{"title":"Association of cardiovascular-kidney-metabolic syndrome with all-cause and cardiovascular mortality: A prospective cohort study","authors":"Jiangtao Li , Xiang Wei","doi":"10.1016/j.ajpc.2025.100985","DOIUrl":"10.1016/j.ajpc.2025.100985","url":null,"abstract":"<div><h3>Background</h3><div>Given evidence on the cardiovascular disease (CVD) risk conferred by comorbidity risk factors, the American Heart Association (AHA) recently introduced a novel staging construct, named cardiovascular-kidney-metabolic (CKM) syndrome. This study examined the association of CKM syndrome stages with all-cause and cardiovascular mortality among US adults.</div></div><div><h3>Methods</h3><div>Data were from the National Health and Nutrition Examination Survey (NHANES) 1999–2018 at baseline linked to the 2019 National Death Index records. For each participant, the CKM syndrome was classified into five stages: stage 0 (no CKM risk factors), 1 (excess or dysfunctional adiposity), 2 (metabolic risk factors and chronic kidney disease), 3 (subclinical CVD), or 4 (clinical CVD). The main outcomes were all-cause and cardiovascular mortality.</div></div><div><h3>Results</h3><div>Among 34,809 participants (mean age: 46.7 years; male: 49.2 %), the prevalence of CKM stages 0 to 4 was 13.2 %, 20.8 %, 53.1 %, 5.0 %, and 7.8 %, respectively. During a median follow-up of 8.3 years, compared to participants with CKM stage 0, those with higher stages had increased risks of all-cause mortality (stage 2: HR 1.43, 95 % 1.13–1.80; stage 3, HR 2.75, 95 % CI 2.12–3.57; stage 4, HR 3.02, 95 % CI 2.35–3.89). The corresponding hazard ratios (95 % confidence interval) of cardiovascular mortality risks were 2.96 (1.39–6.30), 7.60 (3.50–16.5), and 10.5 (5.01–22.2). The population-attributable fractions for advanced (stages 3 or 4) vs. CKM syndrome stages (stages 0, 1, or 2) were 25.3 % for all-cause mortality and 45.3 % for cardiovascular mortality.</div></div><div><h3>Conclusion</h3><div>Higher CKM syndrome stages were associated with increased risks of all-cause and cardiovascular mortality. These findings emphasize that primordial and primary prevention efforts on promoting CKM health should be strengthened to reduce mortality risk.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100985"},"PeriodicalIF":4.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143769100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Torunn Melnes , Martin P. Bogsrud , Jacob J. Christensen , Amanda Rundblad , Kjetil Retterstøl , Ingunn Narverud , Pål Aukrust , Bente Halvorsen , Stine M. Ulven , Kirsten B. Holven
{"title":"LDL cholesterol burden in elderly patients with familial hypercholesterolemia: Insights from real-world data","authors":"Torunn Melnes , Martin P. Bogsrud , Jacob J. Christensen , Amanda Rundblad , Kjetil Retterstøl , Ingunn Narverud , Pål Aukrust , Bente Halvorsen , Stine M. Ulven , Kirsten B. Holven","doi":"10.1016/j.ajpc.2025.100986","DOIUrl":"10.1016/j.ajpc.2025.100986","url":null,"abstract":"<div><h3>Background and aims</h3><div>Familial hypercholesterolemia (FH) is a genetic disorder characterized by elevated low-density lipoprotein cholesterol (LDL-C) and increased risk of premature coronary heart disease (CHD). While current LDL-C levels usually guides therapy, the cumulative exposure to LDL-C (the LDL-C burden) is suggested to offer a more precise estimate of cardiovascular risk in people with FH. Therefore, using real-world data, this study aimed to estimate the LDL-C burden at different ages in elderly FH patients with and without CHD, and to assess the LDL-C burden at CHD onset.</div></div><div><h3>Methods</h3><div>Data was retrospectively collected from the medical records of elderly (>60 years) FH patients at the Lipid Clinic in Oslo. The LDL-C burden (mM-years) was estimated based on repeated LDL-C measurements and information on lipid-lowering medication. Time-weighted average (TWA) LDL-C was calculated as LDL-C burden divided by years.