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Background: We assessed whether hepatic steatosis with or without significant fibrosis (determined by validated non-invasive biomarkers) is associated with an increased 10-year estimated risk for cardiovascular disease (CVD) in people with type 1 diabetes mellitus (T1DM)., Methods: We conducted a retrospective, multicenter, cross-sectional study involving 1,254 adults with established T1DM without pre-existing CVD. We used the hepatic steatosis index (HSI) and fibrosis (FIB)-4 index for non-invasively detecting hepatic steatosis (defined as HSI > 36), with or without coexisting significant fibrosis (defined as FIB-4 index ≥ 1.3 or < 1.3). We calculated the Steno type 1 risk engine and the atherosclerotic CVD (ASCVD) risk score to estimate the 10-year risk of developing a first fatal or nonfatal CVD event., Results: Using the Steno type 1 risk engine, a significantly greater proportion of patients with hepatic steatosis and significant fibrosis (n = 91) had a high 10-year estimated CVD risk compared to those with hepatic steatosis alone (n = 509) or without steatosis (n = 654) (75.8% vs. 23.2% vs. 24.9%, p < 0.001). After adjustment for sex, BMI, diabetes duration, hemoglobin A1c, chronic kidney disease, and lipid-lowering medication use, patients with hepatic steatosis and significant fibrosis had an increased 10-year estimated risk of developing a first fatal or nonfatal CVD event (adjusted-odds ratio 11.4, 95% confidence interval 3.54-36.9) than those without steatosis. We observed almost identical results using the ASCVD risk calculator., Conclusions: The 10-year estimated CVD risk is remarkably greater in T1DM adults with hepatic steatosis and significant fibrosis than in their counterparts with hepatic steatosis alone or without steatosis., (© 2023. BioMed Central Ltd., part of Springer Nature.)

The life history theory assumes that all organisms are under selective pressure to harvest external resources and allocate them to maximise fitness: only organisms making the best use of energy obtain the greatest fitness benefits. The trade-off of energy spans four functions: maintenance, growth, reproduction, and defence against pathogens. The innovative antihyperglycaemic agents glucagon-like peptide 1 (GLP-1) receptor agonists and sodium-glucose cotransporter 2 (SGLT2) inhibitors decrease bodyweight and have the potential to counter low-grade inflammation. These key activities could rewire two components of the life history theory operative in adulthood-ie, maintenance and defence. In this Personal View, we postulate that the benefits of these medications on the cardiovascular system, beyond their glucose-lowering effects, could be mediated by the reduction of the maintenance cost driven by obesity and efforts spent on blunting low-grade inflammation., Competing Interests: Declaration of interests AA received research grants, lecture, and advisory board fees from Mundipharma, Merck Sharp & Dome, AstraZeneca, Novartis, Boehringer Ingelheim, Sanofi, Mediolanum, Novo Nordisk, Eli Lilly, Servier, and Takeda. MLM received lecture fees, advisory fees, and grant support from Mylan, SLA Pharma, Servier Laboratories, Eli Lilly, MSD, and Novo Nordisk. GPF received lecture fees, consultancy fees, grant support, and advisory board fees from Abbott, AstraZeneca, Boehringer Ingelheim, Daiichi Sankyo, Eli Lilly, Novo Nordisk, Sanofi, and Takeda. SDP consulted for Applied Therapeutics, AstraZeneca, Boehringer Ingelheim, Eli Lilly, MSD, Novartis, Novo Nordisk, and Sanofi, and received funding for these consulting services; received grant support from AstraZeneca and Boehringer Ingelheim; and received speaker fees from AstraZeneca, Boehringer Ingelheim, Eli Lilly, MSD, Novartis, Novo Nordisk, and Sanofi. SVdK declares no competing interests., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

In 2020, the Sars-Cov-2 pandemic is causing a huge and dramatic impact on healthcare systems worldwide. During this emergency, fragile patients suffering from other comorbidities, especially patients susceptible to or affected by cardiovascular disease, are the ones most exposed to the poorer outcomes. Therefore, it is still mandatory to continue to strictly adhere to the rules of cardiovascular prevention. This document aims to provide all doctors with simple and clear recommendations in order to spread useful messages to the widest number of subjects in order to continue the battle against cardiovascular diseases even in times of pandemic.

