Management of a left ventricular aneurysm in an adult
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MANAGEMENT OF A LEFT VENTRICULAR ANEURYSM IN ANADULTHom e » Clinical Resources » Clinical Cases
Sorin V. Pusca, MD University of Medicine and
By Sorin V. Pusca, MD, Barry C. Esrig, MD, Preet M.S.
Randhawa, MD, Dusan Knezevic, MD and Muhamed
University of Medicine andDentistry of New Jersey Newark, NJ USA
A 65-year-old female presented to the emergency department
with acute respiratory failure due to pulmonary edema. She
had a history of several months of worsening dyspnea on
exertion. She was admitted to the intensive care unit,
intubated, and received aggressive diuresis and afterload
University of Medicine andDentistry of New Jersey
reduction therapy. After several days, she was successfully
extubated and cardiac catheterization was performed.
Muhamed Saric, MD University of Medicine and
Her past medical history was significant for hypertension,
non-insulin dependent diabetes mellitus, and a remote
myocardial infarc tion. She denied use of tobacco or alcoholand denied history of chest pain, orthopnea, and lowerextremities edema. Her medications after extubation included Lasix, Aldactone, Coreg,Vasotec, Zocor, Aspirin and Glucovance.
On this regimen, she had no orthopnea at bedrest; her heart rate was 60 beats/min,regular, and the blood pressure was 124/60 mm Hg. She had no jugular venous distensionor c arotid bruits. She did not use her accessory respiratory muscles, but she had bibasilarrales in the lower quarter of her lung fields. She had a left parasternal systolic ejec tionmurmur grade II/VI without radiation. She had neither hepatosplenomegaly nor pretibialedema. Her peripheral pulses were normal, and she had no focal neurologic deficits.
Her blood urea nitrogen was 29 mg/dl, and serum creatinine was 0.9 mg/dl. Theelectrocardiogram showed normal sinus rhythm at 69 beats/min and Q waves in leads II, IIIand aVF. Her pulmonary function test showed a vital c apacity of 1.5l (51% predicted), aforc ed expiratory volume in one second of 1.4l (59% predicted), and a maximal voluntaryventilation of 32.9 l/min (37% predicted). Her chest roentgenogram showed small bilateralpleural effusions and pulmonary vascular congestion.
The cardiac catheterization (Videos 1, 2, 3) showed left anterior descending artery (LAD)95% stenosis, obtuse marginal artery (OM) 80% stenosis and proximal right coronary artery(RCA) 85% stenosis. The left ventric ular (LV) ejection fraction was 30% and an apicalaneurysm could be clearly identified (Video 4). The preoperative transthoracicechocardiogram without (Video 5) and with (Video 6) intravenous contrast confirmed a 3.5x1.5 cm left ventricular aneurysm. The left ventricular (LV) ejection fraction was estimatedat 25-30% with a dyskynetic apex, inferior and posterior hypokinesis, grade one LV diastolicdysfunction, and 1+ mitral regurgitation. No intracardiac thrombus was apprec iated. TheLV end-diastolic diameter was 6.2 cm (normal < 5.2cm), the LV end-systolic diameter was4.8 cm (normal < 2.3-3.9 cm) and the LV end-systolic volume index (LVESVI) was 70.1ml/m2. The left atrium measured 4.0 c m in diameter. The aortic, pulmonary, and tricuspidvalves were normal and the estimated pulmonary artery systolic pressure was 20 mm Hg. Preoperative non-invasive vascular studies showed no significant carotid stenosis andnormal ankle-brachial indices.
In summary, this is a patient in class III NYHA secondary to ischemic cardiomyopathy–
6/20/2009 ary, this is a patient in class III NYHA secondary to ischemic ca
Management of a Left Ventricular … rdiomyopathy–
c urrently hospitalized on maximal medical therapy. She has single segment dyskinesia withone-third of the anterior wall dyskinetic/akinetic forming a left ventric ular apic al aneurysm.
She underwent surgical anterior ventricular restoration (SAVER) and coronaryrevascularization (left internal mammary artery to left anterior descending artery, and twosaphenous vein grafts from the aorta to an obtuse marginal and right coronary artery,respectively).
The operation was performed with bi-caval c annulation and an LVvent via the right superior pulmonary vein. Myocardial protectionwas achieved with antegrade aortic and vein graft bloodcardioplegia, as well as retrograde blood cardioplegia. Prior toarresting the heart it was noticed that the apic al aneurysm was anakinetic, but not thinned segment of the heart (Figure 1) and assuch its margins could not be easily identified on the arrestedheart. The aneurysm margins were delineated after completion of
distal anastomoses and cross clamp removal, by opening the apex of
the beating heart. A pursestring Fontan suture was passed through
the base of the aneurysm and the opening closed with a sized Dac ron patch; theaneurysmal tissue was imbricated over the repair. The bypass time was 111 min with ac ross-clamp time of 44 minutes.
