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Thrombosis Journal

, 9:10

First Online: 27 May 2011Received: 05 October 2010Accepted: 27 May 2011

Abstract

BackgroundPatients 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.

MethodsPlasma 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.

ResultsPlasma 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.

ConclusionsDuring 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.

List of abbreviationsVAvasospastic angina

NVAnon vasospastic angina

CADcoronary artery disease

vWFvon Willebrand factor

t-TFPItotal tissue factor pathway inhibitor

f-TFPIfree tissue factor pathway inhibitor

PAI-1plasminogen activator inhibitor-1.

Electronic supplementary materialThe online version of this article doi:10.1186-1477-9560-9-10 contains supplementary material, which is available to authorized users.

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Author: Jaume Figueras - Jasone Monasterio - Enric Domingo - Beatriz Meneses - Elsa Nieto - Josefa Cortadellas - David Garcia-Dorad

Source: https://link.springer.com/article/10.1186/1477-9560-9-10







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