Long-Term Cardiovascular and Noncardiovascular Mortality After Acute Coronary Syndrome: A Nationwide Competing-Risks Analysis of 1.56 Million Patients.

Transcatheter Aortic Valve Replacement in the Immunocompromised: A Systematic Review and Meta-Analysis.

Remnant cholesterol associated with all-cause mortality in oldest-old acute coronary syndrome patients: A cohort study.

Low-density lipoprotein cholesterol longitudinal trajectories and clinical outcomes following an acute coronary syndrome.

The aim of this study is to gain insight into mortality rates and causes of death after major cardiac interventions, using nationwide real-world data from the Netherlands. For this retrospective observational study, data from Statistics Netherlands and the Dutch all-payer claims database in the period 2016-2019 were used to select the intervention groups: coronary artery bypass grafting (CABG), percutaneous coronary intervention, surgical aortic valve replacement (SAVR), SAVR + CABG, mitral valve surgery, transcatheter heart valve intervention, pulmonary vein isolation and minimally-invasive maze surgery. For all interventions, survival status, date, and cause of death were retrieved. Causes of death were clustered for cardiovascular (CV) and non-CV causes by their corresponding ICD-10 code at different time intervals up to 5years after the intervention. Atotal of 203,001 interventions were included, and 13.7% (27,832) of the patients died during the 5‑year follow-up. Of these, 45.1% (12,560) were CV, and 54.9% (15,272) were non-CV deaths. After coronary revascularization, valve intervention, and aortic valve intervention and coronary revascularization combined, respectively, non-CV mortality increased from 14.2%, 12.9% and 20.7% at 30days to 44.5%, 47.0% and 44.5% after 2years. Of all deaths up to 5years, 54.7%, 54.3% and 55.3% were non-CV. Initially main cause of death after cardiac intervention is CV-related. The proportion of non-CV deaths increases during follow-up, impacting survival for all patients up to 5years after intervention. (Fig.1).

Abstract Introduction Obstructive sleep apnea (OSA) is associated with increased risk for recurrent cardiovascular (CV) events and mortality in patients with established CV disease. As many as two-thirds of patients with acute myocardial infarction (MI) may at least have mild OSA. However, if OSA is associated with poor prognosis after an acute MI is not well established. Purpose To investigate the registry reported prevalence of OSA and association with adverse prognosis in patients after first MI. Methods We performed a retrospective cohort study with patients registered in the SWEDEHEART MI registry for first MI 2005-2017. Patients with an ICD-10 OSA diagnosis prior to discharge after first MI were identified by linkage to the Swedish National Patient Register. In adjusted Cox proportional hazards models, the association between OSA diagnosis, mortality, ischemic events, and hospitalization for heart failure were assessed. The no OSA diagnosis subset served as reference. Results The registry reported prevalence of OSA diagnosis prior to discharge after first MI was 1.37 % (2,129 out of 155,332). OSA patients were more likely to be younger (mean age 66.2 years versus [vs] 69.3 years), be male (81.6 % vs 64.1 %), former smokers (42.4 % vs 30.3 %), and more often had prescribed primary prevention therapies: acetylsalicylic acid (28.6 % vs 23.1 %), angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker (48.6 % vs 27.9 %), and statins (32.8 % vs 18.1 %). Further, OSA patients more often presented with non-ST-elevation myocardial infarction (NSTEMI; 65.0 % vs 46.5 %) and had more comorbidities: chronic obstructive pulmonary disease (11.4 % vs 6.1 %); congestive heart failure (11.8 % vs 6.3 %); diabetes mellitus (39.3 % vs 20.4 %); hypertension (68.6 % vs 46.4 %); and obesity (55.6 % vs 20.5 %). During a median follow-up of 4.67 (interquartile range 1.95-7.96) years, those with an OSA diagnosis had an increased risk of all-cause mortality (hazard ratio [HR], 95% confidence interval [CI]; 1.15, 1.04-1.27), non-CV mortality (1.28, 1.13-1.45), and hospitalization for heart failure (1.16, 1.01-1.34). No other associations with the studied outcomes were observed. Conclusions In patients with acute MI, registry reported prevalence of OSA was low, but OSA diagnosis remained independently associated with increased risk of all-cause mortality, non-CV mortality, and hospitalization for heart failure. Further, patients with OSA had higher prevalence of CV comorbidities and more often presented with NSTEMI. Consequently, OSA may constitute an important and potentially underdiagnosed component of the residual risk not affected by the intensive intervention of established risk factors applied after MI.Adjusted analysis of associations Demographic and baseline characteristics