</div></div><div><h3>Results</h3><div>We included 112 FH patients, of which 55 (49 %) had experienced at least one CHD-event, and 58 (52 %) were females. Median age at first and last visit were 50 years and 68 years, respectively, with a median of 9 (range; 2–14) available LDL-C measurements. Subjects with CHD had higher LDL-C burden at all ages tested (45, 50 and 60 years) compared with the non-CHD group (<em>p</em> < 0.01, also after adjusting for sex), and had higher TWA LDL-C before treatment at the Lipid Clinic (<em>p</em> = 0.004), but not during follow-up (<em>p</em> = 0.6). There were no sex differences in LDL-C burden at all ages tested, also after adjusting for CHD (<em>p</em> > 0.1). However, women had higher TWA LDL-C during follow-up at the Lipid Clinic (<em>p</em> = 0.01). Median LDL-C burden at CHD onset was 352 mM-years; numerically lower in women than in men (320 vs. 357 mM-years, respectively. <em>p</em> = 0.1).</div></div><div><h3>Conclusion</h3><div>Elderly FH patients with CHD had higher estimated LDL-C burden compared with FH patients without CHD, due to higher burden <em>prior to treatment</em>, highlighting the importance of early</div><div>detection and treatment.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100986"},"PeriodicalIF":4.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143785296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Rachel M Bond , Kendra Ivy , Tre'Cherie Crumbs , Vikram Purewal , Samed Obang , Dan Inder S Sraow
{"title":"Coronary microvascular dysfunction and its role in heart failure with preserved ejection fraction for future prevention and treatment","authors":"Rachel M Bond , Kendra Ivy , Tre'Cherie Crumbs , Vikram Purewal , Samed Obang , Dan Inder S Sraow","doi":"10.1016/j.ajpc.2025.100983","DOIUrl":"10.1016/j.ajpc.2025.100983","url":null,"abstract":"<div><div>Ischemic heart disease has long been established as the leading cause of heart failure, typically as a result of hemodynamically significant and obstructive coronary anatomy. Since, the role of dysfunctional coronary microvascular pathophysiologic mechanisms have also been associated with the development of congestive heart failure (CHF), most notably heart failure with preserved ejection fraction (HFpEF) although with limited clinical evidence. Conventional cardiometabolic and behavioral risk factors common to HFpEF such as diabetes mellitus (DM), obesity, hypertension, dyslipidemia, smoking, and chronic kidney disease foster a pro-inflammatory environment conducive to endothelial dysfunction and improper regulation of vasoactive substances. The impaired relaxation and increased vasoconstriction of damaged endothelium gives rise to impaired coronary blood flow and episodes of transient ischemia. Such coronary microvascular dysfunction (CMD) has its own implication on cardiovascular pathophysiologic mechanisms beyond symptomatic coronary and myocardial ischemia, and thus its own potential prevention goals and treatment targets for patients with HFpEF, where previous management had been limited. As such, we conducted a literature review to address the current landscape of data which links CMD to HFpEF. Furthermore, we considered the implications of biopsychosocial elements such as race, ethnicity, sex, gender, and the social determinants of health as they relate to the disparate health outcomes of those most at risk for CMD and HFpEF.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100983"},"PeriodicalIF":4.3,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143769093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eleonora Avenatti , Helene DiGregorio , Elia El Hajj , Rakesh Gullapelli , Kenneth Williams , Izza Shahid , Budhaditya Bose , Kobina Hagan , Juan C Nicolas , Shubham Lahan , Nwabunie Nwana , Sara Ayaz Butt , Kanika Monga , Lily Anne Romero Karam , Myriam Guevara , Zulqarnain Javed , Brittany Weber , Sadeer Al-Kindi , Khurram Nasir
{"title":"Disparities in statin use in patients with ASCVD with vs without rheumatologic diseases in a large integrated healthcare system: Houston methodist CVD learning health system registry","authors":"Eleonora Avenatti , Helene DiGregorio , Elia El Hajj , Rakesh Gullapelli , Kenneth Williams , Izza Shahid , Budhaditya Bose , Kobina Hagan , Juan C Nicolas , Shubham Lahan , Nwabunie Nwana , Sara Ayaz Butt , Kanika Monga , Lily Anne Romero Karam , Myriam Guevara , Zulqarnain Javed , Brittany Weber , Sadeer Al-Kindi , Khurram Nasir","doi":"10.1016/j.ajpc.2025.100959","DOIUrl":"10.1016/j.ajpc.2025.100959","url":null,"abstract":"<div><h3>Objective</h3><div>The comorbid presence of Rheumatologic Diseases (RDs) and Atherosclerotic Cardiovascular Disease (ASCVD) substantially accentuates cardiovascular risk. We aimed to compare rates of secondary prevention statin utilization in patients with established ASCVD both with and without underlying comorbid RDs– and to highlight any potential gender, racial, or ethnic disparities in statin use in a contemporary US cohort.