Platelet Activation and Fibrinopeptide Formation in Pulmonary Hypertension

Schulman, Larry L.; Grossman, Betty A.; Owen, John

doi:10.1378/chest.104.6.1690

Cited by 22 publications

(11 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Therefore, in spite of fibrinolytic abnormalities in these patients, the authors did not find a blunted response of t-PA or plasminogen activator activity to venous occlusion to explain the failure to resolve thrombi in pulmonary arteries. Similarly, SCHULMAN et al [48] did not find abnormalities in lytic mechanisms in 10 patients with PPH and seven patients with secondary PH compared to nine normal volunteers. Conversely, HUBER et al [49] found that patients with PPH and CTEPH exhibited a decreased t-PA level and an increased PAI-1 level after venous occlusion compared with healthy subjects (fig.…”

Section: Injured Endotheliummentioning

confidence: 79%

See 1 more Smart Citation

The role of thrombosis in severe pulmonary hypertension

Chaouat¹,

Weitzenblum²,

Higenbottam³

1996

Eur Respir J

116

View full text Add to dashboard Cite

Considering the important surface in pulmonary circulation where blood can interact with the endothelium, the maintenance of blood fluidity through the lung, by antithrombotic pathways and products of the endothelium, is essential. This function appears to be ineffective in primary pulmonary hypertension and in severe secondary pulmonary hypertension. Thrombotic lesions are frequently found in pulmonary arteries in these diseases.Thrombin activity appears to be increased in severe pulmonary hypertension. Antithrombotic pathway disorders may account for this abnormality, particularly in chronic thromboembolic pulmonary hypertension and primary pulmonary hypertension. Injured endothelium, a constant feature in severe pulmonary hypertension, either primary or secondary, enhances thrombus formation in pulmonary vessels. This is probably related to thrombomodulin and tissue factor imbalance, impairment of prostacyclin and nitric oxide release, as well as inefficiency of fibrinolysis. Moreover, platelets appear to be activated in the pulmonary circulation of these patients. They release several mediators acting on vascular tone and as mitogenic agents, and may also contribute to thrombin and clot generation. Long-term oral anticoagulant and continuous infusion of prostacyclin, treatments which impede thrombosis, are known to improve the survival rate in patients with primary pulmonary hypertension.These are the strongest arguments, so far, in favour of the role of thrombosis in severe pulmonary hypertension. However, we do not know whether these abnormalities result from a previous vascular injury or represent the primary disturbance.

show abstract

Section: Injured Endotheliummentioning

confidence: 79%

“…Clinical studies also reveal conflicting results. Two studies [20,39] have shown an increase in amounts of the markers of platelet activation; whereas, another study [48] reported no difference in these markers between patients with primary or severe secondary PH and normal volunteers.…”

Section: Plateletsmentioning

confidence: 98%

The role of thrombosis in severe pulmonary hypertension

Chaouat¹,

Weitzenblum²,

Higenbottam³

1996

Eur Respir J

116

View full text Add to dashboard Cite

show abstract

“…FPA is generated when thrombin cleaves fibrinogen to form a fibrin clot and was previously used as a marker of fibrin generation and degradation prior to the availability of the D-dimer assay. Although a separate smaller study did not confirm the FPA data [18], a more recent study using calibrated automated thrombogram demonstrated that PAH patients have increased thrombin generation and exhibit a hypercoagulable state [19]. A limitation of the thrombogram methodology is its failure to account for fibrinolysis, but it is likely that both fibrin generation and fibrinolysis contribute to the hypercoagulable state in PAH.…”

Section: Evidence For Coagulation In Pahmentioning

confidence: 99%

Thrombosis, platelets, microparticles and PAH: more than a clot

Lannan

Phipps

White

2014

Drug Discovery Today

View full text Add to dashboard Cite

Pulmonary arterial hypertension (PAH) is a progressive disease that involves pathological remodeling, vasoconstriction, and thrombosis. Alterations in hemostasis, coagulation, and platelet activation are consistently observed in PAH patients. Microparticles derived from platelets, inflammatory cells, and the endothelium are an increasingly well-recognized signal in a variety of cardiovascular diseases, including PAH. This review will focus on the role of coagulation, thrombosis, platelet activation, and microparticles in the pathology and progression of PAH.

show abstract

“…Altered endothelial cell and hemostatic markers like endothelin, CD40, selectins, von Willebrand factor, thrombin-antithrombin complex, fragments 1+2, ß-thromboglobulin, and platelet aggregates are present in patients with CTD and in patients with PAH [7][8][9][10][11][12][13] .…”

mentioning

confidence: 99%