Clin Chem Lab Med 2015; 53(7): e153–e155
Letter to the Editor Yuzi Zhou, Qian Zhang, Lirong Yan, Yishi Li and Lu Hua*
Association between red cell distribution width and myocardial infarction in rheumatoid arthritis DOI 10.1515/cclm-2014-0628 Received June 15, 2014; accepted September 16, 2014; previously published online December 9, 2014
Keywords: myocardial infarction; red cell distribution width; rheumatoid arthritis. To the Editor, Red blood cell distribution width (RDW) reflects volume variations in erythrocytes and is an index of the size heterogeneity [1]. This marker has been demonstrated to be strongly associated with C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) in a large cohort of unselected outpatients [2]. Recently, a cross-sectional study on 8513 multi-ethnic adults without pre-existing cardiovascular disease (CVD) demonstrated RDW, independent of other traditional risk factors, was found to be associated with CVD mortality [3], and another article reported that higher RDW was an independent predictor of 12-month major adverse cardiac events after acute myocardial infarction (AMI) [4]. Ten years ago, a review highlighted on the relationship about inflammation and MI in respect of molecular and cellular mechanisms. Rheumatoid arthritis (RA) is a chronic inflammatory disease with increased incidence of CVD morbidity and mortality [5]. Systemic inflammation in RA may accelerate the atherogenic process by accentuating the known plaque formation pathways [6]. However, Radovits et al. failed to find clear evidence supporting *Corresponding author: Lu Hua, Key Laboratory of Clinical Trial Research in Cardiovascular Drugs, Ministry of Health, State Key Laboratory of Cardiovascular Diseases, FuWai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, P.R. China, E-mail: [email protected] Yuzi Zhou, Qian Zhang, Lirong Yan and Yishi Li: Key Laboratory of Clinical Trial Research in Cardiovascular Drugs, Ministry of Health, State Key Laboratory of Cardiovascular Diseases, FuWai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, P.R. China
the concept that disease activity in RA patients carries higher risk of MI [7]. A letter by Lee et al. demonstrated that RDW was associated with inflammatory markers in RA patients [8]. However, associations between RDW and MI in RA patients have not been fully investigated. As such, we conducted a retrospective study including consecutive coronary heart disease (CHD) patients with RA in Fuwai Cardiovascular Disease Hospital from January 2010 to December 2012. The coronary disease was confirmed by coronary angiography, and the RA diagnosis was in accord with the 1987 American College of Rheumatology criteria for the diagnosis of RA [9]. Subjects were screened for any of the following exclusive criteria: other inflammatory diseases, decompensated heart failure, liver and kidney dysfunction, malignance or missing information. In total 106 patients were included in the final sample. The RA disease duration ranged from 1 to 50 years, and the percentage of patients with prior disease modifying antirheumatic drug (DMARDs), glucocorticoid or biological agents was 16.5% (15/91). A total of 46 RA patients developed MI. The diagnosis of MI was made according to the presence of ischemia symptom, ECG changes, and elevated troponin I levels. In total 60 patients free of MI were included in the control group. This study was approved by the Institutional Review Boards of Fu Wai Hospital. Venous blood was drawn by venipuncture from the antecubital vein between 6 am and 8 am after 12 h of overnight fasting on the second day in hospital. Routine hematological testing was performed on the entire study population using identical laboratory instrumentation (Sysmex XE-2100, Sysmex Inc, Japan). Comparisons of parameters between two groups were made by unpaired Student’s t-test, MannWhitney U-test or χ2-test (for dichotomous variables) as appropriate. The following variables were considered as possible predictors for MI: age, gender, body mass index (BMI), hypertension, hypercholesterolemia, diabetes mellitus, smoking, creatinine, uric acid (UA), ESR, CRP, high-sensitivity C reactive protein (Hs-CRP), RDW, cholesterol, triglyceride, high-density lipoprotein (HDL) and low-density lipoprotein (LDL). Variables mentioned above were evaluated by univariable logistic regression
e154 Zhou et al.: RDW and MI in RA and variables that had a p-value of
