|Year : 2018 | Volume
| Issue : 1 | Page : 63-66
Study of platelet count and platelet volume indices in the spectrum of coronary artery diseases and its clinicopathological correlation
Biswajit Majumder1, Himanshu Jain2, Sharmistha Chatterjee3, Tushar Kanti Das2
1 Department of Cardiology, R G Kar Medical College, Kolkata, West Bengal, India
2 Department of Pathology, R G Kar Medical College, Kolkata, West Bengal, India
3 Department of Biochemistry, College of Medicine and Sagore Dutta Hospital, Kolkata, West Bengal, India
|Date of Web Publication||7-May-2018|
Dr. Biswajit Majumder
181B/1 Kabiguru Sarani, Kolkata - 700 038, West Bengal
Source of Support: None, Conflict of Interest: None
Introduction: Larger platelets are enzymatically and metabolically more active and have higher thrombotic ability compared to the smaller one. The mean platelet volume (MPV) and other platelet volume indices quantification have been appreciated as biomarker of cardiovascular disease.
Aims and Objectives: To determine the platelet count, the various platelet volume indices and and to evaluate any statistical difference between these values among the patients of acute myocardial infarction (AMI), unstable and stable angina in age and sex matched control group.
Materials and Methods: 35 cases of AMI/unstable angina, 35 cases of stable angina were compared with 35 non cardiac patients with respect to platelet counts, MPV, PDW and PCT. All the parameters were measured as per standard protocol. Patients with bleeding disorder, thrombocytopenia, liver and kidney disease were excluded.
Result and Analysis: In our study MPV and mean PDW were significantly higher in acute myocardial infarction/unstable angina patients than stable angina (P < 0.05). Statistically significant higher PDW and MPV were also observed in AMI/UA patients than control subjects (P < 0.05).
Conclusion: Measurement of platelet count and platelet volume indices may be of some benefit in detecting those patients at higher risk of an acute coronary syndrome.
Keywords: Coronary artery, disease, platelet, volume indices
|How to cite this article:|
Majumder B, Jain H, Chatterjee S, Das TK. Study of platelet count and platelet volume indices in the spectrum of coronary artery diseases and its clinicopathological correlation. Nig J Cardiol 2018;15:63-6
|How to cite this URL:|
Majumder B, Jain H, Chatterjee S, Das TK. Study of platelet count and platelet volume indices in the spectrum of coronary artery diseases and its clinicopathological correlation. Nig J Cardiol [serial online] 2018 [cited 2019 Aug 22];15:63-6. Available from: http://www.nigjcardiol.org/text.asp?2018/15/1/63/231977
| Introduction|| |
Coronary artery disease (CAD) is an epidemic and is the most common cause of mortality worldwide. Majority of deaths from CAD result from acute coronary syndrome because of rupture or fissuring of an unstable atherosclerotic plaque accompanied by a cascade of platelet reactions, resulting in thrombus formation. The overwhelming importance of platelets in vascular hemostasis and pathogenesis in acute coronary syndrome has triggered plenty of research activities toward understanding of the platelet physiology, function, and the development of antiplatelet drugs. Larger platelets are enzymatically and metabolically more active and have higher thrombotic ability compared to the smaller one.,, The mean platelet volume (MPV) and other platelet volume indices' quantification have been appreciated as a biomarker of cardiovascular disease.,, Compared with healthy controls, increased MPV, platelet distribution width (PDW), platelet large cell ratio (P-LCR), and decreased plateletcrit (PCT) are seen in patients with known CAD risk factors such as smoking, diabetes mellitus, and hypertension.,,, MPV is known to be higher in patients with unstable angina (UA) compared to stable angina patients.,,, In the light of this background, we undertook this study to investigate any possible relation between the various platelet indices and acute myocardial infarction (AMI) and stable and UA.
Aims and objectives
To determine the platelet count, the various platelet volume indices and to evaluate any statistical difference between these values among the patients of AMI, UA, and stable angina in age- and sex-matched control group.
| Materials and Methods|| |
The study was conducted in the Department of Cardiology and Pathology, R G Kar Medical College from April 2015 to March 2016. Thirty-five cases of AMI/UA and 35 cases of stable angina were compared with 35 noncardiac patients with respect to platelet counts, MPV, PDW, and PCT. All the parameters were measured as per standard protocol. Patients with bleeding disorder, thrombocytopenia, and liver and kidney disease were excluded from the study.
