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Mean platelet volume is associated with myocardial perfusion defect in diabetic patients.
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PMID:  25000440     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
AIM: Our aim was to evaluate whether there was a relationship between mean platelet volume and myocardial perfusion defect in diabetic patients using myocardial perfusion imaging.
METHODS: Forty-four diabetic patients with myocardial perfusion defect (group 1) and 44 diabetic patients without myocardial perfusion defect (group 2), matched for age and gender, were retrospectively examined. Levels of mean platelet volume (MPV) in the two groups were assessed.
RESULTS: MPV was higher in group 1 than group 2 patients (8.76 ± 0.76 and 8.25 ± 0.78 fl), respectively, p = 0.003). Levels of glucose, triglycerides (TG), total cholesterol (TC), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, haemoglobin (Hb) and glycosylated haemoglobin (HbA1c), and body mass index (BMI) in the two groups were not statistically significantly different. Multivariate logistic regression analyses showed that MPV was the only variable independently associated with myocardial perfusion defects (OR: 2.401, 95% CI: 1.298-4.440, p = 0.013).
CONCLUSION: This study showed that higher MPV was associated with myocardial perfusion defects. Higher MPV in diabetic patients was independently related to myocardial perfusion defects and may be an indicator of myocardial ischaemia.
Authors:
S Sarikaya; S Sahin; L Akyol; E Borekci; Y K Yilmaz; F Altunkas; K Karaman; S Karacavus; A R Erbay
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Type:  Journal Article    
Journal Detail:
Title:  Cardiovascular journal of Africa     Volume:  25     ISSN:  1680-0745     ISO Abbreviation:  Cardiovasc J Afr     Publication Date:    2014 May-Jun
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Created Date:  2014-07-08     Completed Date:  -     Revised Date:  -    
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Nlm Unique ID:  101313864     Medline TA:  Cardiovasc J Afr     Country:  South Africa    
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Languages:  eng     Pagination:  110-3     Citation Subset:  IM    
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Journal ID (nlm-ta): Cardiovasc J Afr
Journal ID (iso-abbrev): Cardiovasc J Afr
Journal ID (publisher-id): TBC
ISSN: 1995-1892
ISSN: 1680-0745
Publisher: Clinics Cardive Publishing
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www.cvja.co.zaCopyright © 2010 Clinics Cardive Publishing
open-access:
Received Day: 18 Month: 7 Year: 2013
Accepted Day: 13 Month: 3 Year: 2014
Print publication date: Month: 6 Year: 2014
Volume: 25 Issue: 3
First Page: 110 Last Page: 113
PubMed Id: 25000440
ID: 4120130
DOI: 10.5830/CVJA-2014-013

Mean platelet volume is associated with myocardial perfusion defect in diabetic patients
Savas Sarikaya, MD Affiliation: Department of Cardiology, School of Medicine, Bozok University, Yozgat, Turkey
Ali Riza Erbay, MD Affiliation: Department of Cardiology, School of Medicine, Bozok University, Yozgat, Turkey
Safak Sahin, MD Email: drsafaksahin@gmail.com Affiliation: Department of Internal Medicine, School of Medicine, Gaziosmanpaşa University, Tokat, Turkey
Lutfi Akyol, MD Affiliation: Department of Internal Medicine, School of Medicine, Bozok University, Yozgat, Turkey
Elif Borekci, MD Affiliation: Department of Internal Medicine, School of Medicine, Bozok University, Yozgat, Turkey
Yunus Keser Yilmaz, MD Affiliation: Department of Cardiovascular Surgery, School of Medicine, Bozok University, Yozgat, Turkey
Fatih Altunkas, MD Affiliation: Department of Cardiology, School of Medicine, Gaziosmanpaşa University, Tokat, Turkey
Kayihan Karaman, MD Affiliation: Department of Cardiology, School of Medicine, Gaziosmanpaşa University, Tokat, Turkey
Seyhan Karacavus, MD Affiliation: Department of Nuclear Medicine, School of Medicine, Bozok University, Yozgat, Turkey

Abstract

Diabetes mellitus (DM) is considered a coronary artery risk equivalent.1 DM is associated with an increased risk of cardiovascular morbidity and mortality.2,3 DM may cause myocardial perfusion defects involving the main coronary artery and myocardial microvascular circulation. Myocardial perfusion imaging (MPI) is a useful non-invasive tool to determine whether there is a myocardial perfusion defect.4

Platelet volume is a marker of platelet activation and function and is measured as mean platelet volume (MPV).5 MPV has become a prognostic factor in coronary heart disease and may eventually be accepted as a parameter of platelet activity.6 MPV is emerging as a new risk factor for vascular complications of DM of which atherothrombosis plays a crucial role.7

However, to the best of our knowledge, there have been no reports in the literature to evaluate the relationship between MPV and myocardial perfusion defect using MPI in patients with diabetes. Our aim was to evaluate whether there was a relationship between myocardial perfusion defect using myocardial perfusion scintigraphy and MPV in selected diabetic patients.


