Impaired coronary flow after primary percutaneous coronary intervention (PPCI) is associated with short- and long-term morbidity and mortality in patients with acute ST-segment elevation myocardial infarction (STEMI). Recent studies have demonstrated that platelet-to-lymphocyte ratio (PLR) is associated with adverse cardiovascular outcomes. The aim of this study was to assess the relation between admission PLR and angiographic reflow after PPCI. A total of 520 patients with acute STEMI (age 60 ± 13 years; 74% men) occurring within 12 hours of the onset of symptoms who underwent PPCI were enrolled. The PLR and other laboratory parameters were measured before PPCI. The patients were divided into 2 groups based on the postintervention Thrombolysis in Myocardial Infarction (TIMI) flow grade: normal-reflow group (defined as postintervention TIMI grade 3 flow) and none-reflow group (consisted of both patients with angiographic no-reflow defined as postintervention TIMI grades 0 to 1 flow and slow flow defined as postintervention TIMI grade 2 flow). There were 117 patients (22.5%) in the none-reflow group (age 68 ± 13 years and 77% men) and 403 patients in the normal-reflow group (age 58 ± 12 years and 63% men). The none-reflow group had significantly higher PLR compared with the normal-reflow group (219 ± 79 vs 115 ± 59, p <0.001). In logistic regression analysis, PLR (odds ratio 1.818, 95% confidence interval 1.713 to 1.980, p <0.001) and total stent length (OR 1.052, confidence interval 1.019 to 1.086, p = 0.002) were independent predictors of none-reflow after PPCI. In conclusion, preintervention PLR is a strong and independent predictor of slow flow/no-reflow after PPCI in patients with acute STEMI.
Early reperfusion after coronary occlusion in patients with ST-segment elevation myocardial infarction (STEMI) is associated with an improved prognosis. Nevertheless, impaired angiographic reflow is still a challenging major issue in the management of the patients with STEMI who underwent primary percutaneous coronary intervention (PPCI). It is well known that impaired coronary reflow is associated with larger infarct size, worse functional recovery, higher incidence of complications, and short- and long-term mortality in acute STEMI. Several responsible mechanisms for impaired coronary reflow were identified in experimental models, including extravascular compression, microvascular vasoconstriction, and a platelet/leukocyte capillary plugging. The platelet-to-lymphocyte ratio (PLR) has recently been investigated as a new predictor for major adverse cardiovascular outcomes. It has been found that higher PLR is associated with poor coronary collateral development in stable coronary artery disease and long-term mortality after non-STEMI. The aim of our study was to investigate the usefulness of PLR in predicting angiographic reflow after PPCI in acute STEMI.
Methods
From June 2012 to September 2013, a total of 537 consecutive patients with STEMI occurring within 12 hours of the onset of symptoms who underwent PPCI in our institution were enrolled into the study. Medical treatment was decided in 3 patients because of distal lesion at thin vessel. In addition, 14 patients were excluded because of urgent coronary artery bypass grafting surgery because of failed PPCI or coronary anatomy, which is not amenable to PPCI. Finally, 520 patients were enrolled into our study.
STEMI was defined as prolonged chest pain for >30 minutes with ST-segment elevation ≥1 mm in ≥2 contiguous electrocardiographic leads, or with a new left bundle-branch block, and more than twofold increase in serum cardiac markers.
Exclusion criteria included cardiogenic shock on admission, active infections, systemic inflammatory disease history, known malignancy, hematologic disorders, liver disease, and renal failure.
The patients were divided into 2 groups based on the postintervention Thrombolysis in Myocardial Infarction (TIMI) flow grade: normal-reflow group and none-reflow group. Normal-reflow was defined as postintervention TIMI grade 3 flow. None-reflow group consisted of both patients with angiographic no-reflow (defined as postintervention TIMI grades 0 to 1 flow) and slow flow (defined as postintervention TIMI grade 2 flow).
The study protocol was approved by the local ethics committee of the Ankara Education and Research Hospital, and each patient provided written informed consent.
