Mickleborough LL, Carson S, Tamariz M, Ivanov J.
Results of revascularization in patients with severe left ventricular dysfunction.
J Thorac Cardiovasc Surg 2000;119:550-7.
Suma H, Isomura T, Horri T, et al.
Nontransplant cardiac surgery for end-stage cardiomyopathy.
J Thorac Cardiovasc Surg 2000;119:1233-45.
Pasini S, Gagliardotto P, Punta G, et al.
Early and late results after surgical therapy of postinfarction left ventricular aneurysm.
J Cardiovasc Surg 1998;39:209-15.
Dor V, Sabatier M, Di Donato M, Montiglio F, Toso A, Maioli M.
Efficacy of endoventricular patch plasty in large postinfarction akinetic scar and severe left
ventricular dysfunction: comparison with a series of large dyskinetic scars.
J Thorac Cardiovasc Surg 1998;116:50-9.
Elfridi I, Grayburn PA, Panza JA, Oh JK, Zoghbi WA, Marwick TH.
>BR>
Myocardial viability during dobutamine echocardiography predicts survival in patients with
coronary artery disease and severe left ventricular systolic dysfunction.
J Am Coll Cardiol 1998;32:921-6.
Bolling SF, Pagani FD, Deals GM, Bash DS.
Intermediate terms outcome of mitral reconstruction in cardiomyopathy.
J Thorac Cardiovasc Surg 1998;115:381-6.
Di Donato M, Sabatier M, Dor V, Toso A, Maioli M, Fantini F.
Akinetic versus dyskinetic postinfarction scar: relation to surgical outcome in patients undergoing endoventricular
circular patch plasty repair.
J Am Coll Cardiol 1997;29:1569-75.
Sinatra R, Macrina F, Braccio M, et al.
Left ventricular aneurysmectomy; comparison between two techniques: early and late results.
Eur J Cardiothorac Surg 1997;12:291-7.
Shapira OM, Davidoff R, Hilkert RJ, et al.
Repair of left ventricular aneurysm: long-term results of linear repair versus endoaneurysmorrhaphy.
Ann Thorac Surg 1997;63:701-5.
DiCarli MF, Asganzadre F, Schelberth R, et al.
Quantitative relation between myocardial viability and improvement in heart failure symptoms after revascularization in patients with
ischemic cardiomyopathy.
Circulation 1995;92:36-44.
Grossi EA, Chinitz LA, Galloway AC, et al.
Endoventricular remodelling of left ventricular aneurysm: Functional, clinical and electrophysiological results.
Circulation 1995;92(Suppl):II-98-100.
Kawata T, Kitamura S, Kawachi K, et al.
Systolic and diastolic function after patch reconstruction of left ventricular aneurysms.
Ann Thorac Surg 1995;59:403-7.
Mickleborough LL, Maruyama H, Liu P, Mohammed S.
Results of left ventricular aneurysmectomy with a tailored scar excision and primary closure technique.
J Thorac Cardiovasc Surg 1994;107:690-8.
Elefteriades JA, Solomon LW, Salazar AM, Batsford WP, Baldwin JC, Kopf GS.
Linear left ventricular aneurysmectomy: modern imaging studies reveal improved morphology and function.
Ann Thorac Surg 1993;56:242-52.
Mills NL, Everson CT, Hockmuth DR.
Technical advances in the treatment of left ventricular aneurysm.
Ann Thorac Surg 1993;55:792-800.
Couper GS, Bunton RW, Birjiniuk V, et al.
Relative risks of left ventricular aneurysmectomy in patients with akinetic scars versus true dyskinetic aneurysms.
Circulation 1990;82(Suppl):IV-248-56.
Circulation. 1990 Nov;82(5 Suppl):IV248-56.
Relative risks of left ventricular aneurysmectomy in patients with akinetic scars versus true dyskinetic aneurysms.
Couper GS, Bunton RW, Birjiniuk V, DiSesa VJ, Fallon MP, Collins JJ Jr, Cohn LH.
Harvard Medical School, Boston, Mass.
