Background Ejection fraction (LVEF) underpins risk stratification before transcatheter aortic valve replacement (TAVR), yet it does not indicate whether an impaired ventricle will recover once the stenosis is relieved, or what drives death in high-risk patients. We asked whether routine preprocedural data could address both. Methods and Results Among 1212 consecutive patients (1213 procedures) who underwent TAVR for severe aortic stenosis (2012–2026), unsupervised clustering of 18 routine variables (principal components, Ward linkage) defined four phenotypes: low-risk, elderly preserved-EF, reduced-EF, and cardiorenal. Five-year mortality ranged from 13.5% to 44.2% (P < 0.001). Among 180 patients with a baseline LVEF below 50%, a parsimonious model combining LV end-diastolic diameter, mean gradient, and coronary disease predicted a ≥ 10-point LVEF gain (optimism-corrected AUC, 0.75; 0.65 for LVEF alone, a difference that was not statistically significant in this sample), and an integer TAVR-RECOVER score stratified observed recovery from 69% to 98%. Reduced-EF patients recovered from a mean LVEF of 38% to 59% by 1 year. The cardiorenal phenotype carried a 3.4-fold age-adjusted mortality (95% CI, 2.0–5.6) but died chiefly of noncardiovascular causes (5-year incidence, 32% versus 13% cardiovascular); its excess risk became non-significant after adjustment for renal function and other routine laboratories (hazard ratio, 1.60; 95% CI, 0.61–4.17). Phenotype re-stratified mortality within each LVEF category, with an almost 3-fold gradient among preserved-EF patients. Conclusions Routine preprocedural data can estimate which impaired ventricles recover after TAVR and identify a cardiorenal phenotype whose excess, largely noncardiovascular mortality is statistically explained by measurable renal dysfunction rather than captured by ejection fraction. Prospective external validation is warranted.
Background Most mutations causing hypertrophic cardiomyopathy (HCM) affect sarcomeric proteins. Mutations in junctophilin-2 (JPH2) are also implicated, but the underlying mechanisms remain unclear. An A405S variant in JPH2 was identified in a male adolescent patient with interventricular septal (IVS) hypertrophy. The corresponding mouse variant (A399S) produces comparable IVS hypertrophy, establishing causality. Prior data indicated that altered intracellular Ca2+ handling is unlikely to be the primary driver. Methods We generated a CRISPR knock-in mouse model carrying the JPH2-A399S variant. Co-immunoprecipitation mass spectrometry and STED nanoscopy were used to identify JPH2 binding partners. Reactive oxygen species (ROS) were assessed with dihydroethidium in isolated myocytes. Adeno-associated virus serotype 9 (AAV9) was employed to overexpress peroxiredoxin 6 (PRDX6) in mutant hearts. Results PRDX6 was identified as a novel and abundant JPH2-interacting protein. PRDX6 expression was selectively downregulated in the IVS of JPH2-A399S mice and was also reduced in human failing hearts. JPH2-A399S mice exhibited increased ROS levels specifically in IVS myocytes. AAV9-mediated PRDX6 overexpression reversed the IVS hypertrophy phenotype. Conclusions These findings identify PRDX6 downregulation and consequent oxidative stress as a key mechanism driving JPH2-A399S-associated HCM. The results reveal a previously unrecognized role for JPH2 in cardiometabolic regulation and suggest that restoring PRDX6 levels may represent a therapeutic strategy for this form of HCM.
Introduction Human immunodeficiency virus (HIV) infection remains a major global health challenge. People living with HIV are twice as likely to develop cardiovascular disease. Myocardial work is a novel echocardiographic technique that assesses global work index and global work efficiency of the left ventricle, enabling earlier detection of subclinical myocardial dysfunction. Material and methods We conducted a cross-sectional study of patients with long-standing HIV infection without previous cardiovascular disease, aiming to evaluate the prevalence of subclinical cardiac dysfunction determined by an impaired global myocardial work efficiency, and studied its predictors by linear regression. Results 110 HIV patients (78.2% men) were included, median age 53.3 years and median time since diagnosis of 20.5 years. Echocardiographic measurements were compared with matched control participants. HIV patients showed significantly lower values of global longitudinal strain of the left ventricle, right ventricle free wall and left atrial reservoir, although absolute values remained within normal limits. HIV group had consistently reduced global work efficiency values (≤93%) which was associated with by age, diabetes, SCORE2, time from diagnosis, long corrected QT interval, QRS Interval duration, CD4 count nadir, initial and maximum viral load and exposure to didanosine by univariate analysis. After adjustment by SCORE2 and QRS duration, global work efficiency reduction depended on maximum viral load. Conclusions Subclinical myocardial dysfunction is present in long-standing HIV infection. Global work efficiency may represent a sensitive marker of subclinical myocardial dysfunction, even in patients with preserved left ventricular ejection fraction, and it was associated with maximum viral load in our patients.
