IntroductionCongenital fibrinogen deficiency is a rare coagulation disorder usually responsible for hemorrhagic diathesis. However, it can be associated with thrombosis and there have been limited reports of arterial thrombotic complications in these patients.Case presentationA 42-year-old Tunisian man with congenital hypofibrinogenemia and no cardiovascular risk factors presented with new onset prolonged angina pectoris. An electrocardiogram showed features of inferior acute myocardial infarction. His troponin levels had reached 17 ng/L. Laboratory findings confirmed hypofibrinogenemia and ruled out thrombophilia. Echocardiography was not useful in providing diagnostic elements but did show preserved left ventricular function. Coronary angiography was not performed and our patient did not receive any anticoagulant treatment due to the major risk of bleeding. Magnetic resonance imaging confirmed myocardial necrosis. Our patient was managed with aspirin, a beta-blocker, an angiotensin-converting enzyme inhibitor and statin medication. The treatment was well tolerated and no ischemic recurrence was detected.ConclusionAlthough coronary thrombosis is a rare event in patients with fibrinogen deficiency, this condition is of major interest in view of the difficulties observed in managing these patients.

Background: Tako-tsubo cardiomyopathy occurs typicallly after an intrinsic adrenergic hyperstimulation triggered by a psychological or physically stressful event. Exceptionally, it may be caused by an exogenous hyperadrenergism. We report the case of an 85 year old man, hypertensive, with a history of ischemic stroke. He consulted for signs of heart failure with recurrent dizziness two weeks which was explained by an atrioventricular block. Initial echocardiography showed left ventricular ejection fraction to 60% with no wall motion abnormalities. The patient received iso-prenaline (0.02 mcg/kg/mn) for 20 hours before the implantation of a single chamber pacemaker. At 24 hours of admission an acute pulmonary edema occurred. The control echocardiography showed impaired left ventricular ejection fraction of 25% with apical ballooning and akinesis was also found on ventricu-lography. Coronary angiography showed no significant coronary lesions. Troponin level was elevated to 2 ng/ml. The pulmonary edema was then controlled. Subsequent clinical and echocardiographic were favo- rable after two weeks which was consistent with the diagnosis of tako-tsubo cardiomyopathy. Conclusion: This case illustrates an example of tako-tsubo syndrome induced by an exogenous catecholergic stimulation (isoprenaline) combined with an endogenous release after a pacemaker implantation which confirmed the physiopathological hypothesis of a catecholamine-mediated stunning in tako-tsubo cardiomyopathy

Background: In Takotsubo cardiomyopathy (TCM), left ventricular dysfunction is usually reversible within a few weeks. Complete recovery can however be very rapid. We report the case of Mrs. TA, a 53-yearold patient who had a history of hypertension treated with atenolol and captopril. She was admitted with the diagnosis of non ST segment elevation myo-cardial infarction. The electrocardiogram showed anterior sub-and the troponinI level was 3.48 mg/l. Echocardiography revealed a left ventricular (LV) ballooning and LV ejection fraction was 36%. A recent emotional stress was mentioned. TCM was suspected and emergency angiography showed apical ballooning with a normal coronary angiogram. There was a complete recovery in 72 hours with a normalization of regional and global LV function at echocar-diography and angiography. Conclusion: There is a large variability in TCM evolution aspects probably due to a variable physiopathological mechanism which remains to be clarified.

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