T1D youth demonstrated IR, impaired functional exercise capacity and cardiovascular dysfunction. The phenotype of IR in T1D youth was unique, suggesting a pathophysiology that is different from T2D, yet may adversely affect long-term cardiovascular outcomes.

Objectives The primary aim of this systematic review is to objectively evaluate the test performance characteristics of three-dimensional echocardiography (3DE) in measuring left ventricular (LV) volumes and ejection fraction (EF). Background Despite its growing use in clinical laboratories, the accuracy of 3DE has not been studied on a large scale. It is unclear if this technology offers an advantage over traditional two-dimensional (2D) methods. Methods We searched for studies that compared LV volumes and EF measured by 3DE and cardiac magnetic resonance (CMR) imaging. A subset of those also compared standard 2D methods with CMR. We used meta-analyses to determine the overall bias and limits of agreement of LV end-diastolic volume (EDV), end-systolic volume (ESV), and EF measured by 3DE and 2D echocardiography (2DE). Results Twenty-three studies (1,638 echocardiograms) were included. The pooled biases ± 2 SDs for 3DE were −19.1 ± 34.2 ml, −10.1 ± 29.7 ml, and − 0.6 ± 11.8% for EDV, ESV, and EF, respectively. Nine studies also included data from 2DE, where the pooled biases were −48.2 ± 55.9 ml, −27.7 ± 45.7 ml, and 0.1 ± 13.9% for EDV, ESV, and EF, respectively. In this subset, the difference in bias between 3DE and 2D volumes was statistically significant (p = 0.01 for both EDV and ESV). The difference in variance was statistically significant (p < 0.001) for all 3 measurements. Conclusions Three-dimensional echocardiography underestimates volumes and has wide limits of agreement, but compared with traditional 2D methods in these carefully performed studies, 3DE is more accurate for volumes and more precise in all 3 measurements.

Given the strong relationship between decreased cardiopulmonary fitness and increased mortality, these findings in children are especially concerning and represent early signs of impaired cardiac function.

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Background Exercise is recommended as a cornerstone of treatment for type 2 diabetes mellitus (T2DM), however, it is often poorly adopted by patients. Even in the absence of apparent cardiovascular disease, persons with T2DM have an impaired ability to carry out maximal and submaximal exercise and these impairments are correlated with cardiac and endothelial dysfunction. Glucagon-like pepetide-1 (GLP-1) augments endothelial and cardiac function in T2DM. We hypothesized that administration of a GLP-1 agonist (exenatide) would improve exercise capacity in T2DM. Methods and Results Twenty-three participants (64±4 years; mean±SE) with uncomplicated T2DM were randomized in a double-blinded manner to receive either 10mcg BID of exenatide or matching placebo after baseline measurements. Treatment with exenatide did not improve VO2peak (P=0.1464) or VO2 kinetics (P=0.2775). Diastolic function, assessed via resting lateral E:E’, was improved with administration of exenatide compared with placebo (Placebo Pre: 7.6±1.0 vs. Post: 8.4±1.2 vs. Exenatide Pre: 8.1±0.7 vs. Post: 6.7±0.6; P=0.0127). Additionally, arterial stiffness measured by pulse wave velocity, was reduced with exenatide treatment compared with placebo (Placebo Pre: 10.5±0.8 vs. Post: 11.5±1.1 seconds vs. Exenatide Pre: 11.4±1.8 vs. Post: 10.2±1.4 seconds; P=0.0373). Exenatide treatment did not improve endothelial function (P=0.1793). Conclusions Administration of exenatide improved cardiac function and reduced arterial stiffness, however, these changes were not accompanied by improved functional exercise capacity. In order to realize the benefits of this drug on exercise capacity, combining exenatide with aerobic exercise training in participants with T2DM may be warranted. Clinical Trials Registration www.clinicaltrials.gov NCT01364584

Background--Myocardial mechanics are altered in adults with obesity and type 2 diabetes (T2D); insulin resistance and adipokines have been implicated as important risk factors for cardiovascular disease, but these relationships are poorly described in adolescents. We hypothesized that obese adolescents and adolescents with T2D would have abnormal cardiac function compared to lean adolescents. In addition, we hypothesized that insulin sensitivity (IS), adiposity, and adipokines would be associated with altered cardiac strain and cardiopulmonary fitness in adolescents with T2D.

Women with polycystic ovarian syndrome (PCOS) have evidence of subclinical cardiovascular disease (CVD). However, insulin resistance, an important factor in the development of CVD in adults, is common in adolescents with PCOS, yet data in adolescents are limited. Therefore, we sought to measure insulin resistance and CVD markers in obese youth with and without PCOS. Thirty-six PCOS and 17 non-PCOS adolescent girls who were obese, sedentary, and non-hypertensive were recruited from clinics located within the Children's Hospital Colorado. Following 3 days of controlled diet and restricted exercise, fasting plasma samples were obtained prior to a hyperinsulinemic euglycemic clamp. PCOS girls were more insulin resistant than controls (glucose infusion rate 5.24±1.86 mg/kg/min vs 9.10±2.69; p<0.001). Girls with PCOS had blood pressure in the normal range, but had greater carotid intima–media thickness (cIMT) (0.49±0.07 mm vs 0.44±0.06; p=0.038), beta stiffness index (5.1±1.3 U vs 4.4±0.9; p=0.037), and reduced arterial compliance (1.95±0.47 mm2/mmHg × 10−1 vs 2.13±0.43; p=0.047). PCOS girls had a normal mean lipid profile, yet had a more atherogenic lipoprotein cholesterol distribution and had persistent elevations of free fatty acids despite hyperinsulinemia (68±28 μmol/mL vs 41±10; p=0.001), both potential contributors to CVD. Free fatty acid concentrations correlated best with all CVD markers. In summary, adolescent girls with PCOS have greater cIMT and stiffer arteries than girls without PCOS, perhaps related to altered lipid metabolism, even when clinical measures of blood pressure and cholesterol profiles are ‘normal’. Therefore, management of adolescent PCOS should include assessment of CVD risk factor development.

Objective Diabetic cardiomyopathy is a major cause of morbidity, but limited data are available on early cardiac abnormalities in type 1 diabetes (T1D). We investigated differences in myocardial strain in adolescents with and without T1D. We hypothesized that adolescents with T1D would have worse strain than their normoglycemic peers, which boys would have worse strain than girls, and that strain would correlate with glycemic control and adipokines. Methods We performed fasting laboratory measures and echocardiograms with speckle tracking to evaluate traditional echocardiographic measures in addition to longitudinal (LS) and circumferential (CS) strain, and in adolescents (15±2 years) with (19 boys; 22 girls) and without (16 boys; 32 girls) type 1 diabetes. Results Compared to controls, adolescents with type 1 diabetes had significantly lower CS (−20.9 vs. −22.7%, p=0.02), but not LS (p=0.83). Boys with T1D had significantly lower LS than girls with T1D (−17.5 vs. −19.7%, p=0.047), adjusted for Tanner stage. The significant sex differences observed in indexed left ventricular mass, left end-diastolic volume, diastolic septal and posterior wall thickness in our controls were lacking in adolescents with T1D. Conclusions Our observations suggest that youth with T1D have worse myocardial strain than normoglycemic peers. In addition, the relatively favorable cardiac profile observed in girls vs. boys in the control group, was attenuated in T1D. These early cardiovascular changes in youth with T1D are concerning and warrant longitudinal and mechanistic studies.