Abstract 20306: Comparison of Vascular Flow Reserve After Infrapopliteal Intervention Between Patients With Rest Pain and Patients With Tissue Loss
Purpose: Several clinical stages of critical limb ischemia (CLI) are observed in daily practice. Although microcirculatory dysfunction might be correlated in those stages, it is not clear whether the differences of microvascular damage in patients with rest pain or tissue loss are existed. The aim of this study is to compare the physiological parameter in patients with rest pain to that in patients with tissue loss undergoing endovascular treatment (EVT) for isolated infrapopliteal lesions after EVTs.
Methods: A total of 40 limbs of CLI patients with Rutherford-4 (R4) and Rutherford-5 (R5) undergoing EVT for isolated infrapopliteal lesions were included in this study prospectively. All lesions were treated by conventional balloon angioplasty alone. Initial success was defined as ≤30% residual diameter stenosis on angiogram. After the procedure, a pressure/temperature sensor-tipped guidewire was positioned in the proximal popliteal artery. By using thermodilution technique, mean transit time (Tmn) of a thermodilution-curve was obtained after bolus injections of 3 mL saline at baseline and at intra-arterial papaverine induced maximum hyperemia (30mg). It is generally recognized Tmn closely correlates with inverse of blood flow velocities. Vascular flow reserve (VFR) was calculated as resting Tmn divided by hyperemic Tmn.
Results: Procedure success rate was 100%. VFR was successfully measured immediately after EVTs in all patients without complications. All patients were classified into 2 groups according to R4 (n=6) and R5 (n=34). No significant differences existed in baseline lesion characteristics between two groups. Although there was no significant difference in pre-VFR between R4 and R5 (3.9±2.4 versus 3.5±1.6, p=0.67), VFR after EVT was significantly lower R5 than R4 (8.6±3.7 versus 3.5±1.7, p<0.0001).
Conclusions: Post-procedural VFR is restricted in patients with R5 due to the increase of resting flow velocity. Thus, not only reduced vessel flow during hyperemia because of microvascular impairment but also increased resting vessel flow from metabolic abnormalities might be mechanisms of CLI stage. Therefore, advanced lower limb clinical setting might be caused from a poor capability of microvasculature.
Author Disclosures: M. Fukunaga: None. K. Fujii: None. K. Miki: None. M. Nishimura: None. T. Saita: None. T. Horimatsu: None. A. Sumiyoshi: None. H. Tamaru: None. T. Imanaka: None. T. Masuyama: None.
- © 2014 by American Heart Association, Inc.