ABSTRACT
ABSTRACT
Objective Infarct-related artery (IRA) patency yields a better outcome in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). Red cell distribution width (RDW) emerges as a marker of adverse cardiovascular events and mortality in STEMI. Therefore, we aimed to assess the relationship between IRA patency and RDW value on admission in patients with STEMI undergoing primary PCI. Methods A total of 564 patients with STEMI undergoing primary PCI were recruited in this study. According to thrombolysis in myocardial infarction (TIMI) flow grade in the IRA before PCI, the study population was divided into two groups as TIMI 0 or 1 group (occluded IRA, n = 398) and TIMI 2 or 3 group (patent IRA, n = 166). Results RDW was significantly higher in the occluded IRA group (15.1 ± 1.7 versus 13.4 ± 1.3, p < 0.001) as compared to the patent IRA group. White blood cell (WBC) count, platelet count, creatine kinase-myocardial band (CK-MB) and troponin-I levels were also significantly higher in the occluded IRA group (p < 0.05). Moreover, RDW showed positive correlations with troponin-I (r = 0.397, p < 0.001), CK-MB (r = 0.344, p < 0.001) and WBC (r = 0.219, p < 0.001). In multivariate regression analysis, RDW (OR: 0.483, 95% CI: 0.412–0.567, p < 0.001) and WBC count were significantly and independently associated with IRA patency. Conclusions Our findings suggested that RDW value and WBC count on admission were independent predictors of IRA patency in patients with STEMI. As RDW is an easily available, simple and cheap biomarker, it can be used in daily practice as a novel predictor for IRA patency.
Introduction
Although, there were several improvements both in the diagnosis and treatment of atherosclerotic coronary artery disease (CAD), it remains to be the most common cause of death worldwide.[1] As an emergent form of CAD, ST-elevation myocardial infarction (STEMI) is also significantly associated with increased morbidity and mortality.[1] It is already known that immediate restoration of coronary flow in an infarct-related artery (IRA) improves ventricular performance and decreases the incidence of mechanical and electrical complications and also mortality.[2,3] From the view of the pathophysiology of atherosclerosis, inflammation and oxidative stress are landmark mechanisms in plaque formation, progression and acute rupture with superimposed thrombus formation.[4–6]
Red cell distribution width (RDW) is a measurement of variability and size of erythrocytes; that can be easily measured during routine hemogram.[7] RDW is proposed to be an indirect marker of inflammation and oxidative stress.[8,9] Furthermore, increased RDW was shown to be associated with the presence, severity and complexity of CAD and poor clinical outcomes, and higher RDW was also associated with increased mortality in patients with STEMI undergoing primary percutaneous coronary intervention (PCI).[10–12]
In the present study, we hypothesized that STEMI patients with occluded IRA may have higher levels of ischemia that give rise to higher levels of inflammation and oxidative stress that can be reflected by higher levels of RDW. Thus, we aimed to investigate whether RDW level on admission is associated with IRA patency in patients with STEMI undergoing primary PCI.
Methods
Study population
After excluding the patients with a history of coronary artery by-pass graft, previous PCI, admission 12 h after the onset of symptoms, severe valve disease, renal or hepatic dysfunction, acute or chronic infectious or inflammatory disease, anemia or other hematological disorders and presence of malignancy, we retrospectively enrolled 564 patients who underwent coronary angiography with a diagnosis of STEMI between February 2013 and July 2014 in this single-center study. STEMI is a clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent electrocardiographic ST elevation and subsequent release of biomarkers of myocardial necrosis, such as troponin I and creatine kinase-myocardial band (CK-MB). Diagnostic ST elevation in the absence of left ventricular hypertrophy or left bundle-branch block was described as new ST elevation was measured from the J point in ≥2 contiguous leads with at least 2 mm (0.2 mV) in leads V2–V3 or at least 1 mm (0.1 mV) in other contiguous chest leads or the limb leads.[13] Baseline clinical demographic and angiographic characteristics were reviewed. Hypertension was defined as documentation of a systolic blood pressure of ≥140 mmHg and/or a diastolic blood pressure of ≥90 mmHg in at least two measurements or active use of any antihypertensive agent. Diabetes mellitus was defined as a fasting plasma glucose level over 7 mmol/L or glucose level over 11 mmol/L at any measurement or active use of an antidiabetic agent. Smoking was defined as current smoking. Permission for the study was obtained from the institutional review board and ethics committee of our hospital (date: 07/06/2015 number: 332).