</div></div><div><h3>Methods</h3><div>We queried the electronic medical record (EHR)-linked Houston Methodist Learning Health System Outpatient Registry containing data for approximately 1.2 million patients to identify patients with diagnosed ASCVD and RDs using ICD-10 codes. Statin prescription rates and dosage were evaluated via ATC codes.</div></div><div><h3>Results</h3><div>Among 113,021 patients with ASCVD, 7286 (6.4 %) had comorbid RDs. The majority (71.1 %) of patients with ASCVD were prescribed statins, with discernibly lower utilization in patients with comorbid RDs compared to the non-RD population (63.2 % vs. 71.7 %, <em>p</em> < 0.005). High-intensity statins were prescribed in 42,636 (37.7 %) of ASCVD patients, with similarly reduced utilization in RD vs non-RD patients (30.4 % vs. 38.2 %). These trends remained consistent across sociodemographic subgroups. Moreover, women were consistently less likely to receive high intensity statins in both RD and non-RD groups. Reduced statin utilization was not accounted for with non-statin lipid lowering therapies in RD vs non RD subgroups.</div></div><div><h3>Conclusion</h3><div>In this real-world study, co-morbid RDs were associated with significant lower utilization of secondary prevention statin therapy in patients with ASCVD. A multidisciplinary team approach may help to better understand key drivers of statin uptake in this clinically vulnerable population.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100959"},"PeriodicalIF":4.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143817077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Seyedmohammad Saadatagah , Miriam Larouche , Mohammadreza Naderian , Vijay Nambi , Diane Brisson , Iftikhar J. Kullo , P Barton Duell , Erin D. Michos , Michael D. Shapiro , Gerald F. Watts , Daniel Gaudet , Christie M. Ballantyne
{"title":"Recognition and management of persistent chylomicronemia: A joint expert clinical consensus by the National Lipid Association and the American Society for Preventive Cardiology","authors":"Seyedmohammad Saadatagah , Miriam Larouche , Mohammadreza Naderian , Vijay Nambi , Diane Brisson , Iftikhar J. Kullo , P Barton Duell , Erin D. Michos , Michael D. Shapiro , Gerald F. Watts , Daniel Gaudet , Christie M. Ballantyne","doi":"10.1016/j.ajpc.2025.100978","DOIUrl":"10.1016/j.ajpc.2025.100978","url":null,"abstract":"<div><div>Extreme hypertriglyceridemia, defined as triglyceride (TG) levels ≥1000 mg/dL, is almost always indicative of chylomicronemia. The current diagnostic approach categorizes individuals with chylomicronemia into familial chylomicronemia syndrome (FCS; prevalence 1–10 per million), caused by the biallelic combination of pathogenic variants that impair the lipolytic action of lipoprotein lipase (LPL), or multifactorial chylomicronemia syndrome (MCS, 1 in 500). A pragmatic framework should emphasize the severity of the phenotype and the risk of complications. Therefore, we endorse the term “persistent chylomicronemia” defined as TG ≥1000 mg/dL in more than half of the measurements to encompass patients with the highest risk for pancreatitis, regardless of their genetic predisposition. We suggest classification of PC into four subtypes: 1) genetic FCS, 2) clinical FCS, 3) PC with “alarm” features, and 4) PC without alarm features. Although patients with FCS most likely have PC, the vast majority with PC do not have genetic FCS. Proposed alarm features are: (a) history of recurrent TG-induced acute pancreatitis, (b) recurrent hospitalizations for severe abdominal pain without another identified cause, (c) childhood pancreatitis, (d) family history of TG-induced pancreatitis, and/or (e) post-heparin LPL activity <20 % of normal value. Alarm features constitute the strongest risk factors for future acute pancreatitis risk. Patients with PC and alarm features have very high risk of pancreatitis, comparable to that in patients with FCS. Effective, innovative treatments for PC, like apoC-III inhibitors, have been developed. Combined with lifestyle modifications, these agents markedly lower TG levels and risk of pancreatitis in the very-high-risk groups, irrespective of the monogenic etiology. Pragmatic definitions, education, and focus on patients with PC specifically those with alarm features could help mitigate the risk of acute pancreatitis and other complications.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100978"},"PeriodicalIF":4.3,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143769007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hanna M. Knauss , Lara C Kovell , Edgar R. Miller III , Lawrence J. Appel , Kenneth J Mukamal , Timothy B Plante , Stephen P. Juraschek