Methods

Eighty-eight patients with type 2 diabetes who had MPI between January and May 2013 in Bozok and Gaziosmanpaşa universities were retrospectively examined. Eighty-eight patients were enrolled in the study and divided into two groups, matched for age and gender: the myocardial perfusion defect group (group 1) and a group with no myocardial perfusion defect (group 2). Group 1 consisted of 44 subjects (14 men and 30 women, mean age: 61.75 ± 7.86 years). Group 2 consisted of 44 subjects (12 men and 32 women, mean age: 60.48 ± 9.28 years).

Patients with a history of myocardial infarction, unstable angina pectoris, cardiac surgery, angiographically proven coronary artery disease, endocrine disorder without diabetes, systemic inflammatory disease, rhythm disorder, any medication that could affect the MPV, suspicious scintigraphy results due to breast attenuation, and aperture and fixed (scar) perfusion defects were excluded.

The blood samples were withdrawn following a 12-hour fast. Glucose, creatinine and lipid profiles were determined using standard methods. For both groups, we measured the MPV from blood samples that were obtained following venipuncture. The blood was collected in tripotassium EDTA tubes. We analysed the blood samples using an automatic blood counter within one hour of drawing the blood.

The patients underwent a two-day stress/rest single-photonemission tomography and gated GSPECT study using adenosine with a standard weight-based infusion protocol (140 μg/kg/min). The six-minute adenosine infusion was begun and 740 MBq (20 mCi) of MIBI was injected after three minutes. After a 45-minute delay, a stress set of images was acquired.

At rest, before receiving technetium-99m methoxy isobutyl isonitrile (99mTc-MIBI), the patients were given one to two tablets of sublingual nitroglycerin (0.4 mg), five minutes apart and they were injected with 740 MBq (20 mCi) of MIBI. A GSPECT study was performed 45 minutes later.

GSPECT data were acquired in the supine position with the double-head SPECT-γ camera equipped with a high-resolution low-energy collimator. The obtained data were projected as myocardial tomographic slices in short-axis, vertical long-axis and horizontal long-axis views. Electrocardiogram gating was applied to the cardiac cycle with eight frames per cardiac cycle. The myocardium was divided into 17 segments following the American Society of Nuclear Cardiology/American College of Cardiology/American Heart Association guidelines.8

GSPECT dates were processed and analysed using 4D-MSPECT software, which determines the extent and severity of left ventricular perfusion defect size and the extent of reversible (ischaemia) or fixed (scar) perfusion defects.9 The programme assigned a score of 0 to 4 to each segment based on activity level: 0 = normal, 1 = equivocal, 2 = moderate, 3 = severe reduction of radioisotope uptake, and 4 = absence of detectable tracer uptake. Abnormal perfusion, motion and thickening were defined as a score of ≥ 2.

The summed stress score (SSS), summed rest score (SRS), and summed difference score (SDS) were calculated based on the conventional 17-segment model. The summed difference score (SDS), indicating the extent of reversible perfusion defects, was obtained by calculating the differences between the SSS and SRS.


Statistical analysis

Statistical analyses were performed using SPSS 18.0 software. Parametric values are given as mean ± standard deviation and non-parametric values as a percentage. To compare parametric continuous variables, the Student’s t-test was used; to compare non-parametric continuous variables, the Mann–Whitney U-test was used. Categorical data were compared by chi-square distribution. Stepwise multivariate logistic regression models were created to determine independent variables for myocardial perfusion defect. For multivariate regression, variables with a p-value < 0.1 in univariate analysis were selected. Two-tailed p-values < 0.05 were considered to indicate statistical significance.


Results

Baseline characteristic of the patients are given in Table 1. Levels of glucose, triglycerides (TG), total cholesterol (TC), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, haemoglobin (Hb) and glycosylated haemoglobin (HbA1c), and body mass index (BMI) in the two groups were not statistically significantly different. The MPV level was higher in group 1 than in group 2 patients (8.76 ± 0.78 and 8.25 ± 0.78 fl, respectively, p = 0.003). Levels of MPV in the two groups are shown in Fig. 1.

