Erature [1-9].

Erature%20[1-9].%20The%20Methyl 6-bromo-5-fluoropicolinateMethyl 6-bromo-5-fluoropicolinate mechanism of this apparently paradoxical thrombotic tendency, which has long remained problematic, has now been partially clarified [10]. Case presentation We report the case of a 42-year-old Tunisian man, born out of a consanguineous marriage, who had no cardiovascular risk factors and was followed-up for hypofibrinogenemia diagnosed three years previously due to* Correspondence: fathiazghal@yahoo.com 1 Service of Cardiology, Rabta University Hospital, Faculty of Medicine, University of Tunis El Manar, Tunis, Tunisia Full list of author information is available at the end of the articlebleeding after dental care. He had no known family history of fibrinogen deficiency. He was admitted for an acute typical anginal pain which occurred at rest and continued for several hours. On physical examination he had no fever, his blood pressure was 120/70 mmHg, his heart rate was 65 beats per minute and cardiopulmonary auscultation was normal. An electrocardiogram (ECG) on admission, seven hours after the onset of pain (Figure 1A) showed an elevation of the ST segment in inferior leads and an STsegment depression in DI, aVL. His troponin I and creatine phosphokinase levels were elevated to 17 ng/L and 820IU/L respectively. There was no sign of inflammation; his C-reactive protein level was 5 mg/L and white blood cell count, 7000 cells/mL. Bleeding-related tests were carried out. His fibrinogen level was 0.3 g/L using PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/13485127 the Von Clauss method, and < 0.16 g/L using the immunological method. His activated partial thromboplastin time was > 120 seconds (control: 32 seconds), prothombin activity < 10 and thrombin time > 120 seconds (control: 13 seconds). His platelet count?2011 Mghaieth et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Mghaieth et al. Journal of Medical Case Reports 2011, 5:582 http://www.jmedicalcasereports.com/content/5/1/Page 2 ofFigure 1 ECG findings. (A) Electrocardiogram on admission. ST-segment elevation in DIII, aVF and ST- segment depression in DI, aVL. (B) Electrocardiogram on the seventh day. Q wave in inferior leads and apicolateral subepicardial ischemia.(242,000/mm3 ) and bleeding time (140 seconds) were normal. A transthoracic echocardiography estimated his left ventricular ejection fraction at 61 without evidence of segmental motion abnormalities. A coronaryangiography was not performed in view of the major risk of bleeding. Cardiac magnetic resonance imaging (MRI) on day 5 (Figure 2) showed the presence of almost complete transmural enhancement of theMghaieth et al. Journal of Medical Case Reports 2011, 5:582 http://www.jmedicalcasereports.com/content/5/1/Page 3 ofFigure 2 Contrast-enhanced inversion-recovery magnetic resonance study on (A) long axis and (B) short-axis images during the subacute phase (day five). Almost complete PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/12113769 transmural enhancement in the infero-apicolateral wall (arrowheads).apicolateral segment. It is 5-Fluoro-3-nitropyridin-2(1H)-one noteworthy that an etiological investigation for acute myocardial infarction in a young adult was otherwise negative; our patient did not have any protein C or protein S or an antithrombin deficiency; there was neither a Factor V Leiden nor prothrombin G20210 mutation, no anti-phospholipid antibodies (lupus type v inhibitor, antica.