Background Contrast-associated nephropathy is a complication of cardiovascular procedures. Although contrast volume is a risk factor for acute kidney injury, its impact on medium- to long-term renal function remains unknown. This study aimed to investigate this association in patients undergoing repeated percutaneous coronary interventions (PCI). Methods This retrospective single-centre study included patients undergoing repeated PCIs between 2003 and 2023, with intervals of ≥7 and ≤ 365 days between procedures. Renal function was classified by “Kidney Disease: Improving Global Outcomes” (KDIGO) staging system. The maximum allowable contrast dose (MACD) was retrospectively calculated as individual threshold. Primary endpoint was progression to a higher KDIGO stage at readmission. Secondary endpoints included changes in estimated glomerular filtration rate (eGFR). Results In total 6714 patients were included (mean age 67.2 years; 80.2% male; KDIGO stage analysis available for 6611; median interval between procedures 127 days). Baseline mean eGFR was 74.4 mL/min/1.73 m2. Median contrast volume was 220 mL, and median MACD 300 mL. At readmission, mean eGFR was 72.2 mL/min/1.73 m2, 1700 Patients (25.7%) showed KDIGO stage progression. Neither contrast volume nor MACD exceedance was associated with renal deterioration. However, predispositions (diabetes mellitus, arterial hypertension, age), clinical presentation (STEMI, NSTEMI) and the vascular access route were significantly associated with adverse renal outcomes. Conclusions Contrast volume and MACD exceedance during PCI was not associated with deterioration of medium- to long-term renal function. Abbreviations PCI:Percutaneous coronary interventioneGFR:Estimated glomerular filtration rateKDIGO:Kidney Disease: Improving Global OutcomesMACD:Maximum allowable contrast doseCA-AKI:Contrast-associated acute kidney injuryBMI:Body mass indexHR:Hazard ratioCI:Confidence intervalNSTEMI:Non-ST-segment elevation myocardial infarctionSTEMI:ST-segment elevation myocardial infarction
Background Atrial fibrillation (AF) is the most common heart rhythm disorder worldwide. Changes in metabolism and damage to mitochondria affect left atrial structure and electrical function. Few studies have applied multi-omics to plasma from AF patients. Methods We enrolled 37 patients with persistent AF and 36 with supraventricular tachycardia (SVT). Blood samples were drawn from the coronary sinus in all patients. Ten subjects from each group were randomly selected for 4D-DIA proteomics and untargeted metabolomics. ELISA validation was done on 35 patients per group. Four GEO atrial tissue datasets and one single-nucleus RNA-seq dataset were used for external support. Differentially expressed proteins (DEPs) were defined by |fold change| ≥ 1.5 and Benjamini-Hochberg adjusted P < 0.05. Protein-protein interaction networks were built with STRING and Cytoscape. Results We quantified 3268 plasma proteins and identified 217 DEPs in AF. Network analysis showed voltage-dependent anion channel 1 (VDAC1) as a central mitochondrial hub. It connected respiratory chain subunits and autophagy regulators. ELISA confirmed higher plasma VDAC1, citrate synthase(CS) and secreted frizzled-related protein 2(SFRP2) in AF patients (all P < 0.001). Metabolomics identified 505 differentially abundant compounds. Glycerophospholipid and fatty acid pathways were disrupted. Integrated analysis revealed eight shared dysregulated pathways linked to energy metabolism. Four GEO datasets showed higher atrial VDAC1 transcripts in AF (P < 0.05). Single-nucleus RNA-seq localized VDAC1 to cardiomyocytes. Conclusions Plasma protein and metabolite profiles differ between persistent AF and SVT. Mitochondrial and lipid pathways are both affected. VDAC1 is elevated in plasma, atrial tissue. These findings are supported across multiple cohorts.