Abstract Background Chronic Heart Failure (CHF) is associated with sarcopenia in 20% of cases, resulting in a poorer prognosis. CHF and sarcopenia share several pathophysiological mechanisms, including increased oxidative stress, inflammation, insulin resistance, and connective tissue infiltration into muscle tissue. These conditions are further complicated by malabsorption due to gastrointestinal congestion and physical inactivity, which result in enhanced protein catabolism and subsequent muscle mass loss. This bidirectional connection suggests potential benefits of CHF pharmacological treatments for patients with both conditions. Notably, SGLT2-inhibitors (SGLT2i) are strongly recommended for CHF treatment across the left ventricular ejection fraction (LVEF) spectrum and regardless of type 2 diabetes mellitus (T2DM) status. Purpose The aim of this study is to evaluate the association of sarcopenia and the potential role of SGLT2i with the incidence of MACE in outpatients with CHF. Methods In this retrospective observational study we enrolled 670 Caucasian outpatients, 369 were males and the average age was 65.6±12.5 years; 452 are affected by HFpEF while 218 by HFmrEF and HFrEF, 340 patients were sarcopenic, while 330 patients were not sarcopenic. The mean follow-up was 4.7±2.8 years. Study endpoint was MACE incidence and total mortality was also evaluated. We used AUC to evaluate the accuracy of sarcopenia in predicting MACE. Data was processed with Cox univariance and multivariate analysis model to define independent MACE predictors. Results A total of 245 (7.8 events/100 patient-year) MACE were observed; 213 in sarcopenia group and 32 in the no sarcopenia group (13.3 vs 2.1 events/100 patient-year) (p<0.0001). Non-CV mortality was not significantly different between the sarcopenia and no sarcopenic group (18 vs 24 events, 1.1 vs 1.5 events/100 patient-year) (p = 0.291). Total mortality was higher in the sarcopenia group compared to the no sarcopenia group (102 vs 28 events, 6.4 vs 1.8 events/100 patient-year) (p<0.0001). The ROC curve and his relative AUC demonstrated the accuracy of sarcopenia as a predictor of the occurrence of MACE (AUC 0.78; 95% CI 0.749–0.821; p<0.0001). The multivariate analysis model demonstrates that SGLT2i reduces the risk of MACE by 89%. In contrast, sarcopenia increases the risk of MACE by a factor of almost six (HR 5.82). Conclusion This study provides evidence of association between sarcopenia and incidence of MACE in a population of CHF. Early detection and treatment are imperative to improve patient outcomes. SGLT2i reduced the composite endpoint of non-fatal stroke, non-fatal coronary event and cardiovascular death due to CHF by 89%. Total mortality was also reduced.

