Healing process of venous ulcers: the role of microcirculation.

In order to describe adequately the process of healing in the intermediate degrees, we investigated microcirculatory changes in the venous ulcers at well-defined stages of wound repair. We investigated dynamic changes in microcirculation during the healing process of venous ulcers. Ten venous ulcers were investigated in three consecutive clinical stages of wound healing: non granulation tissue (NGTA), GTA and scar. Subpapillary microcirculation was measured by laser Doppler perfusion (LDP) imaging and expressed using LDP values in arbitrary units. Nutritive perfusion by capillary microscopy and expressed as capillary density (CD) - the number of capillaries per square millimetre. Before the development of GTA the LDP was low (median 1·35; lower-upper quartiles 0·71-1·83) accompanied with zero CD in all but one patient who had a density of 1. With the first appearance of GTA in the same area, the LDP was improved (2·22; 1·12-2·33; P = 0·0024) when compared with NGTA, in combination with a significant increase in CD (1·75; 0-3; P = 0·0054). In scar, the LDP was similar to that in the NGTA (1·03; 0·77-1·83; P = 0·278), combined with the highest CD (5·75; 4·5-8) in comparison with the previous stages of the area (for both pairs, P < 0·0001). Venous ulcers are caused by poor nutritive and subpapillary perfusion. Subpapillary perfusion plays a major role in the formation of GTA. In a scar, the increased nutritive perfusion is sufficient to cover the blood supply and keep skin viable while subpapillary perfusion is low.

Covered versus bare self-expanding stents for endovascular treatment of carotid artery stenosis: a stopped randomized trial.

PURPOSE: To investigate whether filter-protected carotid artery stenting (CAS) using a covered self-expanding stent reduces the risk of cerebral embolization. METHODS: Fourteen asymptomatic patients (13 men; median age 77 years, IQR 73-83) were enrolled in a randomized pilot trial comparing the rates of cerebral microembolism during and after filter-protected CAS using either a self-expanding covered (n=8) or a bare (n=6) carotid stent. Transcranial Doppler (TCD) monitoring was done during and for 90 minutes after the procedure. Diffusion-weighted magnetic resonance imaging (DW-MRI) was performed before and 24 hours after CAS. Patients were followed for 6 months for neurological events and occurrence of restenosis. RESULTS: A significant reduction in ipsilateral microembolic signals by TCD was observed with the covered (median 1, IQR 0-4) versus the bare stent (median 6, IQR 3-8; p=0.043). Comparison of the preprocedural and 24-hour postprocedural DW-MRI images showed no new ipsilateral lesions but 1 new lesion in the contralateral hemisphere in the covered stent group, resulting in an overall 7% (95% CI 0%-20%) rate of new ischemic lesions. No neurological complications occurred up to 6 months. Restenosis (>70%) occurred in 3 (38%) of 8 patients with the covered versus none of the bare stents (p=0.21). The trial was stopped when the third restenosis of a covered stent was detected. CONCLUSION: Self-expanding covered stents potentially reduce the risk of cerebral microembolism during and after carotid stenting. However, the problem of in-stent restenosis has to be resolved before these devices can be considered for further investigation.

Vascular dysfunction after coarctation repair is related to the age at surgery.

BACKGROUND: Despite repair of aortic coarctation, hypertension is frequent in adults and premature coronary and cerebrovascular disease remain of concern. Persistent impairment of arterial dilation has been suspected to contribute to abnormal blood pressure regulation. We tested the hypothesis that arterial reactivity is more likely to be impaired in patients corrected at older age. METHODS: We studied changes in brachial artery diameter in response to reactive hyperemia (FMD) and to nitroglycerin (NMD) in 36 patients and 25 controls. Depending on their age at surgery, patients were divided in group A (surgery <9 years) and group B (surgery > or =9 years). RESULTS: Cholesterol levels and percentage of smokers were similar in patients and controls, but 16 patients had arterial hypertension compared to none of the controls. Endothelium-dependent vasodilation, FMD, and endothelium-independent vasodilation, NMD, were significantly impaired in patients vs. controls (8.2+/-6.2% vs. 13.0+/-5.1%, p<0.001 and 12.9+/-8.0% vs. 18.8+/-9.2%, p<0.01, respectively), both, in hypertensives (8.3+/-6.0%, p<0.01 and 11.8+/-6.0%, p<0.05) and in normotensives (8.1+/-6.5% p<0.01 and 13.8+/-9.3%, p<0.05). However, FMD and NMD in patients of group A did not significantly differ from that in controls (10.0+/-6.7% n.s. and 15.0+/-7.6% n.s.), whereas they were lowest in patients of group B (5.5+/-4.3%, p<0.0001 and 9.6+/-7.7% p<0.001). CONCLUSIONS: Persistent impairment of FMD and NMD after repair of coarctation is more likely to be present in patients corrected at older age. It may be an important contributor to abnormal blood pressure regulation and late morbidity and mortality.

