Pulmonary hypertension during exercise underlies unexplained exertional dyspnoea in patients with Type 2 diabetes

Abstract

Aim To compare the cardiac function and pulmonary vascular function during exercise between dyspneic and non-dyspneic patients with type 2 diabetes mellitus (T2DM). Methods 47 T2DM patients with unexplained dyspnea and 50 asymptomatic T2DM patients underwent exercise echocardiography combined with ergospirometry. Left ventricular (LV) function (stroke volume, cardiac output, LV ejection fraction, systolic annular velocity (s’)), estimated LV filling pressures (E/e’), mean pulmonary arterial pressures (mPAP) and mPAP/COslope were assessed at rest, low- and high-intensity exercise with colloid contrast. Results Groups had similar patient characteristics, glycemic control, stroke volume, cardiac output, LV ejection fraction and E/e’ (p > 0.05). The dyspneic group had significantly lower systolic LV reserve at peak exercise (s’) (p = 0.021) with a significant interaction effect (p < 0.001). The dyspneic group also had significantly higher mPAP and mPAP/CO at rest and exercise (p < 0.001) with significant interaction for mPAP (p < 0.009) and insignificant for mPAP/CO (p = 0.385). There was no significant difference in mPAP/COslope between groups (p = 0.706). However, about 61% of dyspneic vs. 30% of non-dyspneic group had mPAP/COslope > 3 (p = 0.009). The mPAP/COslope negatively predicted V̇O2peak in dyspneic group (β= -1.86, 95% CI -2.75, -0.98; multivariate model R²:0.54). Conclusion Pulmonary hypertension and less LV systolic reserve detected by exercise echocardiography with colloid contrast underlie unexplained exertional dyspnea and reduced exercise capacity in T2DM.

Pulmonary disease in diabetes

“…9 Part of the difficulty may be in underdiagnosis, with a study of 53 persons with T2D and unexplained exertional dyspnea showing lower peak oxygen uptake during exercise and higher mean pulmonary artery pressure. 10 The association of IPF severity with diabetes may be related to oxidative stress, to endothelial dysfunction, to inflammation, to obesity, to diaphragmatic muscle dysfunction, to autonomic neuropathy, and to albuminuria. 11,12 Insulin resistance has been proposed as underlying the relationship between diabetes and PH, with consequent inflammation, dyslipidemia, and endothelial dysfunction leading to adverse pulmonary vascular remodeling and to right ventricular dysfunction.…”

“…A meta‐analysis comparing 25 180 persons with IPF to 73 434 controls showed the likelihood of diabetes to be 1.54‐fold greater in the former group, although evidence of diabetes as a risk factor for IPF was not found 9 . Part of the difficulty may be in underdiagnosis, with a study of 53 persons with T2D and unexplained exertional dyspnea showing lower peak oxygen uptake during exercise and higher mean pulmonary artery pressure 10 . The association of IPF severity with diabetes may be related to oxidative stress, to endothelial dysfunction, to inflammation, to obesity, to diaphragmatic muscle dysfunction, to autonomic neuropathy, and to albuminuria 11,12 .…”