{"title":"Dietary sodium reduction lowers 10-year atherosclerotic cardiovascular disease risk score: Results from the DASH-sodium trial","authors":"Hanna M. Knauss , Lara C Kovell , Edgar R. Miller III , Lawrence J. Appel , Kenneth J Mukamal , Timothy B Plante , Stephen P. Juraschek","doi":"10.1016/j.ajpc.2025.100980","DOIUrl":"10.1016/j.ajpc.2025.100980","url":null,"abstract":"<div><h3>Background</h3><div>The Dietary Approaches to Stop Hypertension (DASH) diet lowers estimated 10-year ASCVD (atherosclerotic cardiovascular disease) risk. The effects of dietary sodium reduction on ASCVD risk are uncertain. This study aims to evaluate the impact of sodium reduction, alone and combined with the DASH diet, on 10-year ASCVD risk scores.</div></div><div><h3>Methods</h3><div>The DASH-Sodium trial randomized adults with elevated blood pressure (average systolic blood pressure of 120 to 159 mm Hg and average diastolic blood pressure of 80 to 95 mm Hg) to the DASH diet or typical American diet. Within each arm, individuals consumed 3 different levels of sodium in random order: low, medium, and high. Each period lasted 30 days. Pooled cohort equation-estimated 10-year ASCVD risk scores were calculated at baseline and at the end of each feeding period. The primary outcomes of interest were the absolute and relative differences in 10-year ASCVD risk scores from baseline.</div></div><div><h3>Results</h3><div>Among the 412 participants (mean age 48 ± 10 years; 57 % female, 57 % Black), sodium reduction decreased ASCVD risk scores in both dietary arms. Compared to high sodium intake, low sodium intake changed ASCVD risk by -9.4 % (95 % CI -11.7, -7.0). When compared to a typical American diet, the DASH diet changed 10-year ASCVD by -5.3 % (95 % CI -9.3, -1.2). Compared to a high sodium-control diet, the combination of both low sodium intake with DASH changed ASCVD risk by -14.1 % (95 % CI -18.6, -9.3).</div></div><div><h3>Conclusions</h3><div>Sodium reduction and the DASH diet both independently reduced 10-year ASCVD risk scores. Moreover, the combined impact was additive. These findings support dietary sodium reduction in addition to the DASH diet for ASCVD prevention.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100980"},"PeriodicalIF":4.3,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143817076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Paolo Raggi , Arshed A. Quyyumi , Michael Y. Henein , Viola Vaccarino
{"title":"Psychosocial stress and cardiovascular disease","authors":"Paolo Raggi , Arshed A. Quyyumi , Michael Y. Henein , Viola Vaccarino","doi":"10.1016/j.ajpc.2025.100968","DOIUrl":"10.1016/j.ajpc.2025.100968","url":null,"abstract":"<div><div>Mahatma Gandhi once famously said: “poverty is the worst type of violence”. He was referring to the state of political and social unrest that was pervading his nation, and the impact that humiliating defeat had on those who suffered in dire straits. Today, there is mounting evidence that social disparities cause intense psychosocial stress on those on whom they are imposed and can result in adverse cardiovascular outcomes. In modern society we still witness large disparities in living conditions between races, regions, continents and nations. Even in more privileged nations, we often witness the existence of “food and social deserts” in the middle of large urban centers. Sizable segments of the population are deprived of the comforts and privileges enjoyed by others; food quality and choices are limited, opportunities to exercise and play are scarce or unsafe, physical and verbal violence are prevalent, and racially driven conflicts are frequent. It has become apparent that these conditions predispose to the development of cardiovascular disease and affect its outcome negatively. Besides the increase in incidence of traditional risk factors, such as smoking, hypertension, insulin resistance and obesity, several other pathophysiological mechanisms involving the neuro-endocrine, inflammatory and immune pathways may be responsible for the noted negative outcomes. In this manuscript we review some of the evidence linking social distress with adverse cardiovascular outcomes and the potential subtending mechanisms and therapeutic interventions.