Background: Pericoronary adipose tissue attenuation (PCATa), derived from coronary computed tomography angiography (CCTA), is a novel marker of inflammation in the coronary arteries. Patients with type 2 diabetes mellitus (T2DM) are at elevated risk of coronary artery disease (CAD), potentially due to systemic inflammation. This study evaluated whether baseline PCATa predicts changes in plaque composition and burden over 12 months. Methods: This prospective longitudinal study included 200 participants with T2DM, who had neither symptoms nor a prior diagnosis of CAD (mean age 61 ± 9.4 years, 72% male). PCATa was measured at the baseline scan along the proximal 40 mm of each major coronary artery, and the values were averaged to calculate the participant-level PCATa. High PCATa levels were determined using the validated cut-off of -70.1 Hounsfield units. Compositional plaque changes were quantified as the differences between baseline and 12-month scans, and plaque burden was calculated as the normalized atheroma volume. Multivariable regression analyses assessed the associations between baseline PCATa and compositional plaque changes and evaluated risk factors, including high PCATa, in predicting non-calcified plaque burden progression. Results: Plaque compositional volumes and burden increased over 12 months, while PCATa remained stable. After multivariable adjustments, baseline PCATa was significantly associated with changes in total plaque volume (β = 0.005, p = 0.005), non-calcified plaque volume (β = 0.006, p = 0.007), total plaque burden (β = 1.7, p = 0.007), and non-calcified plaque burden (β = 2.0, p = 0.006), but not with calcified plaque volume or burden. High baseline PCATa was observed in 44 participants (22%) and was the only independent predictor of non-calcified plaque burden progression (odds ratio 3.5, p = 0.002). Conclusions: Baseline PCATa is significantly associated with increases in total and non-calcified plaque volumes and burden over 12 months in participants with T2DM without symptoms or known CAD. High PCATa levels uniquely predict non-calcified plaque burden progression, suggesting that PCATa may serve as a marker for subclinical atherosclerosis progression. This warrants further investigation into PCATa for cardiovascular risk assessment, particularly in high-risk populations such as individuals with T2DM. Trial registration: Trial registration: NCT06644651. Graphical PCATa = Pericoronary Adipose Tissue attenuation. T2DM = Type 2 diabetes mellitus. CAD = Coronary Artery Disease. N = numbers. CCTA = Coronary CT angiography. Created in BioRender. Research insights: What is currently known about this topic? Type 2 diabetes mellitus (T2DM) and coronary artery disease (CAD) share inflammatory mechanisms. Individuals with T2DM face a two- to four-fold increased risk of CAD compared with those without T2DM. Pericoronary adipose tissue attenuation (PCATa) is a novel marker of coronary inflammation. What is the key research question? Can baseline PCATa predict compositional plaque changes over 12 months in T2DM without known CAD? What is new? Baseline PCATa relates to higher total and non-calcified plaque (NCP) volumes after adjustment. Baseline PCATa associates with increased total- and NCP burden after multivariable adjustment. High baseline PCATa (> -70.1 HU) independently predicts NCP burden progression. How might this study influence clinical practice? PCATa may be a marker for subclinical atherosclerosis progression.

Background: Reduced left ventricular function, assessed by global longitudinal strain (GLS), is sometimes observed in asymptomatic patients with diabetes mellitus (DM) and is often present in patients with diabetes-related microvascular complications. Our aim was to assess the association between microvascular complications, coronary artery plaque burden (PB) and GLS in asymptomatic patients with DM and non-obstructive coronary artery disease (CAD). Methods: This cross-sectional study included patients with DM without any history, symptoms or objective evidence of obstructive CAD. All patients were identified in the outpatient Clinic of Endocrinology at Odense University Hospital Svendborg. An echocardiography and a coronary computed tomography angiography were performed to assess GLS and the degree of CAD, respectively. A coronary artery stenosis < 50% was considered non-obstructive. A linear regression model was used to evaluate the impact of potential confounders on GLS with adjustment of body mass index (BMI), mean arterial pressure (MAP), microvascular complications, type of diabetes, tissue Doppler average early diastolic mitral annulus velocity (e’) and PB. Results: Two hundred and twenty-two patients were included, of whom 172 (77%) had type 2 DM and 50 (23%) had type 1 diabetes. One hundred and eleven (50%) patients had microvascular complications. GLS decreased as the burden of microvascular complications increased (P-trend = 0.01): no microvascular complications, GLS (− 16.4 ± 2.5%), 1 microvascular complication (− 16.0 ± 2.5%) and 2–3 microvascular complications (− 14.9 ± 2.8%). The reduction in GLS remained significant after multivariable adjustment (β 0.50 [95% CI 0.11–0.88], p = 0.01). BMI (β 0.12 [95% CI 0.05–0.19]) and MAP (β 0.05 [95% CI 0.01–0.08]) were associated with reduced GLS. In addition, an increased number of microvascular complications was associated with increased PB (β 2.97 [95% CI 0.42–5.51], p = 0.02) in a univariable linear regression model, whereas there was no significant association between PB and GLS. Conclusions: The burden of microvascular complications was associated with reduced GLS independent of other cardiovascular risk factors in asymptomatic patients with DM and non-obstructive CAD. In addition, the burden of microvascular complications was associated with increasing PB, whereas PB was not associated with GLS.

