Risk Of Heart Failure Research Articles

Risk of myocardial infarction and heart failure in gout patients: a systematic review and meta-analysis

BackgroundGout is a metabolic disease caused by decreased blood uric acid excretion and purine metabolism disorders. Long-term and persistent metabolic dysfunction gradually affects other organ functions and is the main factor inducing Myocardial Infarction (MI) and Heart Failure (HF), seriously affecting the health of patients. This study adopts a meta-analysis to analyze the risk of MI and HF in gout patients.MethodsClinical research literature related to gout complicated with MI or HF was searched in databases such as PubMed, Embase, Web of Science, Cochrane Library, etc. through computer retrieval before March 2023. Literature content was carefully read and retrieved, and screening was conducted based on inclusion and exclusion criteria. Relevant data were extracted from the final screened literature, and a forest map was drawn using RevMan 5.3 software for meta-analysis.ResultsAfter searching in various databases, 2519 articles were obtained. After screening, 8 articles were finally included for meta-analysis. Among the 22 included literature, 9 analyzed the risk of gout and MI, and heterogeneity tests showed P = 0.20 and I2 = 28%. Fixing effects analysis showed RR = 4.60, 95%CI = 4.39–4.82, and P < 0.001. Nine articles analyzed the risk of gout and HF, and heterogeneity tests showed that P = 0.13 and I2 = 37%. Fixing effects analysis showed RR = 2.71, 95%CI = 2.61–2.82, and P < 0.001. Eight studies compared the incidence of MI or HF between male gout and non-gout patients. Heterogeneity tests showed P = 0.21 and I2 = 28%, while fixing effects analysis showed RR = 1.98 and 95%CI = 1.89–2.01, with P < 0.001. Four articles statistically compared the incidence of MI or HF between female gout and non-gout patients. Heterogeneity tests showed P = 0.15 and I2 = 43%. Fixing effects analysis showed RR = 1.70, 95%CI = 1.57–1.83, and P < 0.001. Thirteen studies compared the incidence of MI or HF in gout patients of different genders. Heterogeneity tests showed P = 0.37 and I2 = 7%. Fixing effects analysis showed RR = 0.03, 95%CI = 0.03–0.03, and P < 0.001.ConclusionCompared to non-gout patients, gout patients are more prone to MI or HF and are not affected by gender. However, among gout patients, women have a higher risk of MI or HF than men.

Hepcidin, Incident Heart Failure and Cardiac Dysfunction in Older Adults: the ARIC Study.

Hepcidin regulates plasma and tissue iron levels. We studied the association of hepcidin levels with the risk of incident heart failure (HF) and cardiac dysfunction in older adults. We included adults from the ongoing, longitudinal Atherosclerosis Risk in Communities (ARIC) study who were free from prevalent anemia and HF at Visit 5 (2011-2013) and had available hepcidin and covariate data. Associations of plasma hepcidin levels with overall adjudicated incident HF, HF with reduced and HF with preserved ejection fraction (HFrEF and HFpEF) were assessed using multivariable Cox proportional hazards regression models. Cross-sectional associations of hepcidin with echocardiographic measures of cardiac structure and function were estimated using multivariable linear regression models. The mean age was 75±5 years old and 56% were women. In fully adjusted models, lower hepcidin levels were associated with a higher risk of overall incident HF (HR [95% CI] per 50% lower hepcidin: 1.15 [1.05-1.26]; P=0.003) and HFpEF (HR [95% CI]: 1.25 [1.10-1.42]; P=0.001). Plasma hepcidin level was not significantly associated with the risk of incident HFrEF (HR [95% CI]: 1.08 [0.94-1.24]; P=0.30). Lower hepcidin levels were associated with higher E wave (P=0.046), higher E/e' ratio (P=0.002), higher left atrial volume index (P=0.005) and higher pulmonary artery systolic pressure (P=0.02). In community-dwelling older adults without anemia, lower plasma hepcidin levels associate with a higher risk of incident HF (particularly HFpEF) and diastolic dysfunction. The findings imply the importance of monitoring iron metabolism dysregulation, even in absence of anemia, in late life.

Reduced antioxidant high-density lipoprotein function in heart failure with preserved ejection fraction.

