Background—: Patients with type 2 diabetes mellitus are at risk of heart failure. Specific therapeutic interventions for diabetic heart disease are still elusive. We aimed to examine the impact of improved glycemic control on left ventricular (LV) function in these patients. Methods and Results—: A total of 105 subjects with type 2 diabetes mellitus (aged 54±10 years) and poor glycemic control received optimization of treatment for blood glucose, blood pressure, and cholesterol to recommended targets for 12 months. LV systolic and diastolic function, measured by LV global longitudinal strain (GLS) and septal e′ velocities, were compared before and after optimization. At baseline, patients had impaired LV systolic (GLS −14.9±3.2%) and diastolic function (e′ 6.2±1.7 cm/s). After 12 months, glycated hemoglobin (HbA1c) decreased from 10.3±2.4% to 8.3±2.0%, which was associated with significant relative improvement in GLS of 21% and septal e′ of 24%. There was a progressively greater improvement in GLS as patients achieved a lower final HbA1c. Patients achieving an HbA1c of <7.0% had the largest improvement. The 15 patients whose HbA1c worsened experienced a decline in GLS. Patients who improved their HbA1c by ≥1.0% had a significantly higher relative improvement in e′ than those who did not (32% versus 8%; P =0.003). Baseline GLS, decrease in body mass index, and treatment with metformin were additional independent predictors of GLS improvement. Conclusions—: Improvements in glycemic control over a 12-month period led to improvements in LV systolic and diastolic function. This may have long-term prognostic implications.

Background Diabetic cardiomyopathy is an increasingly prevalent health issue, with no specific management options. We examined the impact of weight loss with sleeve gastrectomy on diabetic cardiomyopathy. Methods Eight obese patients with type 2 diabetes undergoing sleeve gastrectomy had left ventricular (LV) systolic and diastolic function assessed by global longitudinal strain (GLS) and septal early diastolic velocity (e’) using echocardiography, before and 9 months after surgery. Results Following surgery, mean weight loss was 28.0 ± 16 kg; body mass index (BMI) decreased from 44 ± 9 to 35 ± 6 kg/m² (p < 0.001). Glycaemic control improved with glycated haemoglobin (HbA1c) improving from 9.2 % at baseline to 6.7 % at follow-up (p = 0.002), with a corresponding improvement in LV GLS from −13.2 ± 3.7 to −19.7 ± 2.2 % (p < 0.001), and LV ejection fraction from 60 ± 5 to 70 ± 4 % (p < 0.001). Improvement in GLS was associated with the amount of weight lost (ρ = 0.81, p = 0.015). LV septal e’ velocities increased, and LV filling pressures decreased after surgery. Conclusions Weight loss with sleeve gastrectomy in obese patients with type 2 diabetes is effective in improving glycaemic control in subjects with type 2 diabetes and results in significant improvement in both systolic and diastolic myocardial function.

Aims: Recent studies have raised concerns regarding increased heart failure in patients on dipeptidyl peptidase-4 inhibitors. We examined whether dipeptidyl peptidase-4 inhibitors, compared to non-incretin–based therapies, have differential effects on left ventricular and endothelial function in patients with type 2 diabetes mellitus. Methods: A total of 25 type 2 diabetes mellitus patients commenced on a dipeptidyl peptidase-4 inhibitor were compared with 50 matched controls. Left ventricular systolic and diastolic function and flow-mediated dilatation were compared before and 12 months after treatment. Results: At baseline, both dipeptidyl peptidase-4 inhibitor and control groups had elevated HbA_1c and comparable subclinical left ventricular dysfunction (left ventricular global longitudinal strain: −15.4% vs −15.9%, p = 0.538; e′ velocities: 6 vs 6 cm/s, p = 0.151, where e′ is the peak mitral annular early diastolic tissue velocity). After 12 months, both groups had similar improvement in HbA_1c. However, patients on dipeptidyl peptidase-4 inhibitors had greater improvement in systolic (ΔGLS: 3.6% vs 1.3%, p < 0.001), despite no significant differences in weight, blood pressure or lipid parameters in both groups. Diastolic (Δe′: 38% vs 17%, p = 0.001) and endothelial function improved in the dipeptidyl peptidase-4 inhibitor group but not the control group (ΔFMD: 5% vs −1%, p = 0.029). Conclusion: We demonstrated significant improvements in LV systolic, diastolic and endothelial function in patients treated with a dipeptidyl peptidase-4 inhibitor over 12 months. These beneficial effects may provide some reassurance regarding the cardiovascular safety of dipeptidyl peptidase-4 inhibitors.

