i n d i a n h e a r t j o u r n a l 6 7 ( 2 0 1 5 ) 4 0 9 e4 1 0
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.elsevier.com/locate/ihj
Correspondence
Mean platelet volume in acute coronary syndrome
Mean platelet volume in acute coronary syndrome We have carefully read the article by Dehghani et al1 entitled “Diagnostic importance of admission platelet volume indices in patients with acute chest pain suggesting acute coronary syndrome” published in the November issue of Indian Heart J. 2014;66:622e62. The authors have found that mean platelet volume (MPV), platelet distribution width (PDW), and platelet large cell ratio (P-LCR) values in the patients with acute myocardial infarction (MI) were higher than the non-acute coronary syndromes (ACS) and control groups. They have also found that MPV is similar between the patients with MI and unstable angina. Unlike the study by Dehghani, in our study MPV values were higher in patients with MI than unstable angina (p < 0.001).2 The question of why the mechanisms of MPV, PDW, and P-LCR are shown to be higher was not well explained in the present study. The MPV may be affected by platelet age and number, thrombopoetin and interleukin-6, coronary risk factors, thyroid and rheumatic diseases, malignancy and medications.3 In a study we compared the total antioxidant capacity levels by MPV values (n ¼ 111, 64% male), and found that in patients with ACS compared to healthy control subjects, plasma total antioxidant capacity levels (1.31 ± 0.33 mmol Trolox equivalent/L versus 1.57 ± 0.38 mmol Trolox equivalent/ L; p < 0.001, respectively) and MPV values (10.7 ± 1.7 fL versus 8.8 ± 1.5 fL; p < 0.001, respectively) were significantly different. The study further showed that there was an important negative correlation between total antioxidant capacity and MPV (r ¼ 0.740, p < 0.001). In multivariate linear regression analysis, MPV was found independently associated with total antioxidant capacity (b ¼ 0.694, p < 0.001) which may indicate that the increased MPV levels in patients with ACS may be responsible for the decreased levels of plasma total antioxidant capacity.3 Thus it may be better to co-relate the increased MPV with other serum inflammatory, oxidative markers and other parameters of platelet function. Whether the increased MPV is a result of ACS or the high MPV values actually led to the ACS require further investigation. On the other hand increased MPV levels may have been related to chronic rather than acute condition. Indeed Martin et al found that MPV starts to increase before the MI and it remains elevated six weeks after MI.4
The sensitivity and the specificities of the MPV, PDW, and P-LCR to predict MI among patients suffering from chest pain are low: 72% and 40%; 73% and 37%; 68% and 44%, respectively. Whereas MPV is well-standardized marker of pathophysiology and of risk stratification in coronary artery disease,5 there are not much information about PDW in the diagnosis of chest pain and the risk stratification of ACS, and the reliability of these parameters is still being questioned. The lines on the receiver operating characteristic curves graph (Fig. 2, in that study) are near the line of zero discrimination with an AUC of 0.563, 0.557, and 0.560, respectively. These results reveal that the test is no better.6 Therefore, it is difficult to say that these parameters are diagnostic tools to detect MI.
Conflicts of interest The authors have none to declare.
references
1. Dehghani MR, Taghipour-Sani L, Rezaei Y, et al. Diagnostic importance of admission platelet volume indices in patients with acute chest pain suggesting acute coronary syndrome. Indian Heart J. 2014;66:622e628. 2. Erkus ME, Altiparmak IH, Kaya Z, et al. Total antioxidant capacity and mean platelet volume in acute coronary sendrome (Akut koroner sendromda total antioksidan kapasite ve ortalama trombosit hacmi). MN Kardiyol. 2015;22, 0e00. 3. Vatankulu MA, Sonmez O, Ertas G, et al. A new parameter predicting chronic total occlusion of coronary arteries: platelet distribution width. Angiology. 2014;65:60e64. 4. Martin JF, Plumb J, Kilbey RS, et al. Changes in volume and density of platelets in myocardial infarction. BMJ Clin Res Ed. 1983;287:456e459. 5. Chu SG, Becker RC, Berger PB, et al. Mean platelet volume as a predictor of cardiovascular risk: a systematic review and metaanalysis. J Thromb Haemost. 2010;8:148e156. 6. Lalkhen AG, McCluskey A. Clinical tests: sensitivity and specificity. Contin Educ Anaesth Crit Care Pain. 2008;8: 221e223.
410
i n d i a n h e a r t j o u r n a l 6 7 ( 2 0 1 5 ) 4 0 9 e4 1 0
Musluhittin Emre Erkus* Recep Demirbag Harran University Faculty of Medicine, Department of Cardiology, Sanliurfa 63100, Turkey
E-mail address: [email protected] (M.E. Erkus)
*Corresponding author. Tel.: þ90 414 318 30 00x2397; fax: þ90 414 318 33 56.