Heart failure (HF) is a heterogeneous clinical syndrome affecting a growing global population. Due to the high incidence of cardiovascular risk factors, a large proportion of the Western population is at risk for heart failure. Oxidative stress and inflammation play a crucial role in the pathophysiology of heart failure with preserved ejection fraction (HFpEF). While previous studies have demonstrated an association between dysfunctional HDL and heart failure, the specific link between oxidized HDL and HF remains unexplored. In this cross-sectional observational study, the antioxidant function of HDL was assessed in 366 patients with suspected heart failure. HFpEF assessment was conducted according to current guidelines. A validated cell-free biochemical assay was used to determine reduced HDL antioxidant function as assessed by increased HDL-lipid peroxide content (HDLox), normalized by HDL-C levels and the mean value of a pooled serum control from healthy participants (nHDLox; no units). Results were expressed as median with interquartile range (IQR). Participants with HFpEF (n = 88) had 15% higher mean relative levels of nHDLox than those without heart failure (n = 180). Using a basic multivariate model adjusted for age, sex, eGFR and a full multivariate model (adjusted for diabetes, hypertension, atrial fibrillation, LDL cholesterol, hsCRP, and coronary artery disease), nHDLox was an independent predictor for HFpEF (p < 0.05). An increase in 1-SD in nHDLox was associated with a 67% increased risk for HFpEF if compared with participants without heart failure (p = 0.02). HDL antioxidant function is reduced in patients with HFpEF. Improving HDL function is a promising target for early heart failure treatment.

The role of exercise in bolstering cardiac resilience during aging

Aging leads to structural and functional deterioration of the heart, reducing its capacity to withstand internal and external stressors and consequently increasing the risk of heart failure. Exercise is a potent modulator of cardiovascular and metabolic health, offering numerous physiological benefits that can persist throughout the aging process. Studies suggest that exercise can decelerate age-related cardiac deterioration and mitigate the risk of heart failure. In this review, we discuss recent advances in our understanding of exercise-mediated molecular and cellular adaptations that could serve as therapeutic targets for age-related cardiac remodeling and functional decline. We also explore how exercise-induced changes may enhance cardiac resilience with age, examine sex differences in cardiac aging and response to exercise, and highlight the value of murine exercise models as research tools for identifying novel therapeutic targets and strategies to combat heart failure.

NT-proBNP for Heart Failure Screening in Primary Care in an Eastern European Country: What We Know and Proposed Steps

Epidemiological studies indicate that heart failure (HF) prevalence and associated mortality are significantly higher among Eastern European countries as compared to their Western European counterparts. The significant financial burden on the healthcare system matches these sobering data. Thus, efficient programs for patients with HF have been called for. N-terminal prohormone of brain natriuretic peptide (NT-proBNP) represents a widely used, cost-effective, and readily available test that can be used to evaluate HF risk. However, it should not be used as a universal assessment, given the existing variability in proposed cut-off scores for various subgroups of patients. Thus, the clinical context needs to always be considered, and alternative diagnoses need to be ruled out. Based upon evidence from the literature for the above assumptions, the advantages and limitations of using NT-proBNP in primary care settings, along with other HF diagnostic modalities, are discussed in this paper. Also, this paper argues that an effective primary care network, in collaboration with specialist providers, may avoid a delay in HF diagnoses, may help provide on-time treatments, and may ultimately cut unnecessary healthcare expenditures associated with HF hospitalizations. Therefore, the present paper proposes an algorithm for diagnosing HF in primary care settings and discusses specific knowledge and skills that family physicians should be well equipped with in order to successfully respond to the needs of their patients with HF.

