The prevalence of type 2 diabetes (T2D) has reached a pandemic scale. Systemic chronic inflammation dominates the diabetes pathophysiology and has been implicated as a causal factor for the development of vascular complications. Heart failure (HF) is regarded as the most common cardiovascular complication of T2D and the diabetic diagnosis is an independent risk factor for HF development. Key molecular mechanisms pivotal to the development of diabetic cardiomyopathy include the NF-κB pathway and renin–angiotensin–aldosterone system, in addition to advanced glycation end product accumulation and inflammatory interleukin overexpression. Chronic myocardial inflammation in T2D mediates structural and metabolic changes, including cardiomyocyte apoptosis, impaired calcium handling, myocardial hypertrophy and fibrosis, all of which contribute to the diabetic HF phenotype. Advanced cardiovascular magnetic resonance imaging (CMR) has emerged as a gold standard non-invasive tool to delineate myocardial structural and functional changes. This review explores the role of chronic inflammation in diabetic cardiomyopathy and the ability of CMR to identify inflammation-mediated myocardial sequelae, such as oedema and diffuse fibrosis.

Background: Type 2 diabetes (T2D) and hypertension commonly coexist and are associated with subclinical myocardial structural and functional changes. We sought to determine the association between blood pressure (BP) and left ventricular (LV) remodeling, systolic/diastolic function, and coronary microvascular function, among individuals with T2D without prevalent cardiovascular disease. Methods: Participants with T2D and age-, sex-, and ethnicity-matched controls underwent comprehensive cardiovascular phenotyping including fasting bloods, transthoracic echocardiography, cardiovascular magnetic resonance imaging with quantitative adenosine stress/rest perfusion, and office and 24-h ambulatory BP monitoring. Multivariable linear regression was performed to determine independent associations between BP and imaging markers of remodeling and function in T2D. Results: Individuals with T2D (n = 205, mean age 63 ± 7 years) and controls (n = 40, mean age 61 ± 8 years) were recruited. Mean 24-h systolic BP, but not office BP, was significantly greater among those with T2D compared to controls (128.8 ± 11.7 vs 123.0 ± 13.1 mmHg, p = 0.006). Those with T2D had concentric LV remodeling (mass/volume 0.91 ± 0.15 vs 0.82 ± 0.11 g/mL, p < 0.001), decreased myocardial perfusion reserve (2.82 ± 0.83 vs 3.18 ± 0.82, p = 0.020), systolic dysfunction (global longitudinal strain 16.0 ± 2.3 vs 17.2 ± 2.1%, p = 0.004) and diastolic dysfunction (E/e’ 9.30 ± 2.43 vs 8.47 ± 1.53, p = 0.044) compared to controls. In multivariable regression models adjusted for 14 clinical variables, mean 24-h systolic BP was independently associated with concentric LV remodeling (β = 0.165, p = 0.031), diastolic dysfunction (β = 0.273, p < 0.001) and myocardial perfusion reserve (β = − 0.218, p = 0.016). Mean 24-h diastolic BP was associated with LV concentric remodeling (β = 0.201, p = 0.016). Conclusion: 24-h ambulatory systolic BP, but not office BP, is independently associated with cardiac remodeling, coronary microvascular dysfunction, and diastolic dysfunction among asymptomatic individuals with T2D. (Clinical trial registration. URL: https://clinicaltrials.gov/ct2/show/NCT03132129 Unique identifier: NCT03132129).

Diabetes mellitus represents a global health concern affecting 463 million adults and is projected to rapidly rise to 700 million people by 2045. Amongst those with type 2 diabetes (T2D), there are recognised differences in the impact of the disease on different sex and ethnic groups. The relative risk of cardiovascular complications between individuals with and without T2D is higher in females than males. People of South Asian heritage are two to four times more likely to develop T2D than white people, but conversely not more likely to experience cardiovascular complications. Differences in the pathophysiological responses in these groups may identify potential areas for intervention beyond glycaemic control. In this review, we highlight key differences of diabetes-associated cardiovascular complications by sex and ethnic background, with a particular emphasis on South Asians. Evidence assessing therapeutic efficacy of new glucose lowering drugs in minority groups is limited and many major cardiovascular outcomes trials do not report ethnic specific data. Conversely, lifestyle intervention and bariatric surgery appear to have similar benefits regardless of sex and ethnic groups. We encourage future studies with better representation of women and ethnic minorities that will provide valuable data to allow better risk stratification and tailored prevention and management strategies to improve cardiovascular outcomes in T2D.

A distinctive pattern of cardiac MRI feature-tracking left ventricular early and late diastolic strain rates was observed across the range of diastolic dysfunction severity.

A previously fit 49-year-old male of South Asian ethnicity, presented to our emergency department at the height of the COVID-19 pandemic with a 2-day history of dyspnoea and a dry cough, preceded by an acute diarrhoeal illness. Clinical examination revealed a temperature of 38.6°C, blood pressure of 150/105 mmHg, heart rate of 129 b.p.m., and a respiratory rate of 40/min with oxygen saturations of 96% on air. A chest radiograph showed bilateral patchy lung opacities (Figure 1A). Initial laboratory tests showed an elevated white cell count of 11.5 [normal range (NR) 4–11 × 10⁹ L], neutrophil count of 9.27 (NR 1.5–7.5 × 10⁹ L), C-reactive protein of 129 (NR < 5mg/L), and a D-dimer of 7.7 (NR < 0.5 µg/mL). International normalized ratio and cardiac troponin were normal. The patient was treated empirically with intravenous clarithromycin 500 mg twice daily, co-amoxiclav 1.2 g three times daily, dexamethasone 6 mg once daily, and continuous positive airway pressure ventilation, along with anti-thrombotic prophylaxis on the intensive care unit. The patient underwent a SARS-CoV-2 polymerase chain reaction test which demonstrated that he had active COVID-19. On Day 6, the patient developed left arm swelling. Ultrasound confirmed a thrombus in the left internal jugular vein and axillary vein and was subsequently anticoagulated with dalteparin 12 500 units once daily. On Day 10, the patient developed central chest pain. Electrocardiogram showed anterior ST-segment elevation and Q-waves ( Supplementary material online , Figure S1), high-sensitive troponin-I was 27 266 (NR < 14 ng/L). An echocardiogram showed moderate left ventricular systolic dysfunction with apical akinesia. A computed tomography pulmonary angiogram showed subpleural organizing areas of consolidation with patchy peripheral ground-glass opacities with multiple bilateral pulmonary emboli (Figure 1B). Cardiac magnetic resonance imaging was undertaken to establish the aetiology of the cardiac injury. T1 mapping showed septal oedema with preserved ejection fraction (63%) but with apical akinesia and late gadolinium enhancement confirming apical myocardial infarction (MI) and patchy micro-infarction in the mid septum on the epicardial right ventricular side (Figure 1C, Video 1). Adenosine stress perfusion, to assess reversible myocardial ischaemia revealed marked hyperaemic myocardial blood flow (up to 5 mL/g/min) with patchy apical and mid septal hypoperfusion (Figure 1D) suggesting microvascular disease. Subsequent coronary angiography revealed unobstructed coronary arteries ( Supplementary material online , Figures S2 and S3). This case highlights the increasingly recognised macrovascular (venous and pulmonary arterial thrombosis, apical MI) and microvascular complications (patchy micro MI with non-matching stress hypoperfusion). The cardiac complications occurred despite 4 days of anticoagulation and there is increasing evidence that the vascular sequalae of COVID-19 are related to immune complex deposition and localized vascular inflammation rather than thromboembolism.