Diabetes is a rapidly growing global health concern projected to affect one in eight adults by 2045, which translates to roughly 783 million people. The profound metabolic alterations often present in dysglycaemia significantly increase the risk of cardiovascular complications. While genetic susceptibility plays a crucial role in diabetes and its vascular complications, identifying genes and molecular mechanisms that influence both diseases simultaneously has proven challenging. A key reason for this challenge is the pathophysiological heterogeneity underlying these diseases, with multiple processes contributing to different forms of diabetes and specific cardiovascular complications. This molecular heterogeneity has limited the effectiveness of large-scale genome-wide association studies (GWAS) in identifying shared underlying mechanisms. Additionally, our limited knowledge of the causal genes, cell types and disease-relevant states through which GWAS signals operate has hindered the discovery of common molecular pathways. This review highlights recent advances in genetic epidemiology, including studies of causal associations that have uncovered genetic and molecular factors influencing both dysglycaemia and cardiovascular complications. We explore how disease subtyping approaches can be critical in pinpointing the unique molecular signatures underlying both diabetes and cardiovascular complications. Finally, we address critical research gaps and future opportunities to advance our understanding of both diseases and translate these discoveries into tangible benefits for patient care and population health.

To explore differences in prevalence and prognosis associated with reduced myocardial flow reserve (MFR) in patients without known coronary artery disease (CAD) based on diabetes status.

Of 2639 patients without known CAD who underwent rubidium positron emission tomography myocardial perfusion imaging (MPI), 818 patients (31%) had diabetes. Reduced MFR was defined as MFR <2.0. Coronary artery calcium (CAC) score was categorized as 0, 1-99, 100-399, and ≥400. Ischemic total perfusion deficit (TPD) was categorized as <1%, 1-<5%, and ≥5%. Outcome variables were all-cause death (ACD) and non-fatal myocardial infarction (MI).

During the median follow-up of 4.1 years, 574 (21.8%) ACD/MI occurred (204 [25.1%] diabetic patients, 370 [20.3%] nondiabetic patients). In multivariable Cox analysis, reduced MFR was associated with increased ACD/MI in patients with diabetes (per .1 decrease: HR: 1.04, 95% CI: 1.02-1.06, P < .001) and patients without diabetes (per .1 decrease: HR: 1.03, 95% CI: 1.02-1.04, P < .001). No interaction existed between diabetes and MFR for ACD/MI risk regardless of CAC or ischemic burden (all P > .05). Adding MFR to the risk prediction model of clinical, conventional MPI findings, and CAC improved the discrimination for clinical outcomes in both groups (DM: .003, non-DM: <.001, respectively).

Reduced MFR was more common in patients with diabetes and an important independent prognostic marker over CAC and clinical variables. The association between MFR and ACD/MI risk did not differ between patients with and without diabetes who had no prior CAD, regardless of CAC and ischemic burden.

The significance of thiamine in human health is linked to its role in several pathways that control different disease processes. Significant improvements in cardiometabolic diseases, substantially impacted by thiamine imbalances, are observed with thiamine supplementation. Diabetic patients could see a reduction in cardiovascular (CV) risk due to thiamine's significant impact on glucose metabolism. Specifically, increased ventricular filling pressures and oxygen consumption, indicative of CV dysfunction, are caused by oxidative and inflammatory damage to blood vessels, diabetic nephropathy, and elevated lactic acid production. Despite promising pre-clinical results for thiamine, clinical trials have yielded conflicting and contradictory findings due to limitations like small sample sizes and insufficient follow-up. To provide a summary of clinical study results, this systematic review assessed the impact of thiamine supplementation on diabetes and its CV complications. The studies included in this systematic review were retrieved from PubMed and Medline databases, in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement and following the Population Intervention Comparison Outcome (PICO) framework. Seven clinical studies were identified, which enlighten the association between thiamine supplementation, hyperglycemia, and cardiovascular disease (CVD). Although large-scale, multicenter studies with longer follow-up periods are needed, the association between thiamine and chronic metabolic dysfunction related to CV risk suggests its crucial role in preventing severe heart failure (HF).

Myocardial oxidative stress increases under conditions of hyperglycemia and ischemia/reperfusion (I/R) injury, leading to cellular damage. Inhibition of oxidative stress is involved in the cardioprotective effects of hydrogen sulfide (H2S) during I/R and diabetes, and H2S has the potential to protect the heart. However, the mechanism by which H2S regulates the level of cardiac reactive oxygen species (ROS) during I/R and hyperglycemic conditions remains unclear. Therefore, the objective of this study was to evaluate the cytoprotective effect of H2S in primary cardiomyocyte cultures subjected to hyperglycemia, hypoxia-reoxygenation (HR), or both conditions, by assessing the PPAR-α/Keap1/Nrf2/p47phox/NOX4/p-eNOS/CAT/SOD and the PPAR-γ/PGC-1α/AMPK/GLUT4 signaling pathways. Treatment with NaHS (100 μM) as an H2S donor in cardiomyocytes subjected to hyperglycemia, HR, or a combination of both increased cell viability, total antioxidant capacity, and tetrahydrobiopterin (BH4) concentrations, while reducing ROS production, malondialdehyde concentrations, 8-hydroxy-2'-deoxyguanosine, and dihydrobiopterin (BH2) concentrations. Additionally, the H2S donor treatment increased the expression and activity of PPAR-α, reversed the reduction in the expression of PPAR-γ, PGC-1α, AMPK, GLUT4, Nrf2, p-eNOS, SOD, and CAT, and decreased the expression of Keap1, p47phox and NOX4. Therefore, the treatment with the H2S donor protects cardiomyocytes from damage caused by hyperglycemia, HR, or both conditions by reducing oxidative stress markers and improving antioxidant mechanisms, thereby increasing cell viability and "cardiomyocyte ultrastructure".

Patients with diabetes are at an increased risk of cardiovascular disease (CVD), including atherosclerotic CVD and heart failure. In addition, diabetes is associated with a higher risk of developing chronic kidney disease, which is considered to be one of the strongest risk factors for CVD and mortality. To address the increased cardiovascular risk of patients with diabetes, dedicated screening strategies for CVD are necessary; conversely, screening for diabetes needs to be performed in all patients with CVD to allow timely identification. Once diabetes is diagnosed, rapid implementation of treatment with therapies to reduce cardiovascular risk on top of standard of care is necessary. This review gives an overview of contemporary therapeutic strategies to reduce cardiovascular risk in patients with type 2 diabetes.

Diabetes mellitus is a substantial global health threat due to its high prevalence and its serious complications. The hyperglycemic state causes damage to vascular endothelial cells and disturbance of lipid metabolism, thus contributing to the development of vascular disorders, especially atherosclerotic diseases. Aggressive glycemic control combined with vascular intervention is critical to the prevention and treatment of diabetes-associated atherosclerosis. It is suggested that metformin should be combined with hypoglycemic agents with proven vascular benefits for treating type 2 diabetes (T2DM) complicated with atherosclerotic diseases. Clinical studies indicates that the preferred combination is metformin with either glucagon-like peptide-1 receptor agonist or sodium/glucose cotransporter-2 inhibitor, which could offer additional vascular benefits and reduce the risk of atherosclerotic complications. Likewise, combination therapy with metformin and hypolipidemic agents has also shown additive effects on glucose control and lipid-lowering in patients with both diabetes and dyslipidemia, whereas extensive clinical trials using atherosclerotic-associated outcomes are required to support the vascular benefits. Moreover, co-administration of metformin with systemic antioxidant or anti-inflammatory therapy may also provide additional vascular benefits as indicated by several animal studies. For instance, a recent study found that additional supplementation of cholecalciferol and taurine enhanced metformin efficacy in controlling diabetes while reducing the risk of associated atherosclerotic complications. However, these potential benefits remain need validation by the evidence from clinical studies. Despite the limitations, such as heterogeneity across different patient populations, and deficiency in long-term outcomes, such efforts can contribute to finding optimal drug combinations to improve the management of T2DM and reduce its atherosclerotic complications.