Serum free 25(OH)D concentrations and cardiovascular disease, heart failure, kidney function decline, and fracture: the health, aging, and body composition study

Abstract Vitamin D deficiency is common across the world. However, the standard clinical biomarker for vitamin D, 25-hydroxyvitamin D, may be a poor marker of vitamin D status, as most of circulating vitamin D is protein bound and not bioavailable. Free (unbound) vitamin D may therefore be a better marker of vitamin D status. We evaluated the relationship of free vitamin D with incident cardiovascular disease (CVD), heart failure (HF), kidney function decline (KFD) and fracture, among 786 participants in the Health Aging and body composition study. We used sequential models to assess hazard ratios (HR) of each outcome that adjusted for age, sex, race, season of blood sampling, and study site, kidney function, serum calcium and phosphate, fibroblast growth factor 23, parathyroid hormone, body mass index, and vitamin D supplementation. The mean age of the 786 participants was 75 ± 3 years, 53% were women, 40% were Black. The median free vitamin D concentration was 5.3 (interquartile range 4.1-6.7) pg/ml. There were 157 cases of incident CVD, 123 cases of incident HF, 382 cases of incident KFD, and 178 fractures over 11 years of follow up. In fully adjusted models, a two-fold greater free vitamin D was associated with lower risk of incident HF [HR 0.75, 95%CI(0.58-0.96)] and greater risk kidney function decline[1.25(1.03-1.52)]. We found no association between free vitamin D and incident CVD or fracture. We did not find evidence that free vitamin D was a superior marker of clinical outcomes compared to total 25-hydroxyvitamin D alone. Further studies are needed to elucidate the relationship of free vitamin D with clinical outcomes.

Heart failure risk stratification using artificial intelligence applied to electrocardiogram images: a multinational study.

Current heart failure (HF) risk stratification strategies require comprehensive clinical evaluation. In this study, artificial intelligence (AI) applied to electrocardiogram (ECG) images was examined as a strategy to predict HF risk. Across multinational cohorts in the Yale New Haven Health System (YNHHS), UK Biobank (UKB), and Brazilian Longitudinal Study of Adult Health (ELSA-Brasil), individuals without baseline HF were followed for the first HF hospitalization. An AI-ECG model that defines cross-sectional left ventricular systolic dysfunction from 12-lead ECG images was used, and its association with incident HF was evaluated. Discrimination was assessed using Harrell's C-statistic. Pooled cohort equations to prevent HF (PCP-HF) were used as a comparator. Among 231 285 YNHHS patients, 4472 had primary HF hospitalizations over 4.5 years (inter-quartile range 2.5-6.6). In UKB and ELSA-Brasil, among 42 141 and 13 454 people, 46 and 31 developed HF over 3.1 (2.1-4.5) and 4.2 (3.7-4.5) years. A positive AI-ECG screen portended a 4- to 24-fold higher risk of new-onset HF [age-, sex-adjusted hazard ratio: YNHHS, 3.88 (95% confidence interval 3.63-4.14); UKB, 12.85 (6.87-24.02); ELSA-Brasil, 23.50 (11.09-49.81)]. The association was consistent after accounting for comorbidities and the competing risk of death. Higher probabilities were associated with progressively higher HF risk. Model discrimination was 0.718 in YNHHS, 0.769 in UKB, and 0.810 in ELSA-Brasil. In YNHHS and ELSA-Brasil, incorporating AI-ECG with PCP-HF yielded a significant improvement in discrimination over PCP-HF alone. An AI model applied to a single ECG image defined the risk of future HF, representing a digital biomarker for stratifying HF risk.

Pro-adrenomedullin as an independent predictive biomarker for heart failure in atrial fibrillation and flutter.