Background Circulating cellular communication network factor 1 (CCN1) improves risk stratification in patients with acute coronary syndrome. We here investigated the association of CCN1 with all-cause mortality in patients with dilated cardiomyopathy (DCM). Methods Patients with a primary diagnosis of DCM, defined as LVEF <45% and increased LVEDD (LVEDD >117%), were included in a derivation (SFB/TR19 Greifswald) and a validation (IKARUS Marburg) cohort. Exclusion criteria comprised primary valvular diseases, acute myocarditis, active infectious diseases, pulmonary diseases, cancer, chronic alcoholism, and heart failure of other origins. CCN1 levels were determined in serum from study inclusion using an enzyme-linked immunosorbent assay. An adjusted multivariable Cox regression model was used to assess the association (hazard ratios) between tertiles of CCN1 concentration and all-cause mortality. Results In the SFB/TR19 cohort and [IKARUS cohort], respectively a total of 283 [236] predominantly male (78% [75%]) DCM patients with a median age of 56 [51] years with a severely reduced LVEF (31% [30%]), increased LVEDD (67.0 [67.0]), and normal eGFR (90.9 [83.6] ml/min) were analyzed. During a median follow-up of 10.6 [14.9] years, a total of 107 (37%) [100 (42%)] patients died. Patients in the highest CCN1 tertile had a significantly higher mortality risk than those in the lower tertile (p = 0.007 [p = 0.004]). In both cohorts, CCN1 remained associated (1.92; 95% CI: 1.14–3.24; p = 0.014 [1.69; 1.00–2.85; p = 0.049]) in adjusted multivariable Cox regression models. Conclusion CCN1 is associated with all-cause mortality in DCM patients, warranting further research into the underlying pathophysiology.
Background and aims:The influence of age, frailty, and non-cardiac comorbidities on long-term survival in a large, real-world cohort of patients undergoing mitral valve edge-to-edge-repair (M-TEER) was investigated. In addition, associated healthcare resource utilization and expenditure were evaluated. Methods:Demographic data, data on frailty and co-morbidities were drawn from the anonymized database of the second largest sickness fund in Germany and analysed in regards of long-term survival. Results:Relevant data was available in 4896 patients. Very old patients (80-99 years) had an impaired survival as compared to younger ones (OR 1.2, 95% CI [1.07;1.49], p = 0.005). With increasing level of frailty (care level 1: OR 1.43, 95% CI [1.19;1.72], p = 0.0001; care level 2: OR 1.63, 95% CI [1.45;1.84], p < 0.0001; care level 3-5: OR 2.09, 95% CI [1.79;2.45], p < 0.0001), and increasing number of non-cardiac comorbidities (one: OR 1.55, 95% CI [1.32, 1.82], p < 0.001; two: OR 2.21, 95% CI [1.90;2.59], p < 0.001, three or more: OR 2.82, 95% CI [2.37;3.36], p < 0.001) survival was significantly impaired. Female sex seems to be protective (OR 0.75, 95% CI [0.68;0.82], p < 0.001), whereas right heart failure at baseline (OR 1.83, 95% CI [1.65;2.03], p < 0.001) has a negative effect on survival. Overall medical expenses 12-months before the procedure were equal to 12-months after M-TEER (12-months before: 5796€ IQR [856.5;14,856.0] vs. 12-months after: 4.184€ IQR [370;15,316]. Conclusion:Age, frailty and comorbidities play a significant role in survival prediction of patients undergoing M-TEER. Overall medical expanses did not change after M-TEER however heart failure hospitalizations were less frequent.
