Usefulness of soluble and surface-bound P-selectin in detecting heightened platelet activity in patients with congestive heart failure

O’Connor, Christopher M.; Gurbel, Paul A.; Serebruany, Victor L.

doi:10.1016/s0002-9149(99)00098-3

Cited by 116 publications

(65 citation statements)

References 28 publications

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“…Several previous studies have reported increased levels of soluble P-selectin in various cardiovascular disorders, supporting the notion that an elevation of P-selectin might constitute a marker of atherosclerosis and endothelial dysfunction. [15][16][17][18][19][20][21][22][23][24][25] Our results in younger patients would support this hypothesis. However, in older patients, the association was reversed.…”

Section: Serum Soluble P-selectin Levels and Cad Risksupporting

confidence: 72%

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Association Between P-Selectin Gene Polymorphisms and Soluble P-Selectin Levels and Their Relation to Coronary Artery Disease

Barbaux

Blankenberg

Rupprecht

et al. 2001

ATVB

105

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Abstract-P-selectin is a cellular adhesion molecule that mediates the interaction of activated endothelial cells or platelets with leukocytes. Increased levels of soluble P-selectin have been reported in various cardiovascular disorders. We measured serum soluble P-selectin levels as well as 3 polymorphisms of the P-selectin gene (C-2123G, A-1969G, and Thr715Pro) in a large cohort of patients with documented coronary artery disease (nϭ869) and a healthy control group (nϭ334). The 3 P-selectin polymorphisms were strongly associated with P-selectin levels and altogether explained 7.3% and 18.6% of the P-selectin variability in patients and controls, respectively. Genotype distributions did not significantly differ between patients and controls. P-selectin levels were increased in patients younger than 55 years of age compared with controls (135.2 vs 114.3 ng/mL, PϽ0.01). On the contrary, patients older than 65 years of age had significantly lower P-selectin levels than did controls (121.5 vs 134.7 ng/mL, PϽ0.02). In intermediate age groups, P-selectin levels did not significantly differ between the 2 groups. In conclusion, this study revealed a strong association between P-selectin gene polymorphisms and serum P-selectin levels and a complex age-dependent relation between soluble P-selectin levels and coronary artery disease, which suggests that this molecule might have different roles in the atherothrombotic process.

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Section: Serum Soluble P-selectin Levels and Cad Risksupporting

confidence: 72%

“…24 In a prospective study, plasma soluble P-selectin levels were recently shown to be predictive of future vascular events in initially healthy women. 25 A number of polymorphisms of the P-selectin gene have been reported that could affect the peptide sequence of the protein and its regulatory sequences.…”

mentioning

confidence: 99%

Association Between P-Selectin Gene Polymorphisms and Soluble P-Selectin Levels and Their Relation to Coronary Artery Disease

Barbaux

Blankenberg

Rupprecht

et al. 2001

ATVB

105

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“…27 It was also reported that the increased expression of platelet P-selectin associated with a reduced NO level, a marker of endothelial dysfunction, was a risk factor for cerebral infarction in patients with atrial fibrillation. 24 Elevated plasma P-selectin has been reported in patients with congestive heart failure, 28 primary pulmonary hypertension 23 and CCHD. 25,29 The platelet activation under these conditions may be due to increased shear stress and/or endothelial dysfunction, but the precise mechanisms for the platelet activation in patients with CCHD remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Increased Thrombogenesity in Patients With Cyanotic Congenital Heart Disease

Kajimoto

Nakazawa

Murasaki

et al. 2007

Circ J

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yanotic congenital heart disease (CCHD) is associated with an increased risk of stroke and thromboembolism. 1 A recent study using contrast-enhanced computed tomography revealed a high prevalence of pulmonary thrombosis in patients with Eisenmenger syndrome. 2 The precise mechanisms of the increased incidence of thromboembolism in patients with CCHD have not yet been determined, but endothelial dysfunction, hemostatic abnormalities and platelet activation may be underlying factors causing hypercoagulability and thromboembolism. [3][4][5] Platelets interact with endothelial cells, leukocytes and other platelets. 6 Intravascular thrombus formation is enhanced by thrombin, which activates the coagulation cascade, platelets and the formation of neutrophil/platelet conjugates. 6-8 P-selectin is an adhesion molecule found in the secretory granules of platelets and Weibel -Palade bodies of endothelial cells, and is mobilized to the plasma membrane on activation. 6,9,10 P-selectin expressed on platelets may be a direct inducer of pro-coagulant activity associated with vascular and thrombotic diseases. 11 Although P-selectin is likely to play an important role in the thrombus formation, 6,11 there have been only a few studies evaluating Pselectin in CCHD. 4,12,13 Thrombomodulin is expressed mainly on the surface of vascular endothelial cells and prevents blood clotting on the internal surface of vessels. Endothelial thrombomodulin is a key component of the protein C anticoagulant pathway that facilitates the activation of protein C by thrombin. 14 Therefore, thrombomodulin acts as an intrinsic anticoagulant barrier between the blood and the endothelium. The plasma thrombomodulin level was elevated in disseminated intravascular coagulation and atheromatous arterial disease. 15,16 It may initially increase with acute vascular injury but decrease with subsequent downregulation of its production during chronic vessel injury. Several reports have shown that reduced thrombomodulin enhances thrombus formation. 17,18,19 We hypothesized that the decreased expression of protein C and the increased expression of Pselectin on platelets due to a reduced thrombomodulin level may contribute to the formation of thrombi in patients with CCHD. To test this hypothesis, we measured plasma levels of thrombomodulin and protein C, and the expression of Pselectin on platelets in patients with CCHD. The plasma thrombin -antithrombin complex III (TAT) level was also measured to evaluate coaguability. Methods PatientsWe enrolled 35 patients with CCHD. The inclusion criterion was the presence of cyanosis due to right-to-left shunt in patients with congenital heart disease. The demography of the patients is summarized in Table 1. There were 19 men and 16 women, with a mean age of 13±11 years, ranging from 1 to 37 years. Twenty-five patients had undergone palliative operations (Balock-Taussig shunt or bidirectional Glenn). Eight patients underwent definitive operations (Fontan operation in 7 and Rastelli operation in 1), but the Circ J 2007; 71: 948...