Abstract Background Insulin resistance (IR), with its myriad proatherogenic effects, is a relevant risk factor for atherosclerosis. The triglyceride-glucose index (TyG) is a marker of IR and subclinical atherosclerosis. Its potential in coronary artery disease (CAD) prognostic assessment has little been explored, but the evidence suggests significant potential. Aim Investigate the association between an IR index, triglyceride-glucose index (TyG), and cardiovascular and non-vascular events in a coronary population. Methods We included 1719 coronary patients with at least 70% stenosis in one or more main coronary arteries or their primary branches after coronary angiography. These patients were in the stabilized phase after an appropriate interventional approach (angioplasty with coronary stenting), coronary artery bypass graft (CABG) surgery and suitable medical therapy despite some residual Ischemia. Cardiovascular (CV) events and non-CV mortality were registered throughout an extended follow-up (average 7.3±6.0 years). TyG was calculated through the formula ln[Triglyceride mg/dl*fast blood glucose (FBG) mg/dl)/2], which was subsequently stratified into terciles. All analyses were performed using the TyG 3rd tercile relative to the 1st. Bivariate analysis evaluated its association with other markers: pulse wave velocity (PWV), fibrinogen, high sensitivity C reactive protein (hsCRP), and clinical variables. A multivariate Cox regression analysis assessed the variables associated with total events. Results TyG was associated with PWV (p<0.0001), hsCRP (p<0.0001), kidney failure (p<0.0001), peripheral vascular disease (p<0.0001), stroke (p<0.0001), CV events (p=0.001), and total events (p<0.0001) in bivariate analysis. After Cox analysis adjusted to age, gender, diabetes, dyslipidemia, hypertension, smoking, alcohol>300/week, obesity, sedentary lifestyle, hsCRP, fibrinogen, lipoprotein(a), PWV and TyG index, this marker remained as a significant and independent risk factor for total events (HR=1.19; p=0.020), together with age (p=0.001), sedentary lifestyle (p<0.0001) and hsCRP (p<0.0001). Conclusion TyG index, cheap and easy to determine, was strongly associated with residual inflammation, atherosclerosis progression, CV events and mortality. Early identification of patients with higher TyG indices before deleterious events occur may be valuable for predicting disease progression in high-risk patients, allowing timely adoption of appropriate preventive measures.

Abstract Background Growth differentiation factor 15 (GDF-15) is a stress responsive member of the transforming growth factor ꞵ (TGF-ꞵ) cytokine superfamily. The circulating GDF-15 level is an independent predictor of cardiovascular (CV) and cancer mortality and morbidity in community-dwelling individuals, and is also an independent marker of all-cause mortality and cardiovascular events in patients with coronary artery disease (CAD). However, the prognostic value of GDF-15 for cause-specific mortality in patients with CAD are not fully confirmed. Methods Serum GDF-15 levels were measured in 3,255 patients enrolled in the EXCEED-J Study and 2,418 patients enrolled in the ANOX Study with suspected or known CAD. The outcomes were all-cause death, CV death, cancer death, and other non-CV death. Patients were followed up over a 6-year period. Results During the follow-up, 518 (15.9%) deaths occurred, including 169 (5.2%) CV deaths, 117 (3.6%) cancer deaths, 170 (5.2%) other non-CV deaths, and 60 (1.8%) undetermined deaths in the EXCEED-J Study, while 536 (22.2%) deaths occurred, including 166 (6.9%) CV deaths, 128 (5.3%) cancer deaths, 198 (8.2%) other non-CV deaths, and 44 (1.8%) undetermined deaths in the ANOX Study. After adjustment for potential clinical confounders (i.e., age, sex, body mass index, hypertension, dyslipidemia, diabetes, current smoker, estimated glomerular filtration rate, the Gensini score, previous myocardial infarction, previous stroke, previous heart failure hospitalization, atrial fibrillation, valvular heart disease, peripheral artery disease, chronic obstructive pulmonary disease, malignancies, anemia, antihypertensive drug use, statin use, and aspirin use) and established CV biomarkers (i.e., N-terminal pro-brain natriuretic peptide, high-sensitivity cardiac troponin I, and high-sensitivity C-reactive protein), log-transformed (Ln-) GDF-15 levels were significantly associated with all-cause death (hazard ratio [HR] for 1-SD increase, 1.58; 95% confidence interval [CI], 1.40–1.78), CV death (HR, 1.40; 95% CI, 1.14–1.72), cancer death (HR, 1.65; 95% CI, 1.29–2.12), and other non-CV death (HR, 1.92; 95% CI, 1.55–2.37) in the EXCEED-J Study; and significantly associated with all-cause death (HR, 1.77; 95% CI, 1.56–2.01), CV death (HR, 1.48; 95% CI, 1.16–1.87), cancer death (HR, 2.32; 95% CI, 1.83–2.95), and other non-CV death (HR, 1.74; 95% CI, 1.40–2.15) in the ANOX Study. The addition of Ln-GDF-15 to the model with potential clinical confounders and established CV biomarkers significantly improved the prediction of all-cause death, cancer death, and other non-CV death (P<0.05 for both continuous net reclassification improvement and integrated discrimination improvement for all comparisons), but not that of CV death, in both studies. Conclusions The GDF-15 level independently predicted all-cause, cancer, and other non-CV mortality, but not CV mortality, in patients with suspected or known CAD.