Cardiovascular prevention represents a cornerstone of modern strategies to reduce the burden of cardiovascular disease. It is of key importance to prevent cardiovascular diseases and associated events, not only to reduce morbidity and mortality, but also to increase the years of wellness in the aging population and to make the growing socio-economic burden imposed by cardiovascular events more sustainable.The current approach to prevention is based on an integrated use of effective lifestyle measures and, whenever appropriate, of antihypertensive and antidiabetic drugs, lipid-lowering agents and antiplatelet drugs.Given that population characteristics, in terms of ethnicity, demography and lifestyle habits, and healthcare system organizations differ among countries, international guidelines are not always applicable to specific countries and, often, are difficult to translate into daily clinical practice.In order to afford the specific features of Italy, 10 Scientific Societies and Research Institutions, mostly involved in preventive strategies, contributed to the present Italian consensus document, which includes brief, practical recommendations to support the preventive actions within the physician community and the general practice setting.

Background: Cardiovascular risk factors cluster in the metabolic syndrome (MS), but it is not known whether the risk associated with the syndrome is higher than the sum of its parts. In this study, we explored the relationship between clustering cardiometabolic risk factors and carotid intima-media thickness (c-IMT)., Methods and Results: Cardiovascular parameters and c-IMT were determined in 240 middle-aged healthy participants, divided into groups according to their number of MS components. Higher number of MS components were associated with higher mean c-IMT. Analysis of synergy revealed that c-IMT increase at component clustering fitted an additive model. Redefinition of cutpoints for MS traits, optimized to detect high c-IMT, did not improve the interaction between components. When metabolic factors were rendered independent, a synergistic interaction between factors in increasing the likelihood of having a high c-IMT was detected. Synergic as well was the interaction between metabolic factors with other risk factors that are not consequence of insulin resistance, such as low-density lipoprotein-cholesterol level and smoking habit., Conclusion: A stepwise approach reveals that the lack of synergy in the interactions between MS components is attributable to their mutual interdependence, possibly owing to the common pathophysiological background. Indeed, if MS is a unique clinical entity, it should be no more than the sum of its parts.

Aims: Circulating progenitor cells are believed to participate in cardiovascular (CV) homeostasis and their exhaustion has been linked to CV damage. As general agreement on their characterization is lacking, this work was carried out to assess the relationships between different antigenic profiles of progenitor cells and CV risk, with special regard to metabolic syndrome (MetSyn)., Methods and Results: CD34, CD133, and KDR were used to quantify circulating progenitors in 214 subjects at different levels of CV risk. In a cross-analysis of six different cell subtypes (CD34(+), CD133(+), CD34(+)CD133(+), CD34(+)KDR(+), CD133(+)KDR(+), and CD34(+)CD133(+)KDR(+)), CD34(+) progenitors showed the best correlation with CV parameters and risk estimates. Components of the MetSyn were all characterized by reduction of CD34(+) cells and acted synergistically in decreasing CD34(+) cell count. Moreover, CD34(+) cell count demonstrated a high performance in detecting high CV risk., Conclusion: These data demonstrate that CD34 identifies progenitor cells linked to CV risk, showing a close negative correlation between CD34(+) cells and CV risk, as well as a synergic detrimental effect of clustered metabolic components. Progenitor cell count may be used as a surrogate marker of CV risk, whereas extensive antigenic characterization may not be useful for this purpose.

