Factors influencing the use of ambulance among patients with acute coronary syndrome: results of two centers in Turkey

Abstract

We are pleased by interest and valuable comments by authors. They correctly pointed out some unclarities in our letter, as some information were not presented due to limited extend of scientific letter format (1). We are glad to supplement this information here.The first remark was about the method used for blood sample collection. EDTA containing tubes were used for mean platelet volume and platelet count examination. All samples were processed in less than 2 hours. According to the literature (2) and our experience in such settings the mean platelet volume increase does not excess 10%. Moreover, using a citrate can result in changes of mean platelet count (2). Samples for aggregometry were collected in hirudine, which seems to produce better results than citrate or lepirudine and is generally available for this method (3).Another remark concerned the potential bias caused by impact of comorbidities on mean platelet volume. In his letter a detailed summary of such confounding factors, namely smoking, obesity, hyperlipidemia, hypertension, coronary artery disease, metabolic syndrome, statin use and atrial fibrillation is presented. These associations correlate with finding that patients with higher mean platelet volume are in higher risk of ischemic heart disease (4) suggests that such bias must be excluded.We analyzed the influence of smoking, diabetes, atrial fibrillation, left ventricle systolic dysfunction (5) [ejection fraction <40% and inflammation (6) (hs-CRP >20 mg/L (7)]. C-reactive protein was measured using CRPL3 Tina-quant C-Reactive Protein Gen. 3 assays by Roche Diagnostics, Germany. Statin use was not added in statistical analysis, because only three patients were not treated using these agents. None of risk factors mentioned above was associated with increased mean platelet volume (Table 1). Regression analysis was not beneficial either.Therefore we expect that the relation of mean platelet volume to both high on-treatment platelet reactivity and increased mortality is rather based on alteration of platelet functions than by concomitant association with another risk factor. Unfortunately, number of patients is insufficient for detailed statistical evaluation. This study also cannot explain the exact etiology of platelet function impairment. Despite these limitations the study suggests that mean platelet volume can be used as marker of high on-treatment platelet reactivity and for risk stratification.