Prothrombotic profile in patients with vasospastic or non vasospastic angina and non significant coronary stenosis
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ORIGINAL CLINICAL INVESTIGATION
Open Access
Prothrombotic profile in patients with vasospastic or non vasospastic angina and non significant coronary stenosis Jaume Figueras*, Jasone Monasterio, Enric Domingo, Beatriz Meneses, Elsa Nieto, Josefa Cortadellas and David Garcia-Dorado
Abstract Background: Patients with vasospastic (VA) or non vasospastic angina (NVA) without significant coronary stenosis have a reduced risk of infarction but is unclear whether or not this may be attributable to a lack of prothrombotic profile - similar to that present in patients with stable coronary artery disease (CAD). Methods: Plasma levels of von Willebrand factor, total and free tissue factor pathway inhibitor, plasminogen activator inhibitor-1, and fibrinogen were analyzed in 15 patients with stable VA and 23 with NVA, all with vasoconstrictive response to acetylcholine although with different severity. Results were compared with those of 20 age-matched controls and 10 patients with CAD. Results: Plasma levels of von Willebrand factor in patients with VA or NVA were higher than in controls (207 ± 62 and 203 ± 69% vs 121 ± 38%, p < 0.001) and tended to be lower than in CAD patients (264 ± 65, p = 0.145). They also presented higher total tissue factor pathway inhibitor (123 ± 18 and 111 ± 25 vs 88 ± 14, ng/ml p < 0.001) and plasminogen activator inhibitor-1 levels than controls (51 ± 30 and 52 ± 31% vs 19 ± 9 ng/ml, p < 0.001) and similar to CAD patients (134 ± 23 and 62 ± 31, respectively, ns). Moreover, free tissue factor pathway inhibitor plasma levels were lower than controls (18 ± 5 and 17 ± 5 vs 23 ± 8 ng/ml, p = 0.002) and similar to CAD patients (14 ± 5, ns). Despite this prothrombotic condition none of VA or NVA patients presented a myocardial infarction during a 9 year follow-up, an observation also reported in larger series. Conclusions: During a stable phase of their disease, patients with VA or NVA present a prothrombotic profile that might eventually contribute to occurrence of myocardial infarction. The rarity of these events, however, may suggests that ill defined factors would protect these patients from coronary plaque rupture/fissure.
Background Endothelial dysfunction has been documented in patients with angina and non significant coronary stenosis, either vasospastic (VA)[1] or non vasospastic (NVA) - including those with syndrome X [2,3]. Overall, endothelial dysfunction appears to be a relevant event for it is often the first step of atherosclerosis [4,5] and may facilitate coronary thrombosis [6,7]. In fact, patients with atherosclerosis may present a protrombotic state characterized by an imbalance in the thrombotic-fibrinolytic equilibrium with abnormal plasma levels of von * Correspondence: [email protected] Unitat Coronària, Àrea del Cor, Laboratori d’Hemostàsia*, Hospital General Vall d’Hebron, Universitat Autònoma de Barcelona, Barcelona. Spain
Willebrand factor (vWF)[8], tissue factor or tissue factor pathway inhibitor (TFPI)[9-11], plasminogen activator inhibitor-1 (PAI-1)[12-15] and fibrinogen
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