Introduction: Evidence on drivers of sudden death (SD) is needed to understand its persistently high incidence and inform prevention interventions. SD studies have been hampered by data limitations and restrictive SD criteria. We conducted a population-based study of all-cause, out-of-hospital SD using Emergency Medical Services (EMS) data from Wake County, a large North Carolina county with >1 million residents. Methods: We screened EMS records of out-of-hospital deaths between 2013-2015 among persons aged 18-64 years, collected medical and death records, and adjudicated 399 SD cases according to a standardized protocol. Deaths occurring in hospices or nursing homes were excluded, as were those due to unnatural death or cancer. Deaths were not excluded by time last seen or coronary artery disease (CAD) criteria. Frequency matched living controls were identified from the same county and time. We compiled and summarized findings based on peer-reviewed papers and published abstracts in Table 1. Results: Cardiovascular disease risk factors were common among decedents, including hypertension (60.4%, 244 of 371), though only 14.8% (55 of 371) had documented CAD. SD cases had lower adjusted mean total cholesterol, low-density lipoprotein and high-density lipoprotein levels compared to controls. Furthermore, left ventricular hypertrophy and inflammation suggested nodes on a common causal pathway. Poor health care management was frequent as well as mental health and substance use problems. Environmental factors such as poverty, air pollution and absence of nearby greenways were associated with SD. Conclusions: Conducting a population-based registry of adjudicated SD cases was feasible and provided high quality data for study. Our findings suggest that SD is not only tied to CAD but a syndrome with potentially different environmental and inflammatory etiologies. Future studies should investigate modifiable risk factors for interventions to prevent SD.

BackgroundSudden death accounts for approximately 10% of deaths among working-age adults and is associated with poor air quality. Objectives: To identify high-risk groups and potential modifiers and mediators of risk, we explored previously established associations between fine particulate matter (PM2.5) and sudden death stratified by potential risk factors.MethodsSudden death victims in Wake County, NC, from 1 March 2013 to 28 February 2015 were identified by screening Emergency Medical Systems reports and adjudicated (n = 399). Daily PM2.5 concentrations for Wake County from the Air Quality Data Mart were linked to event and control periods. Potential modifiers included greenspace metrics, clinical conditions, left ventricular hypertrophy (LVH), and neutrophil-to-lymphocyte ratio (NLR). Using a case-crossover design, conditional logistic regression estimated the OR (95%CI) for sudden death for a 5 μg/m3 increase in PM2.5 with a 1-day lag, adjusted for temperature and humidity, across risk factor strata.ResultsIndividuals having LVH or an NLR above 2.5 had PM2.5 associations of greater magnitude than those without [with LVH OR: 1.90 (1.04, 3.50); NLR > 2.5: 1.25 (0.89, 1.76)]. PM2.5 was generally less impactful for individuals living in areas with higher levels of greenspace.ConclusionLVH and inflammation may be the final step in the causal pathway whereby poor air quality and traditional risk factors trigger arrhythmia or myocardial ischemia and sudden death. The combination of statistical evidence with clinical knowledge can inform medical providers of underlying risks for their patients generally, while our findings here may help guide interventions to mitigate the incidence of sudden death.

Introduction: Out-of-hospital sudden death accounts for over 10% of all deaths among working age adults. Traditional methods of identifying victims by screening Emergency Medical Services (EMS) reports and clinical adjudication are labor intensive. We hypothesize death certificates may provide efficient and reliable information to identify victims of sudden death. This study aims to compare a death certificate-based sudden death screening algorithm to a more time-intensive EMS-screened and cardiologist-adjudicated sudden death method. Methods: Death certificates from four North Carolina counties (Guilford, Mecklenburg, Surry, Wake) were screened by written protocol. Cases were excluded if age under 18 or over 64, hospital death, non-free living, or non-natural cause of death (overdose, gunshot wound, suicide, drowning, cancer, traumatic death without evidence of coronary disease). Census tract data was determined from victim home address. These 2013 death certificate cases were compared to our preexisting dataset of EMS-screened, cardiologist-adjudicated cases identified in Wake County 2013-2015. Demographic data was compared between datasets using Wilcoxon rank sum test for continuous variables and Fisher’s exact test for categorical variables. Results: Death certificate cases included 518 victims and EMS-screened/cardiologist-adjudicated cases included 399 victims. There were 99 overlapping cases in both datasets which were excluded from this comparative analysis. Demographic and social data were similar in the two groups (Table 1). Conclusion: Like previous methods have shown, sudden death occurs predominantly among unmarried individuals and is more common among black race and male sex. Death certificate screening methods are sufficient to identify sudden death victims to allow for efficient, population-based assessment of the epidemiology of sudden death. These methods may allow for identification of high-risk communities to facilitate intervention to reduce the incidence of sudden death.

