Case presentation

We present the case of a 79-year-old male who is former smoker, with a medical history of dyslipidemia and past treatment for paroxysmal atrial fibrillation by pulmonary vein isolation nine years earlier. As a part of the pre-ablation assessment, a cardiac MRI was conducted, revealing an oval structure measuring 27 by 20 mm, in proximity to the left atrium, left atrial appendage and circumflex artery. However, its precise characterization was not possible at that time.

No other cardiac conditions were noted in the patient’s clinical history. The current treatment was bisoprolol and acenocoumarol maintaining INT within target range.

The patient presented to the emergency department complaining of oppressive chest pain, which lasted for one hour and subsided upon arrival at the emergency department. The pain did not radiate and was not associated with vegetative symptoms. He reported experiencing recurrent and transient episodes of retrosternal oppressive chest pain over the past ten days, occurring both during physical exertion and at rest, along with exertional dyspnea. He denied having fever or any other cardiovascular or infectious symptoms.

On arrival at the emergency department, the patient was hemodynamically stable, he had normal vital signs and his physical examination was unremarkable with no signs of overt heart failure. He was eupneic, with no need for oxygen therapy.

The initial electrocardiogram showed sinus rhythm with normal PR segment, narrow QRS with incomplete right bundle branch block and no signs of acute ischemia. Sequential ECG did not change (Figure 1). Laboratory findings included an elevation of high-sensibility cardiac troponin I up to 498 ng/L (N<45 ng/L). The rest of the blood tests (hemogram, renal function, ionogram) were normal.

 

Figure 1: ECG:sinus rhythm at 50 bpm with normal PR, narrow QRS with incomplete right bundle branch block and no repolarization alterations.

An echocardiogram was performed which showed a non-dilated and mildly hypertrophic left ventricle, with a normal ejection fraction despite lateral hypokinesia (LVEF 55%) and no pericardial effusion.

The patient was classified as Killip I class Non-ST-Elevation Myocardial Infarction (NSTEMI), monoantiplatelet therapy with ASA and anticoagulation with enoxaparin was started, and coronary angiography was requested.

Coronary angiography (Image 2) showed right dominance with mild non-obstructive coronary artery disease in the main epicardial arteries. However, a contrast leakage was seen from the proximal Left Circumflex Artery (LCx) to an adjacent round structure causing displacement and compression of the left main and proximal LCx artery (Figure 2, panel A and B). Subsequently, a multi-slice Coronary Computed Tomography Angiography (CCTA) (Figure 2, panel C and D) was ordered to better characterize the nature of the lesion and to describe its location related to other cardiac structures. CCTA confirmed the leakage of contrast iodine from a calcified plaque lesion in the LCx artery into the periphery of a rounded, well-defined and encapsulated extravascular cavity measuring 45 by 40 by 38 mm.

 

Figure 2: Multimodality imaging. Cranial and right-oblique frame projections from the coronary catheterization (panels A and B) and corresponding Maximal Intensity Projection Frames from the CCTA (panels C and D). The location of the pseudoaneurysm is labeled with an Asterisk (*) and the origin of the ruptured calcified plaque in the proximal LCx artery causing contrast leakage is labeled with a white arrow. CCTA: Coronary Computed Tomography Angiography. LCX: Left Circumflex.

The signal intensity in the lesion was slightly heterogenous, showing an attenuation of 75±31 Hounsfield Units, consistent with a thrombus. No signs of malignancy were observed. A tentative diagnosis of coronary pseudoaneurysm arising from the LCx causing extrinsic compression of the left main and proximal segment of the LCx as the cause of myocardial infarction was made.

Comparing the images with the cardiac MRI performed before the pulmonary vein isolation confirmed the presence of the structure at that time, so it was ruled out its relationship with the procedure. However, its previous size was notably smaller (27 by 20 mm).

Based on the above, given the suspicion that compression of the pseudoaneurysm on the left coronary artery tree was the cause of NSTEMI, it was decided to undergo cardiac surgery. The EUROSCORE 2 score predicted low operative risk. A cavitated lesion arising from a calcified plaque in the proximal LCx was confirmed during surgery (Figure 3), requiring an aneurysmectomy and saphenous vein graft to the obtuse marginal branch (Video 1). Surgical findings matched those on the CCTA.