An isolated mid‐anterolateral wall true ventricular aneurysm due to coronary artery disease

Aneurysms following a myocardial infarction usually involve the apical wall segments. We present a case of a rare isolated mid‐anterolateral wall aneurysm due to occlusion of a diagonal branch. We review the echocardiographic criteria for diagnosing a left ventricular (LV) aneurysm and discuss how to differentiate one from a more critical pseudoaneurysm. We demonstrate the utility of using ultrasound enhancing contrast and review imaging protocols for ruling out associated LV thrombus.


CASE REPORT
A 47-year-old female with a history of stage IV chronic kidney disease, hypertension, and medically managed obstructive coronary artery disease (CAD) presented with left sided chest and arm pain.Three years prior, she has a cardiac catheterization (Figure 1) that showed severe   diagonal branch disease was felt to be the culprit for the isolated midanterolateral wall aneurysm imaged over 4 years.

DISCUSSION
An LV aneurysm is a localized protrusion of the LV cavity during A recent review proposed a diagnostic and management approach for LV thrombi following an acute MI.An echo is preformed within 24 h of the acute MI.In the absence of LV thrombus, but in the presence a sizeable anteroapical wall motion abnormality, a repeat contrast echo is recommended in 72 h.If the study is still negative, it is repeated in 1−2 weeks. 6The decision to discontinue anticoagulation with resolved LV thrombus in the setting of persistent flow stasis, especially in the presence of an LV aneurysm, is debatable.
Furthermore, the differentiation between LV aneurysms and pseudoaneurysms is critically important.Aneurysms are usually managed conservatively including medical therapy for heart failure, anticoagulation if thrombus is present, and serial imaging.The risk of rupture is very low.Pseudoaneurysms are contained myocardial ruptures supported by pericardium.The mortality rate is higher, and there is a 30%−45% risk of acute and late rupture requiring urgent cardiac surgery in most patients. 7ere are several echo features that can help to distinguish between aneurysms and pseudoaneurysms.In a 2-D echocardiographic series of 11 patients, the neck to parallel maximal aneurysmal sac diameter ratio was noted to be much smaller in pathologically proven LV pseudoaneurysm (<0.5) compared to true aneurysms (0.9-1.0). 8though relying on a small sample size, the echocardiographic criteria derived from this series continues to be a major differentiator of LV aneurysm versus pseudoaneurysm.The absence of visible myocardium, systolic expansion, associated pericardial effusion, nearly ubiquitous associated thrombus, flow acceleration by color and spectral Doppler at the neck, and a predilection to the inferior wall (due diaphragmatic restraint) all suggest a pseudoaneurysm.Although the location is unusual, none of aforementioned signs were present in our case.Visible myocardium was also seen with LV contrast and confirmed with cardiac MRI.

SUMMARY
We present a rare focal mid-anterolateral wall aneurysm due to progressive disease in a major proximal diagonal branch of the LAD.
LV contrast was crucial to the initial diagnosis.A pseudoaneurysm was excluded by echocardiographic criteria, and the findings were corroborated by cardiac MRI.
branch vessel disease not amenable to intervention including in a major bifurcating diagonal branch of the left anterior descending (LAD).The reference non-contrast echocardiogram from three years ago showed preserved LV wall motion (Video 1).The chest pain resolved during the present hospital course, and troponin I levels were not detectable.A comprehensive echocardiogram (echo) was performed.The apical four chamber window was of fair quality, and there was slight suspicion of an anterolateral wall motion abnormality as noted by the systolic frame of Figure 2. To supplement non-contrast imaging, an echo contrast agent (DEFINITY, Lantheus Medical Imaging) was infused via the diluted bolus technique.The administration of LV ultrasound contrast was instrumental and illustrated a new focal mid-anterolateral wall protrusion shown in Figure 3 in end diastole, Figure 4 in systole, and Video 2. An aneurysm versus pseudoaneurysm was suspected.The neck of the protrusion was broad, even larger than the maximal parallel aneurysmal sac dimension.There was no thrombus or associated pericardial effusion.An aneurysm This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.© 2023 The Authors.Echocardiography published by Wiley Periodicals LLC.

F I G U R E 1 F I G U R E 2
Reference coronary angiogram with cranial projection from 3 years prior to the first presentation shows a bifurcating diagonal branch.was confirmed by cardiac magnetic resonance imaging (MRI), which showed the presence of thinned myocardium in the anterolateral wall in Figure 5.The overall ejection fraction and wall motion in other segments was preserved.She did not undergo cardiac catheterization V I D E O 1 Reference noncontrast echocardiogram from 3 years prior to the first presentation.Apical 4 chamber view shows normal regional wall motion.Apical four chamber view from the first presentation with poorly visualized endocardium.