Univariate analysis showed that MPV, and HbA1c and glucose levels were significantly involved in myocardial perfusion defects. Multivariate logistic regression analyses showed that MPV was the only variable independently associated with myocardial perfusion defect (OR: 2.401, 95% CI: 1.298–4.440, p = 0.013) (Table 2).


Discussion

This study showed that there was a relationship between myocardial perfusion defect and MPV. MPV was higher in the group with myocardial perfusion defects, compared to the one without myocardial perfusion defects. Patients with diabetes develop vascular complications, including macrovascular complications [coronary artery disease (CAD), peripheral vascular disease and stroke] and microvascular complications [diabetic nephropathy (DN), diabetic retinopathy (DR) and peripheral neuropathy].10 Continuous hyperglycaemia may cause endothelial dysfunction and vascular lesions, resulting in diabetic vascular complications. 11,12

Type 2 diabetes is a substantial risk factor in atherosclerotic cardiovascular disease.13,14 Cardiovascular disease (CVD) is the leading cause of death in patients with type 2 DM.15 Asymptomatic CAD is common in patients with DM and is a strong predictor of future poor outcome of coronary vascular events, as well as early death.16,17 DM is associated with generalised endothelial dysfunction and small-vessel abnormalities.18,19

Perfusion defects are substantial predictors of coronary events in patients with known or suspected coronary heart disease (CHD).20 It is proposed that concomitant abnormalities of perfusion imaging scans in patients with diabetes with normal coronary angiograms may be caused by micro-angiopathy or endothelial dysfunction. Accordingly, it reflects an increased likelihood of future coronary events.21

The majority of studies on ischaemia have used SPECT MPI. An analysis of the diagnostic accuracy of pharmacologically induced stress MPI reported a mean sensitivity and specificity of 88 and 77%, respectively.22

Platelet volume is a marker of platelet activation and function, and is measured using MPV.5 Platelets that have dense granules are more active biochemically, functionally and metabolically. Large platelets secrete high levels of prothrombogenic thromboxane A2, serotonin, beta-thromboglobulin and procoagulant membrane proteins such as P-selectin and glycoprotein IIIa.5,23 Platelets secrete a large number of substances that are crucial mediators of coagulation, inflammation, thrombosis and atherosclerosis.24,25 It is also well known that large platelets are a risk factor for developing coronary thrombosis, leading to myocardial infarction.19,23,26,27

Measurement of platelet activation and/or aggregation may provide prognostic information in patients at risk for or following a cardiovascular event.28,29 Reports have revealed that there is a close relationship between MPV and cardiovascular risk factors, including impaired fasting glucose levels, diabetes mellitus, hypertension, hypercholesterolaemia, obesity and the metabolic syndrome.30-32 Increased platelet activity is reported to play a role in the development of vascular complications in diabetic patients.18

MPV was increased in patients with SCF complex and cardiac syndrome X, both being related to microvascular defects and endothelial dysfunction.33,34 In the present study, we showed that MPV was associated with myocardial perfusion defect, using MPI in diabetic patients.

In our study, MPV was increased in the myocardial perfusion defect group compared to those without myocardial perfusion defects. DM not only involves the main coronary artery but also the microvascular circulation, leading to myocardial perfusion defects. Perfusion defects are significant predictors of coronary events in patients with known or suspected CHD.20

The main limitation of our study was the small sample size, which could result in low statistical power for equivalency testing, leading to false-negative results. Second, because of the retrospective nature of data collection, the angiographic results of the patients were not evaluated. MPI may reflect myocardial perfusion defects but it was not able to show the anatomical status of the coronary artery. We cannot extend our results to the general population due to our broad exclusion criteria.


Conclusion

MPV levels were higher in the diabetic patients with myocardial perfusion defects than in those without myocardial perfusion defects. In diabetic patients, increased MPV may be an independent marker of myocardial perfusion defects, which are associated with adverse coronary events.