The standard Judkins technique was used for visualization of the coronary arteries. Each coronary artery was displayed in at least two different plane images. Angiograms and the thrombolysis in myocardial infarction (TIMI) scale were assessed by at least two experienced interventional cardiologists who were blinded to the clinical data of participants. Before the coronary intervention, TIMI flow grade was documented for each patient. The patients were categorized as patients with an absence of early IRA patency (TIMI 0 or 1 group) and patients with the presence of early IRA patency (TIMI 2 or 3 group).[14,15]
Laboratory measurements
The blood samples were collected from the antecubital vein by an atraumatic puncture before the coronary angiography, and Coulter Counter LH Series (Beckman Coulter Ireland Inc. Mervue, Galway, Ireland) was used for complete blood count analysis. Routinely, venous blood was collected in a tube containing K3 EDTA (ethylenediaminetetraacetic acid) for the measurement of hematologic indices in all patients undergoing the coronary angiography. Total cholesterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides, fasting glucose, creatinine and other biochemical markers were evaluated using an automated chemistry analyzer (Abbott Laboratories, Abbott Park, IL). Troponin I levels were measured with a Beckman Image 800 analyzer.
Statistical analysis
The analyses were carried out using the SPSS 20 (SPSS Inc., Chicago, IL). To test the distribution pattern, the Kolmogorov–Smirnov method was used. Continuous data were presented as mean ± SD; categorical variables were given as percentages. Categorical variables were compared with Chi-square test and continuous variables were compared with Student’s t-test. Pearson correlation analysis was performed to define the correlation between RDW, and white blood cell (WBC), troponin I and creatine kinase-myocardial band (CK-MB). Multivariate, stepwise backward conditional logistic regression analysis was used to detect the independent predictors of IRA patency and all significant parameters in the univariate analysis were selected in the multivariate model. A p value of <0.05 was considered statistically significant.
Results
A total of 564 patients with the first STEMI who had been treated with primary PCI of a single IRA were recruited to the present study. On the admission angiography, 398 (71%) patients had TIMI 0 or 1 flow grade (occluded IRA group) and 166 (29%) patients had TIMI 2 or 3 flow grade (patent IRA group) in the IRA. Baseline and angiographic characteristics, and prehospital medications of the study groups are demonstrated in Table 1. There were no significant differences in terms of age, male gender, rate of hypertension, diabetes mellitus, smoking, systolic blood pressure, heart rate and prehospital medications between the groups. Culprit artery for STEMI also did not differ between the groups.
Table 1. Baseline and angiographic characteristics of patients (n = 564).
The laboratory test results are also shown in Table 2. RDW and WBC were significantly higher in the occluded IRA group as compared to the patent IRA group (15.1 ± 1.7 versus 13.4 ± 1.3, p < 0.001 and 10.1 ± 2.8 versus 9.4 ± 2.7, p = 0.007, respectively). Platelet count, troponin-I and CK-MB levels were significantly higher in the occluded IRA group (p = 0.014, p = 0.002, p = 0.008, respectively). Furthermore, there was a significant inverse correlation between RDW and TIMI flow grade. Namely, RDW was highest in the TIMI 0 group and lowest in the TIMI 3 group (TIMI 0: 15.1 ± 1.7%, TIMI 1: 14.8 ± 1.8%, TIMI 2: 13.5 ± 1.5% and TIMI 3: 13.2 ± 1.2%, p < 0.001, respectively) as demonstrated in Figure 1 (the box plot). In Pearson correlation analysis, RDW showed significant but moderate positive correlations with troponin-I (r = 0.397, p < 0.001), CK-MB (r = 0.344, p < 0.001) and WBC (r = 0.219, p < 0.001) as illustrated in Figure 2.
Table 2. Laboratory parameters of patients.
When univariate logistic regression analysis was performed to define possible independent predictors of IRA patency; RDW, WBC and platelet counts, troponin-I and CK-MB remained significant and were included in the multivariate analysis. In the multivariate logistic regression analysis, RDW (OR: 0.483, 95% CI: 0.412–0.567, p < 0.001) and WBC count (OR: 0.900, 95% CI: 0.832–0.974, p = 0.009) remained as negative independent predictors of IRA patency (Table 3).
Published online:
14 December 2015Figure 1. The box plot graphics showing comparison of red cell distribution width (RDW) values according to thrombolysis in myocardial infarction (TIMI) flow rates.
![]({"type":"image","src":"/na101/home/literatum/publisher/tandf/journals/content/icdv20/2016/icdv20.v050.i02/14017431.2015.1119303/20160218/images/medium/icdv_a_1119303_f0001_b.jpg"})
Figure 1. The box plot graphics showing comparison of red cell distribution width (RDW) values according to thrombolysis in myocardial infarction (TIMI) flow rates.
Published online:
14 December 2015Figure 2. Correlation analysis representing a significant positive correlation of RDW with troponin-I, CK-MB and WBC counts.
![]({"type":"image","src":"/na101/home/literatum/publisher/tandf/journals/content/icdv20/2016/icdv20.v050.i02/14017431.2015.1119303/20160218/images/medium/icdv_a_1119303_f0002_c.jpg"})
Figure 2. Correlation analysis representing a significant positive correlation of RDW with troponin-I, CK-MB and WBC counts.
