Özet:

Introduction: Cardiovascular risk factors both affect macrovascular and microvascular systems, resulting in negative results on the entire vascular tree. Aortic stiffness causes augmented systolic pressure, increased pulse pressure, increased myocardial oxygen demand, and consequently, coronary blood flow diminishes because of decreased diastolic augmentation. The aim of our study is to investigate the relation between macrovascular and microvascular hemodynamics. Methods: We have included 58 consecutive patients (29 male, age 54[34-71]) without any epicardial coronary stenosis in coronary angiography. Macrovascular and microvascular parameters were calculated with the measurements of tonometry, coronary flow reserve, and microvascular resistance. Results:Carotid-femoral pulse wave velocity (PWV) and subendocardial viability ratio (SEVR) had an inverse correlation (r=-0.328,p=0.007).The main reason of this correlation was priorly positive correlation between PWV and systolic pressure-time integral (SPTI) (r=0.465, p<0.001).A positive correlation was noted between augmentation index (AI) and PWV (r=0.352,p=0.010); and an inverse significant correlation was noted between AI and SEVR (r=-0.383,p=0.003).PWV had a positive correlation with diastolic/systolic coronary flow velocity (r=0.42,p=0.04) and microvascular resistance (MR) (r=0.44,p=0.03) and a negative correlation with hyperemic mean coronary flow velocity (r=-0.416,p=0.043) and coronary flow reserve (CFR) (r=-0.419,p=0.04) in diabetic patient group (n=27).AI was inversely related to CFR (r=-0.41,p=0.04) in diabetic patient group.SEVR and CFR were well correlated in the same direction (r=0.569, p<0.001).SEVR was significantly lower in the patients with lower CFR (1.41±0.23/1.58±0.24,p=0.01).SEVR had a significant negative correlation with MR (r=-0.321,p=0.016). SEVR was associated with arteriolar resistance index (r=0.413,p=0.002). Conclusion: Cardiovascular events appear as a combined result of the pathologies of the macro and microvascular levels. Aortic wall pathologies, which affect central hemodynamic properties, change subendocardial perfusion and coronary microcirculation.

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