Document Detail

Platelet/lymphocyte ratio and risk of in-hospital mortality in patients with ST-elevated myocardial infarction.
Jump to Full Text
MedLine Citation:
PMID:  24751474     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Background Platelet-to-lymphocyte ratio (PLR) is a new prognostic marker in coronary artery disease. We aimed to evaluate the relationship between PLR and in-hospital mortality in patients with ST-elevated acute myocardial infarction (AMI). Material and Methods The present study included 636 patients with ST-elevated AMI. The study population was divided into tertiles based on their admission PLR. Patients having values in the third tertile was defined as the high PLR group (n=212) and those having values in the lower 2 tertiles were defined as the low PLR group (n=424). Results Risk factors of coronary artery disease and treatments administered during the in-hospital period were similar between the groups. Male patient ratio was found to be lower in the high PLR group (73% vs. 82.8%, p=0.004). In-hospital mortality was increased in the high PLR group when compared to the low PLR group (12.7% vs. 5.9%, p=0.004). The PLR >144 was found to be an independent predictor of in-hospital cardiovascular mortality (HR: 2.16, 95% CI: 1.16-4.0, p=0.014). Conclusions This study showed that PLR is an independent predictor of cardiovascular mortality in patients with ST-elevated AMI.
Authors:
Ahmet Temiz; Emine Gazi; Omer Güngör; Ahmet Barutçu; Burak Altun; Adem Bekler; Emine Binnetoğlu; Hacer Sen; Fahri Güneş; Sabri Gazi
Related Documents :
20009314 - Wellen's syndrome: an ominous ekg pattern.
24509324 - Plasma factor xi and xii activity in patients with slow coronary flow.
21821784 - Intermittent hypobaric hypoxia improves post-ischemic recovery of myocardial contractil...
16777514 - Abnormal intra-qrs potentials associated with percutaneous transluminal coronary angiog...
20428454 - Role of nitric oxide in regulating cardiac electrophysiology.
8800274 - A brief review of epidemiological studies on ischemic heart disease in japan.
Publication Detail:
Type:  Journal Article     Date:  2014-04-22
Journal Detail:
Title:  Medical science monitor : international medical journal of experimental and clinical research     Volume:  20     ISSN:  1643-3750     ISO Abbreviation:  Med. Sci. Monit.     Publication Date:  2014  
Date Detail:
Created Date:  2014-04-22     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9609063     Medline TA:  Med Sci Monit     Country:  United States    
Other Details:
Languages:  eng     Pagination:  660-5     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): Med Sci Monit
Journal ID (iso-abbrev): Med. Sci. Monit
Journal ID (publisher-id): Medical Science Monitor
ISSN: 1234-1010
ISSN: 1643-3750
Publisher: International Scientific Literature, Inc.
Article Information
Download PDF
© Med Sci Monit, 2014
License:
Received Day: 06 Month: 12 Year: 2013
Accepted Day: 23 Month: 1 Year: 2014
collection publication date: Year: 2014
Electronic publication date: Day: 22 Month: 4 Year: 2014
Volume: 20First Page: 660 Last Page: 665
PubMed Id: 24751474
ID: 3999159
DOI: 10.12659/MSM.890152
Publisher Id: 890152

Platelet/lymphocyte ratio and risk of in-hospital mortality in patients with ST-elevated myocardial infarction
Ahmet Temiz1ADF
Emine Gazi1ABCDE
Ömer Güngör2BEF
Ahmet Barutçu1BCF
Burak Altun1CEF
Adem Bekler1BD
Emine Binnetoğlu3CF
Hacer Şen3CD
Fahri Güneş3EF
Sabri Gazi2BC
1Department of Cardiology, Çanakkale Onsekiz Mart University, Çanakkale, Turkey
2Departmentof Cardiology, Çanakkale State Hospital, Çanakkalee, Turkey
3Departmentof Internal Medicine, Çanakkale Onsekiz Mart University, Çanakkale, Turkey
Correspondence: Corresponding Author: Emine Gazi, e-mail: eordulu@hotmail.com
AStudy Design
BData Collection
CStatistical Analysis
DData Interpretation
EManuscript Preparation
FLiterature Search
GFunds Collection