Type 2 diabetes (T2D) and cardiovascular diseases (CVDs) are major public health challenges worldwide. Metabolomics, the exhaustive assessment of metabolites in biological systems, offers important insights regarding the metabolic disturbances related to these disorders. Recent advances toward the integration of metabolomics into clinical practice to facilitate the discovery of novel biomarkers that can improve the diagnosis, prognosis, and treatment of T2D and CVDs are discussed in this review. Metabolomics offers the potential to characterize the key metabolic alterations associated with disease pathophysiology and treatment. T2D is a heterogeneous disease that develops through diverse pathophysiological processes and molecular mechanisms; therefore, the disease-causing pathways of T2D are not completely understood. Recent studies have identified several robust clusters of T2D variants representing biologically meaningful, distinct pathways, such as the beta cell and proinsulin cluster related to pancreatic insulin secretion, obesity, lipodystrophy, the liver/lipid cluster, glycemia, and blood pressure, and metabolic syndrome clusters representing different pathways causing insulin resistance. Regarding CVDs, recent studies have allowed the metabolomic profile to delineate pathways that contribute to atherosclerosis and heart failure, as well as to the development of targeted therapy. This review also covers the role of metabolomics in integrated metabolic genomics and other omics platforms to better understand disease mechanisms, along with the transition toward precision medicine. This review further investigates the use of metabolomics in multi-metabolite modeling to enhance risk prediction models for predicting the first occurrence of major adverse cardiovascular events among individuals with T2D, highlighting the value of such approaches in optimizing the preventive and therapeutic models used in clinical practice.

Purpose To investigate whether pericoronary adipose tissue attenuation (PCATa) provides incremental prognostic value over commonly used coronary CT angiography (CCTA) parameters for predicting major adverse cardiovascular and cerebrovascular events (MACCE) in individuals with diabetes mellitus (DM). Materials and Methods This prospective study included consecutive patients with type 2 DM who underwent CCTA due to suspected coronary artery disease between January 2015 and December 2017. PCATa of three coronary arteries was measured and evaluated. Cox proportional hazards regression was performed to investigate the prognostic value of PCATa for predicting MACCE. The incremental prognostic value of PCATa for MACCE was evaluated by comparing area under the receiver operating characteristic curve (AUC) values of four models (model 1: clinical characteristics, model 2: model 1 + conventional CCTA findings [coronary artery calcium score, Leiden score], model 3: model 2 + advanced CCTA findings [high-risk plaque, CT fractional flow reserve], model 4: model 3 + PCATa). Results Of the 1029 participants (mean age, 60.2 years ± 9.9 [SD]; 539 male) included in the study, 152 (14.8%) experienced MACCE during a median follow-up of 56.5 months. PCATa independently predicted MACCE after adjustment for clinical characteristics and commonly used CCTA findings (hazard ratio, 1.86 [95% CI: 1.24, 2.80]; P = .003). The model incorporating PCATa improved predictive performance for MACCE compared with the model including clinical characteristics and conventional and advanced CCTA parameters (AUC, 0.75 [95% CI: 0.71, 0.79] vs 0.73 [95% CI: 0.68, 0.77]; P = .009). Conclusion PCATa provided incremental prognostic value beyond clinical characteristics and other CCTA findings for prediction of MACCE in individuals with DM. Keywords: CT Angiography, Cardiac, Coronary Arteries, Inflammation, Outcomes Analysis, Coronary Computed Tomography Angiography, Diabetes Mellitus, Coronary Inflammation, Pericoronary Adipose Tissue Attenuation Supplemental material is available for this article. © RSNA, 2025.

Effective glycaemic control following cardiac surgery improves clinical outcomes, and continuous glucose monitoring (CGM) might be a valuable tool in achieving this objective. We investigated the effect of real-time CGM and telemonitoring on postoperative glycaemic control in people with type 2 diabetes (T2D) after coronary artery bypass grafting (CABG).

In this randomized clinical trial (RCT), adults with T2D undergoing CABG were assigned to either a test group utilizing real-time CGM (Dexcom G6) and telemetry for glycaemic control, or a control group with blinded CGM measures, relying on point-of-care measures. The primary outcome was the percentage of time in range (TIR) of blood glucose between 70 and 180 mg/dL (3.9-10.0 mmol/L), measured by CGM.

Among 91 subjects, 48 were in the test group and 43 were in the control group. The least squares (LS) mean ± standard error of TIR was 60.3 ± 2.7%, 50.3 ± 2.9% in the test and control group, respectively. The test group had significantly higher TIR when adjusted with age, sex, body mass index, baseline fasting blood glucose and baseline glycated haemoglobin (LS mean difference, 10.0%; 95% confidence interval, 2.1-18.0; p = 0.014). The test group also had lower time above range and mean glucose levels, with no differences in time below range or hypoglycaemic events.

In this RCT, real-time CGM and telemonitoring improved glycaemic control during postoperative period without increasing hypoglycaemia risk. Given the benefits of effective glycaemic control on perioperative outcomes, CGM may be helpful in managing T2D after CABG.

Familial hypercholesterolemia (FH) is characterized by high levels of low-density lipoprotein cholesterol (LDL-C) and Achilles tendon (AT) thickening. AT thickness (ATT) is useful for diagnosing FH and assessing the risk of coronary artery disease (CAD). Nevertheless, the relationship between AT thickening and lipid profile is not clear. We investigated the association of ATT with lipid Profile and carotid IMT.

We included 450 patients with clinically diagnosed heterozygous FH. ATT was measured by ultrasonography.

The rate of thickening increased for both AT and carotid-IMT according to age (p < 0.001). In the teens, there was no carotid-IMT thickening, but 39 % of the subjects had a thickened AT. The thresholds of cumulative LDL-C values for AT and carotid-IMT thickening based on ROC curves were 9210 mg/dL∗years (AUC: 0.66, 95 % CI: 0.61-0.72) for ATT and 11,255 mg/dL∗years (AUC: 0.79, 95 % CI: 0.75-0.84) for carotid-IMT. For cumulative LDL-C levels ≥ median, untreated HDL-C level was lower in the AT thickened group than in the non-thickened group (AT thickened: 52 (43-63) mg/dL, non-thickened: 63 (52-72) mg/dL). There was a significant correlation between ATT and cumulative LDL-C (Male: R = 0.48 p < 0.001, Female: R = 0.33 p < 0.001).

We clarified that both cumulative exposure to LDL-C and untreated HDL-C levels were closely related to AT thickening. Our results show that in ultrasonographic assessment, ATT is more useful than carotid-IMT for predicting the degree of lipid deposition in tissues, especially in young adults.

