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.