Increased platelet activity in patients with isolated coronary artery ectasia

Yaşar, Ayşe Saatçı; Erbay, Ali Rıza; Ayaz, Selime; Turhan, Hasan; Metin, Fatma; İlkay, Erdoğan; Sabah, İrfan

doi:10.1097/mca.0b013e3282a30665

Cited by 38 publications

(33 citation statements)

References 27 publications

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“…This is very intriguing because the destruction of the musculoelastic component of the vascular media is assumed to be irreversible. Single-antiplatelet therapy may be warranted for primary prevention of cardiovascular events in isolated CAE [52,65,69,70]. Addition of lifetime systemic anticoagulation therapy may be recommended for secondary, but not primary prevention [2,52,65,71].…”

Section: Managementmentioning

confidence: 99%

Coronary Artery Ectasia in Atherosclerotic Coronary Artery Disease, Inflammatory Disorders, and Sickle Cell Disease

Dahhan

2015

Cardiovascular Therapeutics

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SUMMARYCoronary artery ectasia (CAE) or aneurysm is usually defined as dilation ≥1.5-fold the normal vessel diameter. It has an incidence of 1.4-5.3% and is associated with a wide variety of etiologies-mainly congenital, atherosclerotic, and inflammatory ones. CAE is very common in sickle cell disease, and possibly sickle cell trait, with an incidence of 17.7%. It is likely related to the inflammatory process associated with hemoglobin S. Prognosis depends mainly on the underlying etiology. Atherosclerotic CAE does not carry additional risks compared to atherosclerotic coronary artery disease (ACAD) without ectasia. However, isolated CAE in the absence of ACAD carries an increased risk of myocardial infarction (MI) due to vasospasm, slower coronary blood flow, and thrombosis, typically within the dilated segments. Due to lack of studies and guidelines, management recommendations are based on personal experiences. Therapy should be tailored to each individual case after assessment of severity, history of complications, underlying etiology, and comorbidities. Treatment of underlying condition and avoidance of exacerbating factors are essential. Medical therapy in general may include antiplatelets, b-blockers, angiotensin-converting enzyme inhibitors statins, and dihydropyridine calcium channel blockers. In severe CAE or history of MI, the addition of anticoagulation therapy after assessing bleeding risk may be warranted. In acute MI, the large thrombus burden in the dilated segment makes the percutaneous approach very challenging. Aspiration attempts can result in distal thromboembolization. Survival is better in bypass grafting than with medical therapy. Nonetheless, bypass grafting does not improve survival in atherosclerotic CAE. Depending on the physical characteristics of aneurysm, different surgical approaches can be sought; however, the ideal one is unclear.

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Section: Managementmentioning

confidence: 99%

Coronary Artery Ectasia in Atherosclerotic Coronary Artery Disease, Inflammatory Disorders, and Sickle Cell Disease

Dahhan

2015

Cardiovascular Therapeutics

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“…The changes in blood viscosity, platelet activation, activation of coagulation system and the altered flow properties of blood in ectasic segments may cause thrombosis within this segment, consequently, which may be responsible for myocardial ischemia/infarction in patients with CAE. Yasar et al [21] showed that patients with CAE have raised levels of plasma P-selectin, beta-thromboglobulin (b-TG) and PF4 compared with control group, suggesting increased platelet activation in patients with CAE.…”

Section: Discussionmentioning

confidence: 98%

Mean platelet volume in patients with coronary artery ectasia

Varol

Akçay

Özaydın

et al. 2009

Blood Coagulation &Amp; Fibrinolysis

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Coronary artery ectasia (CAE) is a variant of coronary atherosclerosis. Mean platelet volume (MPV), an indicator of platelet activation, has been shown to be elevated in patients with acute coronary syndromes and myocardial infarction in the setting of obstructive coronary artery disease. The aim of this study was to assess the MPV in patients with CAE. We retrospectively studied 366 consecutive patients with CAE (195 men/171 women; mean age 55.4 +/- 10.9 years) and 160 control patients (81 men/79 women; mean age 53.5 +/- 10.2 years). MPV values were recorded in all study and control patients. The MPV values of patients with CAE were found to be significantly higher than those of the controls (9.2 +/- 1.1 versus 8.8 +/- 1.2 fl, respectively; P < 0.001). The platelet count was detected to be significantly lower in patients with CAE group than in patients with control group (233.7 +/- 70.7 versus 264.7 +/- 102.8 (x10(9)/l), respectively; P < 0.0001). We have shown that MPV was significantly elevated in patients with CAE compared with controls.

