Bimodal pattern of coronary microvascular involvement in diabetes mellitus


Atıcı A.

TurkishCardiologyCongresswith International Participation, Antalya, Türkiye, 20 - 23 Ekim 2016, no.108, ss.35

  • Basıldığı Şehir: Antalya
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.35

Özet

Background and Aim: A reduced coronary flow velocity reserve (CFVR) reflecting impaired coronary microcirculation in diabetes mellitus (DM) can be associated with functionally disturbed coronary autoregulatory mechanism (increased baseline coronary flow) and/or structurally impaired microvascular vasodilatory function (decreased hyperemic coronary flow). Moreover, role of the duration of DM in the evolution of these functional and structural coronary microvascular abnormalities over time is not known. Objective of this study was to identify the mechanism behind impaired CFVR in DM in relation to duration of disease. Methods: Coronary flow velocities in distal left anterior descending coronary artery were assessed by transthoracic Doppler echocardiography following coronary angiography revealing normal epicardial coronaries in 55 diabetic and 47 non-diabetic patients. Average peak coronary flow velocities (APV) at rest and under hyperemia, CFVR, coronary microvascular resistance in baseline and hyperemic conditions (BMR and HMR respectively) and arteriolar resistance index (ARI) were assessed. Results: Diabetic patients had significantly lower CFVR (1.86 versus 2.46, p=0.001) primarily driven by decreased hyperemic APV (45.44 cm/s versus 54.51 cm/s, p=0.006) due to increased HMR (1.98 mmHg.cm-1s-1 versus 1.70 mmHg.cm-1.s-1,p=0.019). ARI was also significantly lower (1.82 versus 2.51,p=0.0001) in diabetics than non-diabetics. Reduced CFVR in patients with short duration (<10 years) of DM was primarily driven by increased baseline APV (26.50±5.6 cm/s versus 22.08±4.31cm/s, p=0.008) in the presence of decreased BMR (3.69±0.86 mmHg.cm-1s-1 versus 4.34±0.76mmHg.cm-1s-1, p=0.003). On the contrary, decreased CVFR in patients with long-standing (>10 years) DM was predominantly driven by reduced hyperemic APV (41.57±10.01cm/s versus 53.47±11.8cm/s, p<0.001) along with increased HMR (2.13±0.42 mmHg.cm-1s-1 versus 1.69±0.39 mmHg.cm-1s-1, p<0.001). Conclusions: Both altered coronary autoregulation and impaired microvascular vasodilatory function contribute to diabetes related coronary microvascular impairment in time-dependent manner. Diabetes - induced early functional microvascular autoregulatory impairment resulting in increased coronary flow accompanied by decreased BMR at rest evolves into structural microvascular impairment presented with disturbed vasodilatory function in the initially over-perfused microvascular territory at later stage of disease