Advanced glycation end products (AGEs) and their cellular receptors (RAGEs) play an important role in the pathogenesis of type 2 diabetes mellitus and its progression to cardiovascular disease (CVD). A marker of the AGE-RAGE axis, soluble RAGE (sRAGE), was examined in this study in various glycemic states as well as in low- and high-CVD-risk patients.

In this cross-sectional study, 25 adults were recruited into each of the "Normoglycemic", "Prediabetic", and "Diabetic" groups based on American Diabetes Association 2019 HbA1c% level criteria. Using online American Heart Association Atherosclerotic CVD (AHA ASCVD) risk calculator and guidelines, patients were classified into "Low" and "High" risk categories. Serum sRAGE was assayed using sandwich ELISA technology. Serum markers necessary for calculation of homeostatic model assessment for insulin resistance (HOMA-IR) and atherogenic index of plasma (AIP) were spectrophotometrically estimated. Carotid intima-media thickness (CIMT) was analyzed using B-mode carotid ultrasonography.

Mann-Whitney U analysis showed that sRAGE, AIP, HOMA-IR, CIMT, and %10-year CVD risk values were significantly different in the two ASCVD risk categories. Spearman test showed a significant correlation between sRAGE and other markers. ROC curve analysis demonstrated a higher area under the curve for sRAGE than other known parameters to differentiate between ASCVD risk categories. Finally, odds ratio analysis showed that sRAGE had higher odds of detecting high CVD risk than AIP or CIMT.

Our study has demonstrated the possible role of sRAGE in CVD development and suggests that they may serve as screening markers for future CVD risk.

The growing prevalence of diabetes highlights the urgent need to study diabetic cardiovascular complications, specifically diabetic cardiomyopathy, which is a diabetes-induced myocardial dysfunction independent of hypertension or coronary artery disease. This review examines the role of mitochondrial dysfunction in promoting diabetic cardiac dysfunction and highlights metabolic mechanisms such as hyperglycaemia-induced oxidative stress. Chronic hyperglycaemia and insulin resistance can activate harmful pathways, including advanced glycation end-products (AGEs), protein kinase C (PKC) and hexosamine signalling, uncontrolled reactive oxygen species (ROS) production and mishandling of Ca2+ transient. These processes lead to cardiomyocyte apoptosis, fibrosis and contractile dysfunction. Moreover, endoplasmic reticulum (ER) stress and dysregulated RNA-binding proteins (RBPs) and extracellular vesicles (EVs) contribute to tissue damage, which drives cardiac function towards heart failure (HF). Advanced patient-derived induced pluripotent stem cell (iPSC) cardiac organoids (iPS-COs) are transformative tools for modelling diabetic cardiomyopathy and capturing human disease's genetic, epigenetic and metabolic hallmarks. iPS-COs may facilitate the precise examination of molecular pathways and therapeutic interventions. Future research directions encourage the integration of advanced models with mechanistic techniques to promote novel therapeutic strategies.

We evaluated the surgical outcomes in three groups of individuals with diabetes mellitus (DM), end-stage renal disease (ESRD), and on (ONCAB) vs. off-pump (OPCAB) coronary artery bypass grafting (CABG). We also examined the changes in intraoperative decision-making when ultrasound and transit-time flow measurement was utilized in the operating room. This study will aim to identify the utility of HFUS and TTFM in high-risk patient categories.

Data from the multicenter REQUEST (Registry for Quality assessment with ultrasound imaging and TTFM measurement in cardiac bypass surgery) had recently been compiled in three separate papers examining outcomes in patients with DM, ESRD, and on vs. off-pump bypass grafting. Data was extrapolated to determine the impact of HFUS and TTFM in patients with diabetes, ESRD, ONCAB and OPCAB. The primary outcome measured in in the REQUEST study is any change in planned surgical procedure. Secondary end points include rate of changes, coronary targets, completed grafts, and in-hospital morbidity and mortality.

Outcomes were predicated upon patient population surveyed. The REQUEST registry reported 1016 individuals who underwent CABG. For individuals with DM, any surgical change to the coronary target was slightly lower, measured at a change rate of 11.6% vs. 9.5% (OR 0.80, 95% CI 0.53-1.21, P = 0.288). In diabetics, the aortic component of the operation underwent a higher rate of surgical strategy change with TTFM compared to without (10.2% vs. 6.4%, OR 1.67, 95% CI 1.06-2.65; P = 0.026). In patients with ESRD, TTFM increased the rate of strategy changes compared to no TTFM (33.7% vs. 24.3%, 95% CI 1.01-2.48, P = 0.047) and number of revisions per graft (7.0% vs. 3.4%, OR 2.14, 95% CI 1.17-3.71). In the 1016 individuals who underwent CABG, 402 (39.6%) underwent OPCAB and 614 (60.4%) undergoing ONCAB. When TTFM and HFUS were utilized, OPCAB resulted in greater number of strategy changes for aortic portion of the procedure (14.7% vs. 3.4%, OR 4.03, CI 2.32-7.20) without a difference in coronary target or graft revision. In the REQUEST study, in-hospital mortality was published at 0.6%.

TTFM use demonstrates a statistically significant impact on intra-operative decision making and operative strategy changes in patients with concomitant ESRD, DM and who are undergoing OPCAB relative to ONCAB. This difference in OPCAB vs. ONCAB may be related to higher mean graft flows in OPCAB in the setting of a standardized TTFM cutoff for determination of graft quality. This data cumulatively suggests there a role for TTFM in CABG, namely due to its positive impact on outcome and statistically significant impact on intra-operative decision making.

Zhigancao Decoction (ZGCD) is derived from "Treatise on Febrile Diseases" and is traditionally prescribed for treating a variety of cardiovascular conditions. As of now, there are no data to support its use as a treatment for diabetic cardiomyopathy (DCM) and the mechanism behind the effect is unclear as well. In the present study, clinical evidence for the efficacy of ZGCD in patients with DCM was examined using a meta-analysis and its underlying anti-DCM molecular mechanisms were explored via network pharmacology.

The current study utilized an extensive search strategy encompassing various domestic and foreign databases databases to retrieve pertinent articles published up to June 2024. In light of this, a thorough evaluation of the benefits and safety of Zhigancao decoction (ZGCD) was conducted in this study using RevMan and Stata. Subsequently, a number of active compounds and target genes for ZGCD were gathered from the TCMSP and BATMAN-TCM databases, while the main targets for DCM were obtained from databases such as GenCards, OMIM, TTD, and DrugBank. To select core genes, protein-protein interaction networks were generated using the STRING platform, and enrichment analyses were completed using the Metascape platform.

Meta-analysis results were ultimately derived from 9 studies involving 661 patients in total. In comparison with WM therapy alone, the pooled results showed that ZGCD significantly enhanced overall effectiveness. Additionally, the utilization of ZGCD was leading to a reduction in LVEDV, LVESV and LVDD, also a greater increase in LVEF. Meanwhile, the utilization of ZGCD during intervention was more effective in reducing SBP, and DBP. In addition, the ZGCD showed potential in reducing the occurrence of adverse events. In the context of network pharmacology, five constituents of ZGCD-namely lysine, quercetin, gamma-aminobutyric acid, stigmasterol, and beta-sitosterol-are posited to exert anti-diabetic cardiomyopathy (anti-DCM) effects through interactions with the molecular targets ASS1, SERPINE1, CACNA2D1, AVP, APOB, ICAM1, EGFR, TNNC1, F2, F10, IGF1, TNNI2, CAV1, INSR, and INS. The primary mechanisms by which ZGCD may achieve its anti-DCM effects are likely mediated via the AGEs/RAGE signaling pathway, as well as through pathways related to lipid metabolism and atherosclerosis.

