Explore the vast range of titles available.

Epidemiologic and clinical data from the last 2 decades have shown that the prevalence of heart failure in diabetes is very high, and the prognosis for patients with heart failure is worse in those with diabetes than in those without diabetes. Experimental data suggest that various mechanisms contribute to the impairment in systolic and diastolic function in patients with diabetes, and there is an increased recognition that these patients develop heart failure independent of the presence of coronary artery disease or its associated risk factors. In addition, current clinical data demonstrated that treatment with the sodium glucose cotransporter 2 inhibitor empagliflozin reduced hospitalization for heart failure in patients with type 2 diabetes mellitus and high cardiovascular risk. This review article summarizes recent data on the prevalence, prognosis, pathophysiology, and therapeutic strategies to treat patients with diabetes and heart failure.

Individuals with diabetes mellitus exhibit an increased propensity to develop cardiovascular disorders such as coronary artery disease, stroke and heart failure. Over recent decades, numerous cardiovascular outcome trials in individuals with type 2 diabetes have been published, with data showing a reduction of cardiovascular morbidity and mortality by sodium–glucose cotransporter 2 (SGLT2) inhibitors. These results not only provide novel therapeutic options for this high-risk population but also advance our current understanding of cardiovascular risk reduction in diabetes. The current overview article summarises these aspects and discusses future treatment strategies with SGLT2 inhibitors in diabetic and non-diabetic individuals with chronic kidney disease, liver disease and heart failure.

Background Spontaneous breathing trials (SBTs) on a T-piece can be difficult in patients with prolonged weaning because of remaining de-recruitment phenomena and/or insufficient ventilation. There is no clinically established method existent other than experience for estimating whether an SBT is most probably beneficial. Electrical impedance tomography (EIT) is a clinical useful online monitoring technique during mechanical ventilation, particularly because it enables analysis of effects of regional ventilation distribution. The aim of our observational study was to examine if EIT can predict whether patients with prolonged weaning will benefit from a planned SBT. Methods Thirty-one patients were examined. Blood gas analysis, vital parameter measurements, and EIT recordings were performed at three time points: (1) baseline with pressure support ventilation (PSV) (t0), (2) during a T-piece trial (t1), and (3) after resumption of PSV (t2). Calculation of EIT parameters was performed, including the impedance ratio (IR), the tidal variation of impedance (TIV), the changes in end-expiratory lung impedance (ΔEELI), the global inhomogeneity index (GI), and the regional ventilation delay (RVD) index with use of different thresholds of the percentage inspiration time (RVD40, RVD60, RVD80). The predictive power of the baseline GI with regard to clinical impairment of an SBT was analyzed by means of ROC curves. Clinical deterioration was assumed when tidal volume was decreased by at least 20 ml after the T-piece trial, measured at t2. Results Partial pressure of arterial oxygen significantly decreased at t1 (71 ± 15 mmHg) compared with t0 (85 ± 17 mmHg, p  < 0.05) and t2 (82 ± 18 mmHg, p  < 0.05). The IR trended toward higher values during t1. At t1, TIV and ΔEELI significantly decreased. The GI was significantly increased at t1 (t0 59.3 ± 46.1 vs t1 81.5 ± 62.5, p  = 0.001), as were all RVD indexes. Assuming a GI cutoff value of >40, sensitivity of 85% and specificity of 50% were reached for predicting an increased future tidal volume. Conclusions EIT enables monitoring of regional ventilation distribution during SBTs and is suitable to estimate whether an SBT probably will be beneficial for an individual patient. Therefore, the application of EIT can support clinical decisions regarding patients in the phase of prolonged weaning.

