Abstract 18337: Pulmonary Microvascular Disease in Diabetes Mellitus (DM) Subjects Detected by Exercise Echocardiography is Not Associated With Reduced Exercise Capacity
Introduction: There is limited clinical evidence of pulmonary microvascular disease (PMD) in DM. We hypothesized that (1) a novel echocardiographic marker quantifying the pulmonary transit of agitated colloid contrast bubbles (PTAC) may identify pulmonary capillary disease; and (2) that low-PTAC may be associated with exercise limitation.
Methods: A repeated measures cross-over trial of sixty participants (40 DM and 20 age/sex-matched controls [C]) receiving sildenafil 50 mg or placebo in randomized order prior to each of two exercise tests (VO2max and exercise echocardiography) was performed. PMD was assessed by measuring the degree of PTAC traversing the pulmonary vasculature during incremental exercise. Bubbles reaching the left ventricle were quantified and categorized as low-PTAC or high-PTAC (see Figure 1). Sildenafil’s effect on VO2max was observed, as were non-invasive measures of central hemodynamic parameters including cardiac output (CO) and pulmonary artery systolic pressure (PASP) to derive pulmonary vascular resistance (PVR).
Results: DM and C subjects were of similar age (44 ± 13 vs. 43 ± 13 years, p=0.87) and gender (70% vs. 65% male, p=0.7). Mean DM duration was 16 ± 10 years and glycemic control was moderate (HbA1c: 7.7 ± 1.3%). At peak exercise, low-PTAC was present in more DM than C subjects (low-PTAC: 41 vs. 12.5%, χ2 P=0.041). When only considering DM subjects, there was a further trend to low-PTAC in those with vs. without microvascular complications (low-PTAC: 55% vs. 26.3%, χ2 P=0.069). Sildenafil increased CO and reduced PVR in DM, without altering the frequency of low-PTAC or improving VO2max. On multiple regression, neither PTAC nor sildenafil predicted maximal VO2.
Conclusion: PTAC was lower in DM compared to C subjects thereby suggesting that PTAC may be a novel marker of PMD. However, PTAC was not associated with exercise capacity and nor was it influenced by pulmonary vasodilator therapy.
Author Disclosures: T.J. Roberts: None. A.T. Burns: None. R.J. MacIsaac: None. D.J. Mooney: None. D.L. Prior: None. A. La Gerche: None.
- © 2016 by American Heart Association, Inc.