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“…In HF, there is evidence of reduced platelet survival time, increased mean platelet volume, and greater platelet activation. 19 Patients with HF demonstrate high levels of circulating fibrinogen, fibrinopeptide A, and D-dimer determined by high plasma norepinephrine concentration or low LVEF. 20 Higher levels of angiotensin and endothelin commonly seen in patients with HF patients increase levels of von Willebrand factor (VWF).…”

Section: Pathophysiologymentioning

confidence: 99%

Thromboembolism and Antithrombotic Therapy in Patients With Heart Failure in Sinus Rhythm

Bettari

Fiuzat

Becker

et al. 2011

Circ: Heart Failure

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H eart failure (HF) represents a major and growing public health problem because of its prevalence, incidence, morbidity, mortality, and economic costs. The prevalence of HF is 2% to 3% of the general population. 1 Five million Americans are affected, with Ͼ550 000 cases diagnosed each year. 2 The mortality rate from severe HF remains Ͼ60% within 5 years of diagnosis, and 50% of hospitalized patients with HF require readmission within 6 months of discharge. In the US estimated costs amount to Ͼ $35 billion per year. 3 Although several therapies (eg, ␤-blockers, angiotensinconverting enzyme [ACE] inhibitors, and cardiac resynchronization therapy) have been proven effective in improving HF outcomes, many unanswered questions about optimal treatment remain. One area of ongoing uncertainty is the appropriate role for antithrombotic therapy in patients with HF. Observational data suggest that patients with HF have an increased venous thromboembolism (VTE) risk (deep venous thromboembolism [DVT], pulmonary embolism [PE], peripheral arterial thromboembolism, and stroke). 4 These epidemiological findings are supported by multiple mechanisms that can contribute to a hypercoagulable state in patients with HF. Despite this increased risk of VTE, the role of antithrombotic therapy remains unclear. In this article, we provide an overview of epidemiology, pathophysiology, clinical trial data, and therapeutic recommendations for prevention of thromboembolism in HF. Search StrategyWe searched PubMed for articles published between 1958 and 2010 using the following search terms: epidemiology of heart failure, thromboembolism and heart failure, thrombogenesis and heart failure, anticoagulation in heart failure, antiplatelet agent and heart failure, aspirin and heart failure, bleeding risk and anticoagulation, and aspirin and angiotensin-converting enzyme inhibitors. We also studied abstracts from national and international cardiovascular meetings to identify unpublished studies using the key words anticoagulation and dilated cardiomyopathy. EpidemiologyData from published observational studies and secondary analyses of randomized controlled trials (RCTs) indicate that patients with HF patients have a higher risk for VTE than the general population. Observational CohortsDVT and PE Several case-cohort studies have shown that HF is associated with a 2-to 3-fold increased risk of DVT and PE compared with other medical conditions. 5 Retrospective analyses report an annual VTE incidence of 1.0% to 4.5% in patients with HF. 6 In RCTs of thromboprophylaxis in hospitalized patients with HF followed for 90 days, DVT rates ranged from 4.0% to 14.6%. 7,8 The Prophylaxis in Medical Patients With Enoxaparin trial evaluated VTE incidence in hospitalized patients with (nϭ353) and without (nϭ749) HF during a follow-up of 14 days after discharge and found that 15% of patients with HF not treated with enoxaparin developed VTE. 9 Beemath et al, 4 using data from the National Hospital Discharge Survey, found an increased risk of VTE in hospitalized p...

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Usefulness of soluble and surface-bound P-selectin in detecting heightened platelet activity in patients with congestive heart failure

Cited by 116 publications

References 28 publications

Association Between P-Selectin Gene Polymorphisms and Soluble P-Selectin Levels and Their Relation to Coronary Artery Disease

Association Between P-Selectin Gene Polymorphisms and Soluble P-Selectin Levels and Their Relation to Coronary Artery Disease

Increased Thrombogenesity in Patients With Cyanotic Congenital Heart Disease

Thromboembolism and Antithrombotic Therapy in Patients With Heart Failure in Sinus Rhythm

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