Background:Pulsed field ablation (PFA) is a novel non-thermal ablation modality that may reduce collateral tissue injury compared with conventional thermal ablation. We compared the efficacy, safety, and procedural outcomes of PFA versus thermal ablation in patients with paroxysmal atrial fibrillation (PAF). Methods:We conducted a PRISMA-compliant systematic review and meta-analysis registered in PROSPERO (CRD420261321642). PubMed, Embase, Scopus, MEDLINE, and the Cochrane Library were searched through February 2026. The primary outcome was freedom from atrial arrhythmia at 12 months. Secondary outcomes included freedom from arrhythmia off antiarrhythmic drugs (AADs), procedural complications, and procedural metrics. Random-effects models were used to calculate pooled risk ratios (RR) and mean differences (MD). Results:Twenty-three studies comprising 5755 patients (2266 PFA; 3489 thermal ablation) were included. PFA was associated with higher freedom from atrial arrhythmia (RR 1.07, 95% CI 1.04-1.11; p < 0.0001; I2 = 14.8%) and greater off-AAD success (RR 1.07, 95% CI 1.02-1.12; p = 0.0089). Overall complication rates were similar (RR 0.69, 95% CI 0.47-1.02), with favorable trends toward lower esophageal injury (RR 0.56) and phrenic nerve injury (RR 0.55). Rates of stroke, transient ischemic attack, major bleeding, and cardiac tamponade were comparable. PFA was associated with shorter procedures and reduced fluoroscopy exposure. Conclusions:PFA demonstrated modestly improved efficacy in pooled analyses, although randomized trials showed efficacy comparable to thermal ablation. PFA also showed favorable safety trends and improved procedural efficiency, supporting its role as a promising strategy for PAF while highlighting the need for additional long-term randomized studies.
Background:The efficacy of intravenous amino acids (AA) in preventing cardiac surgery-associated acute kidney injury (CSA-AKI) remains uncertain. Methods:Three libraries were searched for randomized controlled trials (RCTs) comparing intravenous AA versus placebo or standard care to reduce the risk of CSA-AKI after cardiac surgery with cardiopulmonary bypass (CPB). The primary endpoint was the incidence of CSA-AKI, overall and stratified by KDIGO stage. Secondary endpoints were need for renal replacement therapy (RRT), 30-day mortality, and 90-day mortality. Risk ratios (RRs) with 95% confidence intervals (CIs) were pooled using a random-effects model. Results:Five studies were included, comprising 4499 patients, of whom 2247 (50%) were randomized to intravenous AA infusion. Compared with placebo or standard care, intravenous AA administration significantly reduced the risk of CSA-AKI (RR 0.81, 95% CI 0.70-0.94; p = 0.005), predominantly driven by one trial. The relative risk reduction was more important for stage 2 or 3 AKI (RR 0.69, 95% CI 0.48-0.99; p = 0.046). No significant differences were observed in the need for RRT (p = 0.223), 30-day mortality (p = 0.893), or 90-day mortality (p = 0.581). Conclusion:Intravenous AA administration is associated with a reduced risk of CSA-AKI across the spectrum of AKI severity, without showing an association with other major clinical outcomes.
Background:Aortic stenosis (AS) and transthyretin cardiac amyloidosis (CA) may coexist with overlapping clinical and imaging features. Data on the prevalence of this dual pathology (AS-CA) across AS flow groups are limited. This study assessed the likelihood of AS-CA in different AS flow groups and its association with outcomes after transcatheter aortic valve implantation (TAVI). Methods:We retrospectively analyzed 2764 patients (median age 82 years, 55% male) undergoing TAVI for severe native AS between 2017 and 2022). High likelihood of AS-CA was defined as RAISE score ≥ 3 points together with a T-AMYLO score ≥ 3 + red-flag criteria, or a T-AMYLO score ≥ 7 points. Procedural outcomes and long-term survival were evaluated. Results:High AS-CA likelihood was identified in 235 patients (9%). The estimated likelihood was comparable across AS flow groups, including high-gradient (7.4%), classical low-flow low-gradient (10.6%), paradoxical low-flow low-gradient (9.9%), and normal-flow high-gradient AS patients (7.7%) (p = 0.09). Procedural success after TAVI did not differ between patients with AS-CA and lone AS. However, AS-CA likelihood was associated with a higher 3-year all-cause mortality (44% vs. 29%, p < 0.001). This association was attenuated after adjustment for Society of Thoracic Surgeons (STS) risk score (HR 1.2 [95% CI 0.99-1.53], p = 0.065). Conclusion:Dual pathology of AS-CA is likely present in approximately 9% of TAVI patients and is not confined to specific AS flow groups. Although procedural outcomes are comparable, AS-CA is associated with increased mortality, largely driven by baseline risk. Further studies are needed to improve diagnostic strategies and clarify the underlying mechanisms.