The Official Journal of EuroPCR and the European Association of Percutaneous Cardiovascular Interventions (EAPCI)

Background: Endothelial dysfunction is an early feature of vascular disease. Left ventricular (LV) diastolic reserve is the ability of the left ventricle to augment diastolic function with exercise and may be impaired in patients with diabetes mellitus (DM). It is unclear if endothelial dysfunction is related to impaired LV diastolic reserve and diminished exercise capacity. Methods: 96 patients with type 2 DM and 10 controls had brachial artery reactivity testing, followed by exercise echocardiography. The brachial artery diameter was measured at rest and during reactive hyperaemia. LV diastolic reserve was measured as Δe′ with exercise and diastolic reserve index (Δe′/rest e′). Exercise capacity was calculated by metabolic equivalents (METs). Results: Compared with controls, patients with DM had lower rest e′ (7 vs 9 cm/s, p=0.002), lower Δe′(1 vs 4 cm/s, p=0.023), lower Δe′/rest e′ (0.20 vs 0.47, p=0.003) and reduced flow mediated dilation (FMD, 5 vs 15%, p<0.001). FMD was correlated with Δe′ (r=0.65, p<0.001), diastolic reserve index (r=0.61, p<0.001) and post-exercise septal E/e′ (r=−0.50, p<0.001), but not with rest e′ (r=0.13, p=0.177). FMD was an independent predictor of Δe′ (β=0.002, p<0.001, R²=0.47) and diastolic reserve index (β=0.030, p<0.001, R²=0.41). Younger age (p<0.001), male gender (p=0.014), lower body mass index (p<0.001), lower rest E/e′ (p=0.042) and higher FMD (p=0.025) were independent predictors of higher METs (R²=0.52, p<0.001). Conclusions: Patients with DM had impaired endothelial function and LV diastolic dysfunction. LV diastolic reserve and exercise capacity are linked to endothelial function. Targeting vascular risk factors to improve endothelial function may improve LV diastolic reserve and exercise capacity.

Aims Diastolic reserve is the ability of left ventricular filling pressures to remain normal with exercise. Impaired diastolic reserve may be an early sign of diabetic cardiomyopathy. We aimed to determine whether diastolic reserve differs in type 2 diabetes (DM) compared with non-DM, and to identify clinical, anthropological, metabolic and resting echocardiographic correlates of impaired diastolic reserve in patients with DM. Methods and results 237 patients (aged 53±11 years, 133 DM, ejection fraction 68±9%) underwent rest and exercise echocardiography. Mitral E and septal e′ were measured at rest, immediately post, and 10 min into recovery. Analysis of covariance (ANCOVA) and binary regression with continuous outcomes were used to model e′ and E/e′ changes with exercise to identify impaired diastolic reserve defined as post-exercise E/e′ ≥15. After adjusting for baseline differences, patients with DM immediately post-exercise had a lower septal e′, a lower Δe′ (1.2 vs 2.3 cm/s, p=0.006) and a higher Δ septal E/e′ (1.7 vs 0.08, p<0.001) than patients without DM. In patients with normal resting E/e′ of ≤8 (n=130), DM had a significantly higher post-exercise septal E/e′ and a higher Δseptal E/e′ (2.63 vs 0.50, p<0.001). E/e′ in patients with DM remained significantly elevated up to 10 min post-exercise. Hypertension, longer duration of insulin therapy, poorer glycaemic control, worse renal function, larger left atrial volume and lower septal e′ were independent correlates of impaired diastolic reserve in patients with DM. Conclusions Patients with DM have impaired diastolic reserve manifest as a blunted e′ response with exercise, persisting into recovery. Clinical, anthropometric, metabolic and echocardiographic correlates of impaired diastolic reserve in patients with DM were identified. An impaired LV diastolic reserve may be the underlying pathophysiological mechanism in patients with DM with unexplained exertional dyspnoea and may allow earlier detection of DM cardiomyopathy.