F I G U R E 3
at the time due to pain resolution, normal cardiac biomarkers, and advanced renal insufficiency.Four years later, she presented with a myocardial infarction with transient ST elevation.She underwent urgent cardiac catheterization.There were two tandem high grade lesions in the LAD treated with percutaneous coronary intervention.The angiogram also showed development of subtotal occlusion of the same proximal diagonal branch (Figure 6).Video 3 shows an unchanged mid anterolateral wall aneurysm.Image quality was less optimal, but no thrombus was identified in the aneurysm pouch with contrast echo.The progressive Apical four chamber view with administration of LV contrast from the first presentation.A mid-anterolateral wall left ventricular aneurysm is shown in end diastole.LV, left ventricular.

3 V I D E O 2 F I G U R E 5
systole and diastole with akinetic or dyskinetic walls.The vast majority of ventricular aneurysms are secondary to CAD.Chagas disease, F I G U R E 4 Apical 4 chamber with administration of LV contrast from the first presentation.A mid-anterolateral wall left ventricular aneurysm is shown in systole.LV, left ventricular.sarcoidosis,and mid or apical variant hypertrophic cardiomyopathy can also cause aneurysms.1In the prethrombolytic era, ventricular aneurysms were reported in 12.4% of patients with myocardial infarction (MI), 2 although it is likely that the prevalence is now substantially lower with modern reperfusion.Greater than 80% of LV aneurysms involve the anterior wall and apex and are associated with high grade stenosis or complete occlusion of the proximal or mid LAD.1 Days to weeks following an MI, the intraventricular pressure with each systolic contraction causes stretching of the fragile infarcted zone and forms the aneurysm.Echocardiogram from the first presentation.Apical 4 chamber view with LV contrast shows a mid-anterolateral wall aneurysm.LV, left ventricular.Bright blood sequence cardiac MRI from the first presentation shows the aneurysm.MRI, magnetic resonance imaging.The presence of an isolated lateral wall aneurysm, as in our case, is quite infrequent.In a report on 65 consecutive autopsied cases of LV aneurysm, only 1 of 65 was isolated to the lateral wall. 3The rarity is likely related to the dual blood supply of the lateral wall from the obtuse marginal and diagonal branches.Coronary anatomic variations can affect overlapping blood supply.Our patient had obstructive disease of a proximal diagonal branch and a severely diseased circumflex resulting in absent collaterals.Clinicians must also be aware of other LV aneurysm mimickers including rare congenital left ventricular diverticula and clefts.Both diverticula and clefts are congenital abnormalities, and the F I G U R E 6 Coronary angiogram with cranial projection from the second presentation shows occlusion of the same diagonal branch.myocardium has normal systolic contraction.Clefts, which are slit like invaginations in the myocardium, may also characteristically obliterate during systole.This is in contrast to an LV aneurysm that is thinned and abnormally contracting. 4The presence of an LV aneurysm raises suspicion for associated thrombus.Virchow's triad of endothelial injury, blood stasis, and hypercoagulability is responsible for thrombus formation following an acute MI.The vast majority of LV thrombi occur with infarcts resulting in apical or anterior LV akinesis or dyskinesis.There is limited description in the literature regarding post-MI LV thrombi in a non-apical location such as the aneurysm is our case.A study of 201 patients compared the sensitivity of same-day echo versus delayed enhancement cardiac magnetic resonance (DE-CMR) in ST elevation MI patients.LV thrombus was present in 8%, and nearly all thrombi (94%) occurred in the context of an LAD infarct.Interestingly only 18% of thrombi were associated with an LV aneurysm.Using DE-CMR as the reference, V I D E O 3 Echocardiogram from the second presentation.Apical 4 chamber view with LV contrast shows a persistent mid-anterolateral wall aneurysm without definite thrombus.LV, left ventricular.non-contrast echo had limited sensitivity for thrombus (35%) which improved but remained suboptimal (65%) with the use of contrast echo. 5Nevertheless, echocardiography remains the first lime modality due to MRI's limited accessibility, expense, requirement for breath holding, and the difficulty of close space imaging in critically ill patients.Ultrasound enhancing agents (UEAs) can overcome many of the challenges involved in diagnosing LV aneurysms and thrombi.UEAs improve endocardial border definition in technically difficult studies and also minimize false positive or equivocal results due to near field clutter artifact, prominent apical trabeculation, and false tendon.It can be reasoned that all patients with infarcts involving the apical wall segments should receive a contrast echo.