Heart Failure, Anemia and Mortality in Mexican American Older Adults: Sex Differences.

Liver disease, heart failure, and 13-year mortality among Mexican American older adults: Nativity differences

This study sought to investigate the temporal association between changes in physiologic heart failure (HF) sensors, atrial fibrillation (AF) progression, and clinical HF in patients with cardiac resynchronization therapy implantable defibrillators (CRT-D) designed to monitor AF and HF daily. AF is a common comorbidity in HF; however, it is unclear if HF triggers AF, or vice-versa. Current implantable cardiac devices have sensors capable of quantifying HF status, which permits a greater understanding of the impact of AF on HF status and may help guide treatment. The MultiSENSE (Multisensor Chronic Evaluation in Ambulatory HeartFailure Patients) study collected multiple sensor data indicative of HF status in patients with CRT-D followed for up to 12months. Patients were grouped according to their longest daily AF burden: 1) at least 24 hours of AF (HIGH AF); 2) between 6minutes and 24 hours (MID AF); and 3) <6minutes (NO AF). Sensor data were aligned to the first qualifying AF event or a randomly selected day for patients in the NO AF group. Among 869 patients with daily AF data available, 98 patients had HIGH AF, 141 patients MID AF, and 630 patients NO AF. At baseline, history of AF, N-terminal pro hormone B-type natriuretic peptide and device-measured S3 were associated with development of AF. HeartLogic index increased before AF onset (Δ HeartLogic=9.83 ± 2.49; P< 0.001). Multivariable time-dependent Cox regression showed an increased risk for HF events following a 24-hour AF episode compared with no 24-hour AF (hazard ratio: 1.96; 95% confidence interval: 1.03-3.74). Device-measured HF indicators worsened before AF onset, whereas clinical HF deterioration only became apparent after AF occurred. Thus, the sensitivity of methods to ascertain AF and HF status appear to influence the direction of perceived causality. (Multisensor Chronic Evaluation in Ambulatory HeartFailure Patients [MultiSENSE]; NCT01128166).

Introduction AHA/ACC guidelines recommend combination therapy with an angiotensin-converting-enzyme inhibitor (ACEI) or angiotensin-receptor blocker (ARB) and a beta-blocker (BB) at discharge for patients hospitalized for heart failure (HF) with reduced ejection fraction. However, there is little information available to compare outcomes associated with these three treatment options at discharge, and the optimal monotherapy with either an ACEI/ARB or BB for patients who cannot tolerate combination therapy is unknown. Hypothesis We hypothesized that: 1) patients receiving ACEI/ARB or BB monotherapy would have higher rates of mortality and HF re-hospitalization than patients receiving combination therapy; and 2) patients receiving ACEI/ARB monotherapy would experience similar rates of mortality and lower rates of HF re-hospitalization when compared with patients receiving BB monotherapy. Methods We studied 21,849 patients with left ventricular ejection fraction &lt; 40% hospitalized for HF at 144 VA hospitals nationwide and who were assessed for HF quality measures between 2003 and 2007. Patients who received any of the three therapies (n=19,303) were 1:1:1 propensity score matched. We evaluated the association between treatment at hospital discharge and outcomes using the Kaplan-Meier method, pair-wise log-rank tests to test for significant differences in event-free survival, and hazard ratios (HR) and 95% confidence intervals (CI) from Cox proportional hazards regression models. Results Among 4,995 patients in our matched sample, BB monotherapy at discharge was associated with increased 30-day mortality compared with ACEI/ARB monotherapy (HR: 1.62; 95% CI: 1.15, 2.29; log-rank P=0.009), which was not observed at six months (HR: 1.08; 95% CI: 0.91, 1.27; log-rank P=1.00). BB monotherapy at discharge was associated with increased mortality risk when compared with combination therapy at 30 days (HR: 1.67; 95% CI: 1.19, 2.36; log-rank P=0.009) and at six months (HR: 1.28; 95% CI: 1.08, 1.52; log-rank P=0.030). No significant differences in mortality between patients receiving ACEI/ARB monotherapy and combination therapy were observed. No significant association between HF therapy at discharge and risk of HF re-hospitalization was found. Conclusions In this cohort of veterans hospitalized with decompensated HF and reduced ejection fraction, receipt of BB monotherapy at hospital discharge was associated with an elevated risk of mortality when compared with ACEI/ARB monotherapy and combination therapy.

