Secondary prevention of sudden cardiac death.
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ABSTRACT:
SUBMITTER: Chatterjee NA
PROVIDER: S-EPMC8183887 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:There have been tremendous advances in the diagnosis and treatment of heart disease over the last 50 years. Nevertheless, it remains the number one cause of death. About half of heart-related deaths occur suddenly, and in about half of these cases the person was unaware that they had underlying heart disease. Genetic heart disease accounts for only approximately 2% of sudden cardiac deaths, but as it typically occurs in younger people it has been a particular focus of activity in our quest to not only understand the underlying mechanisms of cardiac arrhythmogenesis but also develop better strategies for earlier detection and prevention. In this brief review, we will highlight trends in the recent literature focused on sudden cardiac death in genetic heart diseases and how these studies are contributing to a broader understanding of sudden death in the community.
| S-EPMC5583740 | 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:Wearable cardioverter-defibrillators (WCDs) protect patients from sudden cardiac death (SCD) by detecting and treating life-threatening ventricular tachycardia/fibrillation (VT/VF). Recently, two large studies evaluating WCDs were published. However, the results of older and newer studies have yet to be systematically summarized. The objective of the current study was to conduct a meta-analysis assessing the use and effectiveness of WCDs. We searched MEDLINE and Scopus (January 1998-July 2017) as well as the gray literature. We included registry/observational studies that (1) evaluated adult patients using WCDs; (2) provided data on one or more outcomes of interest; and (3) were full-text studies published in English. We calculated pooled incidence and/or rate [with 95% confidence intervals (CIs)] estimates from nonoverlapping populations using a random-effects meta-analysis model. Statistical heterogeneity was assessed via the I2 statistic. We identified 11 studies (19,882 patients) with nonoverlapping populations/endpoints; seven of them evaluated WCD use across various indications, while the remaining studies restricted their focus to a single indication. Most of the studies were retrospective (82%) and multicenter (64%) in nature, with 45% using manufacturers' registry data. The median duration of WCD use was three or more months in nine (82%) studies, and daily wear time ranged from a mean/median of 17 hours to 24 hours per day across included studies. Seven (64%) studies reported a mean/median daily wear time of more than 20 hours. This meta-analysis showed that the incidences of all-cause and SCD-related mortality among WCD patients were 1.4% (95% CI: 0.7%-2.4%) and 0.2% (95% CI: 0.1%-0.3%), respectively. VT/VF occurred in 2.6% (95% CI: 1.8%-3.5%) of patients. Across patients, 1.7% (95% CI: 1.4%-2.0%) received appropriate WCD treatment, corresponding to a rate of 9.1 patients/100 person-years (95% CI: 6.2-11.9 patients/100 person-years). Successful VT/VF termination following appropriate treatment occurred in 95.5% of patients (95% CI: 92.0%-98.0%) and the incidence of inappropriate treatment was infrequent (0.9%; 95% CI: 0.5%-1.4%). A moderate-to-high degree of statistical heterogeneity was observed in pooled analyses of mortality, VT/VF occurrence, and appropriate/inappropriate treatment (I2 ≥ 41% for all). In conclusion, WCDs appear to be successful in terms of terminating VT/VF in patients with an elevated risk of SCD and are appropriate for use while long-term risk management strategies are being identified.
| S-EPMC7252786 | 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:BackgroundInclusion of 12-lead electrocardiography (ECG) in preparticipation screening of young athletes is controversial because of concerns about cost-effectiveness.ObjectiveTo evaluate the cost-effectiveness of ECG plus cardiovascular-focused history and physical examination compared with cardiovascular-focused history and physical examination alone for preparticipation screening.DesignDecision-analysis, cost-effectiveness model.Data sourcesPublished epidemiologic and preparticipation screening data, vital statistics, and other publicly available data.Target populationCompetitive athletes in high school and college aged 14 to 22 years.Time horizonLifetime.PerspectiveSocietal.InterventionNonparticipation in competitive athletic activity and disease-specific treatment for identified athletes with heart disease.Outcome measureIncremental health care cost per life-year gained.Results of base-case analysisAddition of ECG to preparticipation screening saves 2.06 life-years per 1000 athletes at an incremental total cost of $89 per athlete and yields a cost-effectiveness ratio of $42 900 per life-year saved (95% CI, $21 200 to $71 300 per life-year saved) compared with cardiovascular-focused history and physical examination alone. Compared with no screening, ECG plus cardiovascular-focused history and physical examination saves 2.6 life-years per 1000 athletes screened and costs $199 per athlete, yielding a cost-effectiveness ratio of $76 100 per life-year saved ($62 400 to $130 000).Results of sensitivity analysisResults are sensitive to the relative risk reduction associated with nonparticipation and the cost of initial screening.LimitationsEffectiveness data are derived from 1 major European study. Patterns of causes of sudden death may vary among countries.ConclusionScreening young athletes with 12-lead ECG plus cardiovascular-focused history and physical examination may be cost-effective.Primary funding sourceStanford Cardiovascular Institute and the Breetwor Foundation.
