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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 6  |  Issue : 4  |  Page : 123-126

Mean platelet volume in acute coronary syndrome: Diagnostic implications


1 Department of Medicine, Dr. Rajendra Prasad Government Medical College, Kangra, Himachal Pradesh, India
2 Otolaryngology Head and Neck Surgery, Dr. Rajendra Prasad Government Medical College, Kangra, Himachal Pradesh, India
3 Department of Medicine, IGMC, Shimla, Himachal Pradesh, India

Date of Web Publication17-Dec-2018

Correspondence Address:
Dr. Gaveshna Gargi
Department of Medicine, Dr. Rajendra Prasad Government Medical College, Tanda, Kangra, Himachal Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/heartindia.heartindia_17_18

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  Abstract 


Objective: The aim of the present study was to investigate the association between mean platelet volume (MPV) and platelet count in patients with diagnosis of acute coronary syndrome (ACS).
Materials and Methods: It was a case–control study conducted in a tertiary care hospital. We examined 100 cases of ACS and 100 age- and sex-matched healthy controls. All patients were subjected to focused history, focused clinical examination, vital recording, and baseline 12 lead electrocardiogram. MPV and platelet count were measured by a hemogram device, Melet Schloesing (MS-9) based on the Coulter principle.
Results: The patients with ACS had a higher MPV 7.70 fl as compared to the normal healthy controls 6.64 fl (P < 0.0001). On the other hand, the platelet count was significantly decreased in the patients of ACS 172.44 × 109/L when compared with the healthy control group 204.98 × 109/L, and this difference was statistically significant with P < 0.0001.
Conclusions: We concluded that the patients presenting with features of ACS have a higher MPV and a decreased platelet count as compared to normal population. These simple hematological markers such as MPV and platelet count can help us in reaching the diagnosis of ACS along with traditional tools.

Keywords: Acute coronary syndrome, mean platelet volume, platelet count


How to cite this article:
Gargi G, Saini A, Sharma A, Jaret P. Mean platelet volume in acute coronary syndrome: Diagnostic implications. Heart India 2018;6:123-6

How to cite this URL:
Gargi G, Saini A, Sharma A, Jaret P. Mean platelet volume in acute coronary syndrome: Diagnostic implications. Heart India [serial online] 2018 [cited 2019 Jan 15];6:123-6. Available from: http://www.heartindia.net/text.asp?2018/6/4/123/247567




  Introduction Top


Despite impressive advances in its diagnosis and management over the past four decades, ischemic heart disease continues to be a major public health problem in the developed countries and is becoming an increasingly important problem in developing countries. Acute coronary syndromes (ACSs) encompass a spectrum of unstable coronary artery disease (CAD), from unstable angina (USA) to transmural myocardial infarction (MI).[1]

Platelets have been implicated in the pathogenesis of various disorders since their discovery in 1842 by Donne.[2] Platelets are enucleate cells measuring approximately 1–2 μm in length with an average lifespan of 8–10 days. The platelets are formed via cytoplasmic fragmentation of bone marrow-derived megakaryocytes.

When activated, the platelets are localized, get amplified, and sustain coagulation and inflammatory responses at the site of the ruptured plaque. The platelets then release procoagulant platelet-derived microparticles.[3] They have an important role in the initiation of atherosclerotic lesions and coronary thrombus formation. One study has shown that megakaryocytic changes result in platelet changes which can increase atheroma formation.[4] Given the importance of platelets in vascular hemostasis and its role in the pathogenesis of CAD, there has been enormous research interest directed toward an improved understanding of the platelet physiology and the assessment of platelet function.