Quantification of internal carotid artery stenosis with duplex US: comparative analysis of different flow velocity criteria.

PURPOSE: To compare 13 previously published sets of duplex ultrasonographic (US) criteria with the US criteria used at the authors' institution in terms of agreement with carotid artery angiographic results. MATERIALS AND METHODS: The authors studied 1,006 carotid arteries in 503 patients at duplex US and angiography. The degree of stenosis was determined by using duplex flow US velocities and applying 13 previously published sets of criteria and the criteria used at the authors' institution. Two independent observers evaluated the angiograms according to North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria. kappa statistics, sensitivities, specificities, positive predictive values (PPVs), negative predictive values (NPVs), and generalized linear mixed regression models were used to assess agreement between duplex US and angiographic findings. RESULTS: Stenoses of 0%-29%, 30%-49%, 50%-69%, 70%-99%, and 100% could be differentiated with 73% overall agreement between duplex US and angiographic findings according to flow velocity criteria (kappa = 0.57; 95% confidence interval [CI]: 0.54, 0.60); however, with duplex US, the angiographic degree of stenosis tended to be overestimated. In the differentiation of stenoses of less than 70%, only 45% agreement (kappa = 0.26; 95% CI: 0.23, 0.29) was observed, whereas in the differentiation of high-grade (> or =70%) stenoses, 96% agreement was observed (kappa = 0.85; 95% CI: 0.83, 0.87). The PPV and NPV for the identification of 70%-99% angiographic stenosis were 69% and 98%, respectively, with use of the most sensitive duplex US criteria. CONCLUSION: Duplex US is an excellent examination to screen for high-grade carotid artery stenosis; however, it tends to lead to an overestimation of the degree of stenosis. Exclusion of 70%-99% angiographic stenosis can be achieved with a sensitivity of up to 98%.

Hemostatic markers with bolus versus prolonged heparin after carotid artery stenting.

BACKGROUND: The evolving technique of carotid stenting (CS) requires optimal antithrombotic strategies to reduce periinterventional thromboembolic risk. In animal models of balloon injury, tissue factor (TF) was shown to be the major procoagulant of the atherosclerotic plaque mediating prolonged procoagulant activity. METHODS: We analyzed TF and TF-dependent hemostatic markers before and 2, 6 and 24 h after CS with two antithrombotic drug regimens. Group A (n=20) received prolonged unfractionated heparin (UFH) for 18-20 h starting at intervention next to aspirin and thienopyridine. In group B (n=16), single bolus UFH was administered next to combined antiplatelet therapy. Natural anticoagulants were determined at baseline. RESULTS: Patients with symptomatic and asymptomatic cerebrovascular disease did not differ in plasma TF levels. Furthermore, no statistically significant difference for TF, TFPI/Xa-complex and prothrombin fragment F1.2 was observed between bolus and prolonged heparin treatment. No significant change was found in time course for these parameters. Two patients (5.5%; one in each treatment group) suffered periinterventional minor stroke associated with increased levels of F1.2 and TFPI/Xa-complex. Both were resistant to activated protein C (APC ratio<1.9) due to heterozygous factor V Leiden mutation. CONCLUSIONS: No significant activation of the TF pathway was seen with both antithrombotic regimens suggesting that single bolus UFH combined with antiplatelet therapy is generally sufficient to control TF-dependent procoagulant activity after CS. However, patients with resistance to activated protein C may be at increased periinterventional stroke risk.