| S-EPMC2873148 | biostudies-literature
Project description:BACKGROUND:Blacks have a higher incidence of out-of-hospital sudden cardiac death (SCD) in comparison with whites. However, the racial differences in the cumulative risk of SCD and the reasons for these differences have not been assessed in large-scale community-based cohorts. The objective of this study is to compare the lifetime cumulative risk of SCD among blacks and whites, and to evaluate the risk factors that may explain racial differences in SCD risk in the general population. METHODS:This is a cohort study of 3832 blacks and 11 237 whites participating in the Atherosclerosis Risk in Communities Study (ARIC). Race was self-reported. SCD was defined as a sudden pulseless condition from a cardiac cause in a previously stable individual, and SCD cases were adjudicated by an expert committee. Cumulative incidence was computed using competing risk models. Potential mediators included demographic and socioeconomic factors, cardiovascular risk factors, presence of coronary heart disease, and electrocardiographic parameters as time-varying factors. RESULTS:The mean (SD) age was 53.6 (5.8) years for blacks and 54.4 (5.7) years for whites. During 27.4 years of follow-up, 215 blacks and 332 whites experienced SCD. The lifetime cumulative incidence of SCD at age 85 years was 9.6, 6.6, 6.5, and 2.3% for black men, black women, white men, and white women, respectively. The sex-adjusted hazard ratio for SCD comparing blacks with whites was 2.12 (95% CI, 1.79-2.51). The association was attenuated but still statistically significant in fully adjusted models (hazard ratio, 1.38; 95% CI, 1.11-1.71). In mediation analysis, known factors explained 65.3% (95% CI 37.9-92.8%) of the excess risk of SCD in blacks in comparison with whites. The single most important factor explaining this difference was income (50.5%), followed by education (19.1%), hypertension (22.1%), and diabetes mellitus (19.6%). Racial differences were evident in both genders but stronger in women than in men. CONCLUSIONS:Blacks had a much higher risk for SCD in comparison with whites, particularly among women. Income, education, and traditional risk factors explained ?65% of the race difference in SCD. The high burden of SCD and the racial-gender disparities observed in our study represent a major public health and clinical problem.
| S-EPMC6443438 | biostudies-literature
Project description:Hemodialysis patients carry a large burden of cardiovascular disease; most onerous is the high risk for sudden cardiac death. Defining sudden cardiac death among hemodialysis patients and understanding its pathogenesis are challenging, but inferences from the existing literature reveal differences between sudden cardiac death among hemodialysis patients and the general population. Vascular calcifications and left ventricular hypertrophy may play a role in the pathophysiology of sudden cardiac death, whereas traditional cardiovascular risk factors seem to have a more muted effect. Arrhythmic triggers also differ in this group as compared to the general population, with some arising uniquely from the hemodialysis procedure. Combined, these factors may alter the types of terminal arrhythmias that lead to sudden cardiac death among hemodialysis patients, having important implications for prevention strategies. This review highlights current knowledge on the epidemiology, pathophysiology, and risk factors for sudden cardiac death among hemodialysis patients. We then examine strategies for prevention, including the use of specific cardiac medications and device-based therapies such as implantable defibrillators. We also discuss dialysis-specific prevention strategies, including minimizing exposure to low potassium and calcium dialysate concentrations, extending dialysis treatment times or adding sessions to avoid rapid ultrafiltration, and lowering dialysate temperature.
| S-EPMC5457912 | biostudies-literature
Project description:Sudden cardiac death (SCD), a sudden pulseless condition due to cardiac arrhythmia, remains a major public health problem despite recent progress in the treatment and prevention of overall coronary heart disease. In this review, we examine the evidence for genetic susceptibility to SCD in order to provide biological insight into the pathogenesis of this devastating disease and to explore the potential for genetics to impact clinical management of SCD risk. Both candidate gene approaches and unbiased genome-wide scans have identified novel biological pathways contributing to SCD risk. Although risk stratification in the general population remains an elusive goal, several studies point to the potential utility of these common genetic variants in high-risk individuals. Finally, we highlight novel methodological approaches to deciphering the molecular mechanisms involved in arrhythmogenesis. Although further epidemiological and clinical applications research is needed, it is increasingly clear that genetic approaches are yielding important insights into SCD that may impact the public health burden imposed by SCD and its associated outcomes.
| S-EPMC3501725 | biostudies-literature
Project description:Although the occurrence of sudden cardiac death (SCD) in a young person is a rare event, it is traumatic and often widely publicized. In recent years, SCD in this population has been increasingly seen as a public health and safety issue. This review presents current knowledge relevant to the epidemiology of SCD and to strategies for prevention, resuscitation, and identification of those at greatest risk. Areas of active research and controversy include the development of best practices in screening, risk stratification approaches and postmortem evaluation, and identification of modifiable barriers to providing better outcomes after resuscitation of young SCD patients. Institution of a national registry of SCD in the young will provide data that will help to answer these questions.
| S-EPMC5033115 | biostudies-literature
Project description:To survey recent developments in the field of genetics encompassing discovery of new candidate genes, new diagnostic strategies, and new therapies for sudden cardiac death (SCD) syndromes.In addition to new mutations in known SCD genes, several novel genes not previously implicated in SCD causation have been found, particularly in long QT syndrome (e.g., KCNJ5, AKAP9, SNTA1), idiopathic ventricular fibrillation (e.g., DPP6, KCNJ8), dilated cardiomyopathy (e.g., NEBL), and hypertrophic cardiomyopathy (HCM; e.g., NEXN). Genetic SCD animal models have provided novel insights into the cellular mechanism and pathogenesis of nearly all the major SCD syndromes, which has led to several new drug therapies for patients with genetic arrhythmia syndromes (e.g., flecainide in catecholaminergic polymorphic ventricular tachycardia). Furthermore, genetic contributions to acquired heart diseases are increasingly being recognized. For example, a 21q21 locus is strongly associated with ventricular fibrillation after myocardial infarction. Near this locus is CXADR, a gene encoding a viral receptor implicated in myocarditis and dilated cardiomyopathy. Finally, common variants in cardiac ion channels and proteins likely contribute to common cardiac phenotypes.Major strides have been made in uncovering new genes, mechanisms, and syndromes that have significantly advanced the diagnosis and treatment of genetic SCD disorders.
| S-EPMC3145336 | biostudies-literature