Context: Patients with type 1 diabetes (T1D) have higher cardiovascular disease (CVD) risk than the general population. Objective: This observational study aims to evaluate sex-related differences in CVD prevalence and CVD risk estimates in a large cohort of T1D adults. Methods: We conducted a multicenter, cross-sectional study involving 2041 patients with T1D (mean age 46 years; 44.9% women). In patients without pre-existing CVD (primary prevention), we used the Steno type 1 risk engine to estimate the 10-year risk of developing CVD events. Results: CVD prevalence (n = 116) was higher in men than in women aged ≥55 years (19.2 vs 12.8%, P = .036), but comparable between the 2 sexes in those aged <55 years (P = .91). In patients without pre-existing CVD (n = 1925), mean 10-year estimated CVD risk was 15.4 ± 0.4% without any significant sex difference. However, stratifying this patient group by age, the 10-year estimated CVD risk was significantly higher in men than in women until age 55 years (P < .001), but this risk equalized after this age. Carotid artery plaque burden was significantly associated with age ≥55 years and with a medium and high 10-year estimated CVD risk, without any significant sex difference. Diabetic retinopathy and sensory--motor neuropathy were also associated with higher 10-year CVD risk and female sex. Conclusion: Both men and women with T1D are at high CVD risk. The 10-year estimated CVD risk was higher in men aged <55 years than in women of similar age, but these sex differences disappeared at age ≥55 years, suggesting that female sex was no longer protective. [ABSTRACT FROM AUTHOR]

OBJECTIVE -- Postprandial glycemia is an independent risk factor for cardiovascular disease that is more powerful than fasting glycemia and determines myocardial perfusion defects in type 2 diabetes. We examined the efficacy of two different insulin regimes (regular insulin and insulin analog) in controlling postprandial hyperglycemia and in preventing myocardial perfusion abnormalities. RESEARCH DESIGN AND METHODS -- A total of 20 consecutive type 2 diabetic patients and 20 control subjects were enrolled in this randomized, three-way, cross-over, placebo-controlled study. Myocardial perfusion was assessed by myocardial contrast echocardiography (MCE) in fasting and postprandial (120 min) state. RESULTS -- Insulin analog was associated with lower, but not statistically significant, postprandial glycemia than regular insulin (glucose increase: 116 ± 8 vs. 136 ± 5%, P = NS). However, the area under the curve following insulin analog was significantly lower than regular insulin (18,354 ± 702 vs. 20,757 ± 738 mg per 120 min, P = 0.032). Fasting myocardial flow velocity (β), myocardial blood volume (MBV), and myocardial blood flow (MBF) did not differ between control and type 2 diabetic subjects. Postprandial β (0.67 ± 0.24 vs. 0.92 ± 0.25, P < 0.01), MBV (8.4 ± 2 vs. 10.9 ± 1.2, P < 0.01), and MBF (5.6 ± 2 vs. 9.9 ± 2.8, P < 0.01) increased significantly in control subjects. In type 2 diabetes, during placebo in the postprandial state, β increased (0.65 ± 0.27 vs. 0.89 ± 0.24, P < 0.01), while MBV (8.34 ± 1.2 vs. 4.3 ± 1.3, P < 0.01) and MBF (5.4 ± 1.5 vs. 3.4 ± 0.9, P < 0.01) decreased. Similar changes in MCE variables were observed after regular insulin: β increased (0.65 ± 0.22 vs. 0.92 ± 0.12, P < 0.01) and MBV (8.2 ± 2 vs. 5.2 ± 1.16, P < 0.01) and MBF (5.4 ± 1.9 vs. 4.2 ± 0.86, P < 0.01) were reduced. After insulin analog, postprandial β (0.66 β 0.18 vs. 0.9 β 0.18, P < 0.01), MBV (8.2 ± 1.6 vs. 9.6 ± 1.2, P < 0.01), and MBF (5.4 ± 2 vs. 7.2 ± 1.9, P < 0.01.) increased. Values of postprandial MBV and MBF were higher after insulin analog than regular insulin treatment. CONCLUSIONS -- insulin analog partially reversed myocardial perfusion abnormalities observed in postprandial state by improving glucose control. [ABSTRACT FROM AUTHOR]