Anna Xue and Victor Rodriguez
This chapter is a revision and update of that included in previous editions of the TSRA Review written by Amber Melvin (2nd edition) and Leo M. Gazoni (1st edition).
Definition and Pathophysiology
The classic definition of left ventricular (LV) aneurysm is “a distinct area of LV diastolic contour with systolic dyskinesia or paradoxical bulging.” However, this definition has been broadened by many experts to include any area of akinesia or dyskinesia that reduces EF. True aneurysms involve full thickness bulging of the ventricular wall while pseudoaneurysms or “false aneurysms” are contained cardiac rupture. The most common cause of ventricular aneurysms (95%) is ischemia followed by remodeling of the ventricle after the ischemic event; other, less likely causes are cardiac trauma, Chagas’ disease, sarcoidosis, and congenital diverticula. The incidence of LV aneurysm following myocardial infarction (MI) is varied in the literature and reported to be 8-35%. This incidence is decreasing due to major improvements and widespread rapid intervention of the culprit lesion(s) in acute MI management.
Eighty-five percent of aneurysm formation is associated with an acute MI of the area of the heart supplied by the LAD, with RCA infarcts comprising most of the remainder cases. The incidence is increased in patients with no collateral vessels, transmural infarction, preserved contractility of the surrounding myocardium, history of hypertension, and lack of reperfusion.
During the early phases of remodeling, myocyte death, inflammatory infiltration, and lysis of necrotic myocytes occur. The tensile strength of the ventricular wall is lowest at 5-10 days, making ventricular rupture most common during this time. Large infarct area and surrounding preserved myocardium causes systolic bulging of the infarcted area. The increased preload of the ventricle causes increased muscle fiber shortening and increased oxygen demand of the remaining myocytes, ultimately causing ventricular hypertrophy. Early diastolic dysfunction also occurs due to decreased compliance of the aneurysmal area, thus leading to decreased diastolic filling. Overtime, the left ventricle dilates and heart failure develops. Ventricular arrhythmias are also common in patients with left ventricular aneurysm and may lead to sudden cardiac death. Remodeling begins to occur at 2-4 weeks and the infarcted area is replaced with fibrous tissue at 6-8 weeks, thinning the ventricular wall. Nitrate therapy and ACE inhibitors have been shown to alter ventricular remodeling and reduce ventricular hypertrophy after MI.
Diagnosis
EKG can show Q waves in the anterior leads with or without persistent ST elevation. CXR may show cardiomegaly. Left ventriculography is the gold standard for diagnosis of the aneurysm, showing the area of dyskinesia or akinesia; this is best visualized in the 30ᵒ right anterior oblique view. Echocardiogram is also sensitive and specific for LV aneurysms and can show mitral valve regurgitation or mural thrombus. Cardiac MRI can also be used to assess ventricular aneurysms; this modality is particularly helpful in delineating aneurysm size and anatomy.
Indications for Surgery
Relative indications for operative aneurysm repair include aneurysm expansion/large size, ongoing angina, heart failure despite medical therapy, arrhythmias, ventricular rupture, pseudoaneurysm formation, congenital aneurysm, or associated embolic event. End-systolic volume index >80 mL/m2 and end-diastolic volume >120 mL are also relative indications for aneurysm repair. Preoperatively, all patients should undergo left and right heart catheterizations and echocardiogram to evaluate for valvular abnormality. Contraindications to surgery are RV dysfunction or a small LV cavity, as aneurysm repair will further decrease stroke volume. Small, asymptomatic aneurysms can often be managed medically.
Surgical Intervention
Before intervening on the aneurysm, the coronary anatomy should be well visualized as a ventriculotomy will be performed. Important surgical principles to keep in mind include identification of the akinetic LV segment (will dimple after LV decompression) as well as minimal manipulation of the LV prior to application of the aortic cross-clamp to avoid dislodging any LV thrombus (if present). Coronary artery bypass grafting (CABG) is also typically performed during these operations. The mitral valve may need to be repaired concomitantly and this is generally done with mitral annuloplasty. If necessary, coronary revascularization and mitral repair are typically performed prior to addressing the aneurysm. Ablation therapies may also be considered in patients with malignant ventricular arrhythmias.
There are several surgical techniques that can be used to address a LV aneurysm:
- Plication without opening the aneurysm is performed only on small aneurysms that do not contain mural thrombus. Plication is performed by running a two-layer suture line of large monofilament suture with Teflon felt on either side. The suture line should be oriented as to reconstruct a normal LV chamber and does not have to include all aneurysmal tissue.
- Linear closure is performed by making an incision in the ventricular aneurysm, removing all mural thrombus, and trimming the aneurysm wall to leave a 3 cm rim of scar to reconstruct the ventricle. Anterior aneurysms are closed vertically in two layers with monofilament suture and Teflon pledgets.
- Dacron patch closure is performed by partially excising the aneurysmal portion of the ventricle, leaving a rim of tissue for sewing. The patch is then sewn in with interrupted monofilament sutures with Teflon pledgets on the exterior of the ventricular cavity. The defect may be plicated with a Fontan stitch prior to patch closure. A Fontan stitch is a running, circular, monofilament pursestring stitch that is cinched down to reduce the size of the defect.
- Endoventricular patch technique may also be used although it is not well suited for posterior or inferior aneurysms.
The outcomes of left ventricular remodeling surgery for LV aneurysm show that most patients who undergo surgical remodeling have improvement in ventricular function. The RESTORE study demonstrated that LV aneurysm resection or surgical ventricular reconstruction (SVR) improved postoperative EF, NYHA Class, and LV end-systolic volume. In this study, concomitant CABG and mitral valve repair were performed in 95% and 22% of patients, respectively. The controversial STICH trial showed no difference in mortality of patients undergoing CABG alone versus patients undergoing CABG with LV remodeling. The type of repair did not affect the outcome.
Suggested Readings
- Komeda M, David TE, Malik A, Ivanov J, Sun Z. Operative risks and long-term results of operation for left ventricular aneurysm. Ann Thorac Surg. 1992; 53(1):22.
- Velazquez EJ, Lee KL, Deja MA, et al. Coronary-artery bypass surgery in patients with left ventricular dysfunction. N Engl J Med. 2011;364(17):1607–1616.
- Ruzza A, Czer LSC, Arabia F, et al. Left Ventricular Reconstruction for Postinfarction Left Ventricular Aneurysm: Review of Surgical Techniques. Tex Heart Inst J. 2017;44(5):326-335.