In comparison to WM therapy alone, ZGCD demonstrates greater efficacy and safety in the management of DCM. ZGCD not only significantly reduces blood pressure, but also enhances cardiac function while producing fewer adverse effects. The therapeutic effects of ZGCD on DCM can likely be ascribed to its capacity to modulate the AGEs-RAGE signaling pathway, as well as its efficacy in enhancing lipid metabolism and mitigating atherosclerosis.

identifier (INPLASY202430133).

Rheumatoid arthritis (RA) is associated with heightened cardiovascular disease and increased susceptibility to osteoporosis, with shared underlying mechanisms. This study aimed to investigate the association between vascular function and bone mineral density (BMD).

We conducted a cross-sectional study of 49 patients with RA at Tan Tock Seng Hospital, Singapore. Endothelial function was measured as reactive hyperaemia index (RHI)-endothelial peripheral arterial tonometry and aortic stiffness as carotid-femoral pulse wave velocity (cf-PWV) using SphygmoCor. Univariable and multivariable linear regression analyses were performed to evaluate the associations between BMD and vascular function. We used natural logarithm RHI (lnRHI) and cf-PWV as response variables, and each BMD as covariate, adjusting for body mass index, positive anti-cyclic citrullinated peptide, cumulative prednisolone dose, hydroxychloroquine use and Systematic COronary Risk Evaluation 2.

We recruited 49 patients (mean age 61.08 ± 8.20 years), of whom 44 (89.80%) were women and 39 (81.25%) were Chinese. Significant associations were found between lnRHI and BMD at the lumbar spine (β = 0.4289, P = 0.037) and total hip (β = 0.7544, P = 0.014) in univariable analyses. Multivariable analyses confirmed these associations, showing that lower BMD at the lumbar spine (β = 0.7303, P = 0.001), femoral neck (β = 0.8694, P = 0.030) and total hip (β = 0.8909, P = 0.010) were significantly associated with worse lnRHI. No significant associations were found between BMD and cf-PWV.

Lower BMD is associated with endothelial dysfunction, but not aortic stiffness in patients with RA. Further longitudinal studies are needed to confirm these associations and understand the underlying mechanisms.

Both chronic kidney disease (CKD) and type 2 diabetes mellitus (T2DM) confer a high risk of cardiovascular disease and mortality. These entities frequently coincide. The separate and joint impact of CKD and T2DM on the risk of major cardiovascular events (MACE) and survival is unclear.

In this prospective cohort study, patients with angiographically proven coronary artery disease were investigated according to their CKD and T2DM status (T2DM-/CKD-, T2DM+/CKD-, T2DM-/CKD+, T2DM+/CKD+) and followed for up to 18 years.

A total of 1441 patients were included in the study of whom 39% experienced MACE (T2DM-/CKD-: 31%, T2DM+/CKD-: 43%, T2DM-/CKD+: 53%, T2DM+/CKD+: 61%) and 53% died. A log-rank test revealed significant differences between the event-free time period of the four groups (χ2 (3) = 112.57, p < 0.001). The presence of T2DM and CKD was associated with a 2.72-fold increase [1.98-3.73] in MACE compared to patients who suffered from neither condition (p < 0.001). T2DM alone led to a 1.37-fold increase [1.1-1.7], (p = 0.004), CKD alone to a 1.71-fold increase [1.31-2.25], (p < 0.001).

T2DM and CKD in patients with coronary artery disease are mutually independent predictors of cardiovascular events. Patients with both CKD and T2DM are at an extremely high risk for cardiovascular events.

Background: Patients with peripheral artery disease (PAD) and diabetes face high risks of comorbidities, tissue loss, and cardiovascular events. As global type 2 diabetes (T2DM) prevalence rises, so does its incidence in symptomatic patients with PAD, though this population is under-studied in Australia. This cross-sectional analysis sought to characterize PAD patients with diabetes regarding prevalence, major complications, medication use, and prescribing patterns, comparing them to non-diabetic PAD patients. We also examined PAD complications in relation to diabetic control. Methods: This cross-sectional study looked at the baseline data from 105 PAD participants in the TEAM-PAD randomized controlled trial that were analyzed using descriptive statistics, prevalence odds ratios and regression analysis. Participants were recruited between June 2023 and August 2024 from public clinics, private surgeons, and Concord Repatriation General Hospital, Sydney. Results: Diabetes prevalence was 52.83% (n = 56) with 29.5% (n = 31) of participants with T2DM having uncontrolled hyperglycemia (HbA1c ≥ 7%), which was weakly negatively correlated with age (r = -0.372, p = 0.039). Participants with T2DM were twice as likely to have a history of coronary artery disease (POR 2.43; 95% with a 95% confidence interval (CI) between 1.09-5.43, and over three times as likely to have tissue loss (POR 3.39; 95% CI 1.22-9.43). The odds of polypharmacy (≥5 medications) were 10 times greater in participants with T2DM (POR 10.8; 95% CI 2.31-50.4), affecting 96.4% of this group. Conclusions: Diabetes prevalence and associated complications were higher than previous estimates, underscoring the challenges in managing diabetes and polypharmacy in participants with PAD. A multidisciplinary approach may improve outcomes.

The significance of interrelated risk factors for Type 2 diabetes (T2D) is not easily demonstrated by conventional statistical methods. This study aims to investigate the principal components of T2D risk by employing exploratory factor analysis in Iranian cohort. The analysis encompasses a range of sociodemographic, lifestyle, and health-related variables to uncover clusters of factors associated with the risk of T2D.

Cross-sectional data of 1200 diabetic and 1200 nondiabetic Iranian adults was analyzed using STATA 14.2 (p < 0.05). Pearson's Chi-squared test was used to assess the difference between the two groups. Spearman correlation explored the relationships between variables. Separate factor analyses were conducted for diabetic, non-diabetic, and combined groups. Principal component analysis (PCA) identified the initial components. Crude and adjusted logistic regressions examined the associations between derived factors and T2D risk.

PCA identified eleven components with eigenvalues ≥ 1, accounting for 65.09% of the variance. Logistic regression analysis highlighted several significant associations with T2D risk. Positive associations were observed for PC1 ("drugs, smoking, and alcohol"), PC2 ("chronic diseases", including age, hypertension, dyslipidemia, and coronary heart disease), PC3 ("lipids", such as triglycerides, cholesterol, and low-density lipoprotein), PC4 ("body mass", including BMI, waist circumference, and waist-to-hip ratio), PC5 ("gestational-related risks", such as gestational diabetes and gestational hypertension), and PC6 ("glucose/lipid factors", including fasting glucose, triglycerides, and an inverse relationship with high-density lipoprotein). Conversely, negative associations with T2D risk were found for PC7 ("socioeconomic factors", such as socioeconomic status and education), PC8 (inverse association with age, along with fatty liver, thyroid disorders, and low waist-to-hip ratio), and PC10 (marital status, sleep duration, low fasting glucose, lower age, and an inverse association with fatty liver).