Letter to the Editor Yuzi Zhou, Qian Zhang, Lirong Yan, Yishi Li and Lu Hua*
Association between red cell distribution width and myocardial infarction in rheumatoid arthritis DOI 10.1515/cclm-2014-0628 Received June 15, 2014; accepted September 16, 2014; previously published online December 9, 2014
Keywords: myocardial infarction; red cell distribution width; rheumatoid arthritis. To the Editor, Red blood cell distribution width (RDW) reflects volume variations in erythrocytes and is an index of the size heterogeneity [1]. This marker has been demonstrated to be strongly associated with C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) in a large cohort of unselected outpatients [2]. Recently, a cross-sectional study on 8513 multi-ethnic adults without pre-existing cardiovascular disease (CVD) demonstrated RDW, independent of other traditional risk factors, was found to be associated with CVD mortality [3], and another article reported that higher RDW was an independent predictor of 12-month major adverse cardiac events after acute myocardial infarction (AMI) [4]. Ten years ago, a review highlighted on the relationship about inflammation and MI in respect of molecular and cellular mechanisms. Rheumatoid arthritis (RA) is a chronic inflammatory disease with increased incidence of CVD morbidity and mortality [5]. Systemic inflammation in RA may accelerate the atherogenic process by accentuating the known plaque formation pathways [6]. However, Radovits et al. failed to find clear evidence supporting *Corresponding author: Lu Hua, Key Laboratory of Clinical Trial Research in Cardiovascular Drugs, Ministry of Health, State Key Laboratory of Cardiovascular Diseases, FuWai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing, 100037, P.R. China, E-mail: [email protected] Yuzi Zhou, Qian Zhang, Lirong Yan and Yishi Li: Key Laboratory of Clinical Trial Research in Cardiovascular Drugs, Ministry of Health, State Key Laboratory of Cardiovascular Diseases, FuWai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, P.R. China
the concept that disease activity in RA patients carries higher risk of MI [7]. A letter by Lee et al. demonstrated that RDW was associated with inflammatory markers in RA patients [8]. However, associations between RDW and MI in RA patients have not been fully investigated. As such, we conducted a retrospective study including consecutive coronary heart disease (CHD) patients with RA in Fuwai Cardiovascular Disease Hospital from January 2010 to December 2012. The coronary disease was confirmed by coronary angiography, and the RA diagnosis was in accord with the 1987 American College of Rheumatology criteria for the diagnosis of RA [9]. Subjects were screened for any of the following exclusive criteria: other inflammatory diseases, decompensated heart failure, liver and kidney dysfunction, malignance or missing information. In total 106 patients were included in the final sample. The RA disease duration ranged from 1 to 50 years, and the percentage of patients with prior disease modifying antirheumatic drug (DMARDs), glucocorticoid or biological agents was 16.5% (15/91). A total of 46 RA patients developed MI. The diagnosis of MI was made according to the presence of ischemia symptom, ECG changes, and elevated troponin I levels. In total 60 patients free of MI were included in the control group. This study was approved by the Institutional Review Boards of Fu Wai Hospital. Venous blood was drawn by venipuncture from the antecubital vein between 6 am and 8 am after 12 h of overnight fasting on the second day in hospital. Routine hematological testing was performed on the entire study population using identical laboratory instrumentation (Sysmex XE-2100, Sysmex Inc, Japan). Comparisons of parameters between two groups were made by unpaired Student’s t-test, MannWhitney U-test or χ2-test (for dichotomous variables) as appropriate. The following variables were considered as possible predictors for MI: age, gender, body mass index (BMI), hypertension, hypercholesterolemia, diabetes mellitus, smoking, creatinine, uric acid (UA), ESR, CRP, high-sensitivity C reactive protein (Hs-CRP), RDW, cholesterol, triglyceride, high-density lipoprotein (HDL) and low-density lipoprotein (LDL). Variables mentioned above were evaluated by univariable logistic regression
e154 Zhou et al.: RDW and MI in RA and variables that had a p-value of
