Deniz Şahin

Increased mean platelet volume in patients with infective endocarditis and embolic events.

BACKGROUND Platelet activation appears to play an important role in thromboembolic complications of infective endocarditis (IE). Mean platelet volume (MPV) is a potentially useful marker of platelet activity and a quick and easy determinant of thrombotic risk. Hence the aim of this study was to investigate the baseline platelet volume indices (MPV and platelet distribution width [PDW]) in IE patients who developed embolic events in the follow-up period and who did not. METHODS The study group consisted of 76 consecutive patients (female: 55, male: 21, mean age: 26 years old, ranged: 8-64 years) with definite IE according to Duke Criteria. Thirty four healthy subjects, who were age and gender adjusted, served as the control group. The mean duration of hospital stay was 44 days. RESULTS Among the IE patients, 13 (13/76, 17.1%) had major embolic events. Significantly larger vegetations were observed in patients with embolic events as compared to non-embolic group (1.4 vs. 1.0 cm, p = 0.03). MPV at hospital admission was higher in patients who had embolic events in the follow-up period compared to both those who did not and the control subjects (10.62 ± 1.13 vs. 9.25 ± 0.97 and 8.93 ± 0.82 fL, p < 0.001, respectively). Similarly, the patients with embolic events had increased PDW compared to the non-embolic ones and the control group (16.31 ± 2.42 vs. 14.35 ± 1.97 and 14.04 ± 1.82%, p < 0.001, respectively). CONCLUSIONS The present study demonstrated that IE patients with embolic events had increased MPV and PDW values, compared to non-embolics. Future prospective studies with standardized measurements may clarify the clinical role of platelet volume indices in thrombo-embolic complications of IE.

Increased mean platelet volume in rheumatic mitral stenosis: assessment of clinical and echocardiographic determinants

BACKGROUND AND AIM The aim of this study was to investigate mean platelet volume (MPV) in patients with rheumatic mitral stenosis (RMS) and to define the determinants of a possible platelet activation reflected as platelet volume enlargement. METHODS Peripheral venous plasma value of MPV was measured in 84 consecutive patients (16 men, 68 women; mean age ± SD = 44 ± 13 years) with RMS who had no left atrial thrombus by transoesophageal echocardiography. The control group consisted of 32 healthy subjects (nine men, 23 women; mean age ± SD = 38 ± 7 years). RESULTS The patients had significantly higher MPV values (mean ± SD = 10.07 ± 0.58 fL) compared to the healthy subjects (mean ± SD = 8.15 ± 0.60 fL, p < 0.001). Among many clinical and echocardiographic variables, left atrial spontaneous echo contrast-positivity (beta = 0.426, p < 0.001) and severe mitral regurgitation (beta = 0.577, p < 0.001) appeared as significant predictors of platelet enlargement in RMS in multiple linear regression analysis. CONCLUSIONS Patients with RMS have increased platelet activity reflected as elevated MPV; and the coexistence of severe mitral regurgitation and presence of left atrial spontaneous echo contrast are determinants of this increment.

A new risk scoring model for prediction of poor coronary collateral circulation in acute non-ST-elevation myocardial infarction

BACKGROUND We aimed to investigate the clinical features associated with development of coronary collateral circulation (CCC) in patients with acute non-ST-elevation myocardial infarction (NSTEMI) and to develop a scoring model for predicting poor collateralization at hospital admission. METHODS The study enrolled 224 consecutive patients with NSTEMI admitted to our coronary care unit. Patients were divided into poor (grade 0 and 1) and good (grade 2 and 3) CCC groups. RESULTS In logistic regression analysis, presence of diabetes mellitus, total white blood cell (WBC) and neutrophil counts and neutrophil to lymphocyte ratio (NLR) were found as independent positive predictors of poor CCC, whereas older age (≥ 70 years) emerged as a negative indicator. The final scoring model was based on 5 variables which were significant at p < 0.05 level following multivariate analysis. Presence of diabetes mellitus, and elevated total WBC (≥ 7.85 × 103/μL) and neutrophil counts (≥ 6.25 × 103/μL) were assigned with 2 points; high NLR (≥ 4.5) with 1 point and older age (≥ 70 years old) with -1 point. Among 30 patients with risk score ≤ 1, 29 had good CCC (with a 97% negative predictive value). On the other hand, 139 patients had risk score ≥ 4; out of whom, 130 (with a 93.5% positive predictive value) had poor collateralization. Sensitivity and specificity of the model in predicting poor collateralization in patients with scores ≤ 1 and ≥ 4 were 99.2% (130/131) and +76.3 (29/38), respectively. CONCLUSIONS This study represents the first prediction model for degree of coronary collateralization in patients with acute NSTEMI.