This study aimed to investigate potential biomarkers for predicting incident heart failure (HF) in patients with atrial fibrillation and flutter (AF and AFL), utilizing proteomic data from the UK Biobank Pharma Proteomics Project (UKB-PPP). This study analysed data from AF and AFL patients, split into discovery (n=1050) and replication (n=305) cohorts. Plasma biomarkers were screened using a multivariable-adjusted Cox proportional hazards model. Kaplan-Meier survival analysis and area under the receiver operating characteristic (ROC) curve assessments were conducted to evaluate predictive performance. Over a follow-up of 14.2years, 222 cases (21.1%) of HF were documented in the discovery cohort, while 117 cases (38.4%) occurred over 13.8years in the replication cohort. Out of 2923 proteins measured, only pro-adrenomedullin (pro-ADM) consistently showed a significant association with incident HF in both cohorts. In the discovery cohort, each unit increase in pro-ADM was linked to an increased risk of HF (HR=2.78, 95% CI 1.64-4.71, P<0.001, FDR=0.026), which was confirmed in the replication cohort (HR=3.95, 95% CI 1.97-7.94, P<0.001, FDR=0.012). Kaplan-Meier analysis demonstrated that patients with higher pro-ADM levels had significantly shorter time to HF onset, with median times ranging from 2306 to 3183days across quartiles (P<0.001). The cumulative incidence of HF ranged from 15.3% to 42.7% across quartiles of pro-ADM (log-rank P<0.001). Adding pro-ADM to a model with traditional risk factors, including NT-proBNP, significantly improved predictive accuracy for 3-year (AUC=0.783; integrated discrimination improvement [IDI]=0.010 and net reclassification index [NRI]=0.206, both P=0.002) and 5-year (AUC=0.749, IDI=0.013, NRI=0.179, P=0.001) risk of HF. In sensitivity analyses, the association between pro-ADM and incident HF remained consistent after excluding participants with self-reported AF and AFL, with each unit increase in pro-ADM being associated with an increased risk of HF (HR=1.77, 95% CI 1.02-3.04, P=0.041) and across subgroups of paroxysmal AF (HR=2.80, 95% CI 1.11-7.07, P=0.029) and persistent AF (HR=4.36, 95% CI 1.41-13.43, P=0.010). Pro-ADM is identified as an independent biomarker for predicting incident HF in AF and AFL patients. Its inclusion in risk prediction models enhances the ability to stratify HF risk beyond traditional biomarkers, demonstrating its potential utility in clinical practice.

Impact of Daytime and Nighttime Blood Pressure and Nocturnal Blood Pressure Fall on Heart Failure Risk in Treated Hypertension.

To evaluate the impact of daytime, nighttime and nocturnal blood pressure (BP) fall on heart failure (HF). We analyzed data of five cohorts including 15,526 treated hypertensive patients, experiencing 625 HF events, by study-level meta-analysis. The pooled hazard ratios (HR) and 95% confidence intervals (CI) for 1-SD increase in BP parameters or per group were calculated. When individually analyzed after adjustment for covariates, clinic systolic BP (SBP) (HR 1.20, 95% CI 1.01-1.43), daytime SBP (HR 1.34, 95% CI 1.06-1.70), nighttime SBP (HR 1.43, 95% CI 1.20-1.71), nighttime diastolic BP (DBP) (HR 1.26, 95% CI 1.05-1.52), % of nocturnal SBP fall (HR 0.81, 95% CI 0.75-0.88) and nondipping (HR 1.64, 95% CI 1.54-1.98) were associated with HF. If daytime or nighttime BPs were further adjusted for clinic BP results remained similar. When clinic, daytime and nighttime BPs were mutually adjusted, nighttime SBP (HR 1.43, 95% CI 1.27-1.61) and nighttime DBP (HR 1.37, 95% CI 1.14-1.64) remained associated with outcome. Heterogeneity across cohorts was explained by BP, sex and follow-up duration. In sensitivity analyses, for daytime and nighttime BP, no study had relevant influential effect on overall estimates. Looking for publication bias and adjusting for missing studies by Duval and Tweedie's method, clinic SBP lost significance but daytime SBP, and nighttime SBP and DBP remained significantly associated with HF. daytime and nighttime BPs are stronger than clinic BP in predicting HF, nighttime BP is stronger than daytime BP and a reduced nocturnal BP fall is associated with outcome.

Tissue-Engineered Therapeutics for Lymphatic Regeneration: Solutions for Myocardial Infarction and Secondary Lymphedema.

The lymphatic system, which regulates inflammation and fluid homeostasis, is damaged in various diseases including myocardial infarction (MI) and breast-cancer-related lymphedema (BCRL). Mounting evidence suggests that restoring tissue fluid drainage and clearing excess immune cells by regenerating damaged lymphatic vessels can aid in cardiac repair and lymphedema amelioration. Current treatments primarily address symptoms rather than underlying causes due to a lack of regenerative therapies, highlighting the importance of the lymphatic system as a promising novel therapeutic target. Here cutting-edge research on engineered lymphatic tissues, growth factor therapies, and cell-based approaches designed to enhance lymphangiogenesis and restore lymphatic function is explored. Special focus is placed on how therapies with potential for immediate lymphatic reconstruction, originally designed for treating BCRL, can be applied to MI to augment cardiac repair and reduce heart failure risk. The integration of these novel treatments can significantly improve patient outcomes by promoting lymphatic repair, preventing pathological remodeling, and offering new avenues for managing lymphatic-associated diseases.