Background: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death in the United States. While healthy dietary habits are known to reduce morbidity and mortality, the impact of neighborhood-level healthy food mobility behaviors on mortality in patients with established ASCVD is not well understood. Objective: To evaluate the association between census tract-level healthy food mobility patterns and all-cause mortality among U.S. Veterans with established ASCVD. Design: Retrospective observational cohort study of 770,990 U.S. Veterans (2016–2021) with stable ASCVD—including coronary artery disease (CAD), cerebrovascular disease (CeVD), or peripheral artery disease (PAD)—with a median follow-up of 4.33 years (maximum: 6.33 years). ASCVD was identified using ICD-10 codes. Neighborhood mobility data, obtained from SafeGraph, were linked to Veterans' residential census tracts. The Retail Food Activity Index (RFAI), defined as the proportion of visits to healthy food venues relative to total food-related visits, was used to measure nutrition-related mobility behavior. RFAI was calculated using 2019 origin-destination mobility data from Dewey’s Advanced Research Monthly Patterns datasets, derived from approximately 10% of U.S. GPS-enabled mobile devices. Main Outcomes and Measures: Primary outcomes were all-cause mortality and major adverse cardiovascular events (MACE). Associations between RFAI and all-cause mortality were assessed using Cox proportional hazards models. Competing risk Fine-Gray models were used to evaluate associations with MACE with non-CV mortality as the competitive risk event. Results: Among 770,990 Veterans (mean age 71.7 years; 98% male), higher RFAI was significantly associated with reduced all-cause mortality (HR = 0.5567, p < 0.001) after adjusting for clinical and social covariates, as well as neighborhood-level mobility indicators (average time in greenspaces and recreation facilities). Higher RFAI was also associated with reduced MACE risk (subHR = 0.6287, p < 0.001). Conclusions and Relevance: In this nationwide cohort of U.S. Veterans with stable ASCVD, healthier neighborhood-level food mobility behaviors were associated with significantly lower all-cause mortality and MACE. These findings highlight the potential of improving local access to healthy food as a population-level strategy to enhance cardiovascular outcomes and longevity in vulnerable populations.

The role of adiponectin (ADPN) in stroke remains debatable, despite its significant impact as a major adipocytokine on cardiovascular (CV) diseases. This study aimed to assess the association between ADPN and 5-year mortality, functional outcome and recurrence in Chinese individuals with first ischaemic stroke (IS). This prospective, multicentre study recruited IS patients from 201 hospitals in China between August 2015 and March 2018. Multivariable Cox regression evaluated ADPN's association with mortality/recurrence, while logistic regression analysed poor functional outcomes (modified Rankin Scale score 3-6 and 3-5). Among 8086 patients (median age 62; 31.8% female), there were 710 deaths, 1134 recurrences and 1223 poor functional outcomes (modified Rankin Scale 3-6). Higher baseline ADPN levels were significantly associated with increased risk of 5-year non-CV mortality (adjusted HR Q4 vs Q1=1.47 (95% CI 1.10 to 1.96), p=0.06) after adjustment for age, sex, body mass index and National Institutes of Health Stroke Scale. No independent associations were found between ADPN and CV mortality, stroke recurrence or poor functional outcome. Subgroup analysis revealed a significant association between ADPN and 5-year mortality from various causes among patients with cardioembolism (adjusted HR Q4 vs. Q1=2.39 (95% CI 1.24 to 4.62), p=0.007) and large artery atherosclerosis (adjusted HR Q4 vs Q1=2.16 (95% CI 1.34 to 3.47), p=0.004). Elevated baseline ADPN levels were independently associated with increased 5-year non-CV mortality in Chinese IS patients, especially among those with mild neurological impairment. These findings suggest ADPN may serve as a prognostic biomarker for systemic vulnerability after stroke.

The effect of 0.5 mg dose of colchicine on clinical outcomes in patients with acute myocardial infarction: An updated meta-analysis of randomized controlled trials.