Key metabolic clusters, including "Lipids", "Body Mass", "Chronic Diseases", and "Glucose/Lipid" align with previous findings. These results underscore the multifactorial and interconnected nature of T2D risk, highlighting underlying physiological processes.

Several transitions, or new patterns and dynamics in the contributors and health outcomes, have altered the character and burden of the multi-decade, worldwide growth in prevalence of type 2 diabetes (T2DM). These changes have led to different needs for prevention and care. These dynamics have been driven by diverse demographic, socio-economic, behavioural, and health system response factors. In this Perspective, we describe these transitions and how their attributes have set the stage for multimorbidity, or multiple long-term conditions (MLTCs), to be the next major challenge in the diabetes epidemic. We also describe how the timing and character of these stages differ in high-, middle-, and low-income countries. These challenges call for innovation and a stronger focus on MLTCs across the spectrum of cause, effectiveness, and implementation studies to guide prevention and treatment priorities.

We aimed to analyze the presence and extent of coronary artery disease in patients with newly detected diabetes mellitus.

Clinical health examinations of asymptomatic community-dwelling adults between 2008 and 2018 at a medical center in Taiwan were reviewed. Coronary computed tomography angiography was performed in 444 participants, of which 338, 54, and 52 were categorized as 'without diabetes mellitus', 'newly detected diabetes mellitus', and 'known diabetes mellitus', respectively.

Prevalence of significant coronary artery disease (≥ 50% stenosis) was higher in participants with newly detected diabetes mellitus than in participants without diabetes mellitus (40.7% vs. 20.1%, p < 0.0001). Among those with coronary artery stenosis, the number of coronary vessels with significant obstruction (0.72 vs. 0.42, p = 0.0147) was also higher in participants with newly detected diabetes mellitus. Using multiple logistic regression analysis, new detection of diabetes mellitus was identified as an independent risk factor for significant coronary artery disease (odds ratio: 2.153, 95% confidence interval: 1.112-4.166).

Asymptomatic patients with newly detected diabetes mellitus had higher prevalence and greater extent of coronary artery disease than those without diabetes mellitus. More attention should thus be paid to the assessment of coronary artery disease in patients with newly detected diabetes mellitus.

PM2.5 is an important environmental risk factor for cardiovascular disease (CVD) and poses a threat to global health. This study combines bibliometric analysis, Mendelian randomization (MR), and Global Burden of Disease (GBD) data to comprehensively explore the relationship between PM2.5 exposure and CVD. MR analyses provided strong evidence for causality, reinforcing findings from traditional observational studies. The estimated global burden of PM2.5-related CVD indicated, that there exist significant impacts on the elderly, men, and populations in low and medium socio-demographic index (SDI) areas. This study further found that population growth and aging are the main drivers of this burden with large inequities, although medical advances have mitigated some of the effects. Overall, the opportunity to reduce the burden of CVD remains significant, particularly in medium SDI countries. Projections to 2045 suggested that the absolute burden will increase, while age-standardized rates will decline due to improvements in air quality and health care. These findings emphasized the urgent need for targeted interventions to mitigate the deleterious effects of PM2.5 on global cardiovascular health and to address health inequalities between regions.

Vascular endothelial cells form a single layer of flat cells that line the inner surface of blood vessels, extending from large vessels to the microvasculature of various organs. These cells are crucial metabolic and endocrine components of the body, playing vital roles in maintaining circulatory stability, regulating vascular tone, and preventing coagulation and thrombosis. Endothelial cell injury is regarded as a pivotal initiating factor in the pathogenesis of various diseases, triggered by multiple factors, including infection, inflammation, and hemodynamic changes, which significantly compromise vascular integrity and function. This review examines the causes, underlying molecular mechanisms, and potential therapeutic approaches for endothelial cell injury, focusing specifically on endothelial damage in cardiac ischemia/reperfusion (I/R) injury, sepsis, and diabetes. It delves into the intricate signaling pathways involved in endothelial cell injury, emphasizing the roles of oxidative stress, mitochondrial dysfunction, inflammatory mediators, and barrier damage. Current treatment strategies-ranging from pharmacological interventions to regenerative approaches and lifestyle modifications-face ongoing challenges and limitations. Overall, this review highlights the importance of understanding endothelial cell injury within the context of various diseases and the necessity for innovative therapeutic methods to improve patient outcomes.

Although mortality from myocardial infarction (MI) has declined worldwide due to advancements in emergency medical care and evidence-based pharmacological treatments, MI remains a significant contributor to global cardiovascular morbidity. This study aims to examine the risk factors associated with individuals who have experienced an MI in Türkiye.

Microdata obtained from the Türkiye Health Survey conducted by Turkish Statistical Institute in 2019 were used in this study. Binary logistic regression, Chi-Square, and CHAID analyses were conducted to identify the risk factors affecting MI.

The analysis identified several factors associated with an increased likelihood of MI, including hyperlipidemia, hypertension, diabetes, chronic disease status, male gender, older age, single marital status, lower education level, and unemployment. Marginal effects revealed that elevated hyperlipidemia levels increased the probability of MI by 4.6%, while the presence of hypertension, diabetes, or depression further heightened this risk. Additionally, individuals with chronic diseases lasting longer than six months were found to have a higher risk of MI. In contrast, factors such as being female, having higher education, being married, being employed, engaging in moderate physical activity, and moderate alcohol consumption were associated with a reduced risk of MI.

To prevent MI, emphasis should be placed on enhancing general education and health literacy. There should be a focus on increasing preventive public health education and practices to improve variables related to healthy lifestyle behaviours, such as diabetes, hypertension, and hyperlipidemia.

The impact of diabetes on incident cardiovascular disease in relation to the extent of atherosclerotic disease remains unclear. We aimed to investigate major adverse cardiovascular events (MACE) in patients with or without type 2 diabetes (T2DM) presenting with two extremes of atherosclerotic disease, those with angiographically documented minor coronary atherosclerotic lesions and those with symptomatic peripheral artery disease. We included 1238 patients from two prospective, long-term cohort studies. Patients underwent coronary angiography and/or sonography in order to assess the grade of atherosclerosis and were defined as having no signs of Atherosclerosis (n = 332; Group I), minor atherosclerosis (n = 425; Group II) and major atherosclerosis (n = 481; Group III). Cardiovascular events were recorded over a median follow-up period of 7.1 years (Q1 = 3.6 years, Q2 = 7.1 years, Q3 = 11.3 years), covering a total of 9533 patient years. We tested the hypothesis that T2DM infers the same relative risk increase irrespective of the atherosclerosis stage, considering 3-point MACE as the primary endpoint. Incident MACE was reported in 681 patients (51%). MACE occurred more frequently in patients with T2DM than in patients without T2DM (p < 0.001). Further, MACE occurred more frequently in group III (58.1%), than group II (34.1%) or group I (19.1%) (group I vs. group II vs. group III, p < 0.001). In a cox-regression-model, T2DM was a significant predictor of MACE in univariate analyses (HR = 2.43 [1.88-3.14], p < 0.001) and after multivariate adjustment for cardiovascular risk factors, as well as the different grades of atherosclerosis (HR = 1.37 [1.02-1.84], p = 0.034). Also, atherosclerosis grades predicted MACE (HR = 3.19 [2.75-3.70], p < 0.001) in univariate analyses, and also after multivariate adjustment for known cardiovascular risk factors, including T2DM (HR = 1.61 [1.31-1.98], p < 0.001). Finally, when testing for interactions between T2DM and stages of atherosclerosis on MACE we could not find any significant interaction (HR = 1.14 [0.86-1.52], p = 0.364). We conclude that T2DM infers an increased risk for MACE across anatomically and morphologically distinct stages of atherosclerosis.