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“…13 Additionally, CAE patients exhibited increased platelet activation, with higher levels of plasma P-selectin, b-thromboglobulin and platelet factor 4, in comparison with NCA subjects. 23 C. pneumoniae IgG levels were the only marker of infection, among those that were studied, that were significantly higher in CAE patients than in NCA subjects. C. pneumoniae IgG tests were positive in 98.9% of CAD and 98.5% of CAE patients, compared to 83.5% in NCA subjects.…”

Section: Activation Markers In Peripheral Bloodmentioning

confidence: 99%

“…The search yielded 22 potentially relevant nonrandomized and retrospective studies published from 2000 to 2013. [6][7][8][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29] Exclusion criteria described in the articles selected included the following: recent or current myocardial infarction, acute coronary syndromes, left ventricular dysfunction, left ventricular hypertrophy, cardiomyopathies, congenital heart disease, valvular heart disease, inflammatory arrhythmias or immunologic diseases, active infection, hepatic, renal or thyroid functional abnormalities, immunosuppressive therapy and statin use.…”

Section: Methodsmentioning

confidence: 99%

Inflammatory mediators of coronary artery ectasia

Yuan

2014

J. vasc. bras.

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The exact mechanisms underlying coronary artery ectasia (CAE) remain uncertain. This study aims to investigate whether and how inflammatory mediators play a role in the pathogenesis of CAE. The data sources of this study were located by literature searches on MEDLINE, Highwire Press and Google search engine for the year range 2000-2013. The most sensitive of the four types of plasma inflammatory mediators were cell adhesion molecules and systemic inflammatory markers followed by cytokines, while proteolytic substances were the least sensitive indicators of CAE. Hypersensitive C-reaction protein, homocysteine, intercellular adhesion molecule 1, vascular cell adhesion molecule 1, matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-2, vascular endothelial growth factor and neopterin levels were significantly higher in CAE and coronary artery disease (CAD) patients than in controls without CAE. The percentage of granulocytes was higher in CAE, in comparison with individuals with normal coronary arteries. Polymerase chain reaction determination of angiotensin converting enzyme genotypes showed that the DD genotype was more prevalent in CAE patients than in CAD patients, while prevalence of the I allele was higher in CAD than in CAE patients. CAE is more a result of inflammatory processes than of extracellular matrix degradation, as demonstrated by investigations of plasma inflammatory mediators, activation markers and angiotensin converting enzyme genotypes. Contemporary theories are unable to explain CAE' s predilection for the right coronary artery or the occurrence of multi-vessel and multi-segment involvement.Keywords: coronary aneurysm; extracellular matrix; inflammation mediators. ResumoOs mecanismos exatos da ectasia de artérias coronárias (EAC) não são completamente compreendidos. Este estudo busca verificar, em detalhes, se e como os mediadores inflamatórios funcionam na pathogenesis de EAC. A fonte de dados do presente estudo veio da recuperação de literatura das investigações relevantes em MEDLINE, na Prensa de Highwire e na ativação de pesquisa do Google, do ano 2000 para 2013. Dos quatro tipos de mediadores inflamatórios do plasma, as moléculas de adesão de célula e os marcadores inflamatórios sistêmicos foram os mais sensíveis, sendo que cytokines foram mais sensíveis e substâncias de protease foram menos sensíveis na indicação da presença de EAC. A proteína C reativa hipersensível, o homocysteine, a molécula de adesão intercelular 1, a molécula de adesão de célula vascular 1, a matriz metalloproteinase-9, o nervo inibidor de tecido de metalloproteinase-2, o fator de crescimento endothelial vascular e os níveis de neopterin foram mais altos nos pacientes com EAC do que nos controles sem EAC. A porcentagem de granulocytes foi mais alta no grupo EAC, comparando-se com os indivíduos com a artéria coronária normal. A determinação de genótipo de enzima do angiotensin-conversão utilizando-se a técnica de reação em cadeia da polimerase revelou que o genótipo DD foi prevalecente na EAC, ma...

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Increased platelet activity in patients with isolated coronary artery ectasia

Abstract: In conclusion, we have shown for the first time that patients with isolated CAE have raised levels of plasma P-selectin, beta-TG and PF4 compared with control participants with angiographically normal coronary arteries, suggesting increased platelet activation in patients with CAE.

Cited by 38 publications

References 27 publications

Coronary Artery Ectasia in Atherosclerotic Coronary Artery Disease, Inflammatory Disorders, and Sickle Cell Disease

Coronary Artery Ectasia in Atherosclerotic Coronary Artery Disease, Inflammatory Disorders, and Sickle Cell Disease

Mean platelet volume in patients with coronary artery ectasia

Inflammatory mediators of coronary artery ectasia

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