Atrial fibrillation (AF) is an arrhythmic cardiac disorder with a high and increasing prevalence in aging societies, which is associated with a risk for stroke and heart failure. However, early detection of onset AF can become cumbersome since it often manifests in an asymptomatic and paroxysmal nature, also known as silent AF. Large-scale screenings can help identifying silent AF and allow for early treatment to prevent more severe implications. In this work, we present a machine learning-based algorithm for assessing signal quality of hand-held diagnostic ECG devices to prevent misclassification due to insufficient signal quality. A large-scale community pharmacy-based screening study was conducted on 7295 older subjects to investigate the performance of a single-lead ECG device to detect silent AF. Classification (normal sinus rhythm or AF) of the ECG recordings was initially performed automatically by an internal on-chip algorithm. The signal quality of each recording was assessed by clinical experts and used as a reference for the training process. Signal processing stages were explicitly adapted to the individual electrode characteristics of the ECG device since its recordings differ from conventional ECG tracings. With respect to the clinical expert ratings, the artificial intelligence-based signal quality assessment (AISQA) index yielded strong correlation of 0.75 during validation and high correlation of 0.60 during testing. Our results suggest that large-scale screenings of older subjects would greatly benefit from an automated signal quality assessment to repeat measurements if applicable, suggest additional human overread and reduce automated misclassifications.

The presence of plaque macrophages and microcalcifications are acknowledged features of plaque vulnerability. Experimental data suggest that microcalcifications promote inflammation and macrophages foster microcalcifications. However, co-localization of plaque macrophages and calcification (ColocCaMa) in coronary segments and its impact on plaque phenotype and lesion vulnerability is unexplored. Plaque morphology including ColocCaMa of calcified coronary target segments in patients with stable coronary artery disease (n = 116) was analyzed using optical coherence tomography (OCT) prior to coronary intervention. Therefore we considered macrophages co-localized with calcification if their distance in an OCT frame was <100μm and OCT-defined microcalcifications with a calcium arc <22.5°. ColocCaMa was present in 29/116(25.0%) coronary segments. Calcium burden was greater (calcium volume index:1731±1421°*mm vs. 963±984°*mm, p = 0.002) and calcifications were more superficial (minimal thickness of the fibrous cap overlying the calcification 35±37μm vs. 64±72μm, p = 0.005) in the presence of ColocCaMa. Segments with ColocCaMa demonstrated a higher incidence of newly suggested features of plaque vulnerability, with a 3.5-fold higher number of OCT-defined microcalcifications (0.7±1.0 vs. 0.2±0.6, p = 0.022) and a 6.7-fold higher incidence of plaque inflammation (macrophage volume index:148.7±248.3°*mm vs. 22.2±57.4°*mm, p<0.001). Clinically, intima-media thickness (IMT) in carotid arteries was increased in patients with ColocCaMa (1.02±0.30mm vs. 0.85±0.18, p = 0.021). In a multivariate model, IMT (OR1.76 for 100μm, 95%CI 1.16-2.65, p = 0.007), HDL-cholesterol (OR0.36 for 10mg/dl, 95%CI 0.16-0.84, p = 0.017), calcium volume index (OR1.07 for 100°*mm, 95%CI 1.00-1.14, p = 0.049), macrophage volume index (OR5.77 for 100°*mm, 95%CI 2.04-16.3, p = 0.001) and minimal luminal area (OR3.41, 95%CI 1.49-7.78, p = 0.004) were independent predictors of ColocCaMa. Plaque macrophages co-localize with calcifications in coronary target segments and this is associated with high-risk morphological features including microcalcifications and macrophage infiltration as well as with greater calcification burden. Our data may add to the understanding of the relationship between plaque macrophages, vascular calcification and their clinical impact.

Arterial calcification represents a major burden in chronic kidney disease (CKD) and is an independent risk factor for cardiovascular diseases (CVD). Rodent models are essential for preclinical research on arterial calcification mechanisms and potential therapeutic interventions, permitting longitudinal analysis of disease progression, which is ethically unfeasible in humans. In this study, we specifically focused on rat models as representative rodent models, given their well-established use in cardiovascular research. Through systematic literature screening, we identified 470 studies employing rat models to investigate arterial calcification, with these models designed to simulate various pathological conditions. Our analysis revealed that arterial calcification was predominantly induced through kidney impairment, vitamin D overload, or mechanical and chemical vessel damage. Female rats were significantly underrepresented across studies, highlighting a considerable sex bias in experimental design. Particular emphasis was given to CKD-associated arterial calcification models, which accounted for about 60% of the identified studies. A meta-analysis of 67 CKD-related studies identified several significant factors influencing arterial calcification. Dietary phosphate concentration, male sex, and the use of Sprague-Dawley rats were associated with enhanced arterial calcification development. Nephrectomy-based approaches demonstrated superior efficacy and reliability in arterial calcification induction compared to adenine-based models. However, the analysis was limited by substantial heterogeneity across studies, potential publication bias, and inconsistent reporting of experimental parameters. These findings underscore the critical need for standardized reporting of experimental procedures and results to enhance the applicability of animal studies in meta-analyses and improve their translational value.

