Neutrophil to lymphocyte ratio (NLR) has been proposed as a marker of cardiovascular risk. The potential relation between NLR and periprocedural myocardial damage after percutaneous coronary intervention (PCI) is unclear. We enrolled 502 consecutive patients with stable coronary artery disease undergoing elective PCI. Blood samples were drawn in all patients at baseline, 6 hours, and 24 hours after PCI for complete blood cell count and cardiac biomarkers (creatine kinase-MB and troponin T [Tn-T]) assessment. NLR was calculated as the ratio between the absolute number of neutrophil over the absolute number of lymphocyte. Periprocedural myocardial infarction (PMI) was defined according to the 2012 universal definition of myocardial infarction. In the overall population, a significant postprocedural increase in NLR was observed (3.255 [2.763 to 3.995] at baseline, 4.430 [3.390 to 6.020] at 6 hours, 4.720 [3.940 to 5.750] at 24 hours, p <0.0001). PMI occurred in 33 patients (6.6%). Baseline NLR was similar in patients with and without PMI (3.250 [2.820 to 3.885] vs 3.260 [2.750 to 4.000], p = 0.898); however, patients who developed PMI showed significantly higher NLR both at 6 hours (5.750 [4.360 to 9.095] vs 4.370 [3.370 to 5.950], p <0.001) and 24 hours (5.180 [4.440 to 8.065] vs 4.670 [3.920 to 5.710], p = 0.003). Among patients who developed PMI, periprocedural NLR increase showed a moderate positive correlation with both creatine kinase-MB (rho = 0.377, p = 0.031) and troponin T increase (rho = 0.506, p = 0.003). In conclusion, preprocedural NLR values do not impact on the occurrence of PMI during elective PCI; however, PCI procedures induce a significant increase in NLR that seems to be proportional to the magnitude of periprocedural myocardial damage.
Neutrophil to lymphocyte ratio (NLR), an inexpensive parameter easily acquirable from complete blood count, has been recently proposed as a marker of cardiovascular risk, able to predict clinical outcomes in patients with both stable coronary artery disease (CAD) and acute coronary syndromes, including those treated with percutaneous coronary intervention (PCI). In this study, we tested the hypothesis of an association between high NLR and periprocedural myocardial necrosis in patients undergoing elective PCI.
Methods
In this observational study, we prospectively enrolled a total of 502 consecutive patients with clinically stable CAD undergoing elective PCI from February 2013 to November 2014. Exclusion criteria were acute coronary syndromes with ST-elevation, severe left ventricular dysfunction (ejection fraction <30%), chronic total occlusion, lesions with extensive calcifications requiring rotational atherectomy, bypass surgery in the previous 3 months, severe pulmonary disease, neoplasm, therapy with corticosteroids within the previous year, chronic inflammatory disease, and active infection at time of intervention. A local ethical committee approved the study, and all patients signed written informed consent for participation and data collection. All patients were on chronic aspirin treatment and received either 600-mg clopidogrel loading dose (at least 6 hours before intervention) or were on therapy with clopidogrel 75 mg/day for at least 5 days. Procedural anticoagulation was achieved by administration of unfractionated heparin (100 U/kg) in all patients. Technicalities of the procedure, including the use of glycoprotein IIb/IIIa inhibitors, were left to the operator’s discretion. Procedural success was defined as a reduction in percent diameter stenosis to below 30% and the presence of Thrombolysis In Myocardial Infarction flow grade 3 in the main vessel and all side branches ≥2 mm in diameter. Blood samples were drawn in all patients at pre-PCI (baseline), 6 hours, and 24 hours after intervention for complete blood cell count and cardiac biomarkers assessment. At all time points, NLR was derived for all patients using the whole blood cell count considering for each patient the ratio obtained from the absolute number of neutrophil over the absolute number of lymphocyte. For whole blood cell count, fluorescent flow cytometry and hydrodynamic focusing technologies were used (XT-4000i hematology analyzer Sysmex; Mississauga, Ontario, Canada). Delta NLR was defined as the maximal variation of NLR values from baseline to post-PCI. Cardiac biomarkers creatine kinase-MB [CK-MB] and troponin T [Tn-T] levels were obtained using the Access 2 immunochemiluminometric assay (Beckman Coulter, Fullerton, California). Periprocedural myocardial infarction (PMI) was defined according to the 2012 universal definition of myocardial infarction. Briefly, in patients with normal (<99th percentile upper reference limit) cardiac biomarkers baseline concentration were required elevations of CK-MB or Tn-T >5 × 99th percentile upper reference limit occurring within 48 hours of the procedure plus either evidence of prolonged ischemia (≥20 minutes) or ischemic ST changes or new pathological Q waves or angiographic evidence of a flow limiting complication or imaging evidence of new loss of viable myocardium or new regional wall motion abnormality. If the baseline cardiac biomarkers values were elevated and stable or falling, then an increase of >20% was considered for the diagnosis of PMI. Delta CK-MB and delta Tn-T were defined as the maximal variation of each cardiac biomarker values from baseline to post-PCI.
