Case Presentation:
A 41-year-old man with no previous medical history comprising cardiovascular diseases, hypertension, oral hypoglycemic-treated diabetes, or dialysis-treated renal failure presented as an outpatient with atypical chest pain.
The patient had no known family history of heart disease or any personal history of cardiovascular procedures. Physical examination of the chest was unremarkable, and no murmurs, rubs, or gallops were detected upon auscultation. His ECG was normal as well.
The patient was sent for a nuclear myocardial perfusion stress test, which showed a small reversible perfusion defect in the basal-to-mid inferior wall, suggestive of inducible ischemia in the right coronary artery.
There was also a small, mild-intensity, fixed perfusion defect involving the mid-to-apical anterior segments. According to nuclear imaging results, the patient was a candidate for an outpatient left heart catheterization, which revealed no evidence of coronary artery disease but did show a moderate-sized fistula arising from the LAD to the LV circumflex artery (Figure-1 ) and luminal irregularity of RCA (Figure-2 ).
CTA of the heart was subsequently performed but exhibited no evidence of coronary artery disease or a fistula from the LAD or OM branches (Figure-3 ).
The patient was discharged with instructions to follow up as an outpatient to discuss disease management. Nevertheless, he unfortunately never returned to the clinic.
Since being diagnosed with coronary AV fistula, the patient has been following up with the DMC Sinai Grace Primary Care Center and his private cardiologist on an outpatient basis. He has had three admissions to the hospital with chest pain and shortness of breath. In 2019, the patient was admitted with a troponin level of 0.04 and with ECG findings of T wave inversions in the lateral leads. A transthoracic echocardiogram (TTE) was obtained, which showed no regional wall motion abnormalities but did indicate the interval development of moderate pulmonary hypertension and a small generalized pericardial effusion. As there was no significant increment in troponin level, no cardiac intervention was performed. At his last outpatient clinic visit with the primary care physician, the patient reported having exertional dyspnea and pedal edema but denied any chest pain, palpitations, diaphoresis, or vomiting. On physical exam, the patient had bilateral pitting pedal edema but there were no biochemical abnormalities.