AimsAbdominal aortic calcification (AAC) is a marker of systemic atherosclerosis associated with adverse cardiovascular (CV) outcomes in the general population. This study aimed to evaluate the association of AAC with all-cause and CV mortality in cancer survivors.Methods and resultsUsing 7 years of data from the National Health and Nutrition Examination Survey (NHANES, 2013–2019), we analysed a nationally representative cohort of US cancer survivors. AAC burden was quantified using the Kauppila AAC-24 scores on dual-energy X-ray absorptiometry (DXA) scans. Kaplan–Meier curves and multivariable Cox models were used to assess the associations between AAC and all-cause mortality, while Fine and Gray models assessed associations between AAC and CV mortality, accounting for non-CV mortality as a competing risk. A total of 23 126 424 cancer survivors (aged ≥40 years) were analysed, recording 4 199 131 (114 unweighted) all-cause deaths and 1 160 618 (34 unweighted) CV deaths over a 69-month median follow-up. AAC was present in 46%, with 19.5% of the cohort showing severe AAC (AAC-24 > 6). Each one-unit increase in AAC-24 score was associated with higher risks of all-cause mortality and CV mortality [adjusted hazard ratio, 95% confidence interval of 1.04 (1.00–1.09) and subdistribution hazard ratio 1.07 (1.02–1.12); P = 0.047 and P = 0.002, respectively] after adjustment for demographic, socioeconomic, traditional CV risk factors, baseline comorbidities, and cancer-specific characteristics.ConclusionAAC detected on DXA scans is independently associated with increased all-cause and CV mortality in cancer survivors aged 40 years and older. DXA-based AAC assessment may serve as a valuable tool for risk stratification in cardio-oncology.

BackgroundThe predictive value of the triglyceride-glucose (TyG) index in patients with obstructive sleep apnea (OSA) remains unclear. Therefore, we aimed to investigate the associations between the TyG index and all-cause and non-cardiovascular (non-CV) mortality in an OSA cohort, focusing on age differences.MethodsThis study enrolled 10,274 patients with OSA from the National Health and Nutrition Examination Survey (2005–2008 and 2015–2018). Mortality outcomes were ascertained by linking to National Death Index records through December 31, 2019. Multivariate Cox proportional hazards regression models with restricted cubic splines and interaction tests with age were employed to evaluate the association between the TyG index and all-cause and non-CV mortality. Kaplan-Meier analysis was used to evaluate mortality differences.ResultsDuring a mean follow-up of 88 months, 1027 all-cause deaths occurred, of which non-CV deaths accounted for 77.8% of the total mortality burden. After fully adjusting for potential confounders, our study explored a U-shaped association between the TyG index and all-cause/non-CV mortality (both non-linear p < 0.001), with inflection points at 9.27 and 9.2. Age yielded a statistically significant interaction between the TyG index and mortality. The TyG index was linearly associated with higher risks of all-cause [Hazard Ratio (HR) 1.30, 95% Confidence Interval (CI): 1.09–1.55, p = 0.004] and non-CV mortality (HR 1.33, 95% CI: 1.08–1.62, p = 0.006) in participants aged < 65, but not in participants age ≥ 65. Kaplan–Meier curves indicated that the patients with the higher TyG index had a significantly lower survival probability (All-cause mortality: p for log-rank test < 0.001; non-CV mortality: p for log-rank test = 0.001).ConclusionsThis study identified a U-shaped association between the TyG index and all-cause and non-CV mortality in an OSA population, with a statistically significant interaction with age. A linear relationship was detected between the TyG index and mortality in those aged < 65, while a non-linear association was established in those aged ≥ 65.

