Ischemic heart disease (IHD) and type-2 diabetes mellitus (T2DM) remain major health problems worldwide and commonly coexist in individuals. Gut microbial metabolites, such as trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), have been linked to cardiovascular and metabolic diseases. Previous studies have reported dysbiosis in the gut microbiota of these patients and the prebiotic effects of some components of the Mediterranean diet. Essential oil emulsions of savory (Satureja hortensis), parsley (Petroselinum crispum) and rosemary (Rosmarinus officinalis) were assessed as nutraceuticals and prebiotics in IHD and T2DM. Humanized mice harboring gut microbiota derived from that of patients with IHD and T2DM were supplemented with L-carnitine and orally treated with essential oil emulsions for 40 days. We assessed the effects on gut microbiota composition and abundance, microbial metabolites and plasma markers of cardiovascular disease, inflammation and oxidative stress. Our results showed that essential oil emulsions in mice supplemented with L-carnitine have prebiotic effects on beneficial commensal bacteria, mainly Lactobacillus genus. There was a decrease in plasma TMAO and an increase in fecal SCFAs levels in mice treated with parsley and rosemary essential oils. Thrombomodulin levels were increased in mice treated with savory and parsley essential oils. While mice treated with parsley and rosemary essential oils showed a decrease in plasma cytokines (INFɣ, TNFα, IL-12p70 and IL-22); savory essential oil was associated with increased levels of chemokines (CXCL1, CCL2 and CCL11). Finally, there was a decrease in protein carbonyls and pentosidine according to the essential oil emulsion. These results suggest that changes in the gut microbiota induced by essential oils of parsley, savory and rosemary as prebiotics could differentially regulate cardiovascular and metabolic factors, which highlights the potential of these nutraceuticals for reducing IHD risk in patients affected by T2DM.

Bicuspid aortopathy occurs in approximately 50% of patients with bicuspid aortic valve (BAV), the most prevalent congenital cardiac malformation. Although different molecular players and etiological factors (genetic and hemodynamic) have been suggested to be involved in aortopathy predisposition and progression, clear etiophysiopathological mechanisms of disease are still missing. The isogenic (genetically uniform) hamster (T) strain shows 40% incidence of BAV, but aortic dilatations have not been detected in this model. We have performed comparative anatomical, histological and molecular analyses of the ascending aorta of animals with tricuspid aortic valve (TAV) and BAV from the T strain (TTAV and TBAV, respectively) and with TAV from a control strain (HTAV). Aortic diameter, smooth muscle apoptosis, elastic waviness, and Tgf-β and Fbn-2 expression were significantly increased in T strain animals, regardless of the valve morphology. Strain and aortic valve morphology did not affect Mmp-9 expression, whereas Mmp-2 transcripts were reduced in BAV animals. eNOS protein amount decreased in both TBAV and TTAV compared to HTAV animals. Thus, histomorphological and molecular alterations of the ascending aorta appear in a genetically uniform spontaneous hamster model irrespective of the aortic valve morphology. This is a direct experimental evidence supporting the genetic association between BAV and aortic dilatation. This model may represent a population of patients with predisposition to BAV aortopathy, in which increased expression of Tgf-β and Fbn-2 alters elastic lamellae structure and induces cell apoptosis mediated by eNOS. Patients either with TAV or BAV with the same genetic defect may show the same risk to develop bicuspid aortopathy.

In this work we implement a COVID-19 infection detection system based on chest Xray images with uncertainty estimation. Uncertainty estimation is vital for safe usage of computer aided diagnosis tools in medical applications. Model estimations with high uncertainty should be carefully analyzed by a trained radiologist. We aim to improve uncertainty estimations using unlabelled data through the MixMatch semi-supervised framework. We test popular uncertainty estimation approaches, comprising Softmax scores, Monte-Carlo dropout and deterministic uncertainty quantification. To compare the reliability of the uncertainty estimates, we propose the usage of the Jensen-Shannon distance between the uncertainty distributions of correct and incorrect estimations. This metric is statistically relevant, unlike most previously used metrics, which often ignore the distribution of the uncertainty estimations. Our test results show a significant improvement in uncertainty estimates when using unlabelled data. The best results are obtained with the use of the Monte Carlo dropout method.