The relationship between the Charlson comorbidity index (CCI) and short-term readmission is as yet unknown. Therefore, we aimed to investigate whether the CCI was independently related to short-term readmission in patients with heart failure (HF) after adjusting for other covariates. From December 2016 to June 2019, 2008 patients who underwent HF were enrolled in the study to determine the relationship between CCI and short-term readmission. Patients with HF were divided into 2 categories based on the predefined CCI (low < 3 and high > =3). The relationships between CCI and short-term readmission were analyzed in multivariable logistic regression models and a 2-piece linear regression model. In the high CCI group, the risk of short-term readmission was higher than that in the low CCI group. A curvilinear association was found between CCI and short-term readmission, with a saturation effect predicted at 2.97. In patients with HF who had CCI scores above 2.97, the risk of short-term readmission increased significantly (OR, 2.66; 95% confidence interval, 1.566-4.537). A high CCI was associated with increased short-term readmission in patients with HF, indicating that the CCI could be useful in estimating the readmission rate and has significant predictive value for clinical outcomes in patients with HF.

AimsNutrition and inflammation status play a vital role in the prognosis of patients with heart failure (HF). This study aimed to investigate the association between the advanced lung cancer inflammation index (ALI), a novel composite indicator of inflammation and nutrition, and short‐term mortality among critically ill patients with HF.MethodsThis retrospective study included 548 critically ill patients with HF from the MIMIC‐IV database. ALI was computed using body mass index, serum albumin and neutrophil–lymphocyte ratio. The primary endpoint was all‐cause in‐hospital mortality, and the secondary endpoint was 90 day mortality. Kaplan–Meier survival curve analysis with long‐rank test and Cox proportional hazards regression models were employed to assess the relationship between baseline ALI and short‐term mortality risk. The incremental predictive ability of ALI was evaluated by C‐statistic, continuous net reclassification improvement (NRI) and integrated discrimination improvement (IDI).ResultsThe average age of 548 patients was 72.2 (61.9, 82.1) years, with 60% being male. Sixty‐three patients (11.5%) died in the hospital, and 114 patients (20.8%) died within 90 days of intensive care unit admission. The Kaplan–Meier analysis revealed that the cumulative incidences of both in‐hospital and 90 day mortality were significantly higher in patients with lower ALI (log‐rank test, in‐hospital mortality: P < 0.001; 90 day mortality: P < 0.001). The adjusted Cox proportional hazard model revealed that ALI was inversely associated with both in‐hospital and 90 day mortality after adjusting for confounders [hazard ratio (HR) (95% confidence interval) (CI): 0.97 (0.94, 0.99), P = 0.035; HR (95% CI): 0.62 (0.39, 0.99), P = 0.046]. A linear relationship was observed between ALI and in‐hospital mortality (P for non‐linearity = 0.211). The addition of ALI significantly improved the prognostic ability of GWTG‐HF score in the in‐hospital mortality [C‐statistic improved from 0.62 to 0.68, P = 0.001; continuous NRI (95% CI): 0.44 (0.20, 0.67), P < 0.001; IDI (95% CI): 0.03 (0.01, 0.04), P < 0.001] and 90 day mortality [C‐statistic improved from 0.63 to 0.70, P < 0.001; continuous NRI (95% CI): 0.31 (0.11, 0.50), P = 0.002; IDI (95% CI): 0.01 (0.00, 0.02), P = 0.034]. Subgroup analysis revealed stronger correlations between ALI and in‐hospital mortality in males and patients aged over 65 years (interaction P = 0.031 and 0.010, respectively). The C‐statistic of in‐hospital mortality in patients over 65 years was 0.66 (95% CI: 0.58, 0.74).ConclusionsALI at baseline can independently predict the risk of short‐term mortality in critically ill patients with HF, with lower ALI significantly associated with higher mortality. Further large prospective research with extended follow‐up periods is necessary to validate the findings of this study.