There is a wide range of indices which have been used to quantify platelet function. However, determination of platelet size, usually via quantification of mean platelet volume (MPV), is a simple and easy method of accurately assessing the platelet function. Larger platelets have a greater mass and are both metabolically and enzymatically more active than smaller platelets. Indeed, they have a greater prothrombotic potential, with higher levels of intracellular thromboxane A2 as well as increased levels of procoagulant surface proteins (e.g., P selectin, glycoproteins IIb/IIIa).[5],[6],[7]

MPV is a simple and reliable index of platelet size that correlates with the functional status of platelets. MPV is an emerging risk marker for atherothrombosis. Moreover, previous evidence suggests that MPV may be a risk factor for recurrent MI independent of established risk factors such as hypertension, dyslipidemia, increased fibrinogen, white blood cell count, or plasma viscosity.[8] MPV has been shown to be inversely correlated with the total platelet count. It has been suggested that consumption of small platelets leads to a compensatory production of larger reticulated platelets.[9] Indeed, the MPV has been shown to correlate with both megakaryocyte ploidy and percentage of circulating reticulated platelets. Furthermore, a positive correlation between thrombopoietin levels and MPV values has been demonstrated in CAD.[10]


  Materials and Methods Top


This study was a case–control study conducted in a tertiary care hospital. One hundred consecutive patients diagnosed as ACS admitted to the hospital who fulfilled the inclusion criteria were enrolled for this study. One hundred age- and sex-matched healthy people were included as controls.

Inclusion criteria

The patients who presented in the hospital with pain chest consistent with ACS with any of following features were added in the case group:

  1. Electrocardiogram (ECG) changes:


    1. ST elevation
    2. ST depression
    3. T wave inversion.


  2. Troponin T elevation.


Exclusion criteria

The patients who had any of the following features were excluded from the study.

  1. Patients who were receiving/received anticoagulant, antiplatelet therapy
  2. Patients with bleeding disorders
  3. Patients with preeclampsia and sepsis
  4. Patients with recent blood transfusion.


All the people included in the case group were subjected to focused history to obtain information related to demographic profile, viz., age, sex, educational status, residence, presenting symptoms, focused clinical examination, vital recording, and baseline 12 lead ECG.

For measuring MPV, the following protocol was followed:

The blood samples of patients were taken at the time of hospitalization in case group before starting any treatment. For MPV and platelet count analyses, 2 ml blood was taken in the ethylenediaminetetraacetic acid tubes obtained via antecubital venous access which was examined within 4 h by a hemogram device, Melet Schloesing (MS-9) based on the Coulter principle.

Statistical analysis

All the statistical analyses were done using SPSS 16.0 software. All quantitative values are expressed as mean ± standard deviation (SD). Unpaired student t-test was used to compare results in case and control groups with P < 0.05 being taken as statistically significant.


  Results Top


A total of 200 patients were evaluated comprising 100 cases of ACS and 100 age- and sex-matched healthy controls. The mean age of the case group in the study was 58.45 ± 11.64 years, whereas the mean age in control group was 58.51 ± 11.23 years. The male patients comprised 73% in the case group and 76% in control group. The majority (81%) of the patients belonged to the rural area in both the groups. The patients with elevated total cholesterol (>200 mg) were 10% in case group as compared to 8% in the control group. The baseline characteristics of the study population are summarized in [Table 1].
Table 1: Demographic characteristics of the studied groups

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The MPV was increased in the ACS group 7.70 fl (SD 0.80) as compared to the control group 6.64 fl (SD 0.65). This difference was highly statistically significant with P < 0.0001 [Figure 1].
Figure 1: Comparison of mean platelet volume in case and control groups

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The mean platelet count was decreased in the case group 172.44 × 109/L (SD 59.19) as compared to the controls 204.98 × 109/L (SD 31.98). This decrease in the platelet count was statistically significant with P < 0.0001 [Figure 2].
Figure 2: Comparison of platelet count in case and control groups

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In the case group, 5% of patients were diagnosed as having USA, 16% patients had non-ST-elevated myocardial infarction (NSTEMI), and 79% patients were labeled as having ST-elevated myocardial infarction (STEMI).