Introduction and Objective: Individuals with type 1 diabetes (T1D) have a greater risk of complications and reduced life expectancy compared with those without diabetes. It is hypothesized that age at T1D diagnosis impacts clinical complications and mortality. Methods: A nationwide retrospective cohort study was conducted. Individuals ≥18 years of age with T1D with ≥1 entry in the Swedish National Diabetes Register (NDR) from 1998 through 2019 and matched controls were included. T1D status was based on insulin use and diagnosis at ≤30 years of age. Individuals with T1D with coexisting congenital, metabolic, or neurological disorders were excluded. Relationships between age at T1D diagnosis and fatal and nonfatal outcomes (eg, cardiovascular (CV) mortality, acute myocardial infarction (MI), peripheral arterial disease (PAD), end-stage renal disease) were analyzed using Cox proportional hazards models. Results: Individuals with T1D (n=34,155) had a mean age of 30.7 years and median follow-up of 12.9 years. Younger age at T1D diagnosis was associated with a higher risk of mortality and nonfatal outcomes. T1D diagnosis at &amp;lt; 10 years of age was associated with 16.3 life-years lost. The hazard ratio (HR) per 1-year older age at T1D diagnosis was 0.97 (95% CI: 0.97, 0.98) for CV mortality, indicating a 2.6% lower risk for every 1-year increase in age at diagnosis. The HRs per 1-year older age at T1D diagnosis were 0.99 (95% CI: 0.98, 0.99) for non-CV mortality, 0.96 for end-stage kidney disease (95% CI: 0.96, 0.97), 0.97 (95% CI: 0.96, 0.98) for PAD, 0.97 (95% CI: 0.96, 0.98) for acute MI, 0.97 (95% CI: 0.97, 0.98) for heart failure, and 0.97 (95% CI: 0.97, 0.98) for coronary heart disease. T1D diagnosis before age 10 was associated with the greatest risk of CV mortality (HR 5.7; 95% CI: 4.3, 7.6). Conclusion: Early onset of T1D carries increased risk of serious complications and death. These findings support the premise that delaying T1D onset in young individuals may reduce the risk of future complications. Disclosure A. Rawshani: Consultant; Sanofi. B. Eliasson: Other Relationship; Sanofi, Eli Lilly and Company, Novo Nordisk. Speaker's Bureau; Boehringer-Ingelheim. Other Relationship; Amgen Inc. Advisory Panel; Abbott, Bayer Pharmaceuticals, Inc. D.K. McGuire: Consultant; Novo Nordisk. Advisory Panel; Novo Nordisk. Consultant; Lilly USA LLC. Advisory Panel; Lilly USA LLC. Consultant; Boehringer-Ingelheim. Advisory Panel; Boehringer-Ingelheim, AstraZeneca, ESPERION Therapeutics, Inc., NewAmsterdam Pharma, Pfizer Inc. Consultant; Applied Therapeutics, Lexicon Pharmaceuticals, Inc, Bayer Pharmaceuticals, Inc, Amgen Inc, Kailera, Idorsia, Alveus, Metsera. N. Sattar: Other Relationship; Abbott, AbbVie Inc, Amgen Inc, AstraZeneca, Boehringer-Ingelheim, Eli Lilly and Company. Advisory Panel; Hanmi Pharm. Co., Ltd. Consultant; Carmot Therapeutics, Inc, Menarini. Other Relationship; Novartis AG, Novo Nordisk, Pfizer Inc, Roche Diagnostics. Consultant; GlaxoSmithKline plc, Metsera. Other Relationship; American Diabetes Association, Medscape. H.C. Gerstein: Advisory Panel; Abbott, Bayer Pharmaceuticals, Inc, Eli Lilly and Company, Novo Nordisk. Consultant; Pfizer Inc, Sanofi, Hanmi Pharm. Co., Ltd. Research Support; Eli Lilly and Company, Novo Nordisk, Hanmi Pharm. Co., Ltd. Other Relationship; Eli Lilly and Company, Novo Nordisk, Sanofi, Boehringer-Ingelheim, Abbott, Jiangsu Hansen, Zuellig Pharma, AstraZeneca. J. Isufi: None. N. Cui: None. O. Guenther: Employee; Sanofi. J.H. Zaccai: Employee; Sanofi. A. Mahieu: Employee; Sanofi. A. Rawshani: Consultant; Sanofi. Funding This study was funded by Sanofi. Acknowledgments: Medical writing support was provided by Lauren Poppi, PhD, of IMPRINT Science, New York, NY, and was funded by Sanofi.

