Dina Al Rameni MD, Hashim Sabet MD
Hartford Hospital/UConn Health
August 14th, 2024
Abbreviations & Definitions
CABG – Coronary artery bypass graft
EF – Ejection fraction
EKG – Electrocardiogram
HF – Heart failure
LAD – Left anterior descending artery
LV – Left ventricle
LVA – Left ventricle aneurysm
MI – Myocardial infarction
PDA – Posterior descending artery
RCA – Right coronary artery
SVR – Surgical ventricular reconstruction
Indications & Guidelines for Management
Left ventricular aneurysm (LVA) is a distinct area of LV diastolic contour with systolic dyskinesia or paradoxical bulging. Many experts have broadened this definition to include any area of akinesia or dyskinesia that leads to reduced ejection fraction (EF). LVAs are categorized as either true or false. A true LVA involves the entire thickness of the LV wall and protrudes outward, while a false LVA occurs after ventricular wall rupture and is contained by the surrounding pericardium. Over 95% of LVAs reported in the literature are a result of myocardial infarction (MI) due to coronary artery disease, with a higher prevalence in patients who have experienced acute anterior transmural MI.1 Less common causes include cardiac trauma, Chagas’ disease, sarcoidosis, and congenital diverticula.2 In 90% of cases, LVAs are located at the apex or anterior wall of the heart, while 10% are found in the posterior-inferior wall. The incidence of LVAs is higher in patients with no collateral vessels, transmural infarction, preserved contractility of the surrounding myocardium, a history of hypertension, and lack of reperfusion.
Early diastolic dysfunction occurs due to the decreased compliance of the aneurysmal area, leading to reduced diastolic filling. Over time, the LV dilates, leading to heart failure (HF). Ventricular arrhythmias are also common in patients with LVA and can lead to sudden cardiac death. While mature LVAs are less likely to rupture due to dense fibrous tissue, early immature aneurysms can rupture, potentially causing cardiac tamponade and shock. Blood stasis at the aneurysmal site can increase the risk of mural thrombus formation, which may eventually dislodge and pose a risk of embolization to various organs, including the brain, leading to stroke.3 In patients with LVA, HF is primarily caused by ischemic heart disease, as it leads to progressive ventricular dilation and irreversible myocardial dysfunction. Additionally, mitral insufficiency may develop due to LV dilation or ischemia.
Persistence of ST-segment elevation on EKG for more than three weeks following an acute MI, along with necrosis Q waves in the same region, is suggestive of LVA. Left ventriculography is the “gold standard” for diagnosis, showing a large dyskinetic area, typically in the anterior, apical, and septal walls.3 Two-dimensional echocardiogram, especially with Definity contrast, is sensitive and specific for diagnosing LVA and can detect mural thrombi and mitral regurgitation, while MRI and CT can further identify and delineate aneurysms. Echo and MRI are particularly useful for differentiating true from false aneurysms.4
LVA alone does not justify surgery. Surgery is recommended when persistent angina, refractory HF, thromboembolism, or life-threatening tachyarrhythmias are present. Small asymptomatic LVAs can be safely monitored. Management includes optimizing risk factors for coronary artery disease, reducing afterload, and preventing thromboembolism with anticoagulation. The risk of LV mural thrombus is highest within the first month post-MI, so anticoagulation is advised for the first three months. Long-term anticoagulation should be considered for patients with large, friable thrombi, those who experience systemic embolization beyond three months, or those with globally impaired LV function. Nitrate therapy and ACE inhibitors can also help reduce ventricular remodeling and hypertrophy following MI.5
Surgical Repair
For symptomatic patients with large LVAs unresponsive to medical treatment, surgery might be beneficial. Indications for surgical repair include persistent angina, symptomatic HF, systemic thromboembolism, life-threatening tachyarrhythmias, a diastolic volume index exceeding 880 ml/m², or an end diastolic volume above 120 ml.
Repairing an LVA involves incising the aneurysm, removing any thrombus if present, aneurysmorrhaphy, and ventricular restoration, all of which require cardiopulmonary bypass. Often, extensive pericardial adhesions are attached to the aneurysm, necessitating meticulous dissection. The final size of the LV cavity after repair is linked to patient outcomes. It is recommended that aneurysm resection or patching aim for a postoperative LV end-diastolic volume of approximately 150 mL, as determined by preoperative and postoperative echocardiogram.6
External Plication
There are multiple techniques to repair an LVA; the simplest is external plication, which does not involve opening the aneurysm. It is helpful for smaller aneurysms that do not have thrombi and in patients with less severe LV dysfunction or lower end-diastolic pressure. This repair method involves a double-layered suture across the aneurysm, using Teflon strips on both sides to help restore the normal shape of the ventricle7.
Cooley’s Technique
It involves making a longitudinal incision in the center of the LVA and resecting the aneurysmal wall parallel to either the LAD or PDA, depending on the aneurysm’s location. The thrombus is removed, and a border area of less than 2 cm from the scar tissue is preserved to facilitate the reconstruction of normal LV geometry. Care is taken not to remove too much of the aneurysmal wall to avoid excessively reducing the size of the LV cavity. The resected area is closed vertically with two felt strips of Teflon or pericardium, then secured with a two-layer horizontal mattress suture followed by a two-layer vertical running suture.8 A limitation of this linear repair is that it sutures the lateral and medial (septal) LV walls together, eliminating the natural separation and leaving an akinetic myocardium that may continue to cause LV dysfunction. This technique also does not address the septal area involved.
