Mean platelet volume may be associated with extent of coronary artery disease

LETTER TO THE EDITOR

Mean platelet volume may be associated with extent of coronary artery disease

Sait Demirkol^I; Sevket Balta^I; Ugur Kucuk^I; Hilal Olgun Kucuk^II

^IDepartamento de Cardiologia, Gulhane Medical Academy Ankara, Turquia

^IIDepartamento de Cardiologia, Van Education and Research Hospital, Van, Turquia

^{Mailing Address}

Keywords: Blood Platelet / metabolism; Coronary Artery Disease.

Dear Editor,

We read with interest the article by Guvenç et al¹. MPV is a widely used laboratory marker associated with platelet function based on inflammatory conditions². Recently, increased levels of MPV were demonstrated in atrial fibrillation³, cerebrovascular disease, peripheral artery disease, stroke, thyroid and inflammatory rheumatic diseases⁴. In conclusion, not only MPV but also red cell distribution width, neutrophil lymphocyte ratio⁵, plateletcrit (PCT), platelet lymphocyte ratio, CRP, ferritin and uric acid are easy methods to evaluate the extent of CAD in patients with stable angina. These markers might be useful in clinical practice.

References

Manuscript received May 4, 2013; revised May 8, 2013; accepted May 22, 2013.

Reply

We thank the authors for their constructive comments. Mean platelet volume (MPV) is considered as a promising marker to determine severity and prognosis of a variety of cardiovascular conditions¹. As increased size is a sign of platelet immaturity and immature platelets have a tendency towards increased aggregation, it is generally considered that MPV is a marker of platelet reactivity². It has also been hypothesized that the presence of larger platelets in circulation could be a cause of myocardial infarction, although this concept is not universally accepted³.

To date, a notable exception for the usefulness of MPV was stable coronary artery disease (CAD), where MPV values were not related with the severity and even with the presence of CAD^3,4. The present study is compatible with the previous literature for a wide range of MPV values, as MPV did not correlate with angiographic Gensini score. However, a secondary analysis showed that patients with mean platelet size below normal range (< 6.9 fL) had lower coronary atherosclerotic burden compared to those with normal (within-reference) MPV values⁵. This non-linear relationship of MPV with the severity of chronic CAD could explain why previous studies failed to show an association. From a clinical standpoint, this nonlinear relationship also severely limits MPV usefulness to a rather small number of stable CAD patients. Despite setbacks, our findings indicate MPV could still be a useful marker in chronic CAD, as less severe CAD could be anticipated in patients with MPV value below 6.9 fL. It should be kept in mind that drawing conclusions from a single study could be dangerous and more studies are needed to ascertain this concept.

Mean platelet volume is not, however, the sole useful marker that could be obtained from complete blood count (CBC). Low hemoglobin is a well-known and validated parameter of prognosis in patients with CAD and studies have shown the usefulness of other red-cell related parameters, such as red cell count and red cell distribution width^6,7. White cell count, individual white cell parameters and derivative markers such as neutrophil-lymphocyte ratio, were related with severity and prognosis of CAD⁷. Integrative use of these readily obtainable parameters with each other and with conventional CAD risk factors could give more clinically-relevant information than individual tests.

Although several small-sized or retrospective studies have repeatedly shown the value of MPV in a variety of cardiovascular conditions, clinical usefulness of MPV in large, randomized trials is yet to be demonstrated. This point was correctly emphasized in a recent review by Leader et al⁸. Conduction of properly-sized, prospective and randomized trials should be encouraged to evaluate the usefulness of MPV and similar CBC-based markers in clinical practice.

Sincerely

Tolga Sinan Güvenç

References

2. Balta S, Demirkol S, Celik T, Kucuk U, Unlu M, Arslan Z, et al. Association between coronary artery ectasia and neutrophil-lymphocyte ratio. Angiology. 2013 Mar 7. [Epub ahead of print] .

3. Balta S, Demirkol S, Kucuk U, Unlu M. Hemostatic markers can be pivotal roles of risk factors for new-onset atrial fibrillation. Platelets. 2013 Apr 3. [Epub ahead of print] .