Table 3. Univariate and multivariate logistic regression analysis showing the predictors for the patency in infarct related artery.
Discussion
The main findings of the present study were as follows: (i) RDW was significantly increased in patients with STEMI who had an occluded IRA before primary PCI; (ii) RDW was also positively correlated with troponin-I, CK-MB and WBC counts showing its association with myocardial damage and inflammation; (iii) furthermore, RDW was demonstrated as an independent predictor of IRA patency in patients with STEMI.
Although, there has been a significant improvement in both acute and long-term prognosis of patients with STEMI in parallel with the increased use of secondary prevention treatments and modern reperfusion therapy like primary PCI,[16] the mortality and morbidity are still relatively high in patients with STEMI for the current age.[16,17] Coronary blood flow in IRA plays a major role in both occurrences of clinical symptoms and prognosis of patients with STEMI. The presence of patent IRA before mechanical reperfusion was demonstrated to be an independent predictor of better outcomes in STEMI.[18] Stone et al. showed that patients with an occluded IRA had increased mortality, higher incidence of heart failure and worse clinical outcome at 6-month follow-up compared to patients with a patent IRA.[2] Similarly, in another study, patients with TIMI flow grade 0 or 1 (occluded IRA) before mechanical reperfusion (primary PCI) had higher incidences of in-hospital mortality and other major adverse cardiovascular events.[19] Rakowski et al. showed that early IRA patency at baseline angiography was associated with better reperfusion and improved 1-year clinical outcomes including lower rates of death and stent thrombosis.[15] For these reasons, early restoration of IRA patency is critical for better prognosis. Although, the main pathophysiological mechanism of STEMI is plaque rupture that is the first and leading event in the development of STEMI, some triggering mechanisms remain to be unclear. Proliferating megakaryocytes and relative thrombocytosis are consequences of an ongoing inflammatory response that contribute to a pro-thrombotic state in STEMI. In STEMI group, patients with occluded IRA have larger infarcts and higher inflammatory and oxidative burden than patients with patent IRA.[20,21] As a component of the routine blood cell count, RDW is a quantitative measure of variability in the size of circulating erythrocytes, and RDW emerges as a novel potential inflammatory marker for cardiovascular diseases.[22,23] Lippi et al. demonstrated that there was a strong, graded and independent association between RDW and direct inflammatory markers including hs-CRP and erythrocyte sedimentation rate.[24] Lappe et al. also reported that RDW was associated with increased mortality in patients with coronary artery disease.[25] In a recent study, Uyarel et al. reported that higher RDW levels in patients with STEMI undergoing primary PCI were associated with increased risk of in-hospital and long-term cardiovascular mortality.[26] Additionally, Nabais et al. showed that an elevated RDW level was independently related to mortality and recurrent myocardial infarction within six months after acute coronary syndromes.[27] Furthermore, Polat and colleagues recently demonstrated that high RDW was an independent predictor of high GRACE score, and it was associated with in-hospital mortality in acute coronary syndrome.[28] Therefore, we hypothesized that RDW in association with inflammatory state might play a role in IRA patency in STEMI. Our study findings confirmed that RDW was significantly higher in patients with an occluded IRA and RDW was an independent predictor of better coronary TIMI flow in IRA. Also in our study, RDW positively correlated with WBC counts that support its role in an inflammatory condition. The possible explanation for the association of RDW with adverse outcomes in cardiovascular disease is the presence of the underlying low-grade proinflammatory state. Inflammation may cause changes in red blood cell maturation by deforming the red cell membrane, leading to increased RDW. Therefore, increased RDW value might reflect an underlying inflammation, which would result in an increased risk of cardiovascular diseases. We also observed that RDW was positively correlated with troponin-I and CK-MB, which are reliable indicators of the extent of myocardial infarction. According to our findings, it can be concluded that RDW may be directly associated with IRA patency. Further studies are required to clarify whether increased RDW is a cause or result of occluded IRA.
Study limitations
The primary limitation of our study was that RDW is increased in conditions of ineffective red blood cell production (such as iron deficiency, B12 or folic acid deficiency, anemia of chronic disease and hemoglobinopathies), increased red cell destruction (such as hemolysis), or after blood transfusion. Due to the cross-sectional retrospective design of our study, such a missingness data including iron, vitamin B12 and folate could not be avoided. Secondly, using a spot laboratory value rather than follow-up values was the another limitation of this study. We did not evaluate other cytokines or inflammatory markers, such as C-reactive protein and fibrinogen.