Purpose of ReviewThis review summarizes approaches towards neighborhood characterization in relation to cardiovascular health; contemporary investigations relating neighborhood factors to cardiovascular risk and disease; and initiatives to support community-based interventions to address neighborhood-based social determinants related to cardiovascular health.Recent FindingsNeighborhoods may be characterized by Census-derived measures, geospatial data, historical databases, and metrics that incorporate data from electronic medical records and health information exchange databases. Current research has examined neighborhood determinants spanning racial segregation, access to healthcare and food, educational opportunities, physical and built environment, and social environment, and their relations to cardiovascular health and associated outcomes. Community-based interventions have potential to alleviate health disparities but remain limited by implementation challenges.Consideration of neighborhood context is essential in the design of interventions to prevent cardiovascular disease (CVD) and promote health equity. Partnership with community stakeholders may enhance implementation of programs addressing neighborhood-based health determinants.

Sudden death is a leading cause of deaths nationally. Definitions of sudden death vary greatly, resulting in imprecise estimates of its frequency and incomplete knowledge of its risk factors. The degree to which time-based and coronary artery disease (CAD) criteria impacts estimates of sudden death frequency and risk factors is unknown. Here, we apply these criteria to a registry of all-cause sudden death to assess its impact on sudden death frequency and risk factors. The sudden unexpected death in North Carolina (SUDDEN) project is a registry of out of-hospital, adjudicated, sudden unexpected deaths attended by Emergency Medical Services. Deaths were not excluded by time since last seen or alive or by prior symptoms or diagnosis of CAD. Common criteria for sudden death based on time since last seen alive (both 24 hours and 1 hour) and prior diagnosis of CAD were applied to the SUDDEN case registry. The proportion of cases satisfying each of the 4 criteria was calculated. Characteristics of victims within each restrictive set of criteria were measured and compared to the SUDDEN registry. There were 296 qualifying sudden deaths. Application of 24 hour and 1 hour timing criteria compared to no timing criteria reduced cases by 25.0% and 69.6%, respectively. Addition of CAD criteria to each timing criterion further reduced qualifying cases, for a total reduction of 81.8% and 90.5%, respectively. However, characteristics among victims meeting restrictive criteria remained similar to the unrestricted population. Timing and CAD criteria dramatically reduces estimates of the number of sudden deaths without significantly impacting victim characteristics.

Sudden death (SD) is a leading cause of premature mortality among working-age adults. 1 Mirzaei M Joodi G Bogle B Chen S Simpson Jr., RJ Years of life and productivity loss because of adult sudden unexpected death in the United States. Med Care. 2019; 57: 498-502 Crossref PubMed Scopus (11) Google Scholar Chronic hypertension is a risk factor for SD. 1 Mirzaei M Joodi G Bogle B Chen S Simpson Jr., RJ Years of life and productivity loss because of adult sudden unexpected death in the United States. Med Care. 2019; 57: 498-502 Crossref PubMed Scopus (11) Google Scholar Preeclampsia, a hypertensive disorder of pregnancy, increases risk of chronic hypertension and cardiovascular (CV) disease. 2 Countouris ME Villanueva FS Berlacher KL Cavalcante JL Parks WT Catov JM. Association of hypertensive disorders of pregnancy with left ventricular remodeling Later in life. J Am Coll Cardiol. 2021; 77: 1057-1068 Crossref PubMed Scopus (30) Google Scholar ,3 Wu P Haththotuwa R Kwok CS Babu A Kotronias RA Rushton C Zaman A Fryer AA Kadam U Chew-Graham CA Mamas MA. Preeclampsia and future cardiovascular health: a systematic review and meta-analysis. Circ Cardiovasc Qual Outcomes. 2017; 10e003497 Crossref PubMed Scopus (580) Google Scholar Given the overlap in risk factors, we sought to determine the relation between SD and a history of preeclampsia in women.

