We enrolled 514 STEMI patients who were undergoing primary PCI between January 2008 and June 2015. The patients with malignancy or infectious disease or autoimmune disease or hematologic disease and patients with incompleted data were excluded from this study. The final analysis included 480 patients. Permission of study was obtained by a local ethics committee. STEMI diagnosis was established as typical angina pain lasting > 30 min, with increase in levels of cardiac enzymes (troponin I levels) and electrocardiographic evidence of elevation of the ST segment of > 1 mm in two or more consecutive leads or the presence of new left bundle branch block (LBBB) [13]. We defined hypertension (HT) as the previous use of antihypertensive medication, systolic pressure > 140 mmHg or diastolic pressure > 90 mmHg and Diabetes mellitus as the use of insulin or antidiabetic agents or a fasting glucose level > 126 mg/dL. Hypercholesterolemia was diagnosed as total cholesterol of ≥200 mg/dL. Smoking was defined as a current smoker or not. This study complied with the Declaration of Helsinki.

We defined total mortality as death due to any cause at follow-up and considered as the primary end point. Morever, repeat revascularization, heart failure admission, and stroke/transient ischemic attack (TIA), and 30-day mortality were also evaluated. We obtained follow-up data from the hospital records, patients, and their relatives.

All patients were treated according to the current guidelines.13 Primary PCI was performed using standard techniques via the transfemoral approach by 2-experienced interventional cardiologists. The treatment strategies for each patient were left to the discretion of interventional cardiologists. We obtained angiographic data from the cardiac catheterization laboratory records. The infarct-related artery (IRA) was evaluated based on the thrombolysis in myocardial infarction (TIMI) classification. We defined invasive success in acute phase as reduction to < %20 in IRA obstruction and stenosis with TIMI-3 flow immediately after primary PCI. After angioplasty, all patients were transferred to intensive care unit. Dual antiplatelet therapy, beta-blockers, angiotensin-converting enzyme inhibitors (ACE-I), angiotensin receptor-blocker (ARB), and statins were administered according to current guidelines [13].

The left ventricle ejection fraction (LVEF) was calculated after measuring the end-diastolic and end-systolic left ventricle (LV) volumes in the apical four-chamber and two-chamber views using the modified Simpson’s method.

Peripheral blood was obtained for MPV analysis at admission prior to administration of antiplatelet drugs and 48–72 h after admission. Blood samples were collected into standardized tubes containing dipotassium ethylenediaminetetraacetate powder as anticoagulant and stored at room temperature. All measurements were analyzed within 1 h after collection. Change in MPV was defined as ΔMPV (MPV at 48–72 h minus MPV on admission). An extra blood was collected on admission for biochemical analysis. They were evaluated by standard methods.

Statistical analysis was made using SPSS software (version 16.0; SPSS Inc., Chicago, IL, USA). Variables with normal distribution were analyzed using Kolmogorov-Smirnov test and presented as mean ± standart deviation, while those without normal distribution were presented as medians with a range. Categorical variables were presented as number and percentage. The comparisons between groups was carried out using the chi-square test for categorical variables and Student t tests or Mann-Whitney U test for continuous variables. A multivariate cox regression analysis was carried out to evaluate whether ΔMPV was an independent predictor of mortality. Factors with a p value of < 0.1 by univariate analysis were included in multivariate cox regression analysis. The predictive values of a multivariable model and a combination of ΔMPV with a multivariable model were estimated by comparing the areas under the receivers operating characteristic (ROC) curve. DeLong’s test was used to compare the AUC from each of models [14], which were analysed by use of NCSS 12 software programme. Morever, the increased discriminative value after the addition of ΔMPV to a multivariable model was also estimated using the Net Reclassification Improvement (NRI) and Integrated Discrimination Improvement [15]. Differences were considered significant at the 2-sided p <  0.05 level.

Baseline demographic, and clinical characteristics are shown in Table 1. Median follow-up time was 65.9 (41.9–80.4) months. The non-survivors were significantly older (68 ± 13 vs 58 ± 11, p <  0.001). The histories of diabetes mellitus, HT, stroke/TIA were more common in non-survivors compared with survivors (Table 1). The frequency of Killip class ≥2 and multi-vessel disease were higher in non-survivors than survivors. Compared with survivors there was a higher proportion of women in non-survivors. The rates of usage of ACE-I/ARB and beta-blockers after discharge were lower in the non-survivors than survivors.

Laboratory variables are provided in Table 2. Serum creatinine level at admission was higher in the non-survivors. Compared with survivors, admission hemoglobin level was lower in the non-survivors. There was no significant difference between groups in terms of platelet counts both at admission and at 48–72 h. MPV at 48–72 h was higher in non-survivors than survivors. Compared with survivors, non-survivors had a high ΔMPV value [0.79 (0.30–1.40) vs 0.37 (− 0.1–0.89), p < 0.001]. Baseline MPV was similar between groups.

Thirty-day mortality rate was 20% in the non-survivors (Table 1). The frequencies of TVR, stroke, and MI were comparable between groups. Non-survivors had a higher incidence of HF admission compared with survivors (14% vs 2%, p < 0.001).

ΔMPV (HR: 1.301 [1.070–1.582], p = 0.008), Killip class ≥2, LVEF, history of stroke/TIA and age were independent predictors of long-term mortality in multivariate analysis (Table 3).

The ROC curve analysis of ΔMPV revealed an area under the curve (AUC) of 0.646 for the prediction of long-term mortality. (Fig. 1). Morever, for long-term mortality, the AUC of a multivariable model that included age, LVEF, Killip class, and history of stroke/TIA was 0.781 (95% CI:0.731–0.832, p <  0.001). When ΔMPV was added to a multivariable model, the AUC was 0.800 (95% CI: 0.750–0.848, z = 2.256, difference p = 0.0241, Fig. 1). Also, the addition of ΔMPV to a multivariable model was associated with a significant net reclassification improvement estimated at 24.5% (p = 0.027) and an integrated discrimination improvement of 0.014 (p = 0.0198). Kaplan-Meier survival curves according to a cut-point of ΔMPV (≥ 0.44 fL and < 0.44 fL) are shown in Fig. 2. In the subgroup analysis which was carried out according to the this cut-point, 30-day mortality (2% vs 6%, p = 0.009), long-term mortality (16% vs 30%, p < 0.001), and heart failure admission (3% vs 7%, p = 0.028) were higher in high ΔMPV group compared with low ΔMPV group. There was no significant difference between groups in terms of myocardial reinfarction (8% vs 8%, p = 0.756), stroke (3% vs 3%, p = 0.998) and TVR (12% vs 12%, p = 0.974).