Coronary Artery Fistula From LAD to Pulmonary Artery Causing Stable Angina via Coronary Steal

A 40-year-old Chinese male presented to the emergency department with heavy, retrosternal chest pain lasting 30 minutes, triggered by lifting a 40-pound weight. The pain was associated with dizziness, nausea, and palpitations, and resolved gradually with rest. On further history, the patient disclosed years of similar exertional chest pain — CCS Class II angina — that he had never reported to a physician. He had a 10-pack-year smoking history and GERD but took no medications. He worked in a restaurant kitchen and denied alcohol or illicit drug use.

Physical examination was remarkable for a continuous grade II/VI murmur at the left sternal border — a finding immediately pointing away from atherosclerotic coronary disease. The patient's troponin was negative and EKG showed only sinus tachycardia. The differential for a continuous murmur with chest pain included ruptured sinus of Valsalva aneurysm, patent ductus arteriosus, anomalous coronary origin, aortopulmonary septal defect, ventricular septal defect, Lutembacher syndrome, and coronary artery fistula.

Figure 1

EKG — Sinus Tachycardia

EKG showing sinus tachycardia without ST changes or ischemic features. In the context of a continuous precordial murmur and exertional chest pain, normal EKG findings should lower suspicion for acute coronary syndrome and direct attention toward structural or flow abnormalities not captured by routine electrocardiography.

Exercise stress testing was prematurely terminated at seven minutes when the patient developed dizziness, lateral ST-segment depressions, non-sustained monomorphic ventricular tachycardia, and a transient left bundle branch block — findings confirming significant exertional ischemia despite a negative troponin and lack of atherosclerosis. Cardiac catheterization revealed no significant CAD but identified a fistula running from the left coronary artery near the LAD bifurcation to the main pulmonary artery.

Coronary CT angiography confirmed a tortuous branch distal to the left main bifurcation arising from the LAD, coursing within the epicardial fat along the lateral aspect of the pulmonary outflow tract, with aneurysmal dilatation and multiple fistulous connections to the PA trunk.

Figure 2

CTA — Tortuous Fistula With Aneurysmal Dilatation

Axial CT angiography demonstrating the coronary artery fistula as tortuous vessels with aneurysmal dilatation along the left lateral aspect of the PA trunk. The aneurysmal morphology reflects chronic high-flow state in the fistula — a finding that increases risk of thrombosis, rupture, and coronary steal over time.

Figure 3

CTA — Network of Fistulous Vessels Along PA Trunk

Axial CTA showing a network of vessels along the PA trunk with loss of the intervening fat plane — suggestive of multiple fistulous connections rather than a single feeding vessel. This anatomic complexity precluded transcatheter coil embolization and guided the decision toward surgical ligation.

Transcatheter coiling via the pulmonary circulation failed due to the multiple connections and large fistula diameter. The structural cardiology team assessed the transcatheter approach as unsafe given the proximity to the left main and multiple communicating branches. Robotic-arm assisted ligation by cardiothoracic surgery identified a 1-cm feeding vessel from the LAD with a downstream network of PA-connecting vessels. The fistula was isolated and ligated close to the LAD. Intraoperative TEE and angiography confirmed elimination of flow to the PA before and after ligation. The patient recovered without complications and remained asymptomatic on follow-up.

Discussion

Coronary artery fistula is a rare but increasingly detected anomaly as echocardiography and CT angiography become more widely used in ischemic workup. The incidence is estimated at 0.2–1.2% of the population. Most CAFs arise from the right coronary system and drain into the venous circulation — however, drainage into the pulmonary artery (as seen here) is less common and produces a clinically distinct hemodynamic pattern. The "coronary steal" mechanism explains this patient's symptoms: during exercise, when myocardial demand rises, a portion of coronary blood flow is preferentially diverted through the fistula's low-resistance pathway into the pulmonary artery rather than traversing the myocardial capillary bed. This diverted flow results in relative ischemia in the territory beyond the fistula origin, producing angina even when the epicardial coronary arteries themselves are free of atherosclerosis.

Management of symptomatic CAF is driven by fistula anatomy and patient characteristics. Transcatheter closure with coils, amplatzer plugs, or covered stents is appropriate when a single, narrow draining site is safely accessible — anatomical prerequisites that were not met in this patient, whose fistula had multiple communicating branches and was dangerously close to the left main. Surgical ligation — now facilitated by robotic platforms — provides direct visualization, targeted vessel isolation, and real-time intraoperative imaging confirmation of closure. Both transcatheter and surgical approaches carry similar overall success rates and mortality; the choice is anatomically driven. This case highlights that non-atherosclerotic causes of angina account for a meaningful fraction of CCS Class II presentations, particularly in young patients with a continuous murmur — and that a systematic diagnostic approach including stress testing and CT angiography is essential to avoid attributing symptoms to a missed structural lesion.