0019-4832/$ e see front matter Copyright © 2015, Cardiological Society of India. All rights reserved. http://dx.doi.org/10.1016/j.ihj.2015.05.004
Available online 8 July 2015
Available online at www.sciencedirect.com
ScienceDirect journal homepage: www.elsevier.com/locate/ihj
Correspondence
Mean platelet volume in acute coronary syndrome
Mean platelet volume in acute coronary syndrome We have carefully read the article by Dehghani et al1 entitled “Diagnostic importance of admission platelet volume indices in patients with acute chest pain suggesting acute coronary syndrome” published in the November issue of Indian Heart J. 2014;66:622e62. The authors have found that mean platelet volume (MPV), platelet distribution width (PDW), and platelet large cell ratio (P-LCR) values in the patients with acute myocardial infarction (MI) were higher than the non-acute coronary syndromes (ACS) and control groups. They have also found that MPV is similar between the patients with MI and unstable angina. Unlike the study by Dehghani, in our study MPV values were higher in patients with MI than unstable angina (p < 0.001).2 The question of why the mechanisms of MPV, PDW, and P-LCR are shown to be higher was not well explained in the present study. The MPV may be affected by platelet age and number, thrombopoetin and interleukin-6, coronary risk factors, thyroid and rheumatic diseases, malignancy and medications.3 In a study we compared the total antioxidant capacity levels by MPV values (n ¼ 111, 64% male), and found that in patients with ACS compared to healthy control subjects, plasma total antioxidant capacity levels (1.31 ± 0.33 mmol Trolox equivalent/L versus 1.57 ± 0.38 mmol Trolox equivalent/ L; p < 0.001, respectively) and MPV values (10.7 ± 1.7 fL versus 8.8 ± 1.5 fL; p < 0.001, respectively) were significantly different. The study further showed that there was an important negative correlation between total antioxidant capacity and MPV (r ¼ 0.740, p < 0.001). In multivariate linear regression analysis, MPV was found independently associated with total antioxidant capacity (b ¼ 0.694, p < 0.001) which may indicate that the increased MPV levels in patients with ACS may be responsible for the decreased levels of plasma total antioxidant capacity.3 Thus it may be better to co-relate the increased MPV with other serum inflammatory, oxidative markers and other parameters of platelet function. Whether the increased MPV is a result of ACS or the high MPV values actually led to the ACS require further investigation. On the other hand increased MPV levels may have been related to chronic rather than acute condition. Indeed Martin et al found that MPV starts to increase before the MI and it remains elevated six weeks after MI.4
The sensitivity and the specificities of the MPV, PDW, and P-LCR to predict MI among patients suffering from chest pain are low: 72% and 40%; 73% and 37%; 68% and 44%, respectively. Whereas MPV is well-standardized marker of pathophysiology and of risk stratification in coronary artery disease,5 there are not much information about PDW in the diagnosis of chest pain and the risk stratification of ACS, and the reliability of these parameters is still being questioned. The lines on the receiver operating characteristic curves graph (Fig. 2, in that study) are near the line of zero discrimination with an AUC of 0.563, 0.557, and 0.560, respectively. These results reveal that the test is no better.6 Therefore, it is difficult to say that these parameters are diagnostic tools to detect MI.
Conflicts of interest The authors have none to declare.
references
1. Dehghani MR, Taghipour-Sani L, Rezaei Y, et al. Diagnostic importance of admission platelet volume indices in patients with acute chest pain suggesting acute coronary syndrome. Indian Heart J. 2014;66:622e628. 2. Erkus ME, Altiparmak IH, Kaya Z, et al. Total antioxidant capacity and mean platelet volume in acute coronary sendrome (Akut koroner sendromda total antioksidan kapasite ve ortalama trombosit hacmi). MN Kardiyol. 2015;22, 0e00. 3. Vatankulu MA, Sonmez O, Ertas G, et al. A new parameter predicting chronic total occlusion of coronary arteries: platelet distribution width. Angiology. 2014;65:60e64. 4. Martin JF, Plumb J, Kilbey RS, et al. Changes in volume and density of platelets in myocardial infarction. BMJ Clin Res Ed. 1983;287:456e459. 5. Chu SG, Becker RC, Berger PB, et al. Mean platelet volume as a predictor of cardiovascular risk: a systematic review and metaanalysis. J Thromb Haemost. 2010;8:148e156. 6. Lalkhen AG, McCluskey A. Clinical tests: sensitivity and specificity. Contin Educ Anaesth Crit Care Pain. 2008;8: 221e223.
410
i n d i a n h e a r t j o u r n a l 6 7 ( 2 0 1 5 ) 4 0 9 e4 1 0
Musluhittin Emre Erkus* Recep Demirbag Harran University Faculty of Medicine, Department of Cardiology, Sanliurfa 63100, Turkey
E-mail address: [email protected] (M.E. Erkus)
*Corresponding author. Tel.: þ90 414 318 30 00x2397; fax: þ90 414 318 33 56.
0019-4832/$ e see front matter Copyright © 2015, Cardiological Society of India. All rights reserved. http://dx.doi.org/10.1016/j.ihj.2015.05.004
Available online 8 July 2015
