A 66-year-old female with acute coronary syndrome presented for coronary angiography (cTnI peak 1.15 ug/L; n< 0.04 ug/L). Angiography showed smooth arteries but the unexpected finding of late diastolic opacification… Click to show full abstract
A 66-year-old female with acute coronary syndrome presented for coronary angiography (cTnI peak 1.15 ug/L; n< 0.04 ug/L). Angiography showed smooth arteries but the unexpected finding of late diastolic opacification of the left ventricular (LV) cavity via fistulous drainage from a tortuous left anterior descending artery (LAD) (Panel C, Supplementary material online, Video S1). Left ventriculogram revealed the etiologic cause of presentation as mid wall TakoTsubo cardiomyopathy (Supplementary material online, Video S2). The intercurrent emotional stressor of unexpected spousal death was later recognized, along with lifelong poor exercise tolerance. The patient’s ECG appearance evolved typically for Tako-Tsubo cardiomyopathy with inferolateral T wave inversion and QT prolongation (Panels A and B). A 61-year-old female with progressive exertional dyspnoea, underwent coronary angiography following positive stress echocardiocardiography. Angiography did not reveal obstructive disease but showed a dilated, serpiginous left circumflex artery (LCx), draining to the coronary sinus (CS) (Supplementary material online, Videos S3 and S4). Anatomic characterisation with CT demonstrated LCx dilatation with drainage proximal to the CS orifice (Panels D–F). Coronary artery fistulae are anomalous connections between epicardial coronary arteries and cardiac chambers or systemic/pulmonary vasculature. The prevalence is estimated at 0.2% and the majority involve the right coronary artery and right sided structures, with left to right shunting. Physiologically different causing left to left shunting, left sided fistulae to the left ventricle are very rare and represent abnormal Thebesian venous prominence. The prime pathologic significance of larger fistulae is ‘coronary steal’, with myocardial hypoperfusion distal to the fistulous connection. Progressive ‘steal’ may trigger aneurysmal coronary dilatation with consequences including thrombosis and rupture.
               
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