The MPV and platelet count in these three groups of patients (USA, NSTEMI, and STEMI) were also compared and yielded no significant difference between each group [Table 2].
Table 2: Comparison of mean platelet volume in unstable angina, non-ST-elevated myocardial infarction, and ST-elevated myocardial infarction patients

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  Discussion Top


CAD causes more deaths and disability and incurs greater economic costs than any other illness in the developed world. CAD is the most common, serious, chronic, life-threatening illness in the United States, where 13 million persons have CAD, >6 million have angina pectoris (AP), and >7 million have sustained MI. Given the projection of large increases in CAD throughout the world, CAD is likely to become the most common cause of death worldwide by 2020.[11]

CAD is now growing among low-income groups rather than high-income groups (who are adopting more healthful lifestyles), while primary prevention has delayed the disease to later in life in all socioeconomic groups. Second half of the 20th century has witnessed a global spread of the CAD epidemic, especially in developing countries, including India. Based solely on projected demographic trends, it has been estimated that deaths attributable to CAD would nearly double, in both sexes, in the period 1985–2015 and CAD would emerge, over this period, as the single largest contributor to mortality, accounting for nearly a third of all deaths, globally.[12]

The platelet activation, by favoring thrombus formation and coronary artery occlusion, is thought to play a key pathogenic role in acute myocardial infarction (AMI). Platelets are heterogeneous cells in terms of size, density, and activity.[13] Platelet volume is an important indicator for platelet function and activation. Larger platelets contain more secretory granules and mitochondria and are known to be more active than small platelets.[14]

In the present study, we measured MPV and platelet count in patients suffering from ACS and healthy controls with a mean age of 58.4 ± 11.6 years. Mercan[15] has also studied MPV in ACS. The mean age of the patients in their study was 58.7 ± 11.9 years, which is comparable to our study. The present study comprised 73% male and 27% female patients, which is consistent with the study conducted by Mercan[15] with 71% males and 29% females.

Kishk et al.[16] compared AMI patients to stable AP and control groups and detected that the former group had lower platelet count and higher MPV. They suggested that it was independent of smoking and area or diameter of infarct. They also claimed that increased MPV and decreased platelet count may be a major risk factor for AMI.

Park et al.[17] also considered increased MPV to be a risk factor for platelet activation. Martin et al.[18] reported that platelet volume was significantly increased within first 12 h in post-MI period, which occurred before ACS. Martin et al.[18] also suggested that increased MPV might be an independent risk factor for post-MI recurrence of coronary events and mortality. Ranjith et al.[19] have also concluded in their study that MPV is increased and platelet count decreased in patients of ACS when compared with stable AP and normal population.

The results in all the above studies are consistent with the findings in our population group and reiterate the importance of MPV and platelet count in the diagnosis of ACS.

Butkiewicz et al.[20] conducted a study consisting of 54 patients with unstable AP and found no significant difference between unstable AP patients and controls in terms of MPV. In this study, platelet counts were decreased when unstable AP patients were compared to the control group, yet this difference failed to reach a statistically significant level. Halbmayer et al.,[21] in their study comparing those patients waiting for coronary artery bypass graft surgery to the control group, did not detect any difference in terms of MPV. They claimed that MPV could not be used as a risk indicator for CAD or MI. These few studies provide conflicting results to the present one and points that comprehensive studies should be conducted in the future to include these simple markers in the diagnostic test battery for ACS.


  Conclusions Top


We detected that platelet counts were decreased and MPV were increased in patients presenting with ACS. Based on these findings, we conclude that larger platelet volumes may constitute a high risk for ACS and ischemic complications. For this purpose, we think that MPV and platelet count measurements, which are noninvasive and easy-to-perform methods, may be used as important tools for diagnosis in these patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ross R. Atherosclerosis – An inflammatory disease. N Engl J Med 1999;340:115-26.  Back to cited text no. 1
    
2.
Donne A. De I'origine des globulines du sang. CR Acad Sci 1842;14:366-8.  Back to cited text no. 2
    
3.
Massberg S, Schulz C, Gawaz M. Role of platelets in the pathophysiology of acute coronary syndrome. Semin Vasc Med 2003;3:147-62.  Back to cited text no. 3
    