4. Demirkol S, Balta S, Unlu M, Yuksel UC, Celik T, Arslan Z, et al. Evaluation of the mean platelet volume in patients with cardiac syndrome X. Clinics (São Paulo). 2012;67(9):1019-22.

5. Cingoz F, Iyisoy A, Demirkol S, Sahin MA, Balta S, Celik T, et al. Carotid intima-media thickness in patients with slow coronary flow and its association with neutrophil-to-lymphocyte ratio: a preliminary report. Clin Appl Thromb Hemost. 2013 Apr 23. [Epub ahead of print] .

Correspondência:

Sevket Balta

Gulhane Medical Faculty

Código Postal 66010, Ankara, Turquia

E-mail: [e-mail]

Artigo recebido em 04/05/13; revisado em 08/05/13, aceito em 22/05/13.

Carta-resposta

Agradecemos aos autores por seus comentários construtivos. O volume plaquetário médio (VPM) é considerado como um marcador promissor para determinar a gravidade e prognóstico de uma variedade de doenças cardiovasculares¹. Como o tamanho aumentado é um sinal de imaturidade das plaquetas e plaquetas imaturas possuem uma tendência para maior agregação, geralmente considera-se que o VPM seja um marcador de reatividade das plaquetas^2,3. Tem-se admitido a hipótese de que a presença de plaquetas maiores em circulação possa ser uma causa de infarto do miocárdio, embora esse conceito não seja universalmente aceito³.

Até hoje, uma exceção notável para a utilidade do VPM foi a doença arterial coronária (DAC) estável, onde os valores do MPV não estão relacionados com a gravidade e até mesmo com a presença da DAC^3,4. O presente estudo é compatível com a literatura prévia para uma vasta gama de valores de VPM, já que o VPM não se correlacionou com o escore angiográfico de Gensini. No entanto, uma análise secundária mostrou que pacientes com tamanho médio de plaquetas abaixo da faixa normal (<6,9 fL) apresentaram menor carga aterosclerótica coronariana em comparação com aqueles que tinham valores normais de VPM (dentro-da-referência)⁵. Essa relação não linear do VPM com a gravidade da DAC crônica poderia explicar por que estudos anteriores não conseguiram mostrar uma associação. Do ponto de vista clínico, essa relação não linear também limita severamente a utilidade do VPM a um pequeno número de pacientes com DAC estável. Apesar dos reveses, os nossos resultados indicam que o VPM ainda pode ser um marcador útil na DAC crônica, já que a DAC menos grave pode ser antecipada em pacientes com um valor do VPM abaixo de 6.9 fL. Deve-se ter em mente que tirar conclusões a partir de um único estudo pode ser perigoso e mais estudos são necessários para determinar-se esse conceito.

O volume plaquetário médio não é, no entanto, o único marcador útil que poderia ser obtido a partir do hemograma completo (HC). Baixo nível de hemoglobina é um parâmetro conhecido e validado de prognóstico em pacientes com DAC, e estudos mostram a utilidade de outros parâmetros relacionados com células vermelhas, como a contagem de células vermelhas e distribuição da largura das células vermelhas^6,7. A contagem de células brancas, os parâmetros individuais das células brancas e marcadores derivados, tais como a razão neutrófilos/linfócitos, foram relacionados com a gravidade e o prognóstico da DAC⁷. O uso integrado desses parâmetros facilmente obtidos juntamente com os outros e com os fatores de risco convencionais da DAC, poderia dar informações clinicamente mais relevante do que os testes individuais.

Embora diversos pequenos estudos ou estudos retrospectivos tenham repetidamente demonstrado o valor do VPM em uma variedade de doenças cardiovasculares, a utilidade clínica do VPM em grandes ensaios randomizados ainda precisa ser demonstrado. Este ponto foi enfatizado corretamente em uma recente revisão feita por Leader e cols.⁸. A realização de ensaios de tamanho adequado, prospectivos e randomizados deve ser incentivada para avaliar a utilidade do VPM e marcadores semelhantes baseados no HC na prática clínica.

Sinceramente,

Tolga Sinan Güvenç

Referências

1. 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(1):148-56.