Background Diabetes mellitus (DM) is a common comorbidity in heart failure (HF), but the impact of new-onset DM on HF outcomes remains unclear. This study evaluated the effects of DM status on hospitalization for HF (HHF), major adverse cardiac events (MACEs), and mortality in HF patients. Methods We conducted a retrospective cohort study of patients newly diagnosed HF at Changhua Christian Hospital, Taiwan, from 2011 to 2021. Patients were grouped as non-DM (n = 1477), preexisting DM (n = 1488), and new-onset DM (n = 328). Inverse propensity score weighting was applied to balance covariates. Results Compared to the non-DM group, the preexisting DM was associated with higher risks of HHF [hazard ratio (HR), 1.13; 95% confidence interval (CI), 1.02–1.25], MACEs (HR, 1.22; 95% CI, 1.00–1.49), all-cause mortality (HR, 1.17; 95% CI, 1.01–1.36), and cardiovascular death (HR, 1.54; 95% CI, 1.15–2.06). The new-onset DM group showed a significantly higher risk of HHF (HR, 1.24; 95% CI, 1.01–1.51) and MACEs (HR, 1.22; 95% CI, 1.00–1.49), with nonsignificant trends toward increased all-cause mortality (HR, 1.08; 95% CI, 0.79–1.48) and cardiovascular death (HR, 1.36; 95% CI, 0.74–2.48). Conclusion In HF patients, preexisting DM is associated with worse outcomes across multiple endpoints. New-onset DM also elevates risks of HHF and MACE, though its effect on mortality is less clear. Although our study, utilizing electronic medical record data, revealed a different pattern compared to the Danish registry, the findings emphasize the need for individualized management strategies based on DM status in HF care.

Endothelial dysfunction may be a phenotypic expression of heart failure (HF). Total brachial artery reactivity (TBAR) is a non-invasive measurement of endothelial function that has been associated with increased risk of cardiovascular outcomes. Limited information is currently available on the impact of TBAR on incident HF and its subtypes. The aim of this study was to investigate whether TBAR is associated with overall incident HF, and the two HF subtypes, HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF) in a community-based study. The sample included 5499 participants (45-84years of age) from the Multi-Ethnic Study of Atherosclerosis who were free of cardiovascular disease at baseline. Brachial artery was imaged via ultrasound after five minutes of cuff occlusion at the right forearm. TBAR was calculated as the difference between maximum and minimum brachial artery diameters following cuff release, divided by the minimum diameter multiplied by 100%. A dichotomous TBAR variable was created based on the median value (below or above 7.9%). Participants with EF ≤ 40% were considered HFrEF and those with EF ≥ 50% were considered HFpEF. Cox proportional hazards regression models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI). Over a mean follow-up period of 12.5years, incident HF was diagnosed in 250 participants: 98 classified as HFrEF, 106 as HFpEF, and 46 with unknown or borderline EF (41-49%). Crude analysis revealed that those with TBAR below the median had a significantly greater risk of HF (HR 1.46; 95% CI 1.13-1.88, p < 0.01) and HFrEF (HR 1.61; 95% CI 1.07-2.43, p < 0.05). Following adjustment for known HF risk factors (e.g., age, sex, race, blood pressure), the strength of these relationships was attenuated. Borderline significant results were revealed in those with HFpEF (HR 1.43; 95% CI 0.97-2.12, p = 0.06). Kaplan-Meier curves suggest significantly lower risks of developing HF and HFrEF in those with TBAR above the median (log-rank p ≤ 0.05 for both). When examined as a continuous variable, with a cut point of 50% for EF, every 1-standard deviation (9.7%) increase in TBAR resulted in a 19 and 29% decrease in risk of HF (p < 0.05) and HFrEF (p = 0.05), respectively. Lower TBAR values were associated with higher rates of incident HF and HFrEF, suggesting a possible role of endothelial dysfunction in HF pathogenesis. The impact of other known HF risk factors may mediate this relationship, thus further research is warranted.