Background: Sudden death accounts for approximately 10% of deaths among working age adults. The rate of sudden death among females is one third lower than males, although the burden of chronic medical conditions are similar in victims of both sexes. The reasons for this difference are unclear and may be important in addressing preventive screening underutilization, as preventive screenings have been shown to reduce morbidity and mortality. Research Questions: Does utilization of preventive services differ among sudden death victims and living controls? Do these differences vary by sex? Aims: We aim to describe receipt of preventive screenings and influenza vaccination in sudden death victims and to compare these rates to those of a living control population. Methods: Clinical records from 267 out-of-hospital sudden death victims aged 18-64 in Wake County, North Carolina from 2013-2015 and 1112 demographically matched living controls from the same county and time were compared. Victims were identified by screening Emergency Medical Service records and adjudicated to exclude expected deaths from chronic disease, trauma, suicide, and overdose. Records were systematically reviewed for evidence of influenza vaccination and receipt of colon, cervical, and breast cancer screenings within the past five years, according to USPSTF criteria. Percentage of individuals who received each preventive screening were compared using means difference tests. Binomial regression was performed to investigate the effect of insurance status on preventive care receipt Results: Rates of colonoscopy and influenza vaccination were similar between cases and controls among both sexes. Female victims had low utilization of preventive services and were less likely to have received Pap smears (24.1% vs 50.9%; p<0.001) and mammography (44.0% vs 65.2%; p<0.001) compared to controls. While these differences can be partially explained by insurance status, with both private and public insurance being protective, screening differences remained significant. Conclusion: Significant differences in preventive screenings are present among female sudden death victims and may represent an important behavioral pattern to identify and intervene upon in these vulnerable patients.

