The additional impact of type 2 diabetes on baroreflex sensitivity of coronary artery disease patients might be undetectable in presence of deterioration of mechanical vascular properties

Both deterioration of the mechanical vascular properties of barosensitive vessels and autonomic derangement lead to modification of baroreflex sensitivity (BRS) in coronary artery disease (CAD) individuals. Type 2 diabetes (T2D) reduces BRS as well even in absence of cardiac autonomic neuropathy. The aim of the study is to clarify whether, assigned the degree of mechanical vascular impairment and without cardiac autonomic neuropathy, the additional autonomic dysfunction imposed in CAD patients by T2D (CAD-T2D) decreases BRS further. We considered CAD (n = 18) and CAD-T2D (n = 19) males featuring similar increases of average carotid intima media thickness (ACIMT) and we compared them to age- and gender-matched healthy (H, n = 19) subjects. BRS was computed from spontaneous beat-to-beat variability of heart period (HP) and systolic arterial pressure (SAP) at supine resting (REST) and during active standing (STAND). BRS was estimated via methods including time domain, spectral, cross-spectral, and model-based techniques. We found that (i) at REST BRS was lower in CAD and CAD-T2D groups than in H subjects but no difference was detected between CAD and CAD-T2D individuals; (ii) STAND induced an additional decrease of BRS visible in all the groups but again BRS estimates of CAD and CAD-T2D patients were alike; (iii) even though with different statistical power, BRS markers reached similar conclusions with the notable exception of the BRS computed via model-based approach that did not detect the BRS decrease during STAND. In presence of a mechanical vascular impairment, indexes estimating BRS from spontaneous HP and SAP fluctuations might be useless to detect the additional derangement of the autonomic control in CAD-T2D without cardiac autonomic neuropathy compared to CAD, thus limiting the applications of cardiovascular variability analysis to typify CAD-T2D individuals.