Postoperatively, there were no arrhythmias. The patient was off all inotropes and pressorson postoperative day two and disc harged home on post-operative day six. Seven monthsafter surgery she is in NYHA class I and the echoc ardiogram shows restoration of ventric ulargeometry (Video 7).
CommentsThe concept of excluding the akinetic portion of the ventricle derives from the fact thatwhen a portion of the ventricular wall is transformed into scar tissue, the loss of function ishigher then estimated by the loss of c ontrac tile tissue alone. This is due to changes in theventric ular geometry and loss of synchronization of ejec tion phases that alter fundamentallythe muscle mechanics of the ventricle . It was noted that exc luding that portion of theventric le by resection, plication or resection could improve ventricular function. Cooleydesc ribed a resec tion and linear closure of aneurysms in 1958; for aneurysms in theproximity of the ventric ular septum, he described a septal inclusion technique. Jatenedesc ribed a technique of septal imbrication in 1985 and Cooley described a technique forseptal exclusion in 1988. It was not, however, until Dor in 1985 that the concept ofpreservation of left ventric ular geometry after such resec tions/exc lusions became clear. This began the era of SAVER and made possible excision of myocardial segments thatwere akinetic but had no scar as in this case.
In relatively small aneurysms, survival is influenced by symptoms at presentation;asymptomatic patients have a five-year survival in 85-89% range while symptomaticpatients have a survival in 55-59% range . Medical treatment can extend 50% survivalto 6.5 years (ace-inhibitors), 7.5 years (beta-bloc kers) and 8.5 years (spironolactone) and heart transplantation can extend this further to 9.1 years for advanced class NYHApatients .
Overall 5-year survival after the SAVER operation is 69% . The preoperative leftventric ular end-systolic volume index (LVESVI) is a critical measurement in planning theSAVER operation. Patients with symptoms of heart failure but LVESVI < 60 ml/m2 shouldnot undergo ventricular remodeling, as ventricular size may bec ome too small. In c ontrast,patients with preoperative LVESVI > 100 ml/m2 have a poor long-term outc ome from bypassalone , and when SAVER is indicated, have been shown to have an increased survival. Patients with preoperative LVESVI < 80 ml/m2 have, however, a five-year survival of 79%. This value decreases, however, to 72% and 67% for patients with LVESVI between 80-120ml/m2, and greater then 120 ml/m2 respectively.
Preoperative ejection fraction (EF) is also an important determinant for survival. Patientsthat underwent the SAVER operation and had a preoperative EF > 30% had a 77% 5-yearsurvival while patients with an EF < 30% had a 64% survival .
Patients younger then 70 years of age had a 5-year survival of 70%, while older patientshad only a 59% actuarial survival .
Overall the freedom from readmission to the hospital for heart failure after the SAVERoperation is 78% at five years . Preoperative NYHA class improves from an average of2.9 with 67% of patients in class III and IV to 1.7 with only 15% of patients in class III andIV .
In the current case presentation, the patient was severely symptomatic preoperatively andhad a low ejec tion fraction. However she had a low LVESVI and was in a favorable agegroup. Her postoperative showed that she benefited from the SAVER operation.
In c onclusion, restoring ventricular shape and function in patients with ischemicc ardiomyopathy, especially in patients with anterior myoc ardial infarction and akinesis,c ompares favorably with other treatment modalities for this condition regarding early andlong-term survival as well as postoperative functional status.
References1 . Athanasuleas LC, Buckberg GD, Menicanti L, Gharib M, RESTORE Group. Optimizingventric ular shape in anterior restoration. Semin Thor Cardiovasc Surg 2001;13:459-67
2. Menicanti L, DiDonato M. The Dor procedure: what has c hanged after fifteen years ofc linical practice? J Thorac Cardiovasc Surg 2002;124:886-90.
3. Grondin P, Kretz JG, Bic al O, Donzeau-Gouge P, Peticlerc R, Campeau L. Natural historyof sac cular aneurysms of the left ventricle. J Thorac Cardiovasc Surg 1979;77:57-64.
4. Restore Group – SAVER update meeting, Toronto 2004.
5 . Hosepund JD, Bennett LE, Keck BM, Boucek MM, Novick RJ. The registry of theInternational Society for Heart and Lung Transplanatation: eighteenth official report –2001. J Heart Lung Transplant 2001;20:805-15.
6. Yamaguchi A, Ino T, Adachi H, et al. Left ventricular volume predicts postoperativec ourse in patients with ischemic c ardiomyopathy. Ann Thorac Surg 1998;65:434-8.
7. Athanasuleas LC, Stanley AWH, Buckberg GD, Dor V, Di Donato M, Siler W, RESTOREGroup. Surgical anterior ventricular endocardial restoration (SAVER) for dilated ischemicc ardiomyopathy. Semin Thor Cardiovasc Surg 2001;13:448-58.
Publication Date: 14-Sep-2005Last Modified: 14-Sep-2005
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