BACKGROUND:Coronary artery calcium (CAC) is a robust predictor of cardiovascular risk and is recommended by contemporary prevention guidelines. However, dedicated Agatston scoring is underutilized because of cost and limited availability. Visual assessment using the Weston Score (WS) on routine non-contrast chest CT (NCCT) offers a practical alternative, although data in Asian populations remain limited. METHODS:We retrospectively reviewed 1107 consecutive NCCT studies performed in 2024. After exclusions, 842 patients were included. WS was visually assessed and converted to Agatston-equivalent CAC scores using a validated method. MESA reference data were used to estimate age-, sex-, and race-adjusted CAC percentiles. Interobserver agreement among a resident physician, cardiologist, and medical student was evaluated using intraclass correlation coefficients (ICC) and Bland-Altman analyses. RESULTS:Mean age was 70.8 ± 10.2 years, 51% were female, and 88.5% were Asian. Agatston-equivalent CAC scores were 0 in 17.0%, 1-99 in 20.9%, 100-399 in 34.0%, 400-999 in 17.7%, and > 1000 in 10.5%. Among patients with percentile estimates (n = 830), 52.2% were in the 76th-100th percentile. Interobserver agreement was excellent for WS (ICC 0.88), Agatston-equivalent scores (ICC 0.84), and CAC percentiles (ICC 0.90), with minimal systematic bias. CONCLUSIONS:Visual WS assessment on routine NCCT provides reproducible estimation of CAC burden and MESA percentiles, supporting opportunistic CAC reporting to improve cardiovascular risk stratification in multiethnic populations.
Background:Atrial fibrillation (AF) is associated with an increased risk of ischemic stroke, primarily originating from the left atrial appendage (LAA). Percutaneous LAA closure (LAAC) reduces appendage-borne thromboembolism, while pulmonary vein isolation (PVI) restores sinus rhythm. Observational data on the combined one-stop procedure are heterogeneous, and data on its risk-benefit profile remain scarce. Thus, a meta-analysis was performed to compare the efficacy and safety of combined LAAC+PVI versus LAAC-only. Methods:A structured systematic search of PubMed, MEDLINE, Scopus and Web of Science was performed for studies comparing outcomes of AF patients undergoing combined LAAC+PVI or LAAC-only. Results:Fifteen studies reporting data from 335,013 patients (11,839 LAAC+PVI; 323,174 LAAC-only) were included. Combined LAAC+PVI was associated with significantly fewer systemic thromboembolisms at follow-up (OR = 0.76, 95% CI = 0.60-0.96, I2 = 1%) compared to LAAC-only. However, periprocedural pericardial effusion requiring drainage was significantly more frequent in the combined group (OR = 1.72, 95% CI = 1.26-2.34, I2 = 0%). Peri-device leaks were significantly less common immediately post-procedure (OR = 0.57, 95% CI = 0.35-0.92, I2 = 19%), but significantly more frequent on follow-up echocardiography (OR = 1.56, 95% CI = 1.14-2.12, I2 = 71%). Mortality, major bleeding, device-related thrombus, and pericardial effusion without drainage did not differ significantly between groups. Conclusion:Combined LAAC+PVI was associated with fewer systemic thromboembolisms than LAAC-only, but a higher periprocedural risk of pericardial effusion requiring drainage and divergent temporal behaviour of peri-device leaks. Randomized controlled trials are warranted to confirm these findings.
Cardiovascular diseases account for the highest morbidity worldwide. LR11 (also called SorLA), an LDL receptor family member characterized as a sorting receptor, was initially identified in the brain and has a causative role in the development of Alzheimer's disease. However, LR11, and its circulating shed isoform, sLR11, are also associated to cardiovascular diseases and risk factors for atherosclerosis, such as obesity and diabetes. In the current narrative review, we discuss that elevation of plasma sLR11 levels can result from different forms of vascular injury, but also plays a role in subsequent vascular remodeling. We provide an overview of the mechanisms whereby LR11 promotes vascular remodeling and thereby atherosclerosis and how it could be involved in obesity and diabetes. Furthermore, we discuss the possibilities of (s)LR11 as a biomarker and therapeutic target for cardiovascular diseases.