No abstract

This study shows the electrocardiographic findings of a large sample of Spanish workers from several different employment sectors. The frequencies of many ECG patterns related to an adverse prognosis (left ventricular hypertrophy, complete left bundle branch block, T wave abnormalities, ST segment abnormalities, and atrial fibrillation) were low.

Background: SGLT2i (sodium-glucose cotransporter-2 inhibitors) improve clinical outcomes in patients with heart failure, but the mechanisms of action are not completely understood. SGLT2i increases circulating levels of ketone bodies, which has been demonstrated to enhance myocardial energetics and induce reverse ventricular remodeling. However, the role of SGLT2i or ketone bodies on myocardial ischemia reperfusion injury remains in the dark. The objective of this study is to investigate the cardioprotective potential of empagliflozin and ketone bodies during acute myocardial infarction (MI). Methods: We used a nondiabetic porcine model of ischemia reperfusion using a percutaneous occlusion of proximal left anterior descending artery for 45 minutes. Animals received 1-week pretreatment with either empagliflozin or placebo prior to MI induction. Additionally, a third group received intravenous infusion of the ketone body beta-hydroxybutyrate BOHB (beta-hydroxybutyrate) during the MI induction. Acute effects of the treatments were assessed 4-hour post-MI by cardiac magnetic resonance and histology (thioflavin for area at risk, triphenyltetrazolium chloride staining for MI size). All animals were euthanized immediately postcardiac magnetic resonance, and heart samples were collected. Results: The area at risk was similar in all groups. Empagliflozin treatment increased BOHB levels. Empagliflozin-treated animals showed significantly higher myocardial salvage, smaller MI size (both by cardiac magnetic resonance and histology), less microvascular obstruction, and improved cardiac function (left ventricle ejection fraction and strain). Furthermore, empagliflozin-treated animals demonstrated reduced biomarkers of cardiomyocyte apoptosis and oxidative stress compared with placebo. The BOHB group showed similar results to the empagliflozin group. Conclusions: One-week pretreatment with empagliflozin ameliorates ischemia reperfusion injury, reduces MI size and microvascular obstruction, increases myocardial salvage, preserves left ventricle systolic function, and lowers apoptosis and oxidative stress. Periprocedural intravenous infusion of BOHB during myocardial ischemia also induces cardioprotection, suggesting a role for BOHB availability as an additional mechanism within the wide spectrum of actions of SGLT2i.

The clinical significance of non-obstructive coronary artery disease is the subject of debate. Our objective was to evaluate the long-term cardiovascular prognosis associated with non-obstructive coronary artery disease in patients undergoing coronary angiography, and to conduct a stratification by sex, diabetes, and clinical indication. We designed a multi-centre retrospective longitudinal observational study of 3265 patients that were classified into three groups: normal coronary arteries (lesion <20%, 1426 patients), non-obstructive coronary artery disease (20–50%, 643 patients), and obstructive coronary artery disease (>70%, 1196 patients). During a mean follow-up of 43 months, we evaluated a combined cardiovascular event: acute myocardial infarction, stroke, hospitalization for heart failure, or cardiovascular death. Multivariable-adjusted Cox proportional hazard models showed a worse prognosis in patients with non-obstructive coronary artery disease, in comparison with patients of normal coronary arteries group, in the total population (hazard ratio 1.72, 95% confidence interval 1.23–2.39; p for trend <0.001), in non-diabetics (hazard ratio 2.12, 95% confidence interval: 1.40–3.22), in women (hazard ratio 1.75, 95% confidence interval 1.10–2.77), and after acute coronary syndrome (hazard ratio 2.07, 95% confidence interval 1.25–3.44). In conclusion, non-obstructive coronary artery disease is associated with an impaired long-term cardiovascular prognosis. This association held for non-diabetics, women, and after acute coronary syndrome.

No abstract