All patients were orally pretreated with 300 mg aspirin and 600 mg clopidogrel at the time of diagnosis before the intervention. All patients received 5000 U intravenous bolus of unfractionated heparin before transportation to the PPCI or just in the catheterization laboratory at 40–70 U/kg, targeting an activated clotting time of 200–250 seconds during the procedure. Baseline coronary angiography was performed using standard techniques (Siemens Axiom Artis zee 2011; Siemens Healthcare, Erlangen, Germany). All PPCI procedures were performed with standard femoral approach with a 6-French guiding catheter (Launcher; Medtronic, Minneapolis, MN). After administration of unfractionated heparin conventional wire crossing, direct stenting was implanted whenever possible; in the remaining cases, balloon predilatation was carried out. The use of balloon predilatation or postdilatation, the type of stents (bare metal or drug eluting), and the use of tirofiban and thrombus aspiration were left to the operator’s discretion. The TIMI flow grade was evaluated by 2 independent experienced interventional cardiologists using quantitative cardiovascular angiographic software (Axiom Sensis XP; Siemens, Munich, Germany). The syntax score (SXscore) for each patient was calculated by scoring all coronary lesions with a diameter stenosis of at least 50%, in vessels at least 1.5 mm, using the SXscore algorithm, and is available on the SXscore Web site (available at http://www.syntaxscore.com ).
In all patients, blood samples were drawn on admission in the emergency room. Common blood counting parameters stored in citrate-based anticoagulated tubes were measured by Sysmex K-1000 autoanalyzer within 5 minutes of sampling. Glucose, creatinine, and lipid profile were determined by the standard methods. Cardiac enzymes and high-sensitivity C-reactive protein (Hs-CRP) were also measured in all patients. PLR was calculated as the ratio of platelet count to lymphocyte count.
Transthoracic echocardiography was measured for all patients within 48 hours after PPCI (Vivid 3; GE Medical System, Horten, Norway). Left ventricular ejection fraction (LVEF) was the measurement using the modified Simpson method.
Continuous variables were tested for normal distribution by the Kolmogorov-Smirnov test. We report continuous data as mean and SD. Continuous variables were compared with Student t test between groups. Categorical variables were summarized as percentages and compared with the chi-square test. The receiver operating characteristics (ROC) curve was used to demonstrate the sensitivity and specificity of PLR, optimal cut-off value for predicting postintervention angiographic none-reflow. Univariate logistic regression was used to identify independent predictors of none-reflow. After performing univariate analysis, significantly obtained variables (age, male gender, diabetes, hemoglobin, platelet count, creatinine, PLR, Hs-CRP, Killip class ≥II, and total stent length) were used in multivariate logistic regression analysis. p Value <0.05 was considered as significant. Model discrimination was defined using area under the ROC curve, and calibration was assessed using the Hosmer-Lemeshow statistic. All statistical analyses were performed with the SPSS version 18 (SPSS, Inc., Chicago, IL).
Results
There were 117 patients (22.5%) in the none-reflow group (mean age 68 ± 13 and 77% men) and 403 patients in the normal-reflow group (mean age 58 ± 12 and 63% men).
Baseline clinical characteristics of study patients are listed in Table 1 . The patients with the none-reflow group were significantly older with higher prevalence of male gender, diabetes mellitus, and Killip class ≥II on admission but lower frequency of smoking and lower LVEF compared with those in the normal-reflow group. No significant differences in previous medications and time from pain to intervention were observed between groups. Laboratory findings are summarized in Table 2 . The PLR was significantly higher in the none-reflow group than in the normal-reflow group (219 ± 79 vs 115 ± 59, p <0.001) ( Table 2 and Figure 1 ). The angiographic and interventional characteristics of the patients are presented in Table 3 . Complete ST-segment resolution defined as ≥70% decrement of cumulative ST-segment elevation on the electrocardiogram at 60 minutes of postintervention period was 13.3% and 85.6% in the none-reflow group and normal-reflow group, respectively (p <0.001).