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100968"},"PeriodicalIF":4.3,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143740027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhuo Chen , Jean-Eudes Dazard , Pedro Rafael Vieira de Oliveira Salerno , Santosh Kumar Sirasapalli , Mohamed HE Makhlouf , Sanjay Rajagopalan , Sadeer Al-Kindi
{"title":"Composite socio-environmental risk score for cardiovascular assessment: An explainable machine learning approach","authors":"Zhuo Chen , Jean-Eudes Dazard , Pedro Rafael Vieira de Oliveira Salerno , Santosh Kumar Sirasapalli , Mohamed HE Makhlouf , Sanjay Rajagopalan , Sadeer Al-Kindi","doi":"10.1016/j.ajpc.2025.100964","DOIUrl":"10.1016/j.ajpc.2025.100964","url":null,"abstract":"<div><h3>Background</h3><div>Cardiovascular disease (CVD) is the leading global cause of death, with socio-environmental factors significantly influencing morbidity and mortality. Understanding these factors is essential for improving risk assessments and interventions.</div></div><div><h3>Objective</h3><div>To develop and evaluate the predictive power of a composite socio-environmental (SE) cardiovascular risk score in forecasting major adverse cardiovascular events (MACE) among patients, considering both traditional and novel socio-environmental risk factors.</div></div><div><h3>Methods</h3><div>A Survival Random Forest (RSF) model was used to create a composite socio-environmental (SE) cardiovascular risk score using 22 census-tract level variables from 62,438 patients in the CLARIFY registry undergoing coronary artery calcium (CAC) scoring. A Cox Proportional Hazard (CPH) model was then applied to assess the association between the SE-MACE risk score and MACE in a hold-out test set. SHapley Additive exPlanations (SHAP) values were used to identify variable importance.</div></div><div><h3>Results</h3><div>The study included 62,438 individuals (mean age 59.6 years, 53.2 % female, 87.7 % White). Hypertension (55.4 %), diabetes (15.7 %), and dyslipidemia (72.3 %) were common, with a median CAC score of 168. The RSF model showed a concordance index of 0.58, with significant factors including smoking prevalence, insurance status, and median household income impacting cardiovascular risk. The SE-MACE risk score was robustly associated with MACE (HR, 1.21 [95 % CI, 1.11-1.32]), independent of clinical variables and the CAC score. Kaplan-Meier analysis highlighted clear risk stratification across SE-MACE score quartiles.</div></div><div><h3>Conclusion</h3><div>The SE-MACE risk score effectively incorporates socio-environmental factors into cardiovascular risk assessment, identifying individuals at higher risk for MACE and supporting the need for holistic assessment frameworks. Further validation in diverse settings is recommended to confirm these findings.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100964"},"PeriodicalIF":4.3,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143680966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Niloufar Novin , S. Scott Jones , Elizabeth Cohn , Nisha Parikh , David Zhang , Pey-Jen Yu , Kristie Coleman , Luis David Olivera Leon , Codruta Chiuzan
{"title":"The health effects of housing instability and its association with congestive heart failure","authors":"Niloufar Novin , S. Scott Jones , Elizabeth Cohn , Nisha Parikh , David Zhang , Pey-Jen Yu , Kristie Coleman , Luis David Olivera Leon , Codruta Chiuzan","doi":"10.1016/j.ajpc.2025.100967","DOIUrl":"10.1016/j.ajpc.2025.100967","url":null,"abstract":"<div><div>Housing instability is a critical social determinant of health (SDOH). Prior studies of homelessness and congestive heart failure (CHF) have looked primarily at the association between socioeconomic status and hospitalization. The association between housing instability and the development of CHF has not been fully investigated.