References
1. Whiteley L,Padmanabhan S,Hole D,Isles C,Should diabetes be considered a coronary heart disease risk equivalent? results from 25 years of follow-up in the Renfrew and Paisley survey.Diabetes CareYear: 2005281588159315983305
2. Kannel WB,McGee DL,Diabetes and cardiovascular disease. The Framingham study.J Am Med AssocYear: 197924120352038
3. Nathan DM,Meigs J,Singer DE,The epidemiology of cardiovascular disease in type 2 diabetes mellitus: how sweet it is ... or is it?LancetYear: 1997350(Suppl 1)SI499250276
4. Misko J,Evaluation of myocardial perfusion and viability in coronary artery disease in view of the new revascularization guidelines.Nuclear Med Rev Central Eastern EurYear: 2012154651
5. Martin JF,Shaw T,Heggie J,Penington DG,Measurement of the density of human platelets and its relationship to volume.Br J HaematolYear: 1983543373526860588
6. Erhart S,Beer JH,Reinhart WH,Influence of aspirin on platelet count and volume in humans.Acta HaematolYear: 199910114014410352333
7. Zuberi BF,Akhtar N,Afsar S, Comparison of mean platelet volume in patients with diabetes mellitus, impaired fasting glucose and nondiabetic subjects.Singapore Med JYear: 20084911411618301837
8. Cerqueira MD,Weissman NJ,Dilsizian V,et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical Cardiology of the American Heart Association.CirculationYear: 200210553954211815441
9. Ficaro EP,Lee BC,Kritzman JN,Corbett JR,Corridor4DM: the Michigan method for quantitative nuclear cardiology.J Nucl CardiolYear: 20071445546517679053
10. Murea M,Ma L,Freedman BI,Genetic and environmental factors associated with type 2 diabetes and diabetic vascular complications.Rev Diabet StudiesYear: 20129622
11. Bae SH,Lee J,Roh KH,Kim J,Platelet activation in patients with diabetic retinopathy.Korean J OphthalmolYear: 20031714014414717493
12. Brownlee M,Biochemistry and molecular cell biology of diabetic complications.NatureYear: 200141481382011742414
13. Kitada S,Otsuka Y,Kokubu N,et al. Post-load hyperglycemia as an important predictor of long-term adverse cardiac events after acute myocardial infarction: a scientific study.Cardiovasc DiabetolYear: 201097521070650
14. Nishimura R,Nakagami T,Sone H,Ohashi Y,Tajima N,Relationship between hemoglobin A1c and cardiovascular disease in mild-to-moderate hypercholesterolemic Japanese individuals: subanalysis of a largescale randomized controlled trial.Cardiovasc DiabetolYear: 2011105821714932
15. Morrish NJ,Wang SL,Stevens LK,Fuller JH,Keen H,Mortality and causes of death in the WHO Multinational Study of Vascular Disease in Diabetes.DiabetologiaYear: 200144Suppl 2S142111587045
16. Koistinen MJ,Prevalence of asymptomatic myocardial ischaemia in diabetic subjects.Br Med JYear: 199030192952390590
17. Prevalence of unrecognized silent myocardial ischemia and its association with atherosclerotic risk factors in noninsulin-dependent diabetes mellitus. Milan Study on Atherosclerosis and Diabetes (MiSAD) Group.Am J CardiolYear: 1997791341399193011
18. Demirtunc R,Duman D,Basar M,Bilgi M,Teomete M,Garip T,The relationship between glycemic control and platelet activity in type 2 diabetes mellitus.J Diabetes ComplicatYear: 200923899418358749
19. Senaran H,Ileri M,Altinbas A,et al. Thrombopoietin and mean platelet volume in coronary artery disease.Clin CardiolYear: 20012440540811346249
20. Thomas GS,Miyamoto MI,Morello AP 3rd,et al. Technetium 99m sestamibi myocardial perfusion imaging predicts clinical outcome in the community outpatient setting. The Nuclear Utility in the Community (NUC) Study.J Am Coll CardiolYear: 20044321322314736440
21. Nitenberg A,Ledoux S,Valensi P,Sachs R,Attali JR,Antony I,Impairment of coronary microvascular dilation in response to cold pressor-induced sympathetic stimulation in type 2 diabetic patients with abnormal stress thallium imaging.DiabetesYear: 2001501180118511334424
22. Djaberi R,Beishuizen ED,Pereira AM,et al. Non-invasive cardiac imaging techniques and vascular tools for the assessment of cardiovascular disease in type 2 diabetes mellitus.DiabetologiaYear: 2008511581159318607561
23. Endler G,Klimesch A,Sunder-Plassmann H,et al. Mean platelet volume is an independent risk factor for myocardial infarction but not for coronary artery disease.Br J HaematolYear: 200211739940411972524
24. Coppinger JA,Cagney G,Toomey S,et al. Characterization of the proteins released from activated platelets leads to localization of novel platelet proteins in human atherosclerotic lesions.BloodYear: 20041032096210414630798
25. Gawaz M,Langer H,May AE,Platelets in inflammation and atherogenesis.J Clin InvestigatYear: 200511533783384
26. Rao AK,Goldberg RE,Walsh PN,Platelet coagulant activities in diabetes mellitus. Evidence for relationship between platelet coagulant hyperactivity and platelet volume.J Lab Clin MedYear: 198410382926690642
27. Jakubowski JA,Adler B,Thompson CB,Valeri CR,Deykin D,Influence of platelet volume on the ability of prostacyclin to inhibit platelet aggregation and the release reaction.J Lab Clin MedYear: 19851052712763882862
28. Ault KA,Cannon CP,Mitchell J,et al. Platelet activation in patients after an acute coronary syndrome: results from the TIMI-12 trial. Thrombolysis in Myocardial Infarction.J Am Coll CardiolYear: 19993363463910080462
29. Trip MD,Cats VM,van Capelle FJ,Vreeken J,Platelet hyperreactivity and prognosis in survivors of myocardial infarction.New Engl J MedYear: 1990322154915542336086
30. Tavil Y,Sen N,Yazici HU,Hizal F,Abaci A,Cengel A,Mean platelet volume in patients with metabolic syndrome and its relationship with coronary artery disease.Thromb ResYear: 200712024525017145074
31. Varol E,Akcay S,Ozaydin M,Erdogan D,Dogan A,Altinbas A,Mean platelet volume is associated with insulin resistance in non-obese, non-diabetic patients with coronary artery disease.J CardiolYear: 20105615415820430587
32. Coban E,Bostan F,Ozdogan M,The mean platelet volume in subjects with impaired fasting glucose.PlateletsYear: 200617676916308190
33. Cay S,Biyikoglu F,Cihan G,Korkmaz S,Mean platelet volume in the patients with cardiac syndrome X.J Thromb thrombolYear: 200520175178
34. Gokce M,Kaplan S,Tekelioglu Y,Erdogan T,Kucukosmanoglu M,Platelet function disorder in patients with coronary slow flow.Clin CardiolYear: 20052814514815813623