| Variable | Reflow | p Value | |
|---|---|---|---|
| Normal (n = 403) | None (n = 117) | ||
| Age (years) | 58 ± 12 | 68 ± 13 | <0.001 |
| Male gender | 311 (63%) | 74 (77%) | 0.002 |
| Hypertension | 153 (38%) | 53 (45%) | 0.153 |
| Diabetes mellitus | 114 (28%) | 50 (42%) | 0.003 |
| Smoking | 224 (55%) | 30 (26%) | <0.001 |
| Hyperlipidemia | 168 (41%) | 44 (38%) | 0.753 |
| Family history of coronary artery disease | 98 (24%) | 21 (18%) | 0.149 |
| Prior stroke | 7 (1.7%) | 5 (4.3%) | 0.159 |
| Prior myocardial infarction | 10 (2.5%) | 3 (2.6%) | 0.960 |
| Prior coronary artery bypass grafting | 15 (3.7%) | 2 (1.7%) | 0.281 |
| Systolic blood pressure (mm Hg) | 126 ± 24 | 129 ± 36 | 0.618 |
| Diastolic blood pressure (mm Hg) | 77 ± 13 | 78 ± 13 | 0.508 |
| Left ventricular ejection fraction (%) | 47 ± 9 | 40 ± 10 | <0.001 |
| Killip class ≥II on admission | 17 (4.2%) | 26 (22.2%) | <0.001 |
| Symptom onset to intervention (hours) | 3.5 ± 2.0 | 3.6 ± 2.1 | 0.421 |
| <6 | 322 (82.4%) | 90 (76.9%) | 0.184 |
| ≥6 | 71 (17.6%) | 27 (23.1%) | |
| Previous medications | |||
| Aspirin use | 141 (35%) | 36 (31%) | 0.470 |
| Beta blocker use | 100 (25%) | 30 (26%) | 0.908 |
| Renin angiotensin aldosterone antagonists use | 170 (42%) | 51 (44%) | 0.770 |
| Statin use | 89 (22%) | 25 (21%) | 0.854 |
| Variable | Reflow | p Value | |
|---|---|---|---|
| Normal (n = 403) | None (n = 117) | ||
| Serum glucose (mg/dl) | 137 ± 74 | 159 ± 79 | 0.006 |
| High sensitivity C-reactive protein (mg/dl) | 6.92 ± 4.42 | 8.53 ± 3.92 | 0.007 |
| Peak troponin-T (ng/ml) | 1337 (130–10000) | 2886 (290–10000) | <0.001 |
| Peak creatinine kinase-myocardial band (U/L) | 107 ± 49 | 138 ± 57 | 0.013 |
| Total cholesterol (mg/dl) | 190 ± 43 | 182 ± 49 | 0.111 |
| High density lipoprotein (mg/dl) | 40 ± 9 | 42 ± 11 | 0.104 |
| Low density lipoprotein (mg/dl) | 119 ± 38 | 114 ± 42 | 0.224 |
| Triglyceride (mg/dl) | 144 (37–638) | 124 (39–624) | 0.151 |
| Creatinine (mg/dl) | 1.08 ± 0.24 | 1.19 ± 0.38 | <0.001 |
| Glomerular filtration rate (ml/min/1.73 m 2 ) | 73 ± 19 | 61 ± 19 | <0.001 |
| White blood cell count (×10 9 /L) | 11.68 ± 3.46 | 11.89 ± 3.21 | 0.522 |
| Platelet count (×10 9 /L) | 237 ± 63 | 254 ± 87 | 0.018 |
| Lymphocyte count (×10 9 /L) | 2.5 ± 1.31 | 1.52 ± 0.86 | <0.001 |
| Monocyte count (×10 9 /L) | 0.76 ± 0.29 | 0.74 ± 0.38 | 0.597 |
| Hemoglobin (g/dL) | 14.30 ± 1.74 | 13.46 ± 2.12 | <0.001 |
| Mean platelet volume (fL) | 8.71 ± 1.03 | 8.8 ± 1.0 | 0.416 |
| Platelet-to-lymphocyte ratio | 115 ± 59 | 219 ± 79 | <0.001 |
| Variable | Reflow | p Value | |
|---|---|---|---|
| Normal (n = 403) | None (n = 117) | ||
| Anterior infarct location | 191 (47.8%) | 65 (52.1%) | 0.782 |
| Infarct-related coronary artery | 0.003 | ||
| Left main | 0 (0%) | 1 (0.9%) | |