Conclusion
Our study findings demonstrated that RDW was an independent negative predictor of IRA patency in patients with STEMI, who underwent primary PCI. Higher RDW was associated with lower TIMI flow grade on admission coronary angiogram. Moreover, RDW was significantly and positively correlated with troponin-I, CK-MB and WBC counts. Evaluation of RDW as a part of complete blood count can be useful in daily clinical practice because it is relatively easy, cheap and fast method that is routinely used in clinical practice.
Baseline infarct-related artery | |||
|---|---|---|---|
| Parameters | Occluded group(n = 398) | Patent group(n = 166) | p Value |
| Age, years | 57 ± 10 | 56 ± 10 | 0.340 |
| Male, n (%) | 310 (78) | 123 (74) | 0.331 |
| Hypertension, n (%) | 211 (53) | 81 (49) | 0.361 |
| Diabetes mellitus, n (%) | 83 (21) | 34 (20) | 0.921 |
| Smoking, n (%) | 219 (55) | 98 (59) | 0.382 |
| Systolic blood pressure (mmHg) | 132 ± 24 | 135 ± 21 | 0.338 |
| Heart rate (bpm) | 78 ± 15 | 76 ± 13 | 0.130 |
| Pre-hospital medications, n (%) | |||
| RAS blocker | 107 (27) | 43 (26) | 0.810 |
| β-Blocker | 85 (21) | 36 (22) | 0.931 |
| Calcium channel blocker | 52 (13) | 19 (11) | 0.597 |
| Statin | 35 (9) | 15 (9) | 0.927 |
| Aspirin | 76 (19) | 40 (24) | 0.181 |
| Oral anti-diabetic drug | 77 (19) | 30 (18) | 0.725 |
| Infarct-related artery, n (%) | 0.401 | ||
| LAD | 172 (43) | 65 (39) | |
| LCX | 83 (21) | 43 (26) | |
| RCA | 143 (36) | 58 (35) | |
| TIMI flow in IRA, n (%) | – | ||
| 0 | 359 (90) | – | |
| I | 39 (10) | – | |
| II | – | 65 (39) | |
| III | – | 101 (61) | |
Data were given as mean ± SD or %. IRA: infarct-related artery; LAD: left anterior descending; LCX: left circumflex; RAS: renin–angiotensin system; RCA: right coronary artery; TIMI: thrombolysis in myocardial infarction.
Infarct-related artery | |||
|---|---|---|---|
| Parameters | Occluded group(n = 398) | Patent group(n = 166) | p Value |
| Hemoglobin, g/L | 147 ± 15 | 146 ± 13 | 0.697 |
| RDW (%) | 15.1 ± 1.7 | 13.4 ± 1.3 | <0.001 |
| Platelet, 109/L | 280 ± 85 | 262 ± 68 | 0.014 |
| White blood cell, 109/L | 10.1 ± 2.8 | 9.4 ± 2.7 | 0.007 |
| Creatinine, μmol/L | 82 ± 17 | 79 ± 19 | 0.148 |
| Glucose, mmol/L | 8.6 ± 2.5 | 8.3 ± 2.7 | 0.112 |
| Total cholesterol, mmol/L | 10.4 ± 2.4 | 10.7 ± 2.6 | 0.138 |
| HDL-cholesterol, mmol/L | 2.1 ± 0.5 | 2.2 ± 0.5 | 0.173 |
| LDL-cholesterol, mmol/L | 6.5 ± 2.2 | 6.6 ± 2.4 | 0.475 |
| Triglyceride, mmol/L | 8.6 ± 3.1 | 9.3 ± 3.5 | 0.188 |
| Troponin-I, μg/L | 2.5 ± 4.9 | 1.1 ± 2.6 | 0.002 |
| CK-MB, U/L | 47.1 ± 27 | 40.4 ± 26 | 0.008 |
Data are given as mean ± SD. CK-MB: creatine kinase-myocardial band; HDL: high-density lipoprotein; LDL: low-density lipoprotein; RDW: red cell distribution width.
Univariate | Multivariate | |||
|---|---|---|---|---|
| Variables | Odds ratio (95% CI) | p | Odds ratio (95% CI) | p |
| RDW | 0.506 (0.438–0.585) | <0.001 | 0.483 (0.412–0.567) | <0.001 |
| White blood cell | 0.912 (0.853–0.975) | 0.007 | 0.900 (0.832–0.974) | 0.009 |
| Platelet | 0.997 (0.995–0.999) | 0.015 | 0.998 (0.995–1.001) | 0.130 |
| Troponin I | 0.912 (0.857–0.971) | 0.004 | 1.022 (0.955–1.095) | 0.526 |
| CK-MB | 0.991 (0.983–0.998) | 0.009 | 1.003 (0.994–1.011) | 0.537 |
CI: confidence interval; CK-MB: creatine kinase-myocardial band; RDW: red cell distribution width.
Disclosure ststement
The authors declare no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
Funding information
The authors received no financial support for the research, authorship, and/or publication of this article.
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