Background

Acute myocardial infarction (AMI) results from total coronary artery occlusion, usually due to thrombus formation on complicated atherosclerotic plaque [1]. The patients with AMI have higher mortality rates, especially during the first 30 days [2]. Platelets play an important role in development, destabilization, and rupture of the atherosclerotic plaque, as well as in formation of platelet-fibrin plug at the complicated atherosclerotic plaque [3,4]. Platelet count is associated with increased risk of AMI and short- and long-term mortality after AMI [58]. Lymphocytes play a dominant role in chronic inflammation of atherosclerosis, and lower lymphocyte count is associated with increased cardiovascular risk and mortality in AMI [9,10]. Platelet/lymphocyte ratio (PLR) has been reported as a novel marker of long-term mortality in patients with non-ST-elevated AMI [11].

In the present study, we tested the hypothesis that PLR is associated with in-hospital cardiovascular mortality in patients with ST-elevated AMI (STEMI).


Material and Methods
Study population

Records of patients with AMI who were admitted to the coronary care unit between January 2009 and November 2011 were evaluated retrospectively. We consecutively evaluated 645 patients who were diagnosed with STEMI and excluded 4 patients with intracranial hemorrhage because of the intra-venous thrombolytic treatment (streptokinase, tissue plasminogen activator, or tenecteplase) and 5 patients without eligible laboratory results. A total of 636 patients were enrolled into this study. A diagnosis of STEMI was defined as >30 minutes of continuous typical chest pain and ST-segment elevation ≥2 mm in 2 contiguous electrocardiography leads within 12 hours of symptom onset or within up to 18 hours if there was evidence of continuing ischemia or hemodynamic instability. From medical records, we obtained demographic information, cardiovascular history and risk factors for coronary artery disease (CAD), and treatment received during the in-hospital period. Patients who had been treated with antihypertensive drugs or those whose baseline blood pressure exceeded 140/90 mmHg were diagnosed with hypertension (HT). Diabetes mellitus (DM) was defined as fasting blood sugar level above 126 mg/dl or the use of anti-diabetic medications. The admission glomerular filtration rate (GFR) was estimated by the simplified MDRD (Modification of Diet in Renal Disease) equation [12]. Renal failure was defined as a glomerular filtration rate (GFR) <60 ml/min/m2.

Cardiovascular events during the in-hospital period were investigated from patient records. Ventricular tachycardia or ventricular fibrillation were defined at least 24 hours after the beginning of the symptoms, advanced heart failure was defined as Killip classification ≥2, and cardiovascular death was defined as death due to AMI, heart failure, or arrhythmia. The mean follow-up period was 7 days.

Analysis of blood samples

Complete blood counts and biochemical values were evaluated retrospectively from blood samples obtained by antecubital vein puncture upon admission to the emergency department. Total and differential leukocyte counts were determined with the BeckmanCoulterLH 780device (Beckman Coulter Ireland Inc. Mervue, Galway, Ireland). Other biochemical measurements and electrolyte levels were determined by standard laboratory methods.

Statistical analysis

The study population was divided into tertiles based on admission PLR values. The high PLR group (n=212) was defined as having values in the highest tertile (PLR >144), and the low PLR group (n=424) was defined as having values in the lower 2 tertiles (PLR ≤144).

Quantitative variables are expressed as the mean value ±SD or median (interquartile range), and qualitative variables are expressed as percentages (%). All measurements were evaluated with the Kolmogorov-Smirnov test. A comparison of parametric values between high and low PLR groups was performed using the t test or the Mann-Whitney U-test. Categorical variables were compared by the likelihood-ratio χ2 test or Fisher’s exact test. A backward stepwise multivariate logistic regression analysis, which included variables with p<0.1, was performed to identify independent predictors of in-hospital cardiovascular mortality. Age ≥70, female sex, renal failure (GFR <60 ml/min/m2), time of chest pain, not receiving thrombolytic treatment, NLR>4.1, and PLR>144 were entered into the model. A p value <0.05 was considered statistically significant. All statistical studies were carried out with the SPSS program (version 17.0, SPSS, Chicago, IL, USA).