Sodium-glucose transporters 2 inhibitors (SGLT-2i) and glucagon-like peptide 1 receptor agonists (GLP-1 RAs) are recommended along with metformin for the potential cardiovascular benefits among type 2 diabetes. This meta-analysis aims to evaluate whether the effects of SGLT-2i or GLP-1 RAs on cardiovascular outcomes are consistent with and without baseline metformin use.

PubMed, Cochrane, Web of Science and Embase were searched for randomized placebo-controlled trials with SGLT-2i or GLP-1 RAs as interventions of type 2 diabetes patients up to June, 2024. The main outcomes were major adverse cardiovascular events (MACE), hospitalization for heart failure (HHF) or cardiovascular death. Both random-effects model and fixed model were adopted to estimate pooled hazard ratios (HR) and 95% confidence intervals (95% CI).

A total of 81,738 patients (median age: 62-66 years, 53.7-71.5% men, median follow-up: 1.3-5.4 years) from 11 studies (7 studies of SGLT-2i and 4 of GLP-1 RAs) were included in the study. The metformin-naive portions ranged from 28.90% to 81.98%. Among patients using metformin at baseline, SGLT-2i or GLP-1 RAs reduced MACE risk (HR = 0.95, 95% CI 0.91-0.99, P = 0.02). In metformin-naive patients, similar reductions were observed (HR = 0.79, 95% CI 0.65-0.95, P = 0.01). No statistically significant interaction was found between metformin users and non-users for any outcome (all P values for interaction > 0.05), indicating consistent cardiovascular benefits regardless of baseline metformin therapy.

SGLT-2i and GLP-1 RAs have the effects of cardiovascular benefits for T2DM patients regardless of baseline metformin use.

An aging population combined with a rapidly increasing prevalence of diabetes foreshadows a global epidemic of cardiovascular and kidney disease that threatens to halt improvements in life and health-span and will have particularly severe consequences in older adults. The management of diabetes has been transformed with the recent development of newer anti-hyperglycemic agents that have demonstrated superior efficacy. However, the utility of these drugs extends beyond glycemic control to benefits for managing obesity, cardiovascular disease (CVD), chronic kidney disease, and heart failure. Numerous cardiovascular and kidney outcomes trials of these drugs have played an instrumental role in shaping current guidelines for the management of diabetes and CVD. Older adults with diabetes are diverse in terms of their comorbidities, diabetic complications, and cognitive and functional status. Therefore, there is an unmet need for personalized management of diabetes and CVD in this population. In this review, we provide an overview of the epidemiological burden and management of diabetes and CVD in older adults. We then focus on randomized cardiovascular and kidney outcome trials with anti-hyperglycemic agents to propose an evidence-based approach to the management of diabetes in older adults with high risk of cardiovascular and kidney disease.

Limited data are available on the adverse effects of new-onset diabetes after transplantation (NODAT) in solid organ transplantation (TPL) other than kidney. This study aimed to identify the risk of complications associated with NODAT in recipients of kidney, liver, or heart TPL.

Using the Korean National Health Insurance Service database, recipients of kidney, liver, or heart TPL between 2009 and 2015 were identified. The incidence of coronary artery disease (CAD), cerebrovascular accident (CVA), and malignancy was compared across groups with NODAT, pretransplant diabetes mellitus (DM), and without DM using Cox regression analysis.

A total of 9,632 kidney, liver, or heart TPL recipients were included. During the median follow-up of 5.9 years, NODAT independently increased the incidence of CAD (hazard ratio [HR], 2.46; 95% confidence interval [CI], 1.39 to 4.30) and overall mortality (HR, 1.48; 95% CI, 1.14 to 1.95) compared to the reference group even after adjustment for confounders; this was more prominent in kidney TPL than in liver TPL. The risk of CVA was significantly increased by pretransplant DM but not by NODAT in both kidney and liver TPL (HR, 2.47; 95% CI, 1.68 to 3.65; and HR, 3.18; 95% CI, 1.07 to 9.48, respectively). NODAT increased the risk of malignancy in the crude model, which lost its statistical significance after confounder adjustment.

NODAT independently increases the risk of CAD and mortality after TPL, which is more evident in kidney recipients. There was no additional increased risk of CVA or malignancy with NODAT in solid organ TPL.

There is significant heterogeneity in cardiovascular disease (CVD) risk among patients with diabetes mellitus (DM).

The purpose of this study was to develop risk scores for total CVD and its components from a contemporary pooled, observational cohort of U.S. adults with DM.

CVD-free adults with DM aged 40 to 79 years were pooled from 4 U.S. population-based cohorts (CARDIA [Coronary Artery Risk Development in Young Adults], Framingham Offspring, Jackson Heart Study, and the MESA (Multiethnic Study of Atherosclerosis) studied since 2000. Baseline DM-specific and non-DM-specific CVD risk factors were evaluated as predictors. We developed 10-year DM Risk Scores (DMRS) for total CVD, atherosclerotic CVD (ASCVD), coronary heart disease (CHD), heart failure (HF) and stroke. Score performance was validated internally and externally.

We included 2,174 adults with DM mean age 59.2 ± 10.5 years, 55.4% female and 47.5% Black followed up to 10 years. Age, sex, HbA1c, creatinine, systolic blood pressure, DM medication, and smoking were the most important predictors. The DMRS had good internal discrimination (c-statistics 0.72, 0.72, 0.72, 0.79 and 0.73 for CVD, ASCVD, CHD, HF, and stroke) and calibration (calibration slopes 0.93, 0.95, 0.93, 0.98, and 0.89 for CVD, ASCVD, CHD, HF, and stroke; Greenwood Nam-D'Agostino calibration tests were significant for CHD (P < 0.01) and CVD (P < 0.05) but not for ASCVD, HF, and stroke). From external validation in 2 other cohorts, the DMRS outperformed current risk scores.

Our U.S. pooled cohort DMRS for predicting CVD events demonstrated good predictive performance for assessing CVD risk in adults with DM.

The objective was to assess the protective role of anti-diabetic agent (ADA) in predicting interstitial lung disease (ILD) among patients with diabetes mellitus (DM). We formed a cohort of DM patients between 2009 and 2016 using data from Taiwan. Univariable and multivariable Cox proportion hazards regression models were used to examine the effect of risk factor on the risk of developing ILD, presented as a hazard ratio (HR) with a 95% confidence interval (CI). Cox proportional hazard regression analysis for the risk of DM-associated ILD with joint effect of dipeptidyl peptidase-4 inhibitor (DPP4I), glucagon-like peptide-1 receptor agonist (GLP-1 RA), and sodium-glucose cotransporter 2 inhibitors (SGLT2I) showed that SGLT2I, GLP-1 RA, and DPP-4I had a decreased risk of ILD with adjusted HR of 0.14 (0.11, 0.18), 0.29 (0.24, 0.35), and 0.64 (0.62, 0.67), respectively. DPP4I, GLP-1 RA, and SGLT2I could be considered to be introduced to this DM population for ILD risk reduction in DM, especially with SGLT2I usage.