Guidelines for pulmonary hypertension (PH) continue to evolve to reflect a focus on early disease detection and treatment. This is driven by contemporary data that suggest PH morbidity and mortality exist at smaller hemodynamic parameters than was previously believed. 1 Maron BA Brittain EL Hess E Waldo SW Barón AE Huang S Goldstein RH Assad T Wertheim BM Alba GA Leopold JA Olschewski H Galiè N Simonneau G Kovacs G Tedford RJ Humbert M Choudhary G Pulmonary vascular resistance and clinical outcomes in patients with pulmonary hypertension: a retrospective cohort study. Lancet Respir Med. 2020; 8: 873-884 Abstract Full Text Full Text PDF PubMed Scopus (112) Google Scholar In 2019, the European Society of Cardiology guidelines reduced the threshold for mean pulmonary artery pressure (mPAP) from 25 to 20 mm Hg, and subsequently, in 2022, the threshold for pulmonary vascular resistance (PVR) to qualify for precapillary PH was reduced from 3 to 2 Woods units. 2 Simonneau G Montani D Celermajer DS Denton CP Gatzoulis MA Krowka M Williams PG Souza R Haemodynamic definitions and updated clinical classification of pulmonary hypertension. Eur Respir J. 2019; 531801913 Crossref Scopus (2279) Google Scholar ,3 Humbert M Kovacs G Hoeper MM Badagliacca R Berger RMF Brida M Carlsen J Coats AJS Escribano-Subias P Ferrari P Ferreira DS Ghofrani HA Giannakoulas G Kiely DG Mayer E Meszaros G Nagavci B Olsson KM Pepke-Zaba J Quint JK Radegran G Simonneau G Sitbon O Tonia T Toshner M Vachiery JL Vonk Noordegraaf A Delcroix M Rosenkranz S ESC/ERS Scientific Document Group2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Respir J. 2023; 612200879 Crossref Scopus (255) Google Scholar With these changes, the definition of precapillary PH, or pulmonary arterial hypertension (PAH), is mPAP >20 mm Hg, PVR >2 Woods units, and pulmonary arterial wedge pressure (PAWP) ≤15 mm Hg whereas postcapillary PH, or PH left-sided cardiac disease (PH-LCD ), is defined as mPAP ≥20 mm Hg, PVR ≤2 Woods units, and PAWP >15 mm Hg. 3 Humbert M Kovacs G Hoeper MM Badagliacca R Berger RMF Brida M Carlsen J Coats AJS Escribano-Subias P Ferrari P Ferreira DS Ghofrani HA Giannakoulas G Kiely DG Mayer E Meszaros G Nagavci B Olsson KM Pepke-Zaba J Quint JK Radegran G Simonneau G Sitbon O Tonia T Toshner M Vachiery JL Vonk Noordegraaf A Delcroix M Rosenkranz S ESC/ERS Scientific Document Group2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Respir J. 2023; 612200879 Crossref Scopus (255) Google Scholar As these diagnostic criteria capture a larger population with PH, there is also an increasing number of patients who are qualifying for combined precapillary and postcapillary PH (CpcPH), with mPAP >20 mm Hg, PVR >2 Woods units, and PAWP >15 mm Hg. The pathophysiology of CpcPH is heterogeneous; its genetics likely vary from isolated postcapillary PH, and patients exhibit a broad range of phenotypes between group 1 PAH and group 2 PH-LCD . 4 Miller WL Grill DE Borlaug BA Clinical features, hemodynamics, and outcomes of pulmonary hypertension due to chronic heart failure with reduced ejection fraction: pulmonary hypertension and heart failure. JACC Heart Fail. 2013; 1: 290-299 Crossref PubMed Scopus (237) Google Scholar ,5 Vachiéry JL Tedford RJ Rosenkranz S Palazzini M Lang I Guazzi M Coghlan G Chazova I De Marco T Pulmonary hypertension due to left heart disease. Eur Respir J. 2019; 531801897 Crossref PubMed Scopus (371) Google Scholar It has been shown that CpcPH, carries a greater risk of death than does PH-LCD. This has been driving increased conversation and investigation surrounding the role of diagnostic procedures such as inhaled nitric oxide (iNO) for assessment of vasoreactivity and management of CpcPH with therapies that have only been indicated to be efficacious in PAH. There is a paucity of drug trials that include patients with CpcPH, the most significant of which is the Macitentan in pulmonary hypertension due to left ventricular dysfunction (MELODY-1) study in which the investigators explored the use of macitentan compared with placebo and showed increased fluid retention without improved hemodynamics. 6 Vachiéry JL Delcroix M Al-Hiti H Efficace M Hutyra M Lack G Papadakis K Rubin LJ Macitentan in pulmonary hypertension due to left ventricular dysfunction. Eur Respir J. 2018; 511701886 Crossref Scopus (137) Google Scholar There is no multicentered trial that has shown benefit of PAH-specific medication in PH-LCD. 5 Vachiéry JL Tedford RJ Rosenkranz S Palazzini M Lang I Guazzi M Coghlan G Chazova I De Marco T Pulmonary hypertension due to left heart disease. Eur Respir J. 2019; 531801897 Crossref PubMed Scopus (371) Google Scholar Currently, guidelines recommend "an individualized approach to treatment" in CpcPH given this lack of data and varied tolerance of PAH-specific drugs in this population. 3 Humbert M Kovacs G Hoeper MM Badagliacca R Berger RMF Brida M Carlsen J Coats AJS Escribano-Subias P Ferrari P Ferreira DS Ghofrani HA Giannakoulas G Kiely DG Mayer E Meszaros G Nagavci B Olsson KM Pepke-Zaba J Quint JK Radegran G Simonneau G Sitbon O Tonia T Toshner M Vachiery JL Vonk Noordegraaf A Delcroix M Rosenkranz S ESC/ERS Scientific Document Group2022 ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Respir J. 2023; 612200879 Crossref Scopus (255) Google Scholar The ability to predict disease progression and response to medications has been elusive and lives more within the space of the art rather than the science of medicine. Can Inhaled Nitric Oxide Response Predict Tolerance to Therapies and Survival in Patients With Combined Precapillary and Postcapillary Pulmonary Hypertension?American Journal of CardiologyVol. 207PreviewInhaled nitric oxide (iNO) relaxes the pulmonary circulation and variably increases the left ventricular preload and pulmonary artery wedge pressure (PAWP)—hemodynamic information that may help guide treatment decisions and assess prognosis in patients with combined precapillary and postcapillary pulmonary hypertension (PH). We included consecutive patients with combined precapillary and postcapillary PH (mean pulmonary artery pressure >20 mm Hg, PAWP >15 mm Hg, and pulmonary vascular resistance [PVR] >2 Woods unit [WU]) who underwent right-sided cardiac catheterization with iNO at the Cleveland Clinic Pulmonary Vascular Disease program between 2017 and 2022. Full-Text PDF