Results

A total of 636 patients (505 men and 131 women) were enrolled into the present study. No differences were found between the groups regarding thrombolytic and other treatments received during the in-hospital period. Tobacco use, HT, DM, and CHD history were not significantly different between the groups. Table 1 shows the clinical characteristics of the groups. The rate of male patients ratio was lower in the high PLR group (73% vs. 82.8%, p=0.004). The patients in the high PLR group were older (63.7±12.1 vs. 61.4±12.0, p=0.022). Baseline platelet and neutrophil levels were significantly higher in the high PLR group than in the low PLR group (9.6 [3.2–25.1]×103/mm3vs. 7.3 [2.2–18.4]×103/mm3, p<0.001; 245 [121–779]×103/mm3vs. 215 [43–419]×103/mm3, p=0.001), whereas the baseline lymphocyte level was significantly lower in the high PLR group than in the low PLR group (1, 2 [0.4–3.7]×103/mm3vs. 2.4 [0.6–9.1]×103/mm3, p=0.001). Neutrophil-to-lymphocyte ratio (NLR) was higher in high PLR group (p<0.001) (Table 2).

Cardiovascular events are shown in Table 3. The high PLR group had a significantly higher incidence of in-hospital cardiovascular mortality than the low PLR group (12.7% vs. 5.9%, p=0.003). Advanced heart failure (Killip class ≥2) was more frequent in patients with high PLR values (18.9% vs. 12.3%, p=0.026).

Independent predictors of in-hospital cardiovascular mortality were determined by backward stepwise multivariate logistic regression. Chest pain duration more than 6 hours, female sex, not receiving thrombolytic treatment, renal failure, age ≥70 years, NLR >4.1, and PLR >144 were found to be associated with increased in-hospital cardiovascular mortality in a logistic regression analysis (Table 4). PLR >144 was found to be an independent predictor of in-hospital cardiovascular mortality in multivariate analyses (hazard ratio: 2.16, 95% confidence interval: 1.16–4.0, p=0.014). Table 5 shows other independent predictors of cardiovascular mortality. In ROC curve analyses, an PLR value of 144 was determined as an effective cut-off point in STEMI of in-hospital mortality, with a sensitivity of 51% and a specificity of 69% (area under the curve=0.59, 95% confidence interval 0.50–0.67) (Figure 1).


Discussion

In this study we show that high PLR at admission to hospital is an independent predictor of early cardiovascular mortality in patients with AMI. Older age, renal failure, and not treated with thrombolytic treatment are other independent predictors of mortality. To our knowledge this is the first study to investigate the relationship between PLR and mortality in STEMI.

Atherosclerotic CAD is still the most common cause of mortality and morbidity in developed countries. Inflammation plays a pivotal role in formation and complication of atherosclerosis [13]. Activated platelets precipitate to produce inflammatory substances from endothelial cells and leucocytes that cause monocyte adhesion and transmigration, and thereby increase the inflammatory process and progression of atherosclerotic plaque [14,15]. Furthermore, these activated adhesion molecules and chemokines increase the activation of leucocytes, and produce reactive oxygen molecules and matrix metalloproteinase that cause plaque destabilization in atherosclerotic plaque [16]. AMI usually occurs as a result of coronary artery occlusion due to complication of an atherosclerotic plaque. Platelets play a dominant role in pathogenesis of acute coronary syndromes by formation of platelet-fibrin complexes [17]. Platelet count was found to be associated with development of AMI and presence of CAD [5,17]. Gary et al. concluded that higher platelet volume may change blood viscosity and increase inflammation [18]. Healy et al. reported that expression of CD-49 and plasma myeloid protein in platelets is increased in patients with ST-elevated MI [19]. Davi et al. showed that higher platelet activity is related to higher rates of cardiovascular events [4]. In addition, it was found that platelet count is associated with short- and long-term mortality in patients with ST-elevated and non-ST-elevated AMI, and unstable angina pectoris [2022]. Nikolsky et al. showed a relationship between platelet count and mortality in patients with recurrent AMI in the first year after primary percutaneous intervention [23]. In addition, fibrinogen levels and platelet counts are positively correlated and related to inflammation in AMI patients. These findings suggest that platelets are one of the most important components of CAD and cardiovascular events.

