 participants (1987-1989 and 1994-1995) from the CHS (Cardiovascular Health Study). The main outcome was physician-adjudicated SCD. We used Cox proportional-hazards models with incident coronary heart disease and heart failure as time-dependent covariates to assess the association between echocardiographic variables and SCD, adjusting for Framingham risk score variables, coronary heart disease, and renal function. Cohort-specific results were meta-analyzed. During a median follow-up of 7.3 and 13.1 years, 44 ARIC study participants and 275 CHS participants had SCD, respectively. In the meta-analyzed results, the adjusted hazard ratios (95% confidence intervals) for predictors of SCD were 3.07 (2.29-4.11) for reduced left ventricular ejection fraction; 1.85 (1.36-2.52) for mitral annular calcification; 1.64 (1.07-2.51) for mitral E/A >1.5, and 1.52 (1.14-2.02) for mitral E/A <0.7 (versus mitral E/A 0.7-1.5); 1.30 (1.15-1.48) per 1 SD increase in left ventricular mass; and 1.15 (1.02-1.30) per 1 SD increase in left atrial diameter. A receiver-operating characteristic model for prediction of SCD using Framingham risk score variables had a C statistic of 0.61 for ARIC study and 0.67 for CHS; the full multivariable model including all echocardiographic variables had a C statistic of 0.76 for ARIC study and 0.74 for CHS. CONCLUSIONS:In addition to reduced left ventricular ejection fraction, we identified other echocardiographic-derived variables predictive for SCD that provided incremental value compared with clinical risk factors.
| S-EPMC5010094 | biostudies-literature
Project description:BACKGROUND:Elevated fibroblast growth factor 23 (FGF-23) concentrations are associated with greater risk of cardiovascular events and mortality, especially among people with chronic kidney disease (CKD). Because individuals with CKD are at an increased risk of sudden cardiac death (SCD), we sought to understand whether FGF-23 level is a stronger risk factor for SCD versus non-SCD. STUDY DESIGN:Cohort study. SETTING & PARTICIPANTS:3,244 participants 65 years or older in the community-based Cardiovascular Health Study. PREDICTOR:Plasma FGF-23 concentrations. OUTCOMES:We assessed SCD and non-SCD in these analyses. SCD was adjudicated rigorously and was defined as a sudden pulseless condition of cardiac origin in a previously stable person occurring out of hospital or in the emergency department. MEASUREMENTS:We estimated associations of baseline FGF-23 concentrations with SCD and non-SCD using Cox proportional hazards models after adjustment for demographics, cardiovascular risk factors, comorbid conditions, and kidney function. We also tested whether associations differed by CKD status. RESULTS:During a median follow-up of 8.1 years, there were 118 adjudicated SCD and 570 non-SCD events. After multivariable adjustment for demographics, cardiovascular risk factors, comorbid conditions, and parameters of kidney function, higher FGF-23 concentrations were an independent risk factor for non-SCD (HR [per doubling], 1.17; 95% CI, 1.06-1.30). However, elevated FGF-23 concentrations were not associated independently with SCD (HR [per doubling], 1.07; 95% CI, 0.85-1.35). In stratified analysis by CKD status (36.5% of cohort), doubling of FGF-23 concentrations was associated independently with non-SCD (adjusted HR, 1.26; 95% CI, 1.10-1.45). A similar magnitude of association was observed between FGF-23 level and SCD in the CKD subgroup; however, it was not significant (HR, 1.20; 95% CI, 0.89-1.62). LIMITATIONS:Limited power to detect moderate-sized effects between FGF-23 level and SCD in both the primary and stratified analyses. CONCLUSIONS:In this population-based study, FGF-23 level elevations were associated independently with non-SCD. Among individuals with CKD, the associations between FGF-23 level and SCD and non-SCD were similar.