Diagnosis of heart failure is complex but crucial for patient outcomes and often hindered by the untapped potential of unstructured clinical notes. We introduce a novel end-to-end pipeline for heart failure diagnosis, leveraging electronic health records (EHR) and German clinical notes from 846 patients. Our pipeline synthesizes abbreviation disambiguation, translation of German clinical notes to English, medical entity linking to SNOMED-CT, and subsequent classification. The classification was performed using a Support Vector Machine (SVM) and compared against a fine-tuned medBERT.de neural baseline. We reduced the reliance on training data with zero-shot learning to address limitations with abbreviation disambiguation and entity linking approaches. Validation against benchmark datasets and cardiologists demonstrates high accuracy for real clinical use. Abbreviation disambiguation achieved an accuracy of up to 96.1%. Entity linking achieved competitive performance compared to state-of-the-art approaches on selected evaluation datasets. The SVM classification approach utilizing SNOMED-CT concepts and EHR data achieved an F1-score of 65.3%, on par with the medBERT.de neural baseline using clinical notes and EHR data. Despite challenges regarding limited language-specific resources and reference dataset availability for SNOMED-CT annotations in German, our pipeline demonstrates high potential for real-world clinical use and clinical decision support grounded in the standardized SNOMED-CT ontology.

Observational studies suggest an association between impaired oral health and cardiovascular disease; however, the directionality and underlying mechanisms remain unclear. In particular, whether heart failure (HF) itself adversely affects oral and periodontal health has not been systematically investigated in large populations or experimental models.We examined the association between HF and self-reported oral health indicators in 502,387 participants of the UK Biobank, including 17,356 individuals with HF defined by ICD-9/10 codes. Multivariable logistic regression models adjusted for demographic factors, cardiovascular comorbidities, systemic inflammation, lifestyle, and socioeconomic status were applied. To explore causality and mechanisms, periodontal tissue remodeling and inflammation were assessed in a murine model of pressure overload–induced HF using transverse aortic constriction (TAC). Periodontal ligament (PDL) space and alveolar bone microarchitecture were quantified by micro-computed tomography, and gingival inflammatory gene expression was analyzed by RT–PCR.HF patients exhibited a significantly higher prevalence of oral health burden compared with controls (51% vs. 40%, p<0.001). HF was associated with a 1.6-fold increased risk of impaired oral health, which remained significant after full adjustment (adjusted OR 1.18, 95% CI 1.14–1.22; p<0.001). In mice, reduced left ventricular ejection fraction following TAC was strongly associated with expansion of the maxillary PDL space (R 2 = 0.63, p = 0.009) and alterations in alveolar bone microarchitecture (trabecular thickness R 2 = 0.41 p = 0.061, trabecular number R 2 = 0.38 p = 0.07). These structural changes were accompanied by increased gingival expression of pro-inflammatory cytokines, including Il1b (SHAM vs. TAC: 1.44 ± 1.02 vs. 3.39 ± 1.53,  p  = 0.06) and TNF-α (SHAM vs. TAC: 1.37 ± 0.86 vs. 5.71 ± 1.23,  p  = 0.002 predominantly in the maxilla.HF is independently associated with impaired oral health in a large population cohort and induces site-specific periodontal inflammation and remodelling in experimental HF. These findings support HF as an upstream driver of compromised oral-periodontal health, challenging the prevailing concept that oral disease primarily contributes to cardiovascular pathology.