Lymphocytes are an important part of chronic inflammation in the atherosclerotic process [9]. In AMI, lymphocytes infiltrate to the ischemic and reperfused myocardium and express interleukin-10, which may play a significant role in transmigration of mononuclear cells, and induce the expression of tissue inhibitor of metalloproteinase-1 [24]. Recent studies showed that higher PLR is related to presence of CAD and is correlated with C-reactive protein and fibrinogen levels [18]. Azab et al. reported that PLR above 170 is an independent predictor of long-term mortality in non-ST-elevated AMI patients [11]. In our study, we found that high PLR (above 144) is an independent predictor of in-hospital mortality in patients with STEMI who received thrombolytic treatment.

Prevalence of AMI is increased and prognosis worsens with aging. Complications of AMI, including heart failure, shock, and ventricular rupture, are more frequent in older AMI patients [25,26]. In the present study, patients in the high PLR group were older than in the low PLR group. Additionally, advanced heart failure was more frequent in the high PLR group. Neutrophil count was increased in the high PLR group, suggesting high inflammatory activity. Neutrophils may cause plaque rupture as a result of stimulating the release of proteolytic enzymes, superoxide radicals, and arachidonic acid derivates, and exacerbates the inflammatory condition. Microvascular obstruction due to neutrophil-platelet plug, vasoconstriction due to thromboxanes, and vasoactive molecules may cause no-reflow and cause further myocardial injury. These high inflammatory processes appear to be responsible for high rates of heart failure and mortality. NLR was higher in the high PLR group and was strongly related to cardiovascular mortality in our population, in line with results of previous studies. In multivariate analyses, we found that NLR was not an independent predictor and that PLR is an independent predictor of mortality.

The present study has some limitations. First, this was a retrospective study. Patient long-term survival and cardiac conditions could not be assessed because the patient records and the coronary angiography results of patients were not known. Anti-platelet treatment before AMI is an important factor affecting in-hospital mortality [27], but our data were not able to demonstrate previous antiplatelet use.


Conclusions

AMI is the most important cause of mortality (especially in the first month) and morbidity worldwide. This study showed that high PLR is an independent predictor of in-hospital cardiovascular mortality in patients with STEMI. Complete blood count analysis is a routine and inexpensive method that may be useful for the identification of high-risk patients.

PLR and other inflammatory markers and clinical findings might be helpful in identifying high-risk patients and treatment strategies.


Notes

fn8-medscimonit-20-660Conflict of Interest

There are no conflicts of interest.