Background:Opioid use is frequently reported as a baseline characteristic in transcatheter aortic valve implantation (TAVI) cohorts, yet its prognostic implications have not been examined. Aim:To examine the association between pre-procedural opioid use and post-TAVI outcomes. Methods:Using Danish nationwide registries, we identified patients undergoing TAVI between 2015 and 2022. Patients were categorized according to opioid use within one year before TAVI. We examined one-year all-cause mortality, cumulative days of hospitalization including the composite outcome of death or > 14 cumulative hospitalization days, and a potential opioid dose-response relationship. Adjusted relative risks were estimated using multivariable Cox and logistic regression. Results:We identified 6505 patients: 1265 (19.4%) with opioid use (48.9% male; median age 80 years) and 5240 (80.6%) without (59.4% male; median age 81 years). The two groups were comparable in cardiac comorbidities and malignancy but differed in musculoskeletal (back disorders: 45.9% vs 20.7%; arthropathies 65.3% vs 47.1%) and psychiatric conditions (antidepressants: 18.8% vs. 9.6%; anxiolytics/hypnotics: 23.7% vs. 12.4%). Baseline opioid use was associated with higher post-TAVI mortality (10.4% vs 6.9%; adjusted HR 1.35, 95% CI 1.11-1.66) and increased risk of the composite outcome (OR 1.47, 95% CI 1.25-1.72). A dose-response relationship was observed, with one-year mortality increasing from 7.0% in non-users to 8.8% in low-dose users and 12.1% in high-dose users. Conclusion:Baseline opioid use was associated with increased mortality and hospitalization burden in the year following TAVI, and this relationship was aggravated among high-dose users. The observed associations were most likely driven by the underlying condition of the opioid therapy.
Background:Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are recommended across the heart failure (HF) spectrum, irrespective of diabetes status. However, prescribing patterns in very old adults with multimorbidity, renal dysfunction, and geriatric vulnerability remain insufficiently characterised. Methods:We conducted a single-centre retrospective cross-sectional study in a specialised acute cardiogeriatric unit between January 1, 2025, and February 13, 2026. Consecutive hospitalisations with confirmed HF and documented SGLT2i discharge status were included. The primary outcome was absence of SGLT2i at discharge. Multivariable logistic regression identified factors independently associated with non-prescription. Results:Among 1235 hospitalisations, median age was 88.6 years [IQR 82-92], 54.5% were women, and 32.7% had diabetes. SGLT2i were prescribed in 1016 hospitalisations (82.3%) and absent in 219 (17.7%). Prescription did not differ by diabetes status (80.4% vs 83.2%, p = 0.276) or across HbA1c tertiles. In the prespecified primary model, non-prescription was associated with CKD stage 4 (aOR 2.79 [95% CI 1.97-3.96]), CKD stage 5 (aOR 20.29 [9.67-42.56]), palliative orientation (aOR 1.62 [1.09-2.41]), and HFrEF versus HFpEF (aOR 1.55 [1.08-2.22]). Higher albumin and medication count were associated with lower odds of non-prescription. Diabetes, age, and Charlson Comorbidity Index were not independently associated with the primary outcome. Conclusion:SGLT2i prescription was frequent and similar according to diabetes status and glycaemic control. Advanced CKD and palliative-oriented care were the most consistent correlates of non-prescription. These findings describe prescribing patterns but do not establish the appropriateness of individual decisions.
