Anterolateral retrograde access to the distal popliteal artery and to the tibioperoneal trunk for recanalization of femoropopliteal chronic total occlusions.

OBJECTIVES: To describe and assess the safety of a technique for the percutaneous retrograde access to either the P3 segment of the popliteal artery or the tibioperoneal trunk (TPT) through the anterior muscle compartment of the leg to treat distal femoropopliteal chronic total occlusion (CTO). METHODS: After a failed antegrade attempt of endovascular recanalization of a femoropopliteal CTO, 41 symptomatic patients (29 men; mean age of 75.8 ± 8.4 years) underwent a percutaneous retrograde access by means of the puncture of the TPT in 15 cases (36.6%) and of the P3 tract of popliteal artery in 26 cases (63.4%). The puncture was performed on the anterolateral aspect of the proximal leg through the anterior muscle compartment with the patient in a standard supine position. Access to the vessel was obtained with a sheathless approach. After retrograde recanalization and guidewire rendezvous, the distal wire was retrieved proximally and a standard antegrade endovascular intervention was carried out. RESULTS: Retrograde access was achieved successfully in all patients. Recanalization was carried out in 16 cases (39.0%) with an endoluminal technique and in 25 cases (61.0%) in a subintimal fashion. Hemostasis was successfully attained in 31 patients (75.6%) by inflating a blood pressure cuff at the calf. In 11 cases (26.8%), the hemostasis was accomplished instead by means of a low-pressure ballooning as a bailout strategy for small residual bleedings. The transcutaneous oximetry at the 1-month follow-up from the procedure was significantly increased compared with the preprocedural values (10.4 ± 6.8 vs 42.4 ± 18.7 mm Hg; P < .01). No early or late postoperative access-related complications were observed at a mean follow-up of 12.6 ± 9.5 months. CONCLUSIONS: After a failed antegrade approach, the anterolateral retrograde puncture of the P3 or of the TPT is a valuable and safe technique to treat femoropopliteal CTOs in selected patients, regardless the distal spread of the lesion to the popliteal artery.

Age-adjusted D-dimer for the diagnosis of deep vein thrombosis.

Objective In the diagnosis of deep vein thrombosis, new D-dimer cut-off values were defined by multiplying 10 µg/L × age. The objective of the present study is to define a more specific age-adjusted value, including the pre-test Wells score, without worsening sensitivity. Methods We designed a case-control study in patients attended in the emergency department with clinically suspected deep vein thrombosis. Demographics, Wells score, D-dimer and ultrasound data were collected. In low and intermediate clinical probability cases for deep vein thrombosis, we determined the specificity and sensitivity (false-negative rates) for the following cut-off values of D-dimer: age × 10 µg/L, age × 15 µg/L, age × 20 µg/L, age × 25 µg/L and age × 30 µg/L. The cut-off value with maximum specificity without any false-negative result (sensitivity 100%) was identified. Results We included 138 consecutive patients, 39.9% were men and the mean age was 71.6 years. Deep vein thrombosis was diagnosed in 16.7% of patients and the Wells score was low in 69.6%, intermediate in 21% and high in 9.4% of patients. Applying the conventional cut-off value of 500 µg/L, the specificity was 21.1% with a sensitivity of 100%. Maintaining 100% sensitivity, the highest specificity was reached with a cut-off value for D-dimer equivalent to the age × 25 µg/L in low-risk patients (67.1% specificity) and the age × 10 µg/L (50% specificity) in intermediate-risk patients. Conclusions In patients with low Wells score, the cut-off value can be raised to age × 25 µg/L in order to rule out deep vein thrombosis without jeopardizing safety. In intermediate-risk patients, the D-dimer cut-off value could be raised to age × 10 µg/L as previously suggested.

Targeting the molecular mechanisms of ischemic damage: Protective effects of alpha-crystallin-B.

AIMS: Molecular chaperones constitute protectors of intracellular protein integrity and seem to confer short-term defence against various cell insults. Myocardial damage is associated to a loss of protective chaperones. Ischemic post-conditioning (IPost-Co) is a procedure that seems to protect against reperfusion injury. However, little is known on alpha-crystallin-B-chain (cryab/HspB5) evolution in IPost-Co. Here we have investigated cryab in myocardial ischemia and IPost-Co. METHODS AND RESULTS: Pigs underwent closed-chest 1.5h mid-left anterior descending (LAD) balloon occlusion and were either sacrificed without reperfusion (I;N=10), subjected to 2.5h of reperfusion and sacrificed (I/R; N=5); or subjected to IPost-Co before reperfusion and sacrificed 2.5h afterwards (IPost-Co; N=5). A sham-operated group was included (N=6). Proteomic analysis (2-D-electrophoresis/MALDI-TOF/TOF) revealed cryab as a single spot (20kDa; pI7.6). Myocardial cryab-20-protein and cryab-gene expression levels were decreased after ischemia and I/R(P<0.05). After IPost-Co, cryab-20-protein and cryab-gene expression levels were similar to those found in the heart of sham-operated animals (P<0.05). There was a direct correlation between LVEF-improvement after IPost-Co and myocardial cryab-20-protein levels. In a mice proof-of-principle study, cryab-20-peptide was synthesized and administered 1h before LAD-ligation and ECG-proven MI. A 59% reduction in infarct size was achieved in cryab-20-treated animals (P<0.05). CONCLUSIONS: Ischemia and reperfusion induce a decrease in myocardial cryab-20-protein levels together with a clinical impairment of cardiac function. IPost-Co induces a clinical improvement of cardiac function and a preservation of cryab-20 levels. Intervention studies on a mice-MI model showed that cryab-20-peptide administration reduces infarct size. All together our results show a significant cardioprotective effect of cryab.