The study population was divided into three groups:
- Group 1: Patients with AMI/UA – 35 cases
- Group 2: Patients with chronic stable angina – 35 cases
- Group 3: Healthy controls – 35 cases.
| Results and Analysis|| |
The data obtained from the study were compiled and statistically analyzed by Kruskal–Wallis test (nonparametric K-independent sample test) using SPSS Inc. Released 2007. SPSS for Windows, Version 16.0. (Chicago, SPSS Inc.).
In Group 1, 25 (71%) patients were of AMI and 10 (29%) patients were of UA.
The mean age of all selected patients was 61.30 ± 10.48 years with range from 40 to 84 years. The mean age in Groups 1–3 was 59.49 ± 12.02, 62.40 ± 9.22, and 62.03 ± 10.48, respectively. Out of 105 patients, 57 (54%) were males and 48 (46%) were females. In Groups 1 and 3, 20 (57%) patients were males and 15 (43%) were females. In Group 2, 17 (49%) were males and 18 (51%) were females. The mean platelet count in all randomly selected cases was 216.80 ± 105.36 × 103/cmm. The mean platelet count of Group 1 (177.20 ± 73.22 × 103/cmm) was significantly lower than Group 2 (228.40 ± 106.30 × 103/cmm). The mean platelet count of Group 2 was also lower than Group 3 (244.80 ± 121.38 × 103/cmm). No significant difference was noted between the mean platelet count of male and female patients [Table 1]. The MPV of all randomly selected patients was 11.24 ± 1.41fl. The MPV of Group 1 (11.99 ± 1.62fl) was significantly higher than Group 2 (10.93 ± 1.22fl). The MPV of Group 2 was also higher than Group 3 (10.80 ± 1.05). The difference of MPV between Group 2 and Group 3 was statistically nonsignificant [Table 2]. The PDW of all patients was 15.69 ± 3.85%. The PDW of Group 1 (18.20 ± 3.87%) was significantly higher than Group 2 (14.73 ± 3.69%) and control Group 3 (14.14 ± 2.63%). The PDW of Group 2 was higher than Group 3, but it was not statistically significant. The mean PDW among females (16.15 ± 3.85%) was higher than in males (15.30 ± 3.85%) [Table 3]. The mean P-LCR of all patients was 36.58 ± 10.11%. The mean P-LCR of Group 3 (31.73 ± 7.13) was significantly lower than Group 1 (42.62 ± 9.17%) and Group 2 (35.38 ± 10.69%) [Table 4]. The mean PCT of all patients was 0.23 ± 0.13%. The PCT of Group 1 (0.18 ± 0.10%) was significantly lower than that of Group 2 (0.25 ± 0.14%) and control Group 3 (0.23 ± 0.13%). The difference of PCT in Group 2 and Group 3 was not statistically significant [Table 5]. The PCT of females was slightly higher than males.
| Discussion|| |
In our study, MPV and mean PDW were significantly higher in AMI/UA patients than stable angina and statistically significant higher PDW and MPV were also observed in AMI/UA patients than controls. Our results are similar to that of Khandekar et al., who also showed higher MPV and mean PDW in AMI or UA patients than stable CAD.
The mean P-LCR was significantly lower in stable angina patients compared to AMI/UA patients. Statistically significant lower P-LCR was also observed in controls compared to AMI/UA patients. We did not find any significant association of mean P-LCR in patients with stable angina and healthy control group. Our results are comparable to study of Khandekar et al. and Manchanda et al.
The mean PCT was significantly lower in AMI/UA patients than stable angina. Statistically significant lower PCT was also observed in AMI/UA patients compared to healthy control groups. We did not find any statistically significant association of mean PCT in patients with stable angina and healthy control. Results are similar to other published studies.,,,
This study showed significantly lower platelet counts and lower PCT in AMI/UA patients in comparison to stable angina patients. Our study shows increased platelet volume indices, i.e., (MPV, PDW, and P-LCR) in AMI/UA patients than stable angina patients and healthy controls. Activation of platelets occurs before acute coronary syndrome and consumption of platelets at ruptured atherosclerotic plaque site probably release larger sized platelets from bone marrow. Although some studies have shown higher MPV in patients with UA than AMI, we found no such difference in our study like Senaran et al. Although in our study we have found higher values of MPV, PWD, P-LCR in patients with UA and AMI compared to stable angina, majority of other studies showed stronger correlation of higher MPV rather than PDW and P-LCR in patients with UA/AMI compared to stable angina. However, there is certain limitation of our studies. The sample size of our study was low. The MPV is influenced by many factors such as ethnicity, medication, illness, obesity, smoking, aging, diabetes, aspirin, clopidogrel, and inflammatory bowel disease.,,, The majority of patients in Groups 1 and 2 were getting aspirin and clopidogrel which may interfere with the determination of MPV. MPV is a simple and economic laboratory measurement and it might be very useful in conjunction with other conventional biochemical cardiac markers in the early prediction of acute coronary syndrome in high-risk patients. However, it should be substantiated with further well-designed studies.