Figures

[Figure ID: F1]
Fig. 1. 

MPV levels in the two groups.



Tables
[TableWrap ID: T1] Table 1  Baseline characteristic of the patients.
Group 1 Group 2 p-value
Age (years) 60.02 ± 9.28 60.81 ± 8.02 0.660
Women (%) 72.7 68.2 0.408
HT (%) 72.7 86.4 0.093
HL (%) 47.7 56.8 0.281
Aspirin (%) 34.1 29.5 0.410
BMI (kg/m2) 31.41 ± 6.23 30.41 ± 5.7 0.446
Glucose (mg/dl) 131.79 ± 40.553 151.16 ± 54.213 0.070
TG (mg/dl) 192.36 ± 116.48 171.71 ± 87.321 0.600
TC (mg/dl) 190.04 ± 42.25 178.83 ± 46.73 0.258
HDL-C (mg/dl) 40.58 ± 5.911 38.68 ± 6.08 0.167
LDL-C (mg/dl) 118.77 ± 28.75 108.28 ± 33.82 0.133
Hb (g/dl) 13.16 ± 1.40 13.42 ± 1.46 0.399
MPV (fl) 8.76 ± 0.76 8.25 ± 0.78 0.003
HbA1c (%) 8.67 ± 0.68 8.35 ± 0.86 0.094

HT: hypertension; HL: hyperlipidaemia TG: triglycerides; TC: total cholesterol; HDL-C: high-density lipoprotein cholesterol; LDL-C: lowdensity lipoprotein cholesterol; Hb: haemoglobin; MPV: mean platelet volume; HbA1c: glycosylated haemoglobin.


[TableWrap ID: T2] Table 2  Univariate and multivariate regression analyses of independent variables for MPD .
Variables Univariate Multivariate
OR 95% CI p-value OR 95% CI p-value
MPV (fl) 2.401 1.298–4.440 0.005 2.484 1.215–5.081 0.013
Glucose (mg/dl) 1.009 0.999–1.029 0.072 1.008 0.997–1.019 0.178
HbA1c (%) 1.800 0.993–3.474 0.08 1.984 0.980–4.018 0.064
Age (years) 1.011 0.963–1.061 0.664
Gender 1.244 0.497–3.16 0.641
HT (mg/dl) 2.375 0.801–7.043 0.119
BMI (km/m2) 0.991 0.92–1.067 0.820
TC (mg/dl) 0.994 0.984–1.004 0.256
TG (mg/dl) 0.998 0.994–1.002 0.360
HDL-C (mg/dl) 0.948 0.878–1.023 0.167
LDL (mg/dl) 0.989 0.975–1.003 0.134
Hb (%) 1.138 0.845–1.534 0.395


Article Categories:
  • Cardiovascular Topics

Keywords: myocardial perfusion defect, mean platelet volume, diabetes mellitus.

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