To examine the effect of co-occurring depressive symptoms and functional disability on mortality in older Mexican-American adults with diabetes mellitus. Longitudinal cohort study. Hispanic Established Populations for the Epidemiological Study of the Elderly (HEPESE) survey conducted in the southwestern United States (Texas, Colorado, Arizona, New Mexico, California). Community-dwelling Mexican Americans with self-reported diabetes mellitus participating in the HEPESE survey (N = 624). Functional disability was assessed using a modified version of the Katz activity of daily living scale. Depressive symptoms were measured using the Center for Epidemiologic Studies Depression Scale. Mortality was determined by examining death certificates and reports from relatives. Cox proportional hazards regression analyses were used to examine the hazard of mortality as a function of co-occurring depressive symptoms and functional disability. Over a 9.2-year follow-up, 391 participants died. Co-occurring high depressive symptoms and functional disability increased the risk of mortality (hazard ratio (HR) = 3.02, 95% confidence interval (CI) = 2.11-4.34). Risk was greater in men (HR = 8.11, 95% CI = 4.34-16.31) than women (HR = 2.21, 95% CI = 1.42-3.43). Co-occurring depressive symptoms and functional disability in older Mexican-American adults with diabetes mellitus increases mortality risk, especially in men. These findings have important implications for research, practice, and public health interventions.

BackgroundPatients with psoriatic arthritis and psoriasis, collectively termed psoriatic disease (PsD), have an increased risk for cardiovascular (CV) disease.ObjectivesWe aimed to identify traditional CV risk factors and PsD-related risk factors...

Mid-term Prognostic Implication of hospitalized COVID-19 patients with Prior Heart Failure diagnosis

The association between heart failure and incident cancer in women: an analysis of the Women's Health Initiative.

Canagliflozin reduced kidney disease progression in participants with type 2 diabetes in the CANagliflozin cardioVascular Assessment Study (CANVAS) Program. This analysis explored potential mediators of the effects of canagliflozin on kidney outcomes. The percent mediating effect of 18 biomarkers indicative of disease was determined by comparing the hazard ratios for the effect of randomized treatment from an unadjusted model and from a model adjusting for the average post-randomization level of each biomarker. Multivariable analyses assessed the joint effects of biomarkers that mediated most strongly in univariable analyses. The kidney outcome was defined as a composite of 40% estimated glomerular filtration rate decline, end-stage kidney disease, or death due to kidney disease. Nine biomarkers (systolic blood pressure [8.9% of effect explained], urinary albumin:creatinine ratio [UACR; 23.9%], gamma glutamyltransferase [4.1%], hematocrit [51.1%], hemoglobin [41.3%], serum albumin [19.5%], erythrocytes [56.7%], serum urate [35.4%], and urine pH [7.5%]) individually mediated the effect of canagliflozin on the kidney outcome. In a parsimonious multivariable model, erythrocyte concentration, serum urate, and systolic blood pressure maximized cumulative mediation (115%). Mediating effects of UACR, but not other mediators, were highly dependent upon the baseline level of UACR: UACR mediated 42% and 7% of the effect in those with baseline UACR 30 mg/g or more and under 30 mg/g, respectively. The identified mediators support existing hypothesized mechanisms for the prevention of kidney outcomes with sodium glucose co-transporter 2 inhibitors. Thus, the disparity in mediating effects across baseline UACR subgroups suggests that the mechanism for kidney protection with canagliflozin may vary across patient subgroups.

Relation of Baseline Systolic Blood Pressure and Long-Term Outcomes in Ambulatory Patients With Chronic Mild to Moderate Heart Failure