Introduction: Sudden death is often attributed to coronary artery disease. Demonstrating that sudden death exhibits a different circadian profile than coronary artery disease would support the emerging concept that sudden death is a syndrome, with multiple etiologies. Hypothesis: Sudden death will demonstrate a circadian peak with deaths more frequent in the morning hours. Methods: The study analyzed 399 sudden death victims aged 18-64 attended by Wake County Emergency Medical Services (EMS) from 2013 to 2015. Time of death was determined using EMS records and medical examiner reports. When time of death could not be reliably determined for a victim, the victim was removed from the study. Only 169 deaths (42.3%) where time of death was reliably known to within one hour were included in the final analysis. Bayesian hierarchical modeling identified the location and/or absence of peak times for sudden death victims overall and subgroups with heart failure (19), coronary artery disease (40), hypertension (89), and respiratory disorders (48). Results: Time of death for all-cause sudden death victims spanned from 6:30 AM to noon, with no evidence of a specific, circadian peak. However, sudden death victims with underlying chronic heart failure displayed a strong circadian peak around 7:00 AM, while respiratory disorder cases showed a limited peak in the mid to late morning. Victims with coronary artery disease and hypertension exhibited no peak (Figure 1). Conclusions: Sudden death victims lack a distinct overall pattern for time of death. However, individuals with underlying heart failure and possibly respiratory diseases demonstrate a circadian pattern. These findings support the notion that sudden death has multiple causes beyond coronary artery disease. Future preventive interventions should consider the diverse etiologies of sudden death.

Background: In the United States, former incarceration is a risk factor for chronic conditions and sudden death (SD) due to poor healthcare continuity after release and lack of community support. During the COVID-19 pandemic, all-cause mortality increased, and preexisting risk factors and social limitations of having an incarceration history were exacerbated. We hypothesized that sudden deaths among the formerly incarcerated increased during the pandemic. Methods: North Carolina death certificates from pre-COVID-19 (2014) and during the COVID-19 pandemic (2020) were screened for presumed SD. Individuals were excluded based on age (<18 or >65), violent or expected deaths, and deaths in hospitals or care facilities. Deaths were matched to the North Carolina Department of Public Safety Criminal Offender Database for a history of incarceration. ICD-10 codes for hypertension, diabetes, chronic respiratory disease, obesity, mental health, and substance abuse were extracted from the top four causes of death on the death certificates. Results: We found no significant difference in the prevalence of former incarceration in SD victims from 2014 to 2020. In 2020, the odds of substance abuse among SD victims with a history of incarceration were significantly greater compared to those without a history of incarceration (OR (95CI): 2.29 (1.91-2.73)). The odds of substance abuse among the formerly incarcerated were greater in 2020 SD victims compared to 2014 SD victims (2.29 (1.76-2.99)). Conclusion: Sudden death

Although cardiovascular death is a growing source of mortality for people living with human immunodeficiency virus (HIV), the risk factors and circumstances surrounding sudden death in this population are poorly understood. We compared 399 adult sudden death victims reported by Emergency Medical Services in North Carolina to 1,114 controls. Sudden death was more common among HIV-positive than HIV-negative individuals (OR: 2.59, 95% CI: 1.15-5.83). In a multivariable model of sudden death victims including Black race, BMI, and history of divorce, incarceration, substance abuse, and respiratory disease, HIV-positive individuals were more likely to be Black (adjusted OR [aOR]: 6.04, 95% CI: 1.08-33.7) or divorced (aOR: 4.71, 95% CI: 1.04-21.3), adjusted for all other variables in the model. Compared to controls with HIV, sudden death victims with HIV were more likely to have a history of incarceration, divorce, respiratory disease, alcohol abuse, or dyslipidemia. A qualitative assessment of victims suggested that many died in isolation, suffering from past and current substance abuse and depression. HIV infection appears to be an important risk factor for sudden death, and incarceration history, social isolation, and medical comorbidities contribute to sudden death risk for HIV-positive individuals.