4.
Bath PM, Missouris CG, Buckenham T, MacGregor GA. Increased platelet volume and platelet mass in patients with atherosclerotic renal artery stenosis. Clin Sci (Lond) 1994;87:253-7.  Back to cited text no. 4
    
5.
van der Loo B, Martin JF. A role for changes in platelet production in the cause of acute coronary syndromes. Arterioscler Thromb Vasc Biol 1999;19:672-9.  Back to cited text no. 5
    
6.
Pizzulli L, Yang A, Martin JF, Lüderitz B. Changes in platelet size and count in unstable angina compared to stable angina or non-cardiac chest pain. Eur Heart J 1998;19:80-4.  Back to cited text no. 6
    
7.
Martin JF, Trowbridge EA, Salmon G, Plumb J. The biological significance of platelet volume: Its relationship to bleeding time, platelet thromboxane B2 production and megakaryocyte nuclear DNA concentration. Thromb Res 1983;32:443-60.  Back to cited text no. 7
    
8.
Martin JF, Bath PM, Burr ML. Influence of platelet size on outcome after myocardial infarction. Lancet 1991;338:1409-11.  Back to cited text no. 8
    
9.
Sewell R, Ibbotson RM, Phillips R, Carson P. High mean platelet volume after myocardial infarction: Is it due to consumption of small platelets? Br Med J (Clin Res Ed) 1984;289:1576-8.  Back to cited text no. 9
    
10.
Senaran H, Ileri M, Altinbaş A, Koşar A, Yetkin E, Oztürk M, et al. Thrombopoietin and mean platelet volume in coronary artery disease. Clin Cardiol 2001;24:405-8.  Back to cited text no. 10
    
11.
Eckel RH. The metabolic syndrome. In: Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Loscalzo J, et al., editors. Harrison's Principle of Internal Medicine. 17th ed. New York: McGraw-Hill; 2008. p. 1509-14.  Back to cited text no. 11
    
12.
Singh SP, Sen P. Coronary heart disease: The changing scenario. Indian J Prev Soc Med 2003;34:74-80.  Back to cited text no. 12
    
13.
Karpatkin S. Heterogeneity of human platelets. II. Functional evidence suggestive of young and old platelets. J Clin Invest 1969;48:1083-7.  Back to cited text no. 13
    
14.
Thompson CB, Jakubowski JA, Quinn PG, Deykin D, Valeri CR. Platelet size as a determinant of platelet function. J Lab Clin Med 1983;101:205-13.  Back to cited text no. 14
    
15.
Mercan R. Mean platelet volume in acute coronary syndromes. Van Tıp Derg 2010;17:89-95.  Back to cited text no. 15
    
16.
Kishk YT, Trowbridge EA, Martin JF. Platelet volume subpopulations in acute myocardial infarction: An investigation of their homogeneity for smoking, infarct size and site. Clin Sci (Lond) 1985;68:419-25.  Back to cited text no. 16
    
17.
Park Y, Schoene N, Harris W. Mean platelet volume as an indicator of platelet activation: Methodological issues. Platelets 2002;13:301-6.  Back to cited text no. 17
    
18.
Martin JF, Plumb J, Kilbey RS, Kishk YT. Changes in volume and density of platelets in myocardial infarction. Br Med J (Clin Res Ed) 1983;287:456-9.  Back to cited text no. 18
    
19.
Ranjith MP, Divya R, Mehta VK, Krishnan MG, KamalRaj R, Kavishwar A, et al. Significance of platelet volume indices and platelet count in ischaemic heart disease. J Clin Pathol 2009;62:830-3.  Back to cited text no. 19
    
20.
Butkiewicz AM, Kemona H, Dymicka-Piekarska V, Bychowski J. Beta-thromboglobulin and platelets in unstable angina. Kardiol Pol 2003;58:449-55.  Back to cited text no. 20
    
21.
Halbmayer WM, Haushofer A, Radek J, Schön R, Deutsch M, Fischer M, et al. Platelet size, fibrinogen and lipoprotein(a) in coronary heart disease. Coron Artery Dis 1995;6:397-402.  Back to cited text no. 21
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2]



 

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