Proteomic signature of HIV-associated subclinical left atrial remodeling and incident heart failure

People living with HIV are at higher risk of heart failure and associated left atrial remodeling compared to people without HIV. Mechanisms are unclear but have been linked to inflammation and premature aging. Here we obtain plasma proteomics concurrently with cardiac magnetic resonance imaging in two independent study populations to identify parallels between HIV-related and aging-related immune dysfunction that could contribute to atrial remodeling and clinical heart failure. We discover a plasma proteomic signature that may in part reflect or contribute to HIV-associated atrial remodeling, many features of which are associated with older age and time to incident heart failure among an independent community-based cohort without HIV. This proteomic profile was statistically enriched for immune checkpoint proteins, tumor necrosis factor signaling, ephrin signaling, and extracellular matrix organization, identifying possible shared pathways in HIV and aging that may contribute to risk of heart failure.

Assessing the risk of heart failure in type 2 diabetes: a prediction algorithm to sustain the evaluation of NT-proBNP in primary care.

Heart failure (HF) is a disease that leads to approximately 300,000 fatalities annually in Europe and 250,000 deaths each year in the United States. Type 2 Diabetes Mellitus (T2DM) is a significant risk factor for HF, and testing for N-terminal (NT)-pro hormone BNP (NT-proBNP) can aid in early detection of HF in T2DM patients. We therefore developed and validated the HFriskT2DM-HScore, an algorithm to predict the risk of HF in T2DM patients, so guiding NT-proBNP investigation in a primary care setting. Using a primary care database, we formed a cohort of patients aged ≥18 years diagnosed with T2DM between 2002 and 2022. A multivariate Cox model was adopted to assess the determinants associated with the occurrence of HF to combine them to form an individual score. Within a cohort of 167,618 patients (52.3% males; mean age 64.4 (SD: 14.4); HF rate equal to 6.7 cases per 1000 person-years), we developed the HFriskT2DM-HScore. When it was applied to the validation sub-cohort we found an explained variation and discrimination value of 43% (95% CI: 42-44) and 81% (95% CI: 0.80-0.83), respectively. Calibration slope was equal to 0.93 (95% CI: 0.81-1.1; p = 0.3123). The HFriskT2DM-HScore might be implemented as a decision support system for primary care to appropriately ease the prescription of NT-proBNP and early identification of HF.

Weight Changes and Heart Failure Risk After Breast Cancer Development

Weight Changes and Heart Failure Risk After Breast Cancer Development

Long-term changes in frailty and incident atrial fibrillation, heart failure, coronary heart disease, and stroke: A prospective follow-up study.

People with frailty have increased prevalence and incidence of atrial fibrillation (AF). The study aimed to further investigate the association of long-term changes in frailty with risk of new-onset AF. Its associations with heart failure (HF), coronary heart disease (CHD), and stroke were also evaluated as a secondary aim. Over 50,000 participants from UK Biobank cohort were included, with frailty index (FI) data and free of AF, HF, CHD or stroke in baseline and follow-up assessments. Frailty status of the participants was categorized into non-frail, pre-frail and frail based on their FI scores. FI in baseline and follow-ups are used to calculate the trajectories of frailty (ΔFI). During a median of 5.1 years of follow-up from the final assessment, 1729 cases of AF were recorded. Frailty trajectory analysis showed that even a 0.01 point/year increase in ΔFI was associated with 14% (95% CI 1.08-1.20) higher risk of AF, independent of baseline FI after adjusting for potential confounders. Compared with maintained non-frail participants, those with sustained frail status had the highest risk of incident AF (HR 1.95, 1.61-2.36). The risk declined by 30% (95% CI 0.53-0.94) when frail participants regressed to non-frail or pre-frail status, compared with sustained frail participants. These associations were similar in HF and CHD, however, not significant in stroke. In middle-aged and elderly individuals, frailty remission or non-frailty maintenance was associated with lower risk of AF, HF and CHD compared to persistent frailty, regardless of prior frailty status and established risk factors.