fn9-medscimonit-20-660Source of support: Departmental sources

References
1. Davies MJ,Thomas AC. Plaque fissuring: the cause of acute myocardial infarction, sudden ischaemic death, and crescendo anginaBr Heart JYear: 198553363733885978
2. Fauci AS,Braundwald E,Kasper DL,et al. 17th edMcGraw-Hill: chapter of disorders of the cardiovascular system (Part 9)Harrison’s principle of internal medicineYear: 2008151416
3. Falk E. Pathogenesis of atherosclerosisJ Am Coll CardiolYear: 200647712
4. Davi G,Patrono C. Platelet activation and atherothrombosisN Engl J MedYear: 200735724829418077812
5. Klovaite J,Benn M,Yazdanyar S,Nordestgaard BG. High platelet volume and increased risk of myocardial infarction: 39,531 participants from the general populationJ Thromb HaemostYear: 20119495620942852
6. Ly HQ,Kirtane AJ,Murphy SA,et al. Association of platelet counts on presentation and clinical outcomes in ST-elevation myocardial infarction (from the TIMI Trials)Am J CardiolYear: 2006981516784909
7. Kilicli-Camur N,Demirtunç R,Konuralp C,et al. Could mean platelet volume be a predictive marker for acute myocardial infarction?Med Sci MonitYear: 2005118CR3879216049381
8. Glud T,Schmidt EB,Kristensen SD,Arnfred T. Platelet number and volume during myocardial infarction in relation to infarct sizeActa Med ScandYear: 198622040153812027
9. Horne BD,Anderson JL,John JM,et al. Which white blood cell subtypes predict increased cardiovascular risk?J Am Coll CardiolYear: 20054516384315893180
10. Frangogiannis NG,Smith CW,Entman ML. The inflammatory response in myocardial infarctionCardiovasc ResYear: 200253314711744011
11. Azab B,Shah N,Akerman M,McGinn JT Jr. Value of platelet/lymphocyte ratio as a predictor of all-cause mortality after non-ST-elevation myocardial infarctionJ Thromb ThrombolysisYear: 2012343263422466812
12. Levey AS,Bosch JP,Lewis JB,et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study GroupAnn Intern MedYear: 19991304617010075613
13. Libby P,Ridker PM,Maseri A. Inflammation and AtherosclerosisCirculationYear: 2002105911354311877368
14. Gawaz M,Langer H,May AE. Platelets in inflammation and atherogenesisJ Clin InvestYear: 200511533788416322783
15. Lindemann S,Krämer B,Seizer P,Gawaz M. Platelets, inflammation and atherosclerosisJ Thromb HaemostYear: 20075Suppl 12031117635728
16. Libby P. Current concepts of the pathogenesis of the acute coronary syndromesCirculationYear: 20011043657211457759
17. Falk E. Pathogenesis of atherosclerosisJ Am Coll CardiolYear: 2006478 Suppl712
18. Gary T,Pichler M,Belaj K,et al. Platelet-to-lymphocyte ratio: a novel marker for critical limb ischemia in peripheral arterial occlusive disease patientsPLoS OneYear: 2013867688
19. Healy AM,Pickard MD,Pradhan AD,et al. Platelet expression profiling and clinical validation of myeloid-related protein-14 as a novel determinant of cardiovascular eventsCirculationYear: 200611322788416682612
20. Ly HQ,Kirtane AJ,Murphy SA,et al. Association of platelet counts on presentation and clinical outcomes in ST-elevation myocardial infarction (from the TIMI Trials)Am J CardiolYear: 2006981516784909
21. Mueller C,Neumann FJ,Hochholzer W,et al. The impact of platelet count on mortality in unstable angina/non-ST-segment elevation myocardial infarctionAm Heart JYear: 20061511214 e1–7. 16781221
22. Slavka G,Perkmann T,Haslacher H,et al. Mean platelet volume may represent a predictive parameter for overall vascular mortality and ischemic heart diseaseArterioscler Thromb Vasc BiolYear: 20113112151821330610
23. Nikolsky E,Grines CL,Cox DA,et al. Impact of baseline platelet count in patients undergoing primary percutaneous coronary intervention in acute myocardial infarction (from the CADILLAC trial)Am J CardiolYear: 20079910556117437727
24. Frangogiannis NG,Smith CW,Entman ML. The inflammatory response in myocardial infarctionCardiovasc ResYear: 200253314711744011
25. Gurwitz JH,Col NF,Avorn J. The exclusion of the elderly and women from clinical trials in acute myocardial infarctionJAMAYear: 19922681417221512909
26. Rich MW,Bosner MS,Chung MK,et al. Is age an independent predictor of early and late mortality in patients with acute myocardial infarction?Am J MedYear: 1992927131731513
27. Akpek M,Kaya MG,Lam YY,et al. Relation of neutrophil/lymphocyte ratio to coronary flow to in-hospital major cardiac events in patients with ST elevated myocardial infarction undergoing primary coronary interventionAm J CardiolYear: 201211056212722608360

Article Categories:
  • Clinical Research

Keywords: MeSH Keywords Myocardial Infarction, Hospital Mortality, Platelet/Lymphocyte Ratio.

Previous Document:  Assessment of the acute effects of different pep levels on respiratory pattern and operational volum...
Next Document:  Second order sliding mode control for a quadrotor UAV.