As a neurological disorder, epileptic seizures have been documented to correlate with structural and functional cardiac alterations in prior studies. However, the long-term risk association between epilepsy and cardiovascular diseases (CVDs) remains incompletely elucidated. This prospective population-based cohort study utilized individual-level data from the UK Biobank. The primary composite endpoint comprised incident CVDs, including ischemic heart disease (IHD), heart failure (HF), atrial fibrillation (AF), stroke, and cardiovascular death. Cox proportional hazards regression models with covariate adjustments, complemented by Fine-Gray competing risk analyses, were employed to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for assessing epilepsy-CVD associations. A total of 448,487 participants, including 7,220 patients with epilepsy, were included in the analyses. Over a median follow-up of 13.4 years (IQR: 12.5-14.1; range: 3.0-16.2 years), 2,097 (29.0%) and 64,341 (14.6%) participants experienced CVDs in the epilepsy and non-epilepsy cohorts, respectively. Epilepsy was associated with higher risks of overall CVDs (HR: 1.97, 95% CI: 1.88-2.06) and specific cardiovascular outcomes including IHD (HR: 1.63, 95% CI: 1.53-1.74), HF (HR: 1.89, 95% CI: 1.72-2.09), AF (HR: 1.78, 95% CI: 1.65-1.91), stroke (HR: 4.32, 95% CI: 4.01-4.64), and cardiovascular mortality (HR: 2.55, 95% CI: 2.26-2.88), after adjustment for available common variant-based genetic predisposition scores. Furthermore, patients with status epilepticus exhibited a significantly higher CVDs risk compared to those with epilepsy alone (HR: 1.70, 95% CI: 1.43-2.02). Epilepsy was associated with higher risks of incident CVDs, including IHD, HF, AF, stroke, and cardiovascular mortality. These findings suggest that patients with epilepsy may represent a population at elevated cardiovascular risk, although causal inference cannot be established.

Introduction: Contralateral differences in systolic blood pressure (SBP) are a risk assessment tool and indicative of underlying cardiovascular issues. Most of the available studies focused on brachial blood pressure and its clinical impact. This study evaluated whether interankle SBP differences and contralateral differences in pulse wave velocity (PWV) are associated with incident heart failure (HF) and all-cause and cardiovascular mortality in a community-dwelling sample of older adults. Methods: Sample included 5,077 participants (75.2 ± 5.1 years old) of the Atherosclerosis Risk in Communities (ARIC) study. The OMRON VP-1000 plus was used to measure PWV and blood pressure in the ankles. PWV was assessed between the brachial artery and ankle (baPWV) and heart and ankle (haPWV) on the right and left sides. Cut points for contralateral differences in PWV were set at the 90th percentile in our sample. Outcomes included incident HF (first definite or probable hospitalization for acute decompensated HF), all-cause and cardiovascular mortality (until December 31, 2020). Cox proportional hazards regression models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI). Results: Over a mean follow-up of 7.5 ± 2.1 years, incident HF was diagnosed in 457 participants, and 1,275 all-cause and 363 cardiovascular deaths occurred. The prevalence of interankle SBP difference ≥10 and ≥15 mmHg was 24.9% (1,268) and 12.0% (605), respectively. The prevalence of contralateral differences in baPWV (&gt;240 cm/s) and haPWV (&gt;80 cm/s) was 10.1% (513) and 9.1% (464), respectively. Interankle SBP difference ≥10 mmHg (HR 1.13; 95% CI 1.00-1.29), ≥15 mmHg (HR 1.25; 95% CI 1.06-1.48), contralateral difference in baPWV &gt;240 cm/s (HR 1.18; 95% CI 1.00-1.41), and haPWV &gt;80 cm/s (HR 1.21; 95% CI 1.01-1.44) were each independently associated with all-cause mortality after adjustment for demographics, traditional cardiovascular risk factors, and extreme values of ankle-brachial index ≤0.9 or &gt;1.40. Contralateral differences in ankle SBP ≥15 mmHg (HR 1.55; 95% CI 1.16-2.06), and haPWV &gt;80 cm/s (HR 1.40; 95% CI 1.02-1.91) were both independently associated with cardiovascular mortality. Crude analysis revealed that those with contralateral differences in ankle SBP ≥10 and ≥15 mmHg, baPWV &gt;240 cm/s, and haPWV &gt;80 cm/s had a significantly higher risk of HF (p&lt;0.05 for all). However, these HF relationships were no longer statistically significant after adjustment for confounders. Conclusions: Contralateral differences in ankle SBP and PWV were independently associated with all-cause and cardiovascular mortality risk even after accounting for traditional cardiovascular risk factors and the ankle-brachial index. These results underscore the significance of evaluating contralateral differences in ankle SBP and PWV as potential markers of increased mortality risk among older adults.