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.