P635Type 2 diabetes mellitus and cardiopulmonary exercise capacity in patients with ischemic heart disease. Relationship between glycated haemoglobin levels and respiratory muscle impairment

Abstract

Introduction: Growing evidence supports that hyperglycaemia and insulin resistance may promote myocardial hypertrophy and fibrosis, leading to ventricular stiffness and myocardial dysfunction. Besides, impaired lung function has been reported in patients with type 2 diabetes mellitus (T2DM), suggesting the lung to be another target organ of diabetes. However, studies evaluating whether glycemic control affects exercise tolerance in patients with T2DM have shown conflicting results. Purpose: The aim of this study was to assess the impact of glycemic status, as reflected by HbA1c levels, on cardiopulmonary exercise (CPE) capacity in patients with IHD. Methods: We included 91 consecutive patients (57±10 years, 90% men) who underwent a CPE testing at the beginning of an exercise-based standard phase- II cardiac rehabilitation program, 2-3 months after an acute coronary syndrome (ACS). All tests were performed in accordance with ATS/ACCP Statement on CPET recommendations. Results: There were 24 (29%) T2DM subjects among IHD patients included in the study. HbA1c levels showed a weak negative linear correlation with vital capacity (VC) (r=-0.352; P=0.001), forced expiratory volume at the end of the first second (FEV1) (r=-0.347; P=0.001) and peak expiratory flow (PEF) (r=-0.288; P=0.006). Minute ventilation (VE) and tidal volume (VT) were negatively correlated with HbA1c levels (r=-0.351; P<0.001 and r=-0.320; P<0.001, respectively). No significant correlation was found between HbA1c levels and respiratory rate at peak exercise. HbA1c levels were independent predictor of FEV1 (P=0.013), VC (P=0.02), VE (P=0.001) and VT (P=0.007), after adjustment using multivariate analysis where we included age, waist circumference (WC) and β-blocker therapy. No significant association was found between HbA1c levels and ventilationperfusion mismatch parameters. Patients included in the study were divided into three groups according to previous diagnosis of T2DM and HbA1c levels above or below the current DM diagnosis cut-off point (6.5%). Oxygen uptake (VO2) (P trend <0.001), anaerobic threshold (AT) (P trend =0.002) and pulse O2 trajectory (P trend =0.004) decreased alongside the presence or not of a previous diagnosis of T2DM and glycemic control status (Figure). (Figure Presented) Conclusion: HbA1c levels were negatively correlated with static lung volumes (VC), dynamic spirometric (FEV1) and maximum flow (PEF) parameters. HbA1c levels were also negatively correlated with VE and VT, regardless of age and central obesity. All these results suggest that hyperglucemia could be implicated in respiratory muscle impairment leading to a decreased aerobic capacity. Poor glycemic control, as reflected by elevated HbA1c levels, may further deteriorate aerobic capacity in T2DM patients by an additional impairment in respiratory mechanics. (Figure Presented).