Association of periprocedural neurological deficit in carotid stenting with increased anticardiolipin antibodies.

INTRODUCTION: Carotid stenting (CS) has become a therapeutic alternative to endarterectomy in selected patients. Periinterventional plaque thromboembolism leading to neurological ischemic events remain the major risk of the procedure. We prospectively studied the potential role of thrombophilic conditions including anticardiolipin antibodies (ACA, IgG and IgM isotype), lupus anticoagulants, activated protein C resistance, antithrombin, and protein C and S. MATERIAL AND METHODS: The study was approved by the local ethics committee, and written informed consent was obtained from all patients. In total, 236 consecutive patients were included (158 men, 78 woman; median age 73 years). Prothrombotic markers were quantitated on the day of admission. Periprocedural neurological deficits (PND) occurring within 48 hours of the intervention were recorded and classified by an independent neurologist as transient ischemic attack, minor or major stroke. Uni- and multivariable logistic regression analysis were performed to test for the influence of thrombophilic conditions, demographic factors and lesion characteristics on PND. RESULTS: Neurologic complications occurred in 18 interventions (7.6%). In 4 (36.4%; 3 minor, 1major stroke) out of 11 patients with elevated IgG-ACA neurological events were observed as compared to 14 (6.2%; 6 TIA, 5 minor stroke, 3 major stroke) out of 225 patients with normal IgG-ACA levels. In multivariable analysis, two variables were independently associated with PND: elevated IgG-ACA (OR 6.09, 95% CI 1.49-25.88; P=0.012) and lesion length >10 mm (OR 4.36, 95% CI 1.19 to 16.01; P=0.027). CONCLUSIONS: A thrombophilic condition due to elevation of anticardiolipin antibodies increases the risk of periinterventional neurological complications during CS.

Asymmetric dimethylarginine is increased in chronic thromboembolic pulmonary hypertension.

RATIONALE: Asymmetric dimethylarginine (ADMA), a potent endogenous nitric oxide synthase (NOS) inhibitor, is increased in idiopathic pulmonary arterial hypertension and associated with unfavorable outcome. OBJECTIVES: Chronic thromboembolic pulmonary hypertension (CTEPH), although principally amenable to surgical removal of major pulmonary arterial obstructions by pulmonary endarterectomy, may show a small-vessel pulmonary arteriopathy similar to idiopathic pulmonary arterial hypertension. We hypothesized that ADMA plasma levels are increased in patients with CTEPH. METHODS: We measured ADMA by high-performance liquid chromatography at the time of diagnosis in 135 patients with CTEPH. Inoperability in 66 patients was based on an imbalance between severity of pulmonary hypertension and morphologic lesions. MEASUREMENTS AND MAIN RESULTS: ADMA plasma levels were significantly elevated in patients, compared with 40 matched control subjects (0.62 [0.51-0.73] vs. 0.51 [0.45-0.6] micromol/L, P = 0.0002). At baseline, ADMA plasma concentrations correlated with mixed venous saturation (r = -0.25, P = 0.005), right atrial pressure (r = 0.35, P < 0.0001), and cardiac index (r = -0.21, P = 0.01). Patients who underwent surgery demonstrated lower ADMA levels at baseline than inoperable patients (0.60 [0.5-0.68] vs. 0.63 [0.53-0.85] micromol/L, P = 0.02), with a further decrease 12 +/- 1 months after pulmonary endarterectomy (P = 0.02). Endothelial NOS expression in endothelial cells was low in patients with elevated ADMA plasma levels. Survival of patients with ADMA plasma levels >/= 0.64 micromol/L was worse than in patients with ADMA plasma levels < 0.64 micromol/L. CONCLUSIONS: ADMA plasma levels correlate with the severity of pulmonary vascular disease and predict outcome in patients with CTEPH. Measurement of ADMA plasma levels may be useful for estimating the degree of small-vessel arteriopathy in CTEPH.