Low-dose aspirin for primary prevention is determined by the balance of risks of cardiovascular events and adverse effects. We assessed the long-term gastrointestinal symptoms or bleeding with low-dose aspirin in diabetic patients.

The Japanese Primary Prevention of Atherosclerosis with Aspirin for Diabetes (JPAD) trial was a randomized clinical trial to evaluate the efficacy and safety of low-dose aspirin in patients with type 2 diabetes. As a post hoc analysis, we investigated the incidence of upper gastrointestinal symptoms or bleeding in aspirin (100 mg enteric-coated aspirin or 81 mg buffered aspirin daily) and no-aspirin groups within and beyond 3 years.

Of 2535 patients (mean age 65 years, 55% male) followed for a median of 11.2 years, 1258 were included in the aspirin group (951 enteric-coated, 208 buffered, 99 unknown) and 1277 were included in the no-aspirin group. The cumulative incidence of upper gastrointestinal symptoms or bleeding was higher in the aspirin group than the no-aspirin group (8.8% vs. 5.7% at 18 years; p < 0.0001). The increased risk in the aspirin group was prominent within 3 years, and the hazard ratio (HR) [95% confidence interval (CI)] of the aspirin group was 7.10 [3.21-15.7], but attenuated beyond 3 years (HR 1.20 [0.76-1.89]). In 1159 patients in the aspirin group, the cumulative incidence was lower in the enteric-coated than in the buffered aspirin groups (2.9% vs. 7.3%; p = 0.003) within 3 years, and the adjusted HR of enteric-coated aspirin was 0.38 [0.20-0.72] compared with the buffered aspirin group.

The upper gastrointestinal symptoms or bleeding of low-dose aspirin within 3 years, and the aspirin formulations, were relevant for decision making of initiation and continuation of low-dose aspirin for primary prevention.

The aim was to evaluate the acute effect of drinking tomato juice preloaded with lemon and perilla oil 10 min before consuming carbohydrate on postprandial blood glucose, insulin, and lipids concentrations in young healthy women. In this randomized controlled crossover study, 21 women (age 21.1±0.6 y, HbA1c 5.2±0.2%, mean±SD) consumed either 200 g of tomato juice, tomato juice with 10 g of lemon juice and 5 g of perilla oil (n-3 PUFA-rich oil), or water 10 min before consuming 200 g of boiled white rice for 3 separate days. The energy and fat in tomato juice with lemon/n-3 PUFA-rich oil were higher (energy 402 kcal, fat 5.6 g) than tomato juice (354 kcal, 0.6 g) and water (315 kcal, 0.6 g). The blood parameters were measured at 0, 30, 60, and 120 min after carbohydrate consumption and compared among 3 d. The plasma glucose at 30 min in tomato juice with lemon/n-3 PUFA-rich oil was significantly lower than that of water (103.1±3.4 mg/dL vs. 127.8±4.0 mg/dL, p<0.001, mean±SE) and tended to be lower than that of tomato juice (113.9±4.9 mg/dL, p=0.078). The serum insulin at 30 min was also significantly lower in tomato juice with lemon/n-3 PUFA-rich oil than that of tomato juice (p<0.01). Adding lemon and n-3 PUFA-rich oil to tomato juice before carbohydrate meal can be practical method to lower early postprandial glucose and insulin responses in young healthy women.

The classification of major adverse cardiovascular event (MACE) endpoints in patients with type 2 diabetes mellitus (T2DM) and either confirmed coronary artery disease (CAD) or high CAD risk, as well as the extent of the association between T2DM and coronary plaque characteristics, remains uncertain.

This meta-analysis aims to compare MACE endpoints between patients with diabetes and patients without diabetes based on coronary artery plaques.

We searched studies from Web of Science, PubMed, Embase, and the Cochrane Library up until September 1, 2023. Two independent researchers evaluated the quality and bias of the included studies. We used odds ratio (OR) and standardized mean difference (SMD) with 95% confidence interval (CI) to assess the effect of individual lesion parameters and coronary artery plaque characteristics on MACE endpoints.

Seven studies covered 1218 patients with diabetes and 3038 patients without diabetes. The follow-up time ranged from 2 to 5.4 years. The pooled results indicated that in all CAD lesions, DM was more strongly associated with MACE, myocardial infarction (MI), revascularization, and rehospitalization for unstable or progressive angina. The pooled OR was 1.82 (95% CI: 1.42 to 2.33, I2 = 0%, P < 0.00001) for MACE, 2.36 (95% CI: 1.47 to 3.79, I2 = 0%, P = 0.0004) for MI, 1.83 (95% CI: 1.33 to 2.53, I2 = 0%, P = 0.0002) for revascularization, and 1.65 (95% CI: 1.20 to 2.27, I2 = 0%, P = 0.002) for rehospitalization respectively. Subgroup analysis of culprit lesions (CLs) revealed significant differences between DM and non-DM for MACE, MI, revascularization, and stent thrombosis. While non-culprit lesions (NCLs) showed differences for MACE, MI, revascularization, and rehospitalization between the two groups.

The rates of MACE, MI, and revascularization are greater in DM than in non-DM patients in terms of all lesions, CLs, and NCLs. Except for CLs, the readmission rate is greater for unstable or progressive angina. Plaque characteristics are similar between patients with and without diabetes. Prospero registration number CRD42023474226.

Prognostic markers for long-term outcomes are lacking in patients with deferred (nonculprit) coronary artery lesions. This study aimed to identify the morphological criteria for predicting adverse outcomes and validate their clinical impact. Using deep learning models, we extracted geometrical parameters and maximal attenuation (or calcium) burden index (ABI-max or CBI-max) from the intravascular ultrasound (IVUS) images of nonculprit vessels in 1115 patients. The endpoints included cardiac death, myocardial infarction, and target vessel revascularization of nonculprit vessel. Cardiac death occurred in 27 (2.4 %) patients at 3 years and 39 (3.5 %) patients at 5 years. At 5 years, the cardiac death-free survival rate was significantly lower with ABP-max ≥11.37 % vs. < 11.37 % (90.0 % vs. 98.7 %), CBI-max ≥13.40 % vs. < 13.40 % (92.8 % vs. 98.4 %), and percent atheroma volume ≥ 51.35 % vs. < 51.35 % (94.0 % vs. 97.7) (all log-rank p < 0.001). The independent predictors of 5-year cardiovascular mortality were age (hazard ratio [HR] 1.21), female sex (HR 0.33), history of heart failure (HR 6.06), chronic kidney disease (HR 18.28), ABI-max (HR 1.04), and CBI-max (HR 1.05). The independent determinants of 5-year target vessel revascularization of nonculprit vessel were fractional flow reserve (HR 0.95 per 0.01 increase), minimal lumen area (HR 0.63), and plaque burden (HR 1.15). In patients with nonculprit coronary artery lesions, a large burden of attenuated or calcified plaques predicted cardiac mortality, while IVUS geometry was associated with repeat revascularization. Thus, deep learning-based IVUS analysis of the whole target vessel may help clinicians identify high-risk lesions.

