P642 Coronary arteriovenous fistulas

Abstract

Abstract Clinical case A 53 years woman in good health and un uneventful clinical history except for a mild hypercholesteremia was evaluated for palpitations. At the clinical examination she had a systolic murmur 3/6 Levine, with no signs of heart failure. The ECG showed normal sinus rhythm with a normal heart rate (62bpm), normal atrio-ventricular and intraventricular conduction and normal repolarisation, one supraventricular premature beat. The echocardiography showed normal biventricular dimension and function, no valvular heart diseases, no septal defects, regular aortic dimensions. A giant right coronary was evidenced (Figure, panel a) with an arteriovenous fistula originating from the right coronary artery and draining through the coronary sinus into the right atrium (Figure, panel b). The CT coronary angiogram evidenced an dilated right coronary artery communicating with the coronary sinus (arteriovenous fistula) draining into the right atrium. A smaller arteriovenous fistula was evidenced between the circumflex artery (slightly dilated) and the great cardiac vein. (Figure, panel c-e) The Treadmill test didn’t evidence an induced ischemia; however the patient didn’t perform a maximal exercise (double product 20400mmHb*bpm). Moreover, during the first steps of recovery frequent supraventricular premature beats were registered with phases of bigeminies followed by a junctional rhythm phase. Thus, a Gated myocardial Perfusion SPECT was performed evidenced a mild stress induced ischemia of the inferolateral and apical left ventricle wall with normal rest perfusion and normal left ventricle volumes (125ml during exercise and 134ml at rest) with a normal ejection fraction ( > 65%). (Figure, panel f)An elective coronarography was planned. The patient is on therapy with beta-blockers and aspirin. The patient is asymptomatic for angina. Antibiotic prophylaxis was recommended for dental, gastrointestinal, or urologic procedures. Discussion: Coronary arteriovenous fistula (CAVF), first described in 1865 by Krausein (1), are a rare congenital heart disease representing less than 0.5% of all congenital heart diseases with an extremely rare prevalence 0.002% in the general population (2). Moreover, therapy of CAVF is still controversial with previous data showing a relatively high rate of myocardial infarction after surgical repair (3). The recent AHA/ACC guideline for the management of adults with Congenital heart disease recommend a review by a knowledgeable team that may include congenital or noncongenital cardiologists and surgeons to determine the role of medical therapy and/or percutaneous or surgical closure (4) Conclusion: CAVF is a very rare congenital heart defect and might be asymptomatic and evidenced by hazard in adults patients. Therapy strategy demands a multidisciplinary team evaluation and should be be individualized according to the clinic presentation, the presence or absence of myocardial ischemia or ventricular dysfunction. Abstract P642 Figure.