Endovascular revascularization below the knee: 6-month results and predictive value of C-reactive protein level.

PURPOSE

To determine the association between pre- and postintervention serum C-reactive protein (CRP) levels and 6-month restenosis after endovascular treatment of atherosclerotic lesions in arteries below the knee.

MATERIALS AND METHODS

Eighty-nine patients with peripheral arterial disease underwent primary successful percutaneous transluminal angioplasty (PTA) of the distal popliteal, anterior tibial, posterior tibial, and fibular arteries. Six-month patency was evaluated with the ankle brachial index (ABI) and color-coded duplex ultrasonography (US). The association between restenosis and preintervention and 48-hour postintervention CRP levels was assessed with multiple logistic regression analysis.

RESULTS

ABI improved from a preintervention median of 0.54 to a postintervention median of 0.75 (P <.001). The primary technical success rate was 94% (100 of 106). In 50 patients, a suboptimal technical result was achieved with 30%-40% residual stenosis at the dilated segment. The median ABI at 6 months was 0.65, and it was inversely correlated with preintervention (r = -0.27, P =.009) and 48-hour postintervention (r = -0.40, P <.001) CRP levels. With duplex US at 6 months, restenosis (> or =50%) occurred in 36 patients. Patients with a preintervention CRP level of 0.23-0.92 mg/dL (2.3-9.2 mg/L) had a 3.7-fold increased adjusted risk for restenosis (P =.05); patients with a preintervention CRP level greater than 0.92 mg/dL (9.2 mg/L) had a 4.7-fold increased adjusted risk (P =.03). Postintervention CRP values greater than 2.42 mg/dL (24.2 mg/L) were associated with a 10.7-fold adjusted risk for restenosis (P =.002). Suboptimal PTA result was the only other parameter associated with an increased risk for restenosis (odds ratio, 3.7; P =.03).

CONCLUSION

Pre- and postintervention CRP levels were associated with restenosis after PTA of the distal popliteal and tibioperoneal arteries, which indicates that inflammation plays a crucial role in the pathophysiology of this process.