</div><div>We examined data from 4,408 participants with annual household income below $50,000 in the All of Us Research Program, a national cohort study enriched for individuals underrepresented in biomedical research. Within the inceptive survey, participants were asked if they were worried or concerned about not having a place to live in the past 6 months. We assessed the association between this self-reported housing concern and CHF occurrence, finding that individuals with low income and housing instability had a 44 % higher risk of diagnosis of CHF than those with stable housing (HR 1.44; 95 %CI 1.03–2.01). The increased risk remained significant after adjusting for cardiovascular risk factors as potential confounders (HR 1.73; 95 %CI 1.19–2.51) such as cholesterol, history of diabetes, and older age categories aged 55–64 years, 65–74 years, 75 years and older.</div><div>Compared with men, women in the study were estimated to be at lower risk of CHF diagnosis (HR 0.52; 95 %CI 0.38–0.70) with 5.3 % of men and 2.9 % of women eventually diagnosed. We found that participants with housing instability had a higher risk of diagnosis of CHF compared to those with stable housing, highlighting the potential health impact of this healthcare disparity. Housing instability disrupts the essentials of effective management of cardiovascular risk factors (diabetes, obesity, hypertension) including consistent management, reliable access to care, and access to basic needs like kitchen and bathroom. This exacerbates their severity and increasing the risk of being diagnosed with CHF.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100967"},"PeriodicalIF":4.3,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143724982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ying Li , Donghui Jin , Sidong Li , Hao Wu , Jiangang Wang , Pingting Yang , Xue He , Lu Yin
{"title":"The dose-response relationships between all-cause and cardiovascular mortality and the accrual of various dietary habits","authors":"Ying Li , Donghui Jin , Sidong Li , Hao Wu , Jiangang Wang , Pingting Yang , Xue He , Lu Yin","doi":"10.1016/j.ajpc.2025.100963","DOIUrl":"10.1016/j.ajpc.2025.100963","url":null,"abstract":"<div><h3>Objective</h3><div>To evaluate the potential dose-response relationships of all-cause and cardiovascular death with the accumulation of various dietary habits.</div></div><div><h3>Setting</h3><div>A prospective cohort study.</div></div><div><h3>Methods</h3><div>Twenty-three dietary habits were assessed through face-to-face interviews with 57,737 participants in health check-up programs from 2015 to 2021. The total score of various dietary habits was calculated as the sum of each dietary habit multiplied by its own full-adjusted coefficient (β) for all-cause mortality in Cox proportional hazard models. Cox proportional hazard models were fitted for the associations of total and cause-specific mortality with the scores of various dietary habits.</div></div><div><h3>Results</h3><div>1,692 deaths occurred after the earliest check-ups in our center, followed up for a median time of 2.14 years (range: 1.01–7.71 years). Total mortality was 11.23/1,000 person-years, and the mean scores of dietary habits were 2.83±2.14. All-cause mortality increased significantly with the cumulative score of dietary habits (the highest quartile vs. lowest quartile: adjusted hazard ratio [AHR], 1.72; 95 % confidence interval [CI], 1.49–1.99; <em>P<sub>linear</sub></em><0.01). Significance was also found for cardiovascular disease (CVD) mortality (HR, 1.82; 95 % CI, 1.47–2.27; <em>P<sub>linear</sub></em><0.01), cancer mortality (AHR, 1.59; 95 % CI, 1.23–2.04; <em>P<sub>linear</sub></em><0.01), and other-cause mortality (AHR, 2.00; 95 % CI, 1.46–2.73; <em>P<sub>linear</sub></em><0.01). These dose-response trends were more significant in total mortality and CVD mortality among middle-aged adults, and non-obese population.</div></div><div><h3>Conclusions</h3><div>The greater the accumulation of diverse dietary habits, the higher the total mortality, CVD mortality, cancer mortality, and other mortality. This additive effect was particularly pronounced in the risk of death among middle-aged individuals and those with average body statures.</div></div>","PeriodicalId":72173,"journal":{"name":"American journal of preventive cardiology","volume":"22 ","pages":"Article 100963"},"PeriodicalIF":4.3,"publicationDate":"2025-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143680917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}