DISCUSSION
The term ”coronary artery aneurysms” (CAAs) refers to localized irreversible dilatation of a coronary artery to a diameter more than 1.5 times that of the adjacent normal coronary segments. In contrast, coronary artery ectasias (CAE) occur as widespread arterial dilations wherein the length of the dilated segment is more than 50% of the diameter [2, 3]. Morgagni published the first pathological description of a coronary artery aneurysm [2]. With the advanced application of coronary tomography (CT) and invasive coronary angiography, an anticipated increase in detection rate of CAAs exists.
Although the exact prevalence of CAAs is difficult to determine due to their asymptomatic nature, it is likely underestimated – reported prevalence ranges from 0.3–5%. RCA is most affected (40–70%), followed by the LAD (32.3%) and LCx (23.4%) [3, 4,]. An aneurysm in the left main coronary artery aneurysm (LMCAA) is a very rare finding occurring in 0.1% cases as reported by Topaz et al. [5]. A review recently published identifies atherosclerosis (40%) as the most common cause of LMCAAs, followed by inflammatory (12%) and congenital (9%) factors. Compared to stable angina (43%) and acute coronary syndromes (ACS) (32%), which were more often the first clinical signs, 14% of LMCAA were incidental observations. 18.6% of the patients were presented as STEMI [6].
Atherosclerosis is the leading cause of CAAs, accounting for approximately half of the cases. Other potential causes include vasculitis (Kawasaki disease and Takayasu arteritis), infections (bacterial, fungal, mycobacterial, Lyme, syphilitic, septic emboli, mycotic aneurysm, and HIV), connective tissue disorders (Marfan syndrome and Ehlers-Danlos syndrome), congenital conditions, fibromuscular dysplasia, and traumatic (post PCI).
While most patients are asymptomatic and are diagnosed incidentally, symptomatic patients often present with either effort angina or ACS owing to concurrent obstructive atherosclerotic disease or local thrombosis and embolisation [7, 8]. Rarely, it can present as cardiac tamponade due to CAA rupture or symptoms due to compression of adjacent structures. LMCAAs might even manifest as an incidental anterior mediastinal mass and syncope [9, 10]. Occasionally, a systolic murmur can be detected over the precordial region [3].
The most effective diagnostic approach for CAAs likely involves coronary angiography coupled with IVUS. IVUS can help address drawbacks such as underestimation of CAA size due to intraluminal thrombi and differentiation between true and false aneurysms. Transthoracic echocardiography (TTE) is particularly helpful in the detection of abnormalities in the proximal LMCA and RCA, especially in children with Kawasaki disease. Computed tomography (CT) angiography is valuable for assessing larger CAAs and those with saphenous vein graft aneurysm. Optical coherence tomography (OCT) has limitations due to its narrow scanning diameter. OCT capabilities are constrained by the infrared scan’s narrow diameter [7, 8].
Given the rarity of this cardiac entity and the lack of standard treatment guidelines, management approaches typically involve anticoagulation-based medical therapy, stenting using covered stents, or surgical intervention. Treatment decisions should be tailored to patient characteristics, clinical presentation, and the location and morphology of the aneurysms. According to a recent review, 53% of LMCAA patients received surgical treatment, while only 7% received percutaneous intervention. CAAs, especially LMCAAs, are associated with poor prognosis, with a reported 15% mortality rate after a median 8-month follow-up, when longitudinal data (n = 81) were reported for LMCAA [6]
In the present case, as the patient suffered an acute AWMI with a completely occluded LMCA, it was decided to assess the anatomy of the LAD and LCx and then pursue revascularization. A planned approach to cross the lesion and wire the LAD resulted in inadvertent wiring of the diagonal artery. After discovering the LMCA aneurysm after pre-dilation, another wire was placed in the LAD and RI, however wiring and visualization of LCx proved unsuccessful. Consequent RCA angiography revealed complete LCx occlusion, filling retrogradely through the RCA. It was decided to stent LM-LAD up to LAD and the Diagonal bifurcation with a covered stent. Drug-eluting stents in such a LMCA aneurysm have a high chance of stent thrombosis. At the three-month follow-up, the patient’s symptoms improved, and angiography revealed TIMI III flow and aneurysm completely obliterated. To the best of our knowledge, this case appears to be the first successful percutaneous treatment of a completely obstructed aneurysmal LMCA.