Desmoplakin Cardiomyopathy: Role of Inflammation and Potential Role of Disease-Modifying Therapies.

To summarize the available data on the use of immunosuppression therapies for the management of hot phases of disease and recurrent myocarditis in patients with desmoplakin cardiomyopathy (DSP-CMP). Occurrence of myocarditis episodes has been associated with worsening of outcomes in DSP-CMP. Multiple case reports and small case series have described potential benefit in using anti-inflammatory and immunosuppressive medications for the treatment of those episodes. Recently published translational data has shown a clear link between DSP variants and a propensity to inflammation. The presence of acute myocarditis episodes have been clearly demonstrated as a manifestation of DSP-CMP. These episodes are marked by myocardial inflammation and subsequent fibrosis, and, moreover, contribute to a heightened future risk of subsequent arrhythmias and heart failure. Identifying optimal strategies to prevent and/or interrupt myocardial inflammation is therefore a critical priority of patients with DSP-CMP.

Revolutionizing Cardiac Care: Artificial Intelligence Applications in Heart Failure Management.

Recent advancements in artificial intelligence (AI) have revolutionized the diagnosis, risk assessment, and treatment of heart failure (HF). AI models have demonstrated superior performance in distinguishing healthy individuals from those at risk of congestive HF by analyzing heart rate variability data. In addition, AI clinical decision support systems exhibit high concordance rates with HF experts, enhancing diagnostic precision. For HF with reduced as well as preserved ejection fraction, AI-powered algorithms help detect subtle irregularities in electrocardiograms and other related predictors. AI also aids in predicting HF risk in diabetic patients, using complex data patterns to enhance understanding and management. Moreover, AI technologies help forecast HF-related hospital admissions, enabling timely interventions to reduce readmission rates and improve patient outcomes. Continued innovation and research are crucial to address challenges related to data privacy and ethical considerations and ensure responsible implementation in healthcare.

A retrospective analysis of cardiovascular outcomes of clozapine treated individuals within Hunter New England.

Clozapine has demonstrated superiority in improving both positive and negative symptoms of treatment-resistant schizophrenia; however, there are associated treatment-limiting side effects, including myocarditis, cardiomyopathy and agranulocytosis. This retrospective cohort study describes the prevalence of myocarditis, left ventricular (LV) dysfunction, cardiovascular risk factors and outcomes in a cohort of patients maintained on clozapine therapy. Data were retrospectively collated from patients who had a diagnosis of schizophrenia, had been managed with clozapine at any stage during their care and undergone at least one echocardiogram. Between March 2020 and September 2021 674 patients were identified, 71% were male, with a mean age of 47 years old (interquartile range (IQR) 40-57). The mean duration of clozapine use was 7 years (IQR 4-13). The overall mortality was 5.54% during the follow-up period. Myocarditis was identified in one patient (0.15%) within the first 30 days, and an additional five cases were identified over the follow-up period (0.89%). The combined incidence of heart failure (HF) and myocarditis was 1.6% during the follow-up period. There was no association between LV size and function at baseline or during follow-up and adverse cardiac outcomes (comprising death, myocarditis, HF). Older age at initiation of therapy and baseline E/e' ratio were associated with risk of HF and myocarditis. The overall incidence of myocarditis and HF during follow-up was low, with surveillance echocardiography offering limited predictive value. Patients maintained on clozapine are at risk of significant cardiovascular sequelae, likely reflecting an adverse risk factor profile.

Metabolic dysfunction-associated steatotic liver disease is associated with increased risks of heart failure.

