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- W3159598906 abstract "Presentation, Investigation and Management of Coronary fistula and its arrhythmic complications. A 40-year-old male patient with no past medical history was admitted to hospital with a brief history of loss of consciousness while jogging. He was in atrial fibrillation (Figure 1) with a ventricular rate of 131 bpm and complained of no symptoms. Cardioversion was attempted with an intravenous infusion of flecainide. However, the patient developed a broad complex tachycardia followed by ventricular fibrillation from which he was successfully resuscitated via DC Cardioversion with one shock of 150 Joules. An initial echocardiogram and subsequent cardiac MRI confirmed good LV and RV systolic function with no regional wall motion abnormality. There was a left circumflex artery to coronary sinus fistula. Both ventricles were, however, dilated, with an LV end diastolic volume of 216 ml and an RV end diastolic volume of 227 ml, consistent with a hyperdynamic circulation. Left ventricular ejection fraction was normal at 68%, with LV end systolic volume of 70 ml. The left atrium was not dilated. Invasive coronary angiography (Figure 2) demonstrated retrograde filling of the distal left anterior descending artery and obtuse marginal branches from the right coronary artery. CT coronary angiography (Figure 3) did not show any obstructive coronary disease and confirmed the presence of a dilated circumflex artery to coronary sinus fistula. Ten days later the patient underwent an exercise treadmill test in which he managed 14 minutes of the Bruce protocol stopping because of fatigue. His resting blood pressure and heart rate were 145/ 58 mmHg and 86 bpm, respectively. Figure 4A shows his resting 12 lead ECG. At peak exercise, blood pressure increased to 170/70 mmHg and heart rate to 187 bpm. He developed >2 mm ST depression in the inferolateral leads at peak exercise (Figure 4B). Immediately after the end of the test he dropped his blood pressure to 79/49 mmHg and at 9 minutes into recovery he developed a broad complex tachycardia (Figure 4C) which then deteriorated into ventricular fibrillation. The patient was once again successfully electrically cardioverted. Immediately following his arrest, electrophysiology studies demonstrated no accessory pathways and VT stimulation was negative. The patient developed atrial fibrillation during his EP study which was internally cardioverted. The patient underwent surgical ligation of the coronary cameral fistula and 4 weeks later cardiopulmonary exercise testing failed to induce any arrhythmias and 5 years later the patient remains free of symptoms. Repeat cardiac MRI demonstrated normal biventricular function with no evidence of myocardial necrosis or fibrosis on delayed hyperenhancement images. The end diastolic volumes of the left and right ventricle were 168 ml and 172 ml, respectively, a 25% reduction in size compared with preoperative MRI findings. Coronary Cameral fistulae are rare congenital communications between a coronary artery and cardiac chamber. Patients with coronary cameral fistula are often asymptomatic; however, young patients presenting with arrhythmias such as atrial fibrillation may rouse suspicion of anatomical variants and, therefore, warrant investigation for structural abnormalities. Myocardial ischemia can occur in patients with fistulae as a result of “steal” syndrome in which there is a reduction in coronary blood flow as a result of pressure differences between the two arterial beds. Retrograde filling of the LAD from the RCA in the absence of any coronary stenosis as shown in Figure 2 is consistent with coronary steal. The patient’s initial rise in heart rate associated with exercise could have precipitated coronary ischemia to the left atrium in view of the coronary filling demonstrated in Figure 2. This ischemia may have initiated atrial fibrillation, and thus a further increase in the heart rate caused by fast ventricular response causing yet more coronary “steal”. The degree of such “steal” may have then led to ventricular arrhythmia. The second ventricular arrhythmic episode, in recovery, after the treadmill test, is likely to have been caused by reperfusion injury as demonstrated by the ischemic ECG changes at peak exercise. The morphology of the ventricular tachycardia at this time, showing ST elevation in aVR, right bundle branch block (RBBB), and left axis deviation, correlates with occlusion of the left main trunk. Another explanation could be that during recovery, the physiological vagal response post exercise with the drop in blood pressure could have enhanced the coronary “steal”. Fistulae presenting with exercise-induced arrhythmias such as described here are rare. This case highlights a rare cause of exercise-induced ventricular arrhythmia, and how the consequences of abnormal coronary blood flow can have life-threatening consequences. Surgical intervention for patients with symptomatic fistulae should be considered. None. Authors have no conflicts of interest." @default.
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- W3159598906 date "2021-05-06" @default.
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- W3159598906 title "Exercise‐induced ventricular arrhythmia in coronary cameral fistula: A manifestation of reperfusion injury" @default.
- W3159598906 doi "https://doi.org/10.1002/joa3.12543" @default.
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