Mindfulness training has gained increasing attention as a potential intervention to improve cardiovascular health, particularly in populations with chronic conditions, such as type 2 diabetes. Given the heightened cardiovascular risk associated with type 2 diabetes, identifying effective non-pharmacological strategies to mitigate these risks is crucial. This critical review assessed the current evidence on the impact of mindfulness training on cardiovascular health in individuals with type 2 diabetes. A comprehensive literature search was conducted using the PubMed database, and studies were selected based on stringent inclusion and exclusion criteria. The search strategy was meticulously designed to filter out high-quality articles and ensure that only the most relevant and rigorous studies were included in the analysis. The findings from this review suggest that while mindfulness training has the potential to improve cardiovascular health in individuals with type 2 diabetes, evidence remains mixed. Some studies have reported significant improvements in cardiovascular markers, such as blood pressure and inflammation, while others have shown limited or no effects. This variability highlights the need for further research to better understand the mechanisms underlying these outcomes and identify the most effective mindfulness interventions for this population. In conclusion, mindfulness training appears to be a promising approach for enhancing cardiovascular health in Type 2 diabetes patients, yet the current evidence is inconclusive. Future research should focus on standardizing mindfulness interventions, conducting larger clinical trials, and exploring the long-term benefits of these interventions on cardiovascular outcomes in high-risk populations.

Diabetes mellitus, a metabolic syndrome characterized by hyperglycemia and insulin dysfunction, often leads to serious complications such as neuropathy, nephropathy, retinopathy, and cardiovascular disease. Incretins, gut peptide hormones released post-nutrient intake, have shown promising therapeutic effects on these complications due to their wide-ranging biological impacts on various body systems. This review focuses on the role of incretin-based therapies, particularly Glucagon-like peptide-1 (GLP-1) agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors, in managing diabetes and its complications. We also discuss the potential of novel agents like semaglutide, a recently approved oral compound, and dual/triple agonists targeting GLP-1/GIP, GLP-1/glucagon, and GLP-1/GIP/glucagon receptors, which are currently under investigation. The review aims to provide a comprehensive understanding of the beneficial impacts of natural incretins and the therapeutic potential of incretin-based therapies in diabetes management.

Chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) have a syndemic relationship with shared risk factors and complex interplay between genetic, environmental, socioeconomic, and pathophysiological mechanisms. CVD is among the most common comorbidities in patients with COPD and vice versa. Patients with COPD, irrespective of their disease severity, are at increased risk of CVD morbidity and mortality, driven in part by COPD exacerbations. Despite these known interrelationships, CVD is underestimated and undertreated in patients with COPD. Similarly, COPD is an independent risk-enhancing factor for adverse cardiovascular (CV) events, yet it is not incorporated into current CV risk assessment tools, leading to under-recognition and undertreatment. There is a pressing need for systems change in COPD management to move beyond symptom control towards a comprehensive cardiopulmonary disease paradigm with proactive prevention of exacerbations and adverse cardiopulmonary outcomes and mortality. However, there is a dearth of evidence defining optimal cardiopulmonary care pathways. Fortunately, there is a precedent to support systems-level change in the field of diabetes, which evolved from glycemic control to comprehensive multi-organ risk assessment and management. Key elements included integrated multidisciplinary care, intensive risk factor management, coordination between primary and specialist care, care pathways and protocols, education and self management, and disease-modifying therapies. This commentary article draws parallels between the cardiometabolic and cardiopulmonary paradigms and makes a case for systems change towards multidisciplinary, integrated cardiopulmonary care, using the evolution in diabetes care as a potential framework.

Type 2 diabetes mellitus (T2DM) is characterised by endothelial dysfunction, leading to increased risk of cardiovascular disease. Emerging evidence suggest that HWI may favourably improve vascular function but data are limited in individual with T2DM. The aim was to investigate whether repeated hot water immersion (HWI) improved macrovascular, microvascular and central haemodynamic function in individuals with T2DM. Fourteen individuals completed a pre-post experimental study where participants were assessed pre- and post-8-10 × 1 h HWI sessions (40 °C water) undertaken within a 14-day period. During HWIs, body position was adjusted to clamp rectal temperature at 38.5-39.0 °C for the duration of the immersion. Stroke volume index (SVi), cardiac index (Q˙ i), resting heart rate (HR), systolic blood pressure (SBP), diastolic BP (DBP), brachial flow-mediated dilation (FMD) and cutaneous microvascular endothelial function (via transdermal iontophoresis) and plasma [nitrate] and [nitrite] (NOX; via ozone chemiluminescence) were assessed pre- and post HWI. Neither brachial FMD measures of macrovascular endothelial function (p = 0.43) or forearm microvascular function (ACh max, p = 0.63; ACh area under curve (AUC), p = 0.63; insulin max, p = 0.51; insulin AUC, p = 0.86) or NOX (p = 0.38) were changed. Q˙ i (p < 0.01), SVi (p < 0.02) and resting HR (p < 0.01) were all significantly reduced following the 10-days HWI intervention. SBP was reduced (p = 0.03), whereas DBP was unchanged (p = 0.56). HWI may represent an appropriate intervention to improve Q˙ I, SVi and BP in individuals with T2DM, but not macrovascular endothelial or cutaneous microvascular function.

Visit-to-visit blood pressure variability is a factor for a series of cardiovascular diseases in hypertensive patients. Hypertension is a common complication of patients with type 2 diabetes mellitus. Our research demonstrated that blood pressure variability is more important than systolic blood pressure to be associated with the occurrence of coronary artery disease and stroke. However, the importance of visit-to-visit blood pressure variability was easily overlooked. The results aimed to inform the health professionals the significance of stability blood pressure variability in the blood pressure management for patients with type 2 diabetes.

To investigate the effect of sodium-glucose cotransporter 2 inhibitors (SGLT2i) on cardiovascular outcomes in patients with acute coronary syndrome (ACS) and type 2 diabetes (T2D).

The clinical data of 88 patients with ACS and T2D who were treated with SGLT2i between January 2020 and December 2021 were collected as the case group through convenience sampling. Patients taking other hypoglycaemic drugs were included as the control group in a 1:1 ratio matched with the case group using retrospective propensity score matching. Relevant data were subsequently collected from both groups for comparison.

Statistically significant differences were observed in glycated haemoglobin (HbA1c) between the two groups (8.11[6.93, 9.41] vs 7.51[6.52, 9.14]%; Z=2.109; P=0.035). The SGLT2i group showed a decrease in major adverse cardiovascular events (MACEs) (P<0.001), secondary composite endpoint events (P=0.024), heart failure readmission (P=0.042) and unplanned revascularisation (P=0.014) compared with the control group. Moreover, the multivariate analysis showed that SGLT2i significantly reduced the risk of MACEs (hazard ratio [HR], 0.472; 95% CI, 0.321-0.694; P<0.001) and unplanned revascularisation (HR, 0.422; 95% CI, 0.212-0.842; P=0.014). In patients with reduced ejection fraction, SGLT2i significantly reduced the risk of MACEs (HR, 0.258; 95% CI, 0.106-0.626; P=0.003) compared with the control group. By contrast, in patients without reduced ejection fraction, SGLT2i significantly reduced the risk of MACEs (HR, 0.640; 95% CI, 0.412-0.996; P=0.048) and unplanned revascularisation (HR, 0.464; 95% CI, 0.222-0.969; P=0.041) compared with the control group.

In addition to significantly reducing the risk of adverse cardiovascular events and unplanned revascularisation in patients with ACS and T2D, the use of SGLT2i can reduce the risk of adverse cardiovascular events regardless of the presence of reduced ejection fraction.