Metabolic dysfunction-associated steatotic liver disease (MASLD), defined by steatotic liver disease (SLD) and cardiometabolic factors, is increasing in prevalence, but its association with heart failure (HF) is unclear. Patients with SLD without a history of HF from 2006 to 2021 were retrospectively included and were classified into MASLD and non-MASLD groups that were followed longitudinally. The primary outcome was the new development of HF, which was sub-classified by echocardiography. Multivariable and propensity score matching analyses were conducted to adjust for confounding factors. Overall, 26 676 patients with SLD were included, with a median age of 51 years and 71% classified as MASLD. During a median follow-up of 6 years, 429 (1.61%) patients developed HF, and 76% were HF with preserved ejection fraction (HFpEF). The risk of HF was significantly higher in patients with MASLD than in those without (sub-distribution hazard ratio [SHR] 2.59, 95% confidence interval [CI] 1.84-3.64) after adjustment of competing mortality. There was a dose-dependent increase in HF risks in patients with more cardiometabolic risk factors (SHR 1.12, 95% CI 1.04-1.22). MASLD was also associated with higher risk of HF-related hospitalization (SHR 2.30, 95% CI 1.31-4.04) and specifically, the risk of HFpEF (SHR 1.91, 95% CI 1.27-2.86). In propensity score-matched cohorts, MASLD was also associated with a 2.52-fold higher risk of HF. In patients with SLD, those with MASLD show a higher risk of HF, specifically HFpEF. Future studies are warranted to validate the association between HF and MASLD.

Impact of TCF7L2 rs7903146 on clinical presentation and risk of complications in patients with type 2 diabetes.

TCF7L2 rs7903146 is the most impactful single genetic risk variant for type 2 diabetes. However, its role on disease progression, complications and mortality among people with type 2 diabetes at diagnosis remains unclear. We assessed the per allele impact of the rs7903146 T-allele on clinical characteristics and complication risk in 9231 individuals with type 2 diabetes at diagnosis and over a 10-year follow-up period. Log-binomial and robust Poisson regression analyses were used to estimate prevalence ratios for clinical characteristics and macro- and microvascular complications at diabetes onset, while Cox regression was applied to estimate the risk of complications post-diagnosis. Analyses were adjusted for sex, calendar year at birth, age at enrollment and diabetes duration. The per T-allele impact was associated with 0.6 kg/m2 (95% CI: 0.4, 0.8) lower BMI, 1.4 cm (95% CI: 1.0, 1.8) smaller waist circumference, 5.6% (95% CI: 4.2, 7.0) lower insulin secretion and 5.0% (95% CI: 3.3, 6.7) higher insulin sensitivity. Over 10 years, the per T-allele impact was associated with lower risks for major adverse cardiovascular events (0.87 [95% CI 0.79, 0.95]), myocardial infarction (0.82 [95% CI: 0.72, 0.93]) and heart failure (0.85 [95% CI 0.73, 1.00]), with no significant impact on microvascular complications. The TCF7L2 variant is associated with less obesity, lower insulin secretion and higher insulin action at diabetes onset, and decreased risk of cardiovascular events following type 2 diabetes onset.

High and Low Adherence to Mediterranean and DASH Diet Patterns and the Risk of Heart Failure: A Meta-Analysis of Observational Studies

Background. The relationship between heart failure (HF) and Mediterranean and DASH diets is not well delineated. This meta-analysis aimed to assess the effectiveness of high adherence to Mediterranean and DASH diets compared to low adherence in reducing the risk of incident HF (primary prevention of HF) and reducing all-cause mortality in patients with HF (secondary prevention of HF). Methods. The reporting stages of this meta-analysis closely adhered to the PRISMA guidelines. A comprehensive literature search was undertaken for published papers in PubMed, Embase, EBSCO, ICTRP, and the NIH clinical trials databases. Results. A total of 16 reports from 14 studies were included in this paper. A significant inverse association was identified between high adherence to the Mediterranean diet model (compared to low adherence) and the risk of incident HF (OR = 0.77, 95% CI: 0.63–0.93, p = 0.007) among patients without previous diagnosis of HF. Similarly, there was a significant and inverse relationship between high adherence to the DASH diet (compared to low adherence) and the risk of incident HF (OR = 0.83, 95% CI: 0.70–0.98, p = 0.03) among patients without previous diagnosis of HF. High adherence to the Mediterranean diet model (compared to low adherence) was associated with lower all-cause mortality (OR = 0.88, 95% CI: 0.78–0.99, p = 0.03) among patients with HF. Conclusions. This paper demonstrated that high adherence to Mediterranean and DASH diets significantly reduced the risk of incident HF among individuals without a previous diagnosis of HF, whereas only high adherence to the Mediterranean diet was associated with lower all-cause mortality among patients with HF.