Aims Inflammation accompanies heart failure (HF) and elevated levels of inflammatory biomarkers are linked to new onset of HF. However, whether the prognostic relevance of inflammatory biomarkers is different in HF with reduced (HFrEF) and preserved ejection fraction (HFpEF) is unclear. The aim of the current study is to explore the role of inflammation on the mortality risk in patients with HF. Methods We analysed interleukin‐6 and hsCRP levels by ELISA and immunonephelometry, respectively, in HFpEF and HFrEF patients referred for coronary angiography and assessed the prognostic value in the Ludwigshafen Risk and Cardiovascular Health (LURIC) study. Results HF was present in 1086 patients (N = 506 HFpEF; N = 580 HFrEF; mean age 65 ± 10 years; 28% female). Increasing IL‐6 levels were significantly associated with increased CV mortality in HFpEF [1.5 (95% CI: 1.1–2.2), P = 0.018] but not HFrEF [HR 1.3 (95% CI: 1.0–1.7), P = 0.06] patients. High‐sensitive CRP followed a similar pattern but failed to reach statistical significance after full‐adjustment (HFpEF: HR 1.4 95%C I: 1.0–2.0; P = 0.065; HFrEF HR: 1.0 95% CI: 0.7–1.3; P = 0.800). Interaction analysis in patients stratified by IL‐6 and N terminal pro brain natriuretic peptide (NT‐proBNP) above and below the median revealed a stepwise increase in CV‐mortality in HFpEF (P = 0.036) but not HFrEF patients (P = 0.220). To investigate the relationship between IL‐6 and NT‐proBNP, we assessed the genetic IL6‐Receptor variant p.Asp358Ala (rs2228145) which is linked to impaired IL‐6 receptor signalling. Homozygous carriers with HFpEF but not HFrEF exhibited significantly lower NT‐pro‐BNP levels compared with wildtype carriers (HFpEF 779 pg/mL ± 787 vs. 1180 pg/ mL ± 1532; P = 0.008; HFrEF 2289 pg/ mL ± 3439 vs. 2326 pg/ mL ± 3386; P = 0.94), raising the hypothesis that IL‐6 signalling may play a pathophysiological role in HFpEF. Conclusions These data suggest a predictive value of elevated IL‐6 for CV‐mortality in HFpEF but not in HFrEF patients.

Background Patients with type 2 diabetes (T2DM) are at high risk for cardiovascular events, which usually arise from the rupture of a vulnerable coronary plaque. The minimal fibrous cap thickness (FCT) overlying a necrotic lipid core is an established predictor for plaque rupture. Recently, coronary calcification has emerged as a relevant feature of plaque vulnerability. However, the impact of T2DM on these morphological plaque parameters is largely unexplored. Therefore, this study aimed to compare differences of coronary plaque morphology in patients with and without T2DM with a particular focus on coronary calcification. Methods In 91 patients (T2DM = 56, non-T2DM = 35) with 105 coronary de novo lesions (T2DM = 56, non-T2DM = 49) plaque morphology and calcification were analyzed using optical coherence tomography (OCT) prior to coronary intervention. Results Patients with T2DM had a lower minimal FCT (80.4 ± 27.0 µm vs. 106.8 ± 27.8 µm, p < 0.001) and a higher percent area stenosis (77.9 ± 8.1% vs. 71.7 ± 11.2%, p = 0.001) compared to non-diabetic subjects. However, patients with and without T2DM had a similar total number of calcifications (4.0 ± 2.6 vs. 4.2 ± 3.1, p = ns) and no significant difference was detected in the number of micro- (0.34 ± 0.79 vs. 0.31 ± 0.71), spotty (2.11 ± 1.77 vs. 2.37 ± 1.89) or macro-calcifications (1.55 ± 1.13 vs. 1.53 ± 0.71, all p = ns). The mean calcium arc (82.3 ± 44.8° vs. 73.7 ± 31.6), the mean thickness of calcification (0.54 ± 0.13 mm vs. 0.51 ± 0.15 mm), the mean calcified area (0.99 ± 0.72 mm 2 vs. 0.78 ± 0.49 mm 2 ), the mean depth of calcification (172 ± 192 μm vs. 160 ± 76 μm) and the cap thickness overlying the calcification (50 ± 71 μm vs. 62 ± 61 μm) did not differ between the diabetic and non-diabetic groups (all p = ns). Conclusion T2DM has an impact on the minimal FCT of the coronary target lesion, but not on localization, size, shape or extent of calcification. Thus, the minimal FCT overlying the necrotic lipid core but not calcification is likely to contribute to the increased plaque vulnerability observed in patients with T2DM.