2. Kamath S, Blann AD, Lip GY. Platelet activation: assessment and quantification. Eur Heart J. 2001;22(17):1561-71.

3. De Luca G, Santagostino M, Secco GG, Cassetti E, Giuliani L, Franchi E, et al. Mean platelet volume and the extent of coronary artery disease: results from a large prospective study. Atherosclerosis. 2009;206(1):292-7.

4. Ihara A, Kawamoto T, Matsumoto K, Shouno S, Hirahara C, Morimoto T, et al. Relationship between platelet indexes and coronary angiographic findings in patients with ischemic heart disease. Pathophysiol Haemost Thromb. 2006;35(5):376-9.

5. Güvenç TS, Hasdemir H, Erer HB, Ilhan E, Ozcan KS, Calık AN, et al. Lower than normal mean platelet volume is associated with reduced extent of coronary artery disease. Arq Bras Cardiol. 2013;100(3):255-60.

6. Ilhan E, Guvenç TS, Altay S, Çagdas M, Calik AN, Karaca M, et al. Predictive value of red cell distribution width in intrahospital mortality and postintervention thrombolysis in myocardial infarction flow in patients with acute anterior myocardial infarction. Coron Arter Dis. 2012;23(7):450-4.

7. Madjid M, Fatemi O. Components of the complete blood count as risk predictors for coronary heart disease: in-depth review and update. Tex Heart Inst J. 2013;40(1):17-29.

8. Leader A, Pereg D, Lishner M. Are platelet volume indices of clinical use? A multidisciplinary review. Ann Med. 2012;44(8):805-16.

• 2. Balta S, Demirkol S, Celik T, Kucuk U, Unlu M, Arslan Z, et al. Association between coronary artery ectasia and neutrophil-lymphocyte ratio. Angiology. 2013 Mar 7. [Epub ahead of print]
• 3. Balta S, Demirkol S, Kucuk U, Unlu M. Hemostatic markers can be pivotal roles of risk factors for new-onset atrial fibrillation. Platelets. 2013 Apr 3. [Epub ahead of print]
• 4. Demirkol S, Balta S, Unlu M, Yuksel UC, Celik T, Arslan Z, et al. Evaluation of the mean platelet volume in patients with cardiac syndrome X. Clinics (São Paulo). 2012;67(9):1019-22.
• 5. Cingoz F, Iyisoy A, Demirkol S, Sahin MA, Balta S, Celik T, et al. Carotid intima-media thickness in patients with slow coronary flow and its association with neutrophil-to-lymphocyte ratio: a preliminary report. Clin Appl Thromb Hemost. 2013 Apr 23. [Epub ahead of print]
• 1. 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(1):148-56.
• 2. Kamath S, Blann AD, Lip GY. Platelet activation: assessment and quantification. Eur Heart J. 2001;22(17):1561-71.
• 3. De Luca G, Santagostino M, Secco GG, Cassetti E, Giuliani L, Franchi E, et al. Mean platelet volume and the extent of coronary artery disease: results from a large prospective study. Atherosclerosis. 2009;206(1):292-7.
• 4. Ihara A, Kawamoto T, Matsumoto K, Shouno S, Hirahara C, Morimoto T, et al. Relationship between platelet indexes and coronary angiographic findings in patients with ischemic heart disease. Pathophysiol Haemost Thromb. 2006;35(5):376-9.
• 6. Ilhan E, Guvenç TS, Altay S, Çagdas M, Calik AN, Karaca M, et al. Predictive value of red cell distribution width in intrahospital mortality and postintervention thrombolysis in myocardial infarction flow in patients with acute anterior myocardial infarction. Coron Arter Dis. 2012;23(7):450-4.
• 7. Madjid M, Fatemi O. Components of the complete blood count as risk predictors for coronary heart disease: in-depth review and update. Tex Heart Inst J. 2013;40(1):17-29.
• 8. Leader A, Pereg D, Lishner M. Are platelet volume indices of clinical use? A multidisciplinary review. Ann Med. 2012;44(8):805-16.

Publication Dates

• Publication in this collection
  20 Sept 2013
• Date of issue
  Sept 2013