| Left anterior descending | 166 (41.2%) | 68 (58.1%) | |
| Left circumflex | 69 (17.1%) | 10 (8.5%) | |
| Right | 168 (41.6%) | 38 (32.5%) | |
| Initial occluded infarct artery | 234 (58.1%) | 94 (80.3%) | <0.001 |
| Total stent length (mm) | 22.07 ± 9.36 | 26.27 ± 13.6 | <0.001 |
| Stent diameter (mm) | 3.19 ± 0.4 | 3.15 ± 0.39 | 0.395 |
| Multivessel disease | 194 (48.1%) | 72 (61.5%) | 0.011 |
| Chronic total occlusion | 52 (13.3%) | 23 (21.7%) | 0.026 |
| Number of used stent | 1.31 ± 0.57 | 1.42 ± 0.61 | 0.070 |
| Direct stenting | 213 (52.9%) | 28 (23.9%) | <0.001 |
| Syntax score | 14.4 ± 7.8 | 20.3 ± 9.5 | <0.001 |
| Tirofiban use | 140 (37.8%) | 41 (38%) | 0.981 |
| Use of thrombus aspiration | 20 (5.1%) | 8 (7.2%) | 0.762 |
Univariate and multivariate logistic regression analyses of the association between the angiographic none-reflow and multiple parameters are listed in Table 4 . In multivariate analyses, PLR (odds ratio 1.818, 95% confidence interval [CI] 1.713 to 1.980, p <0.001) and total stent length (odds ratio 1.052, 95% CI 1.019 to 1.086, p = 0.002) were independent predictors of angiographic none-reflow. Hosmer-Lemeshow test showed that the model fit the data well (p = 0.44). Area under the ROC curve showed that the model has good discrimination capability (area under the curve: 0.883, 95% CI 0.826 to 0.939, p <0.001). Some of the possible interactions (platelet-PLR, age-PLR, Hs-CRP-PLR, gender-PLR, creatinine-PLR, and diabetes-PLR) were also assessed; however, they found to be nonsignificant.
| Variable | Univariate | Multivariate | ||
|---|---|---|---|---|
| Odds Ratio (95% CI) | p Value | Odds Ratio (95% CI) | p Value | |
| Age | 1.065 (1.046–1.084) | <0.001 | 1.002 (0.962–1.044) | 0.917 |
| Male gender | 1.964 (1.263–3.056) | 0.003 | 0.796 (0.288–2.200) | 0.661 |
| Killip class ≥II on admission | 1.487 (1.387–1.559) | <0.001 | 1.070 (0.951–1.197) | 0.397 |
| Diabetes mellitus | 1.923 (1.254–2.950) | 0.003 | 1.505 (0.528–4.293) | 0.445 |
| Hemoglobin | 0.794 (0.712–0.886) | <0.001 | 0.954 (0.735–1.237) | 0.724 |
| Platelet count | 1.003 (1.001–1.006) | 0.020 | 0.994 (0.088–1.107) | 0.257 |
| Creatinine | 3.291 (1.647–6.576) | 0.001 | 1.039 (0.236–4.566) | 0.959 |
| Low density lipoprotein | 0.996 (0.991–1.002) | 0.224 | ||
| High density lipoprotein | 1.018 (0.996–1.040) | 0.105 | ||
| Triglyceride | 0.998 (0.995–1.001) | 0.152 | ||
| Hemoglobin A1c | 1.107 (0.984–1.244) | 0.090 | ||
| High sensitivity C-reactive protein | 1.089 (1.022–1.162) | 0.009 | 1.028 (0.926–1.141) | 0.603 |
| Platelet-to-lymphocyte ratio | 1.013 (1.011–1.017) | <0.001 | 1.818 (1.713–1.980) | <0.001 |
| Stent length | 1.034 (1.014–1.054) | 0.001 | 1.052 (1.019–1.086) | 0.002 |
| Stent diameter | 0.783 (0.446–1.376) | 0.395 | ||
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