Preprocedural high-thrombus burden (HTB) of infarct-related artery (IRA) is a harbinger of procedural complications following primary percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI). The HTB of IRA can lead to poor outcomes by various mechanisms, including no-reflow phenomenon, increased myocardial necrosis and with subsequent reduced survival benefit at follow-up. In this study, we investigated the relationship between all platelet indices on admission and thrombus burden and the no-reflow phenomenon after primary PCI of IRA in patients with STEMI. We retrospectively enrolled 475 patients with STEMI undergoing primary PCI. Study population was divided into two groups according to the thrombolysis in myocardial infarction thrombus grade of IRA as low-thrombus burden or HTB. There were no statistically significant differences in platelet indices, including platelet count, platelet-large cell ratio (P-LCR), mean platelet volume (MPV) and platelet distribution with (PDW) among the groups. However, in the subgroup analysis, P-LCR, MPV and PDW were significantly higher in the no-reflow patients than reflow patients despite similar platelet count (P for all < 0.001). The cutoff value of P-LCR for predicting no-reflow was 26.5% with a sensitivity of 67.0% and a specificity of 62% (area under the curve, 0.689; 95% confidence interval, 0.614-0.765; P < 0.001). Furthermore, P-LCR, MPV and PDW had similar AUC (0.689, P < 0.001; 0.688, P < 0.001; and 0.677, P < 0.001; respectively) for predicting no-reflow phenomenon after primary PCI. As a result, all of the platelet indices have no effect on thrombus load of IRA, however, these parameters seem to impair epicardial perfusion after primary PCI.

In patients with CTO, a poor coronary collateral status and multivessel disease may further impair electrical homogeneity. Our results indicate that successful CTO PCI reduces the arrhythmic vulnerability of the myocardium on the basis of an analysis of the TpTe, the TpTe/QT ratio, and QTc dispersion.

A dilated CS was associated with moderate to severe pulmonary hypertension, and RA area and PASP were independent predictors of CS diameter.

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Adult T cell leukemia/lymphomas are aggressive disorders, which infiltrate not only the bone marrow but extensively the visceral organs as well. A case with left ventricular systolic dysfunction with myocardial infiltration and massive pericardial effusion which was demonstrated with echocardiography is discussed. The patient responded well to pericardial drainage and subsequent chemotherapy. The dramatic improvement in echocardiographic findings after chemotherapy gave a clue to investigate suspected patients with aggressive leukemia and lymphomas for exclusion of leukemic infiltration of myocardium. KEYWORDSAdult T cell leukemia/ lymphomas; Echocardiography; Pericardial effusion; Left ventricular dysfunction Case reportA 19 year old male patient was admitted to our center with ongoing dyspnea for 3-4 days. His physical examination revealed hepatosplenomegaly but no skin lesions or peripheral lymphadenopathy. His chest X-ray revealed massive mediastinal enlargement and signs of massive pericardial effusion. In ECG we observed sinusal tachycardia, incomplete left bundle branch block and nonspecific T-wave abnormalities. In echocardiographic examination left ventricular end diastolic diameter was 5.6 cm, and there was an increase in left ventricular thickness with heterogeneous echogenicity. Left ventricular posterior wall thickness was 3.0 cm, apical thickness was 3.1 cm, and anterior wall was 2.0 cm. There was segmental wall motion abnormality and ejection fraction was calculated as 40%. There was a significant interventricular dyssynchronization of the left ventricle in the tissue synchronization imaging. Additionally, myocardial velocities, peak systolic strain and strain rate values were lower in the myocardial segments with hypoechogenic areas in comparison to the same parameters detected on the normoechogenic areas. Both valvular functions were normal and only a mild mitral regurgitation was detected.Emergency pericardiocentesis and underwater tube drainage was performed because of progressive cardiac tamponade. Cytology of the pericardial fluid was negative for malignancy. However, the microscopical exam showed atypical lymphoid cells. Cultures and the PCR for mycobacterium were negative. On admission he showed a hemoglobin level of 14.4 g/dl, platelet count of 44 Â 10 9 /L and WBC count of 44.6 Â 10 9 /L. Coagulation studies were: partial thromboplastin time, 15.3 s; fibrinogen, 2.21 g/l. Other laboratory tests revealed calcium of 3.69 mmol/dl (range, 2.15-2.55 mmol/dl), LDH of 5245 U/L (range, 240-480 U/dl), CK-MB of 39 U/L (range, 0-24 U/L). The patient was referred to the hematology department of a university hospital.Peripheral blood smear revealed neutropenia and 90% blasts. Bone marrow biopsy was hypercellular with blastic infiltration destroying the normal hematopoietic architecture. Flow cytometric analysis demonstrated that the blasts were positive for CD, TdT, CD, cytoplasmic CD, CD, CD, CD, CD and negative for CD, HLA-DR and surface CD. These findings were consistent with adult T cell leukemia...