No evidence of reduced exercise capacity or ‘diabetic cardiomyopathy’ in type 1 diabetes subjects (#216)
Introduction
Reduced exercise capacity and VO2max have been reported in Type 1 diabetes (T1D) subjects which some attribute to the so-called ‘diabetic cardiomyopathy’.
Aims
To assess whether people with T1D have reduced exercise capacity and cardiac reserve during exercise, and whether sildenafil improves non-invasive measures of exercise performance.
Methods
Twenty T1D patients (ten with microvascular complications - retinopathy - and ten without) were recruited through St Vincent’s Hospital Melbourne. Participants performed a cardiopulmonary exercise test (VO2max) and semi-supine bicycle ergometer stress echocardiogram and were randomised to sildenafil 50 mg orally or placebo in a double blind fashion. Both tests were later repeated with the alternative therapy prescribed. Age and body mass index were similar in both groups. Those with microvascular complications had a statistically significant longer duration of diabetes (27.3 +/- 5.8 yrs vs. 11.6 +/- 7.3; p = 0.0007), and higher HbA1c (8.9 +/- 1.7% vs. 7.3 +/- 0.6%; p = 0.005) at the time of study.
Cardiopulmonary exercise test data was collected and analysed using Oxycon Alpha (Jager, Germany) software. Echocardiography analysis was performed off-line using commercial software (Echopac BT11, GE, Horten Norway). Statistical analysis was performed using SPSS Version 22 (IBM, USA).
Results
Exercise capacity was above average in those with or without complications, with no significant difference between the two groups in maximum load (218W, 121% predicted vs. 254W, 141% predicted; p = 0.23) and VO2max (36 ml/min/kg, 112% predicted vs. 40 ml/min/kg, 121% predicted; p = 0.16). There was no significant difference in LV systolic function between groups at increasing levels of exercise intensity based on echocardiography measures. Interestingly, right ventricular fractional area change (RVFAC) was significantly lower at all stages of exercise (p = 0.03) in those with microvascular complications. Overall there was a non-significant trend to improved cardiac output at maximal exercise with sildenafil.
Conclusion
We found no evidence of reduced exercise capacity or ‘diabetic cardiomyopathy’, however there was reduction in RV augmentation in the microvascular disease group. Further assessment is required to evaluate whether subclinical RV dysfunction could be an early marker of exercise intolerance, or diabetic pulmonary microvascular disease.