1999 - 2000 : Süleyman Demirel University, ISPARTA

2002 - 2006 : Atatürk Training and Research Hospital, İZMİR

2006 - 2010 : Private Ege Sağlık Hospital, İZMİR

2010 -          : Private Tınaztepe Hospital, İZMİR

DOES "SMOKER'S PARADOX" EXIST IN CLOPIDOGREL-TREATED TURKISH PATIENTS WITH ACUTE CORONARY SYNDROME

By

Edem, E (Edem, Efe) [1] ; Kirdök, AH (Kirdok, Ali Hikmet) [1] ; Kinay, AO (Kinay, Ahmet Ozan) [1] ; Tekin, ÜI (Tekin, Umit Ilker) [1] ; Tas, S (Tas, Sedat) [2] ; Alpaslan, E (Alpaslan, Erkan) [2] ; Pabuccu, MT (Pabuccu, Mustafa Turker) [2] ; Akdeniz, B (Akdeniz, Bahri) [2]

 (provided by Clarivate) 

Source

PLATELETS

Volume

27

Issue

3

Page

240-244

DOI

10.3109/09537104.2015.1083544

Published

APR 2 2016

Indexed

2016-04-27

Document Type

Article

Abstract

Previously conducted studies revealed that smoking enhanced the efficacy of clopidogrel by increasing formation of the active metabolite (AM) from the prodrug through induction of the cytochrome CYP1A2. The expression of cytochrome enzymes depends on genotype and no data exists in literature conducted in Turkish patients comparing the clopidogrel responsiveness between active smokers and non-active smokers treated with clopidogrel. In this study, our aim was to investigate the clopidogrel responsiveness in clopidogrel-treated Turkish acute coronary syndrome (ACS) patients according to their smoking status. We retrospectively enrolled 258 patients who were hospitalized due to ACS. Clinical variables of the patients, especially smoking status were recorded. Clopidogrel resistance was evaluated by using adenosine diphosphate (ADP) induced platelet aggregometry. Clopidogrel resistance was detected as a change in maximal aggregation <= 20% from baseline. A total of 139 patients were active smokers while 12 were former smokers. 107 patients did not have a history of smoking. Ten of the smokers were hyporesponsive to clopidogrel, whereas 36 of non-smokers were hyporesponsive to clopidogrel (p < 0.001). Receiver-operating characteristic curve analysis demonstrated that Au-min value >612.5 predicted the clopidogrel resistance with a sensitivity of 60% (OR: 100.65, %95 CI = 19.996-506.615 p < 0.001). Results of this study demonstrated that ADP responses were lower in smokers receiving clopidogrel and aspirin than in non-smokers receiving the same drug regimen. This finding indicates that smoking was related to an enhanced clopidogrel responsiveness in Turkish patients hospitalized due to ACS, suggesting that "smoker's paradox" probably exists in Turkish ACS patients.

Keywords

Author Keywords

2-oxo-clopidogreldrug resistanceclopidogrelAcute coronary syndrome
 

Keywords Plus

CIGARETTE-SMOKINGGENE POLYMORPHISMSCYP1A2RELATEDNESSPOPULATIONDISEASE

PREDICTIVE VALUE OF PLATELET-TO-LYMPHOCYTE RATIO IN SEVERE DEGENERATIVE AORTIC VALVE STENOSIS

By

Edem, E (Edem, Efe) [1] ; Reyhanoglu, H (Reyhanoglu, Hasan) [2] ; Küçükukur, M (Kucukukur, Murat) [4] ; Kirdök, AH (Kirdok, Ali Hikmet) [1] ; Kinay, AO (Kinay, Ahmet Ozan) [1] ; Tekin, ÜI (Tekin, Umit Ilker) [1] ; Özcan, K (Ozcan, Kaan) [2] ; Ertürk, M (Erturk, Murat) [2] ; Sentürk, Ç (Senturk, Cagin) [3] , [7] ; Kirilmaz, B (Kirilmaz, Bahadir) [5] ; 

 (provided by Clarivate) 

Source

JOURNAL OF RESEARCH IN MEDICAL SCIENCES

Volume

21

DOI

10.4103/1735-1995.192509

Article Number

93

Published

2016

Indexed

2017-03-24

Document Type

Article

Abstract

Background: Aortic valve stenosis (AVS) is the most common cause of left ventricular outflow obstruction, and its prevalence among elderly patients causes a major public health burden. Recently, platelet-to-lymphocyte ratio (PLR) has been recognized as a novel prognostic biomarker that offers information about both aggregation and inflammation pathways. Since PLR indicates inflammation, we hypothesized that PLR may be associated with the severity of AVS due to chronic inflammation pathways that cause stiffness and calcification of the aortic valve. Materials and Methods: We retrospectively enrolled 117 patients with severe degenerative AVS, who underwent aortic valve replacement and 117 control patients in our clinic. PLR was defined as the absolute platelet count divided by the absolute lymphocyte count. Severe AVS was defined as calcification and sclerosis of the valve with a mean pressure gradient of > 40 mmHg. Results: PLR was 197.03 +/- 49.61 in the AVS group and 144.9 +/- 40.35 in the control group, which indicated a statistically significant difference (P < 0.001). A receiver operating characteristic (ROC) curve analysis demonstrated that PLR values over 188 predicted the severity of aortic stenosis with a sensitivity of 87% and a specificity of 70% (95% confidence interval = 0.734- 0.882; P < 0.001; area under ROC curve: 0.808). Conclusion: We suggest that the level of PLR elevation is related to the severity of degenerative AVS, and PLR should be used to monitor patients' inflammatory responses and the efficacy of treatment, which will lead us to more closely monitor this high-risk population to detect severe degenerative AVS at an early stage.

Keywords

Author Keywords

Aortic valve stenosisbiomarkersplatelets
 

Keywords Plus

CORONARY-ARTERY-DISEASEPROGNOSTIC MARKERASSOCIATIONINFLAMMATIONPREVALENCE