Epicardial fat thickness is associated with aortic intima-media thickness in patients without clinical manifestation of atherosclerotic cardiovascular disease.

BACKGROUND: Although the relationship between epicardial fat thickness (EFTh) and coronary atherosclerosis is well established, this relation in the early periods of atherosclerosis has not been fully demonstrated. On the other hand, thoracic aortic intima-media thickness (IMT) rather than carotid IMT was reported as an earlier marker of preclinical atherosclerosis. OBJECTIVE: We aimed to assess the relationship between thoracic aortic IMT and EFTh in patients undergoing transesophageal echocardiography (TEE) examination for different indications. METHODS: We included 104 patients (mean age 38±11.4 years), who underwent TEE for various indications. The patients were divided into two groups according to the median thoracic aortic IMT values (IMT normal group<10 mm and IMT abnormal group≥10 mm). EFTh was obtained using two-dimensional transthoracic echocardiography on the right ventricular free wall during systole and diastole. RESULTS: The highest EFTh values (3.3±0.96 mm vs. 4.51±0.66 mm, P<.001) were observed in the abnormal aortic IMT group. Multivariate linear regression analysis showed that aortic IMT was independently correlate with EFTh (ß=0.423, P<.001). Moreover, EFTh was found to be associated with history of transient ischemic attack (r=.403, P<.001) and abnormal IMT (r=.643, P<.001) in bivariate analysis. CONCLUSION: Epicardial fat thickness is independently related to the extent of subclinical thoracic aortic atherosclerosis. Increase in EFTh may be crucial marker for initial atherosclerosis.

Initial dose effect of 5-fluorouracil: rapidly improving severe, acute toxic myopericarditis.

5-Fluorouracil (5-FU) has a significant antineoplastic activity and has been used for the management of various malignant neoplasms. Cardiotoxicity of 5-FU is rare but may be life-threatening. A 55-year-old female patient was admitted to our hospital with atypical chest pain. Her electrocardiogram revealed widespread ST-segment elevations, and she had an elevated troponin level. Transthoracic echocardiography revealed global myocardial hypokinesia with impaired left ventricular systolic function (ejection fraction, 20%). Coronary angiography revealed normal coronary arteries with no vasospasm, and therefore, she was hospitalized with the diagnosis of acute toxic myopericarditis and was treated medically. In literature, this case is the first case of acute toxic myocarditis occurring because of the first dose of 5-FU.

Impact of Nonalcoholic Fatty Liver Disease on Myocardial Perfusion in Nondiabetic Patients Undergoing Primary Percutaneous Coronary Intervention for ST-Segment Elevation Myocardial Infarction.

Limited data exist on the role of nonalcoholic fatty liver disease (FLD) as a potential independent risk factor in the setting of acute coronary syndromes. The aim of this study was to evaluate the impact of FLD on myocardial perfusion and inhospital major adverse cardiac events (MACE) in the setting of ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). We examined 186 consecutive nondiabetic patients (mean age 58 ± 11 years and 76% men) who underwent primary PCI for STEMI by ultrasound within 72 hours of admission. FLD was graded according to a semiquantitative severity score as mild (score <3) or moderate to severe (score ≥3). Myocardial perfusion was determined by measuring myocardial blush grade (MBG) and ST-segment resolution (STR) analysis. Patients were divided into 2 groups according to FLD score (<3 or ≥3). There were no differences with regard to postprocedural Thrombolysis In Myocardial Infarction 3 flow grade between the 2 groups (89% vs 83%, p = 0.201). Patients with FLD score ≥3 were more likely to have absent myocardial perfusion (MBG 0/1, 37% vs 12%, p <0.0001), absent STR (27% vs 9%, p = 0.001), and higher inhospital MACE rate (31% vs 8%, p <0.0001). By multivariate analysis, FLD ≥3 score was found to be an independent predictor of absent MBG 0/1 (odds ratio [OR] 2.856, 95% confidence interval [CI] 1.214 to 6.225, p = 0.033), absent STR (OR 2.862, 95% CI 1.242 to 6.342, p = 0.031), and inhospital MACE (OR 2.454, 95% CI 1.072 to 4.872, p = 0.048). In conclusion, we found that despite similar high rates of Thrombolysis In Myocardial Infarction 3 after primary PCI, patients with FLD score ≥3 are more likely to have impaired myocardial perfusion which may contribute to adverse inhospital outcome.

From wide QRS tachycardia to a diagnostic surprise.

A 29-year old male patient presented with a hemodynamically significant ventricular tachycardia. Despite a comprehensive examination, the correct diagnosis was unfortunately established after two years. We discuss why the correct diagnosis was initially overlooked in physical examination, electrocardiogram, echocardiography and cardiac magnetic resonance imaging, and which findings led the cardiologists to misdiagnose the patient. We have organized this report in a format that the information is presented to a consultant physician by a resident physician to simulate the way such information emerges in the real life as we have encountered. The consultant physician responds as new information is presented, expressing his reasoning with the reader.

Acute myocardial infarction after capecitabine treatment: not always vasospasm is responsible.

Capecitabine is an orally available chemotherapeutic agent that is converted to 5-fluorouracil (5-FU) after absorbtion. Capecitabine and its active metabolite, 5-FU, have cardiotoxic effects with reported instances of acute coronary syndromes caused due to coronary vasospasm. However, these agents exert toxic effects on cardiovascular system and beyond vasospasm provacation. We report a 46-year-old patient diagnosed as acute inferior infarction who is treated with capecitabine for 3 months due to metastatic breast carcinoma, in whom thrombotic coronary occlusion was observed in angiography. This case demonstrates that apart from vasospasm, coronary thrombosis could be observed after capecitabine treatment, with a possible direct effect of this drug.