Epstein-Barr virus-positive mucocutaneous ulcer is a newly recognized clinicopathologic entity in the spectrum of Epstein-Barr virus-positive lymphoproliferative disorders. This entity is characterized by a self-limited, indolent course. We report the case of a 74-year-old, type 2 diabetic man who presented with an ulceroinfiltrative skin lesion on the left side of his neck. Histological examination showed that the lesion consisted of large atypical cells, some with Hodgkin-Reed-Sternberg-like morphology, in the midst of reactive lymphocytes, plasma cells, eosinophils and histiocytes. The atypical cells were partially positive for CD45, CD20, CD79a, CD30, B-cell lymphoma 2 and latent membrane protein 1 (CS.1-4), and negative for CD15, B-cell lymphoma 6 and CD10. In situ hybridization for Epstein-Barr virus-encoded ribonucleic acid was positive. Two years before, the patient had been diagnosed with a self-limited subcutaneous abscess in the same anatomic area that healed after antibiotic therapy. Older patients with positive Epstein-Barr virus serology may develop B-cell lymphoproliferations due to age-related immune suppression. Epstein-Barr virus-encoded ribonucleic acid testing and clonality analysis, eventually complemented with close clinical follow-up, should be performed for suspicious inflammatory lesions in older patients.

During acute myocardial infarction, phosphorylated TnI levels, Ca2+ sensitivity and ATPase activity are decreased in the myocardium, and the subsequent elevation in Ca2+ levels activates protease I (caplain I), leading to the proteolytic degradation of troponins. Concurrently, the levels of apelin and APJ expression are increased by limiting myocardial injury. In this prospective observational study, 100 consecutive patients with ST-elevation acute myocardial infarction were included. Patients meeting the following criteria were included in our study: (1) continuous chest pain lasting for >30 min, (2) observation of ST-segment elevation of more than 2 mm in two adjacent leads by electrocardiography (ECG), (3) increased cardiac troponin I levels, and (4) patients who underwent reperfusion therapy. We evaluated the levels of apelin-12 and troponin I on the first and seventh days after reperfusion therapy in all patients. Apelin-12 was inversely correlated with troponin I levels (Spearman’s correlation = −0.40) with a p value 2.2 for the association of apelin with MACE was determined, and the AUC was 0.71 (95% CI, 0.58–0.84). Survival analysis using the Kaplan-Meier method showed a lower rate of MACE among patients with apelin levels >2.2 (p = 0.002), and the ROC curve analysis showed a statistically significant difference in the area under the curve (p = 0.004). The influence of apelin levels on troponin levels in the acute phase of STEMI is inversely correlated, whereas in the non-acute phase, low apelin values were associated with a high rate of MACE.

Background: Increased level of high‐sensitivity C‐reactive protein (hs‐CRP) is associated with no‐reflow phenomenon. Therefore, even when timely coronary revascularization is performed through the primary percutaneous coronary intervention (pPCI), the process can induce reperfusion injury. Purpose: We evaluated the influence of hs‐CRP level on the no‐reflow phenomenon in patients with ST‐segment elevation myocardial infarction (STEMI). Methods: In this study, we included one hundred and eighty‐two consecutive patients with STEMI of onset < 12 h, who underwent pPCI. The levels of creatine kinase (CK), the MB fraction of creatine kinase (CK‐MB), troponin I, hs‐CRP, and other routine laboratory parameters were measured. Measurement of hs‐CRP was done on the day of admission by Cobas assay (particle‐enhanced immunoturbidimetric assay) on Cobas c501 (Roche). Thereafter, patients were divided in two groups according to the thrombolysis in myocardial infarction (TIMI) flow grade. Results: From a total of 182 STEMI patients who underwent pPCI, the median value of hs‐CRP of the patients with TIMI grade flow 3 (successful reperfusion) was 8.5 (0.4–268) and of the patients with no‐reflow phenomenon (unsuccessful reperfusion, TIMI flow grade ≤ 2) was 37.90 (1.8–271.20), p < 0.0001. Receiver operating characteristics (ROC) curve of hs‐CRP plots the true positive rate against the false positive rate at different cutoff points, AUC = 0.73 (95% CI, 0.64–0.81), and the cutoff value for the hs‐CRP was 18.0 mg/L, p = 0.0001. Conclusions: hs‐CRP may be associated with no‐reflow phenomenon in STEMI patients. The cutoff value for hs‐CRP may be used to identify patients at risk for reperfusion injury.

