Cardiac autonomic dysfunction (CAD) is characterized by sympatho-vagal imbalance (reduced vagal activity and relative sympathetic overdrive). This condition might shorten diastole duration (DD) and thus impair coronary perfusion. Arterial stiffness is also considered to impair coronary perfusion. The aim was to investigate the influences of CAD and arterial stiffness on subendocardial myocardial viability (SVI) and in particular the relation between the severity of CAD, DD and SVI in patients with type 2 diabetes (T2D).

In 42 T2Ds (55.2±12.6 yrs, BMI 33.4±7.3kg/m², HbA1c 8.04±1.58%) free of cardiovascular history, we measured noninvasively heart rate (HR) and blood pressure (Finapres^®) continuously during 5minutes in supine position. We calculated then DD and arterial stiffness (augmentation index AIx and pulse wave velocity with a recently validated method: a Mac Apple dedicated software that reconstructs the central aortic pressure curve from the peripheral one (measured on finger) by a transfer function). Pulse wave velocity (PWV) was calculated from the equivalent index SI-DVP derived from the pulse pressure profile. The percentage of DD [DD%=(DD/duration of heart period)×100] and SVI (area under aortic pressure curve during diastole/area during systole) were calculated as well. CAD was assessed using standard tests (deep-breathing, lying-to-standing, Valsalva), which mostly depend on vagal control.

CAD was absent in 7 patients (Autonomic score 0: AS0), early (AS1: 1 abnormal test) in 14 patients, definite (AS2: 2 abnormal tests) in 15 patients and severe (AS3: 3 abnormal tests) in 6 patients. Mean HR in AS0 was 70.1±11.6 bpm, in AS1: 74.9±8.1, in AS2: 77.8±11.2, in AS3: 95.0±16.0 with a statistical significance (P<0.05) between AS0 vs. AS3, AS1 vs. AS3, AS2 vs. AS3. DD% correlated negatively with HR (r=−0.747, P<0.0001) and was lower in patients with higher AS. DD% differed significantly in AS3 and AS2 compared to AS0 (AS3: 52.8±3.6%, AS2: 56.7±4.1% and AS1: 59.7±3.9% vs. AS0: 61.7±3.3%; P=0.0008, P=0.011 and P=0.25, respectively). Furthermore, the patients with AS2 or AS3 considered together showed lower DD% compared with the patients with AS0 or AS1 even after adjusting DD% with regression analysis at a conventional HR of 75 bpm (CAD+: 57.8±3.3% vs. CAD−: 59.9±2.6%; P=0.030). SVI showed the same trend as DD%, with lower values in the patients with higher AS and reached the statistical significance in AS3 compared to AS0 (AS0: 1.23±0.2; AS1: 1.16±0.1, P=0.41 vs. AS0; AS2: 1.02±0.2, P=0.056 vs. AS0; AS3: 0.88±0.1, P=0.006 vs. AS0). A strong positive linear correlation was found between SVI and DD% (r=0.921, P<0.0001); conversely SVI showed a moderate negative linear correlation with aortic AIx adjusted at HR 75 bpm (r=−0.489, P<0.001). No correlations were found with pulse wave velocity.

In T2Ds CAD, expressed as reduced vagal activity, leads to HR acceleration and thus to diastole shortening, but it seems that CAD may shorten DD per se, independently of the effect on heart rate. Since DD influences strongly SVI, CAD plays a primary role in addition to arterial stiffness in the impairment of subendocardial myocardial viability and may thus worsen cardiovascular prognosis.