| S-EPMC4485528 | biostudies-literature
Project description:Sudden cardiac death (SCD) is a leading cause of death in the United States, but the relative public health burden is unknown. We estimated the burden of premature death from SCD and compared it with other diseases.Analyses were based on the following data sources (using most recent sources that provided appropriately stratified data): (1) leading causes of death among men and women from 2009 US death certificate reporting; (2) individual cancer mortality rates from 2008 death certificate reporting from the Centers for Disease Control and Prevention's National Program of Cancer Registries; (3) county, state, and national population data for 2009 from the US Census Bureau; and (4) SCD rates from the Oregon Sudden Unexpected Death Study (SUDS) population-based surveillance study of SCD between 2002 and 2004. Cases were identified from multiple sources in a prospectively designed surveillance program. Incidence, counts, and years of potential life lost for SCD and other major diseases were compared. The age-adjusted national incidence of SCD was 60 per 100 000 population (95% confidence interval, 54-66 per 100,000). The burden of premature death for men (2.04 million years of potential life lost; 95% uncertainty interval, 1.86-2.23 million) and women (1.29 million years of potential life lost; 95% uncertainty interval, 1.13-1.45 million) was greater for SCD than for all individual cancers and most other leading causes of death.The societal burden of SCD is high relative to other major causes of death. Accordingly, improved national surveillance with the goal of optimizing and monitoring SCD prevention and treatment should be a high priority.
| S-EPMC4041478 | biostudies-literature
Project description:ImportanceQT-prolonging medications (QTPMs) are a reported risk factor for sudden cardiac death (SCD) when defined by consensus criteria that presume an arrhythmic cause. The effect of QTPM on autopsy-defined sudden arrhythmic death (SAD) is unknown.ObjectiveTo evaluate the association between QTPM and autopsy-defined SAD vs nonarrhythmic cause of sudden death.Design, setting, and participantsThis prospective countywide case-control study included World Health Organization-defined (presumed) SCD cases who underwent autopsy as part of the San Francisco Postmortem Systematic Investigation of Sudden Cardiac Death Study (POST SCD) to determine arrhythmic or nonarrhythmic cause, and control deaths due to trauma (hereinafter referred to as trauma controls) in San Francisco County, California, from February 1, 2011, to March 1, 2014. Multivariate regression was used to evaluate the association of QTPM with the risk of presumed SCD, autopsy-defined SAD, and non-SAD compared with trauma controls. Medication exposure, determined by prescription lists and postmortem toxicologic findings, was used to calculate a summative QTPM exposure score (range, 0-20). Data were analyzed from September 1, 2018, to June 15, 2019.ExposureQT-prolonging medication exposure, as measured by QTPM score (1 indicated low; 2-4, moderate; and >4, high).Main outcomes and measuresDeath due to trauma, presumed SCD, and autopsy-defined non-SAD and SAD with no postmortem findings of extracardiac cause.ResultsA total of 629 patients (mean [SD] age, 61.4 [15.7] years; 439 men [69.8%]) were included, 525 with presumed SCDs and 104 traumatic death controls. Individuals with presumed SCDs had higher exposure and were more likely to be taking any QTPM (291 [55.4%] vs 28 [26.9%]; P?<?.001) than trauma controls. Use of QTPMs was associated with increased risk of presumed SCD in low (odds ratio [OR], 2.25 [95% CI, 1.03-4.96]; P?=?.04) and high (OR, 6.70 [95% CI, 1.47-30.67]; P?=?.01) exposure groups. After autopsy adjudication, use of QTPMs was associated with increased risk of non-SAD (low-risk OR, 2.88 [95% CI, 1.18-6.99; P?=?.02]; moderate-risk OR, 2.62 [95% CI, 1.20-5.73; P?=?.02]; and high-risk OR, 14.22 [95% CI, 2.91-69.30; P?=?.001]) but not SAD in all exposure groups. This association was attenuated by the exclusion of occult overdose non-SADs in the highest exposure group.Conclusions and relevanceThese findings confirm the association between QTPMs and presumed SCD; however, after autopsy, this risk was specific for nonarrhythmic causes of sudden death. Studies using consensus SCD criteria may overestimate the association of QTPMs with the risk of SAD.
| S-EPMC7052791 | biostudies-literature