ObjectiveThis study aimed to investigate the associations between the Dietary Inflammatory Index (DII) and cardiovascular (CV)/non-CV mortality in hypertensive individuals, and to explore sex-specific differences.MethodsSixteen thousand six hundred twenty-three individuals with hypertension were selected from the National Health and Nutrition Examination Survey (NHANES) from 2001 to 2018 and divided into groups of males and females. We used multivariate Cox proportional hazards models, competing risk regression, restricted cubic splines (RCS), propensity score matching (PSM), and decision curve analysis (DCA) to evaluate the associations between the DII and CV/non-CV mortality.ResultsAfter fully adjusting for potential confounders, individuals with the highest DII score had a 35 percent higher CV mortality than those with the lowest DII score, observed in females but not in males. Across the cohort, there was a significant association between DII and non-CV mortality. RCS results showed that DII had an S-shaped association with CV mortality and a J-shaped association with non-CV mortality in hypertensive individuals.ConclusionsIn patients with hypertension, we found sex differences in the association between DII and CV mortality. High DII was only associated with increased CV mortality in females with hypertension, but not in males. Higher DII was also associated with increased non-CV mortality.

Cardiovascular disease (CVD) is a leading cause of death worldwide, and infections often worsen the clinical condition of these patients. Respiratory infections, either bacterial or viral sources, are important causes of high morbidity and mortality in older adults. Beyond the burden of infection-related complications, they are also associated with non-infection-related complications such as cardiovascular (CV) events. For example, herpes zoster is associated with an increased risk of stroke and myocardial infarction. Vaccination is an effective preventive strategy for patients with CVD by reducing viral and bacterial infections, and minimizing systemic inflammatory responses to support plaque stability and reduce the likelihood of CV events in high-risk patients, thereby reducing the risks of CV and non-CV hospitalizations and mortality. Despite evidence on the effectiveness, safety, and benefits of vaccines and recommendations to vaccinate older patients and those with risk factors, vaccination rates remain sub-optimal in this population. The Taiwan Society of Cardiology and the Infectious Diseases Society of Taiwan recently appointed a task force to formulate a consensus on vaccinations for adults with high CV risk or CVD. Based on the most up-to-date information, the consensus provides current evidence-based important recommendations.

Abstract Background Hypertrophic cardiomyopathy (HCM) is a heterogeneous disorder with varying risks of clinical outcomes, including sudden cardiac death (SCD). Purpose We aimed to identify distinct phenotypes among patients with HCM in relation to SCD risk factors, interpret their clinical characteristics, and examine their outcomes. Methods This retrospective study analyzed 1,231 consecutive patients with HCM from two tertiary hospitals. We performed latent class analysis (LCA) to categorize patients into phenotypic groups, which is a probabilistic modeling technique that reveals hidden patterns and subgroups within a dataset. Results Three distinct phenotypic groups were identified using LCA. Group 1 (n=554) consisted of young patients with HCM with minimal SCD risk factors and favorable cardiac remodeling. Group 2 (n=114) comprised young patients with HCM and a high prevalence of SCD risk factors, whereas Group 3 (n=563) included older patients (median age, 68 years). Over a median 6.5-year follow-up, 34 SCD-related events, 131 cardiovascular (CV) events, 133 all-cause mortality, and 70 non-CV mortality were observed. Group 2 exhibited the highest rate of SCD-related events (5-year SCD rate: Group 1 vs. 2 vs. 3: 0.8% vs. 8.2% vs. 4.0%, respectively, p&amp;lt;0.001), and CV events were more frequent in Group 2 and 3 compared to Group 1 (Figure 1). All-cause and non-CV mortality were the most frequent in Group 3. A simplified decision tree was developed for the straightforward assignment of phenotypic group membership, demonstrating fair concordance. The phenotypic categorization and the decision tree is shown in Figure 2. Conclusions This study identified three distinct clinical phenotypes in patients with HCM, each associated with different SCD risks and outcomes. Data-driven phenotyping of patients with HCM offers effective risk stratification and may optimize patient management.