Heart failure with preserved ejection fraction (HFpEF) is more prevalent in women, whereas heart failure with reduced ejection fraction (HFrEF) predominates in men. Despite these well-established epidemiological differences, sex-specific alterations in vascular function in heart failure (HF) remain poorly characterised. This systematic review, using a narrative synthesis approach, evaluated sex-related differences in vascular function in individuals with HF. The review was prospectively registered with PROSPERO (CRD42024617745). MEDLINE and CINAHL were searched from inception to 26th November 2024 for studies reporting sex-stratified measures of arterial stiffness among individuals with HF. Nine studies met the eligibility criteria for inclusion (n = 2820; men: n = 1390, women: n = 1430). Of the included studies, 78% were characterised as HFpEF. Compared with men, women exhibited a higher pulsatile arterial load and lower arterial compliance. Representative findings from individual studies showed that women exhibited a higher augmentation index (28.9 ± 13.7% vs 21.7 ± 11.9%, p < 0.001) and augmentation pressure (19.1 ± 12.4 vs 13.7 ± 10.1 mmHg, p = 0.003). Body mass index (BMI) showed variable relationships with arterial stiffness indices, including positive associations with pulse wave velocity (r = 0.24, p < 0.01), central pulse pressure (r = 0.33, p < 0.001), and augmentation index (r = 0.23, p = 0.01), but an inverse relationship was found with cardio-ankle vascular index (r = -0.204, p < 0.001). Importantly, sex differences in HFpEF remained significant after adjustment for BMI. Women with HF exhibit higher pulsatile arterial load and reduced arterial compliance compared with men, which remain after adjustment for BMI. Sex-specific vascular dysfunction contributes to HF pathophysiology and supports the need for sex-informed assessment.
Background:Heart failure (HF) is a common complication in diabetes mellitus (DM), affecting approximately 40% of HF patients. While inflammation plays a crucial role in both conditions, the prognostic value of inflammatory markers in patients with both DM and HF remains unestablished. Objective:To examine the associations of neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), and (neutrophil + monocyte)/lymphocyte ratio (NMLR) with 30-day mortality in ICU patients with both DM and HF. Methods:This retrospective cohort study analyzed 1318 patients with both HF and DM from the MIMIC-IV database. NLR, MLR, and NMLR were calculated from complete blood counts within 24 h of ICU admission. Multivariate Cox regression, restricted cubic spline analysis, and ROC curves assessed predictive performance. Results:Among 1318 patients, 239 died within 30 days. The deceased group had significantly higher median values of NLR (10.9 vs. 6.5), MLR (0.9 vs. 0.4), and NMLR (12.1 vs. 7.0) compared to survivors (all P < 0.001). After adjustment, each one-unit increase in MLR was associated with 11% increased mortality risk (HR = 1.11, 95% CI: 1.04-1.19, P = 0.002), while NMLR and NLR showed 1% increases, respectively (NMLR: HR = 1.01, 95% CI: 1-1.01; NLR: HR = 1.01, 95% CI: 1-1.01; both P < 0.001). MLR demonstrated the highest discriminative capacity (AUC = 0.672), followed by NMLR (AUC = 0.658) and NLR (AUC = 0.650). Conclusion:NLR, MLR, and NMLR are independent predictors of 30-day mortality in ICU patients with DM and HF, with MLR showing superior discriminative capacity.
Background:Despite advances in percutaneous coronary intervention (PCI), patients with obstructive coronary artery disease (CAD) continue to experience recurrent ischemic symptoms and adverse cardiovascular events. Skin post-occlusive reactive hyperemia (PORH) is a noninvasive measure of systemic microvascular function that may add prognostic information beyond epicardial coronary anatomy, but its relation to long-term cardiovascular outcomes after PCI has not been well defined. Methods:We performed a retrospective analysis of a prospectively established CAD registry that included 197 patients with obstructive CAD who underwent PCI and baseline assessment of the skin PORH response. Long-term composite cardiovascular outcomes were evaluated over follow-up of up to 5 years using Kaplan-Meier methods and Cox proportional hazards regression, with propensity score matching used as a sensitivity analysis. Results:The median age of the cohort was 66 years, and 84.8% of patients were male. Compared with those in the higher PORH group, patients with a lower PORH index had more cardiometabolic comorbidities and experienced significantly higher rates of long-term composite cardiovascular events. In multivariable Cox analysis, a higher PORH index was independently associated with a lower risk of composite cardiovascular events (adjusted hazard ratio, 0.422; 95% confidence interval, 0.198-0.898), and this inverse association was preserved in the propensity score-matched cohort. Conclusions:In patients with obstructive CAD undergoing PCI, impaired skin PORH was independently associated with an increased risk of long-term composite cardiovascular events. These findings support a potential role for skin microvascular assessment in cardiovascular risk stratification, and warrant confirmation in larger prospective studies.