Left ventricle mass (LVM) can be influenced by various conditions including hypertension and/or inherent cardiomyopathies. Dysglycemia is also thought to exert an anabolic effect on heart tissue by hyperinsulinemia and thereby promoting increased LVM. The primary aim of this study was to assess the influence of dysglycemia on LVM evaluated by an oral glucose tolerance test (OGTT) in patients admitted with a first myocardial infarction (MI) without hypertension. The secondary aim was to assess the impact of dysglycemia on major adverse cardiovascular events (MACE) and all-cause mortality during long-term follow-up. Patients admitted with a first MI without known history of hypertension were included. All patients without previously known type 2 diabetes mellitus (T2DM) had a standardized 2-hour OGTT performed and were categorized as: normal glucose tolerance (NGT), impaired fasting glucose (IFG)/impaired glucose tolerance (IGT) and newly detected T2DM (new T2DM). LVM was measured by echocardiography using Devereaux formula and indexed by body surface area. Multivariate linear regression analysis was used to assess the impact of confounders (dysglycemia by OGTT, known T2DM, age, sex and type of MI) on LVM. Cox proportional hazard model was used to assess the impact of dysglycemia on all-cause mortality and a composite endpoint of MACE (all-cause mortality, MI, revascularisation due to stable angina, coronary artery bypass graft, ischemic stroke or hemorrhagic stroke). Two-hundred-and-five patients were included and followed up to 14 years. In multivariate regression analysis, LVM was only significantly increased in patients categorized as new T2DM (β = 25.3; 95% CI [7.5–43.0]) and known T2DM (β = 37.3; 95% CI [10.0-64.5]) compared to patients with NGT. Patients with new T2DM showed higher rates of MACE and all-cause mortality compared to patients with IFG/IGT and NGT; however no significantly increased hazard ratio was detected. Dysglycemia is associated with increasing LVM in normotensive patients with a first acute myocardial infarction and the strongest association was observed in patients with new T2DM and patients with known T2DM. Dysglycemia in normotensive patients with a first MI is not an independent predictor of neither MACE nor all-cause mortality during long-term follow-up compared to normotensive patients without dysglycemia.

Aim: Insulin resistance (IR) and hyperglycemia have been associated with increased risk of heart failure (HF) in patients with and without diabetes. Global longitudinel strain (GLS) has been shown to be superior in the detection of left ventricular (LV) systolic dysfunction when compared to ejection fraction (EF). In this study, we aimed to assess GLS in relation to IR and pre-diabetes. Method: All participants underwent an echocardiography to assess LV systolic function using GLS. IR was evaluated using homeostatic model assessment for IR (HOMA-IR), and the participants were divided into tertiles based on their HOMA-IR values. An oral glucose tolerance test (OGTT) was performed to divide participants into normal glucose tolerance (NGT) and pre-diabetes. A multivariable linear regression model was used to assess GLS in relation to IR and glycemic groups. Results: In total, 359 men without significant coronary artery disease (CAD) and without diabetes were enrolled. Participants in the higher HOMA-IR tertile had significantly reduced GLS when compared with participants in the lower HOMA-IR tertile (−17.9% vs. −18.7%, p < 0.01). A significant trend was observed towards reduced GLS with increasing HOMA-IR tertile (p-trend 0.005). However, in the multivariable regression model, only waist-to-height-ratio (WH) (β 7.1 [95% CI 3.1–11.1, p = 0.001) remained significantly associated with GLS, whereas HOMA-IR tertile and pre-diabetes were not. Conclusions: In asymptomatic elderly men with no diabetes or CAD, neither IR nor pre-diabetes was associated with GLS in the adjusted regression model. Increased WH seems to be associated with reduced systolic function by GLS measurement.

Background: Left ventricular mass (LVM) is known to be influenced by various conditions including hypertension. Dysglycaemia in type 2 diabetes (DM2) is characterized by an increased endogenous production of insulin, but an impaired function of insulin (insulin resistance). Previous research suggests, that dysglycaemia can exert an anabolic effect on tissue thereby promoting increased LVM.