| Conclusion|| |
Hence, it can be concluded from our study that larger platelets are hemostatically active and act as risk factors for developing coronary thrombosis leading to myocardial infarction. Platelet count and platelet volume indices can provide a signature for the prethrombotic state in ischemic heart disease. Measurement of platelet count and platelet volume indices may be of some benefit in detecting those patients at higher risk of acute coronary syndrome.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Trip MD, Cats VM, van Capelle FJ, Vreeken J. Platelet hyperreactivity and prognosis in survivors of myocardial infarction. N Engl J Med 1990;322:1549-54.
Boos CJ, Lip GY. Platelet activation and cardiovascular outcomes in acute coronary syndromes. J Thromb Haemost 2006;4:2542-3.
Boos CJ, Lip GY. Assessment of mean platelet volume in coronary artery disease - what does it mean? Thromb Res 2007;120:11-3.
Gurney D, Lip GY, Blann AD. A reliable plasma marker of platelet activation: Does it exist? Am J Hematol 2002;70:139-44.
Kamath S, Blann AD, Lip GY. Platelet activation: Assessment and quantification. Eur Heart J 2001;22:1561-71.
Harrison P. Platelet function analysis. Blood Rev 2005;19:111-23.
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.
Yang A, Pizzulli L, Lüderitz B. Mean platelet volume as marker of restenosis after percutaneous transluminal coronary angioplasty in patients with stable and unstable angina pectoris. Thromb Res 2006;117:371-7.
Bluteau D, Lordier L, Di Stefano A, Chang Y, Raslova H, Debili N, et al.
Regulation of megakaryocyte maturation and platelet formation. J Thromb Haemost 2009;7 Suppl 1:227-34.
Italiano JE Jr. Shivdasani RA. Megakaryocytes and beyond: The birth of platelets. J Thromb Haemost 2003;1:1174-82.
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.
Chu SG, Becker RC, Berger PB, Bhatt DL, Eikelboom JW, Konkle B, et al.
Mean platelet volume as a predictor of cardiovascular risk: A systematic review and meta-analysis. J Thromb Haemost 2010;8:148-56.
Dalby Kristensen S, Milner PC, Martin JF. Bleeding time and platelet volume in acute myocardial infarction – A 2 year follow-up study. Thromb Haemost 1988;59:353-6.
Martin JF, Bath PM, Burr ML. Influence of platelet size on outcome after myocardial infarction. Lancet 1991;338:1409-11.
Trowbridge EA, Martin JF. The platelet volume distribution: A signature of the prethrombotic state in coronary heart disease? Thromb Haemost 1987;58:714-7.
Khandekar MM, Khurana AS, Deshmukh SD, Kakrani AL, Katdare AD, Inamdar AK, et al.
Platelet volume indices in patients with coronary artery disease and acute myocardial infarction: An Indian scenario. J Clin Pathol 2006;59:146-9.
Manchanda J, Potekar RM, Badiger S, Tiwari A. The study of platelet indices in acute coronary syndromes. Ann Pathol Lab Med 2015;2:A30-5.
Kario K, Matsuo T, Nakao K. Cigarette smoking increases the mean platelet volume in elderly patients with risk factors for atherosclerosis. Clin Lab Haematol 1992;14:281-7.
Papanas N, Symeonidis G, Maltezos E, Mavridis G, Karavageli E, Vosnakidis T, et al.
Mean platelet volume in patients with type 2 diabetes mellitus. Platelets 2004;15:475-8.
Coban E, Ozdogan M, Yazicioglu G, Akcit F. The mean platelet volume in patients with obesity. Int J Clin Pract 2005;59:981-2.
Nadar S, Blann AD, Lip GY. Platelet morphology and plasma indices of platelet activation in essential hypertension: Effects of amlodipine-based antihypertensive therapy. Ann Med 2004;36:552-7.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]