Endoventricular Circular Patch Plasty
Endoventricular circular patch plasty, or the so-called Dor’s technique, involves incising the aneurysm and assessing the extent of the endocardial scar to identify the junction between the scar and viable myocardium around the aneurysm’s circumference. A running suture is placed at this junction, deep enough in the endocardium to prevent tearing when tightened. The suture tension controls the size of the remaining ventricular opening and the patch size, typically 2 to 3 cm in diameter, made from Dacron or pericardium.9 After suturing the patch inside the LV cavity to close the endocardial opening, surgical adhesive glue is applied to reinforce the suture line.10 The Dor technique has several advantages: it excludes the akinetic segment of the interventricular septum, creates a more physiologic ventricular shape, preserves the LAD for potential grafting, and avoids external prosthetic materials that may cause persistent pericardial adhesions. Additionally, it helps realign myofiber cells in the remaining viable myocardium.11
Summary Table1. Surgical techniques.
| Plication | Cooley’s Technique | Dor’s Technique | |
|---|---|---|---|
| Feasibility | Technically simple | Complex | |
| Resection | No resection, native tissue is preserved | Aneurysmectomy is performed | |
| LV thrombus | Not addressed | Thrombus is accessible and removed if present | |
| Patch | No patch used | Circular patch is used with at least 2 cm overlap | |
| Post-repair LV volume | Markedly decreased due to invagination of the aneurysm into the ventricular cavity | Decreased as a result of the resection of the aneurysmal tissue | Relatively preserved as the patch aims to restore the natural geometry of the ventricle |
Ongoing Trials/Recent Publications
There are no active ongoing trials concerning LVAs specifically. The STICH (Surgical Treatment for Ischemic Heart Failure) trial was a major clinical study designed to evaluate the best surgical approach for patients with ischemic HF. It specifically investigated whether adding SVR to CABG provided additional benefits compared to CABG alone. The trial found no significant difference in overall outcomes, such as survival rates or improvements in heart function, between patients who underwent CABG alone and those who had CABG combined with SVR. The trial results for both groups (CABG alone vs. CABG + SVR) were almost identical across various measures, suggesting that the selection process by surgeons led to comparable outcomes. The key takeaway from the trial is that SVR should be avoided in patients with poor ventricular function and mild aneurysmal dilation, as it offers no clinical benefit and may increase suffering. However, the trial should not be interpreted to suggest that CABG alone is always sufficient for patients with LVAs, as this could lead to inappropriate treatment decisions.12
Expert Commentary
At our institution, we have seen a significant decline in the number of LVAs, largely due to the success of PCI. We take an aggressive approach in managing large LVAs with paradoxical motion at the time of CABG, aiming to prevent progression to HF. Whenever feasible, we perform concomitant CABG if the target vessel is patent and not atretic, as it must be supplying some viable myocardium. In our experience, isolated LVA surgery does not significantly improve survival outcomes.
Sources
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- Mills NL, Everson CT, Hockmuth DR. Technical advances in the treatment of left ventricular aneurysm. Ann Thorac Surg 1993;55(3):792-800.
- Goh VYS, Yew MS. Multimodality Imaging of an Idiopathic Left Ventricular Aneurysm Presenting With Frequent Premature Ventricular Beats. CASE (Phila). 2023 Jul 6;7(9):377-382. doi: 10.1016/j.case.2023.05.007. PMID: 37791125; PMCID: PMC10543177.
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- El Ouazzani J, Jandou I. Aneurysm and pseudoaneurysm of the left ventricle. Ann Med Surg (Lond). 2022 Feb 24;75:103405. doi: 10.1016/j.amsu.2022.103405. PMID: 35386778; PMCID: PMC8977915.
- Cherniavsky AM, Karaskov AM, Marchenko AV, Mikova NV. Preoperative modeling of an optimal left ventricle volume for surgical treatment of ventricular aneurysms. Eur J Cardiothorac Surg. 2001 Oct;20(4):777-82. doi: 10.1016/s1010-7940(01)00901-0. PMID: 11574224.
- Mukaddirov M, Demaria RG, Perrault LP, Frapier JM, Albat B. Reconstructive surgery of postinfarction left ventricular aneurysms: techniques and unsolved problems. Eur J Cardiothorac Surg 2008;34(2):256-61.
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- Dor V. Surgical management of left ventricular aneurysms by the endoventricular circular patch plasty technique. Oper Techn Cardiac Thorac Surg 1997;2(2):139-50
- Di Donato M, Sabatier M, Toso A, Barletta G, Baroni M, Dor V, Fantini F. Regional myocardial performance of nonischaemic zones remote from anterior wall left ventricular aneurysm. Effects of aneurysmectomy. Eur Heart J 1995;16(9): 1285-92.
- Zivkovic I, Mihajlovic V, Zdravkovic D, Krstic D, Krasic S, Lesanovic J, Peric M, Milacic P. Surgical Reconstruction of a Left Ventricular Aneurysm Using an Extracellular Matrix Patch. Braz J Cardiovasc Surg. 2022 May 2;37(2):259-262. doi: 10.21470/1678-9741-2021-0045. PMID: 35503698; PMCID: PMC9054139.
- Velazquez EJ, Lee KL, Deja MA, Jain A, Sopko G, Marchenko A, Ali IS, Pohost G, Gradinac S, Abraham WT, Yii M, Prabhakaran D, Szwed H, Ferrazzi P, Petrie MC, O’Connor CM, Panchavinnin P, She L, Bonow RO, Rankin GR, Jones RH, Rouleau JL; STICH Investigators. Coronary-artery bypass surgery in patients with left ventricular dysfunction. N Engl J Med. 2011 Apr 28;364(17):1607-16. doi: 10.1056/NEJMoa1100356. Epub 2011 Apr 4. PMID: 21463150; PMCID: PMC3415273.