Categorical variables are reported as frequencies and percentages. Continuous variables are reported as mean ± SD or as median (lower and upper quartiles). Comparisons between categorical variables were evaluated using the Fisher’s exact test or the Pearson’s chi-square test, as appropriate. Comparisons between continuous variables were performed using the Student t test or Mann–Whitney U test, as appropriate. NLR values at different time points were compared using the Friedman test. Correction for multiple comparisons was applied where appropriate. A mixed-design repeated-measures analysis of variance followed by pairwise comparisons was used to detect changes in NLR over time in the different study groups. The Pearson test was used to assess correlations between normally distributed variables, and the Spearman test was used to assess correlations between nonnormally distributed variables. Statistical analysis was performed using Stata/IC, version 12.0 (STATA Corp., College Station, Texas), and p values <0.05 (2 tailed) were considered significant.
Results
PMI occurred in 33 patients (6.6%). Clinical and procedural characteristics of the overall population and of patients with and without PMI are reported in Tables 1 and 2 , respectively. Patients who developed PMI were more frequently treated for bifurcation lesions. No other differences between the 2 groups were detected.
| Variable | All patients (n=502) | Periprocedural MI | p value | |
|---|---|---|---|---|
| Yes (n=33) | No (n=469) | |||
| Mean age (years) | 67.0 ± 9.8 | 67.5 ± 11.7 | 66.9 ± 9.6 | 0.724 |
| Men | 393 (78%) | 29 (88%) | 364 (78%) | 0.196 |
| Body mass index (kg/m 2 ) | 27.8 ± 4.1 | 26.8 ± 4.5 | 27.9 ± 4.0 | 0.207 |
| Hypertension ∗ | 409 (81%) | 26 (79%) | 382 (82%) | 0.681 |
| Dyslipidemia † | 357 (71%) | 23 (70%) | 334 (71%) | 0.852 |
| Diabetes Mellitus | 208 (41%) | 11 (33%) | 197 (42%) | 0.328 |
| Smoker | 100 (20%) | 6 (18%) | 94 (20%) | 0.796 |
| LV ejection fraction (%) | 55.4 ± 7.9 | 56.6 ± 6.0 | 55.3 ± 8.0 | 0.382 |
| Prior myocardial infarction | 188 (37%) | 14 (42%) | 174 (37%) | 0.541 |
| Prior percutaneous coronary intervention | 209 (42%) | 11 (33%) | 198 (42%) | 0.312 |
| Prior coronary bypass | 31 (6%) | 2 (6%) | 29 (6%) | 1.000 |
| Chronic kidney disease | 90 (18%) | 4 (12%) | 86 (18%) | 0.484 |
| Clinical presentation | 0.569 | |||
| Stable angina pectoris | 331 (66%) | 20 (61%) | 311 (66%) | |
| NSTE-ACS | 171 (34%) | 13 (39%) | 158 (34%) | |
| N° of narrowed coronary arteries | 1.76 ± 0.79 | 1.79 ± 0.78 | 1.75 ± 0.79 | 0.817 |
∗ Systolic blood pressure: >140 mm Hg and/or diastolic blood pressure >90 mm Hg or current antihypertensive treatment.
| Variable | All patients (n=502) | Periprocedural MI | p value | |
|---|---|---|---|---|
| Yes (n=33) | No (n=469) | |||
| Multivessel PCI | 96 (19%) | 4 (12%) | 92 (20%) | 0.611 |
| Lesion Type | 0.117 | |||
| A | 91 (15%) | 3 (8%) | 88 (15%) | |
| B1 | 231 (38%) | 10 (27%) | 221 (39%) | |
| B2 | 191 (32%) | 18 (49%) | 173 (31%) | |
| C | 89 (15%) | 6 (16%) | 83 (15%) | |
| Bifurcation Lesion | 44 (7%) | 7 (19%) | 37 (7%) | 0.013 |
| No. of stent implanted | 1.41 ± 0.91 | 1.55 ± 0.83 | 1.40 ± 0.91 | 0.382 |
| Total stent length (mm) | 18.79 ± 8.32 | 19.82 ± 8.16 | 18.71 ± 8.34 | 0.460 |
| Stent diameter (mm) | 2.94 ± 1.31 | 2.94 ± 0.87 | 2.94 ± 1.35 | 0.972 |
| Glycoprotein IIb/IIIa inhibitors | 38 (6%) | 3 (8%) | 35 (6%) | 0.501 |
| Procedural success | 499 (99%) | 32 (97%) | 494 (99%) | 0.176 |
| Neutrophil count | ||||
| Pre-PCI (cells/microl) | 3962 ± 1392 | 4090 ± 1265 | 3952 ± 1401 | 0.582 |
| 6 hours (cells/microl) | 5240 ± 2104 | 6583 ± 2765 | 5144 ± 2018 | <0.001 |
| 24 hours (cells/microl) | 5391 ± 1759 | 6591 ± 1977 | 5305 ± 1713 | <0.001 |
| Lymphocyte count | ||||
| Pre-PCI (cells/microl) | 1143 ± 324 | 1214 ± 373 | 1138 ± 320 | 0.196 |
| 6 hours (cells/microl) | 1104 ± 346 | 1054 ± 397 | 1107 ± 342 | 0.390 |
| 24 hours (cells/microl) | 1118 ± 368 | 1168 ± 438 | 1115 ± 363 | 0.425 |
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