Patients with transthyretin (ATTR) cardiac amyloid infiltration are increasingly diagnosed at earlier disease stages with no heart failure (HF) symptoms and a wide range of cardiac amyloid infiltration. To characterize the clinical phenotype and natural history of asymptomatic patients with ATTR cardiac amyloid infiltration. This cohort study analyzed data of all patients at 12 international centers for amyloidosis from January 1, 2008, through December 31, 2023. Inclusion criteria were asymptomatic ATTR cardiac amyloid infiltration, defined as an absence of HF history, HF signs and symptoms, diuretic therapy, and plasma cell dyscrasia with evidence of myocardial uptake on bone scintigraphy. If plasma cell dyscrasia was present, histologic confirmation of ATTR amyloid was required. Asymptomatic ATTR cardiac amyloid infiltration. The primary outcomes were all-cause and cardiovascular (CV) mortality. The secondary outcomes were unplanned HF hospitalization, unplanned CV-related hospitalization, and a composite outcome of CV mortality and HF hospitalization. The study comprised 485 patients with asymptomatic ATTR cardiac amyloid infiltration (mean [SD] age, 74.9 [9.9] years, 85.8% male, 112 [23.1%] with hereditary ATTR amyloidosis), with 369 (76.1%) having grade 2 or 3 and 116 (23.9%) having grade 1 cardiac uptake at baseline. Patients with grade 2 or 3 uptake exhibited significantly more cardiac functional and structural abnormalities vs patients with grade 1 uptake. At 3 years, compared with grade 1 uptake, patients with grade 2 or 3 uptake had greater development of HF (54.3% [95% CI, 47.7%-61.3%] vs 23.1% [95% CI, 14.8%-35.1%]), greater outpatient diuretic initiation and N-terminal pro-B-type natriuretic peptide progression (35.0% [95% CI, 28.0%-43.2%] vs 12.4% [95% CI, 6.3%-23.7%]), and greater HF hospitalization (8.7% [95% CI, 5.9%-12.9%] vs 0%) and unplanned CV hospitalization (20.0% [95% CI, 15.7%-25.3%] vs 4.3% [95% CI, 1.6%-11.3%]). Over a median follow-up of 37 months (IQR, 20-64 months), the all-cause death rate was similar between patients with grade 1 vs 2 and 3 uptake; however, those with grade 2 or 3 compared with grade 1 uptake had a significantly higher risk of CV mortality (unadjusted hazard ratio, 5.30; 95% CI, 1.92-14.65). This study shows that asymptomatic ATTR cardiac amyloid infiltration encompasses a wide spectrum of disease severity, with patients with grade 2 or 3 cardiac uptake experiencing an increased rate of CV events and CV mortality and patients with grade 1 uptake experiencing a lower CV event rate and predominantly non-CV mortality. These findings support the use of disease-modifying treatments in asymptomatic patients with grade 2 or 3 uptake and highlight the need of large-scale studies to assess their role in grade 1 uptake.

The temporal changes in clinical profiles and outcomes of high-risk myocardial infarction survivors enrolled in clinical trials are poorly described. This study compares mortality rates, baseline characteristics, and the prognostic impact of therapies among participants of the VALIANT and PARADISE-MI trials. Exclusively VALIANT participants who matched the inclusion criteria of the PARADISE-MI trial were included in the analysis. Risk of death was compared between trials using Cox regression models. The impact of baseline characteristics and therapies on mortality was estimated by the magnitude reduction of β coefficients using Cox proportional hazards regression models. A total of 9617 VALIANT participants matched the inclusion criteria of the PARADISE-MI trial (n = 5661). All-cause mortality in PARADISE-MI was less than half that in VALIANT (4.2 vs 9.9 per 100 patient-years; hazard ratio [HR] 0.41, 95% confidence interval [CI] 0.37-0.46). This difference was reduced after adjustment for clinical variables but remained substantial (adjusted HR 0.68, 95% CI 0.58-0.80). The most important mediator of this reduction related to covariate adjustment was the use of percutaneous coronary intervention (PCI), accounting for almost half of the attenuation observed. Similar results were found for cardiovascular (CV) death, while no between-trial significant differences were found in the non-CV mortality risk. Cardiovascular mortality following high-risk myocardial infarction has significantly declined over time, while the risk for non-CV death has remained unchanged. This improvement is partially attributable to advancements in CV care, particularly the use of PCI. Continued efforts to implement guidelines and standardize the quality of care are needed to sustain this positive trend.