BACKGROUND:The aim of this study was to determine the correlation between the size of acute myocardial infarction (AMI) and the time of initiation of reperfusion therapy with cardiac perfusion scintigraphy. MATERIAL AND METHODS:Overall, 80 patients with acute ST elevation myocardial infarction (STEMI) were examined. All patients were treated with primary percutaneous coronary intervention (pPCI). Data on patient and system delay expressed in minutes were recorded and compared with recommended timelines. Cardiac scintigraphy was performed with 99m Tc-sestamibi single-photon emission computed tomography (SPECT). The median time of cardiac scintigraphy was 20 days. The correlation between the size of infarction and the time of initiation of reperfusion therapy was evaluated. RESULTS:The mean age of patients was 60.5±11.5 years, and 72.5% were male. The average system delay was 348 min, and the average patient delay was 173 min. The mean total ischemic time was 800 min. There was a correlation between time delays of reperfusion therapy and infarct size. Patients with a shorter time delay to patent artery after FMC showed smaller infarct size when compared to the patients with longer delay times. Multiple linear regression analysis showed that FMC, being male, and smokers had statistical significance when predicting infarct size. CONCLUSIONS:There is a correlation between the size of myocardial infarction and the time of initiation of reperfusion therapy determined by perfusion myocardial scintigraphy. The study showed that there are time delays in starting the treatment of AMI with pPCI when compared to the recommended time, which requires an action plan in the near future to ensure earlier treatment for our patients.

Immature teratoma in a mediastinal location is a rare disease that might present as a valve pathology. Germ cell tumors with mediastinal locations account for up to 6% of immature teratoma cases. We present a case of an immature teratoma located primarily in the anterior mediastinum that manifested solely through symptoms of pulmonary stenosis. We report a case of a 20-year-old white man with an immature teratoma who presented with progressive exertional dyspnea. During a cardiac examination, an ejection systolic murmur was observed, and echocardiography findings at an Emergency Centre revealed high velocity flow at the level of the pulmonary artery, indicating pulmonary stenosis. He was hospitalized in our Cardiology Department for further investigation. A chest X-ray revealed a mediastinal mass, and repeated echocardiography indicated the presence of a large mediastinal mass compressing his main pulmonary artery. Magnetic resonance imaging confirmed the tumor in the mediastinum, and a histopathological diagnosis of immature teratoma was established following biopsy. Immature teratoma causing cardiac-related complaints might shift the diagnosis toward cardiovascular diseases, thus requiring prompt examination by standard and sophisticated methods to clarify the diagnosis.

Coronary artery fistulas are anomalous connections between one or two coronary arteries with either a cardiac chamber or any major blood vessels (coronary sinus, superior vena cava, pulmonary veins and pulmonary artery). It is rarely reported, occurring only in 0.1%-0.2% of patients who undergo coronary angiography. We report a very rare case where myocardial ischaemia may have resulted from the presence of coronary artery fistula, significant coronary artery stenosis and severe aortic valve stenosis. Transthoracic echocardiography showed severe aortic stenosis, while coronary angiography showed a tortuous coronary artery fistula originating from the proximal left anterior descending artery, with a single opening in the main pulmonary artery. Angiography also showed significant stenosis in the middle of the left anterior descending artery. Coronary artery fistula with concomitant significant coronary atherosclerosis and severe aortic stenosis requires optimal therapeutic planning.