PP-097 Mild Hypereosinophilia During Warfarin Therapy: Report of Two Cases and a Short Review of the Literature

A B S T R Objective: Warfarin is widely used in clinical practice. Its most known side effects are hemorrhage and skin adverse reactions.We report two cases in whom mild eosinophilia appeared after initiation of warfarin therapy. Methods-Results: A 43-year-old man presented with dyspnea, hemoptisis and chest pain. The final diagnosis was acute pulmonary thromboembolism following acute deep venous thrombosis(DVT). He was treated with low molecular weight heparin (LMWH) and warfarin. The eosinophil count was normal before initiation of warfarin. However the eosinophil ratio gradually increased to 10% (800/mm) in the first week. The examination for ova and parasites was negative. Blood biochemistry and several kinds of allergen tests were normal. IgE level was slightly increased. The INR value of the patient increased very quickly and daily need was 1.25 mg to stabilize INR between 2-3. With 8.75 mg/week dosing, the eosinophil count was stabilized at 600/mm. The patient was heterozygos for factor V Leiden and he was experiencing a second attack of DVT. Therefore he had a lifelong oral anticoagulation (OAC) therapy indication. A second 55-year-old male patient presented with rapid ventricular response lone atrial fibrillation(AF). During discharge 27.5 mg/week warfarin was started. On his first control 10 days later,the INR was 17. He was hospitalized to receive vitamin K and fresh frozen plasma. Hemogrambefore AF attackwas normal, but when hewas hospitalized for warfarin overdose he had 10% (appr. 800/mm) eosinophils in the peripheral blood.Allergy and parasites testswere negative.He was not on any medications other than warfarin. During discharge we started 20mg/day rivaroxaban and 25 mg carvediolol. The eosinophil count decreased to 400/mm one month after cessation of warfarin. Conclusions: Besides hemorrhage, skin adverse reactions, hipersensitivity or liver disorders, there are reports that warfarin can cause eosinophilia.Normal eosinophil count is up to 600 cells/mm.Mild eosinophilia is 600-1500 eosinophils, moderate is 1500-5000 and severe is 5000 eosinophils per microlitre. Drugs can be responsible for eosinophilia. The most commondrugs are aspirin, penicillin, gold compoundsor sulfa agents. In 1981, first report on severe hypereosinophilia related with warfarin use was published. Similar several cases followed this index report. The common point in our two patients was a propensity for warfarin overdose.The approach to this clinical entity is not known. Warfarin therapy should be ceased in symptomatic severe hypereosinophilia. In one patient we switched to rivaroxaban, but in the other we continued warfarin due to economical issues. NewOACs are not an alternative for all patients,such as those having metallic heart valves. We should be aware of this adverse effect of warfarin. We can periodically check hemogram together with hemostasis panel, because the eosinophil counts can increase to deleterious numbers.

OP-010 Increased Mean Platelet Volume in Patients with Infective Endocarditis and Embolic Events

Background: Platelet activation appears to play an important role in thromboembolic complications of infective endocarditis (IE). Mean platelet volume (MPV) is a potentially useful marker of platelet activity and a quick and easy determinant of thrombotic risk. Hence the aim of this study was to investigate the baseline platelet volume indices (MPV and platelet distribution width [PDW]) in IE patients who developed embolic events in the follow-up period and who did not. Methods: The study group consisted of 76 consecutive patients (female: 55, male: 21, mean age: 26 years old, ranged: 8–64 years) with definite IE according to Duke Criteria. Thirty four healthy subjects, who were age and gender adjusted, served as the control group. The mean duration of hospital stay was 44 days. Results: Among the IE patients, 13 (13/76, 17.1%) had major embolic events. Significantly larger vegetations were observed in patients with embolic events as compared to non-embolic group (1.4 vs. 1.0 cm, p = 0.03). MPV at hospital admission was higher in patients who had embolic events in the follow-up period compared to both those who did not and the control subjects (10.62 ± 1.13 vs. 9.25 ± 0.97 and 8.93 ± 0.82 fL, p < 0.001, respectively). Similarly, the patients with embolic events had increased PDW compared to the non-embolic ones and the control group (16.31 ± 2.42 vs. 14.35 ± 1.97 and 14.04 ± 1.82%, p < 0.001, respectively). Conclusions: The present study demonstrated that IE patients with embolic events had increased MPV and PDW values, compared to non-embolics. Future prospective studies with standardized measurements may clarify the clinical role of platelet volume indices in thromboembolic complications of IE. (Cardiol J 2015; 22, 1: 37–43)