From 1971 to 1988, 303 patients underwent left ventricular aneurysm resection. We analyzed preoperative and procedure-related variables to ascertain risk factors for surgery. A distinction was made between akinetic and dyskinetic aneurysms to assess potential relation with postoperative outcome. Indications for surgery were arrhythmia in 20 patients, congestive heart failure in 81, angina in 133, congestive heart failure and angina in 42, and other combinations in the remaining 27 patients. The left ventricular aneurysm was dyskinetic in 180 patients and akinetic in 121. Risk factors and surgical procedures were similar in both groups. Left ventricular ejection fraction was less than or equal to 30% in 98 patients. Coronary bypass grafting was performed in 269 patients, with an average of 2.3 grafts per patient. Mitral valve replacement, the most common concomitant procedure, was performed in 16 patients. Intra-aortic balloon assist was required postoperatively in 47 patients. Overall operative mortality was 13% (38 patients) and was due to low cardiac output in 23 patients and arrhythmia in 12 patients. Univariate and multivariate analyses related early mortality to New York Heart Association functional classification of heart failure, the predominant indications of arrhythmia or congestive heart failure, left ventricular ejection fraction less than or equal to 30%, the need for intra-aortic balloon support, and the excision of an akinetic (18%) rather than dyskinetic (8%) left ventricular aneurysm. Over a follow-up period averaging nearly 5 years, the actuarial survival at 5 years was 63% in the dyskinetic group and 51% in the akinetic group.
Pfeffer MA, Braunwald E.
Ventricular remodelling after myocardial infarction: experimental observations and clinical implications.
Circulation 1990;81:1161-72.
Circulation. 1990 Apr;81(4):1161-72.
Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications.
Pfeffer MA, Braunwald E.
Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.
An acute myocardial infarction, particularly one that is large and transmural, can produce alterations in the topography of both the infarcted and noninfarcted regions of the ventricle. This remodeling can importantly affect the function of the ventricle and the prognosis for survival. In the early period, infarct expansion has been recognized by echocardiography as a lengthening of the noncontractile region. The noninfarcted region also undergoes an important lengthening that is consistent with a secondary volume-overload hypertrophy and that can be progressive. The extent of ventricular enlargement after infarction is related to the magnitude of the initial damage to the myocardium and, although an increase in cavity size tends to restore stroke volume despite a persistently depressed ejection fraction, ventricular dilation has been associated with a reduction in survival. The process of ventricular enlargement can be influenced by three interdependent factors, that is, infarct size, infarct healing, and ventricular wall stresses. A most effective way to prevent or minimize the increase in ventricular size after infarction and the consequent adverse effect on prognosis is to limit the initial insult. Acute reperfusion therapy has been consistently shown to result in a reduction in ventricular volume. The reestablishment of blood flow to the infarcted region, even beyond the time frame for myocyte salvage, has beneficial effects in attenuating ventricular enlargement. The process of scarification can be interfered with during the acute infarct period by the administration of glucocorticosteroids and nonsteroidal antiinflammatory agents, which result in thinner infarcts and greater degrees of infarct expansion. Modification of distending or deforming forces can importantly influence ventricular enlargement. Even short-term augmentations in afterload have deleterious long-term effects on ventricular topography. Conversely, judicious use of nitroglycerin seems to be associated with an attenuation of infarct expansion and long-term improvement in clinical outcome. Long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions on the left ventricle and reduce progressive ventricular enlargement as demonstrated in both experimental and clinical studies. With the former therapy, this attenuation of ventricular enlargement was associated with a prolongation in survival. The long-term clinical consequences of long-term angiotensin converting enzyme inhibitor therapy after myocardial infarction is currently being evaluated. Although studies directed at attenuating left ventricular remodeling after infarction are in the early stages, it does seem that this will be an important area in which future research might improve long-term outcome after infarction.
Dor V, Saab M, Coste P, Kornaszewski M, Montiglio F.
Left ventricular aneurysm: a new surgical approach.
J Thorac Cardiovasc Surg 1989;37:11-9.
Cooley DA.
Ventricular endoaneurysmorrhaphy: a simplified repair for extensive postinfarction aneurysm.
J Card Surg 1989;4:200-5.
Cosgrove DM, Lytle BW, Taylor PC, et al.
Ventricular aneurysm resection: trend in surgical risk.
Circulation 1989;79(Suppl):I-97-101.
Circulation. 1989 Jun;79(6 Pt 2):I97-101.
Ventricular aneurysm resection. Trends in surgical risk.
Cosgrove DM, Lytle BW, Taylor PC, Stewart RW, Golding LA, Mahfood S, Goormastic M, Loop FD.
Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic Foundation, Ohio 44195-5066.
From 1972 to 1987, 1,183 patients underwent ventricular aneurysm resection. At 4-year intervals, this series was divided into four subsets that differed in patient and management-related variables. Comparison of patients seen from 1972 to 1975 with those seen in 1984-1987 shows a significant increase in mean age to 59.4 years, with 31.6% older than 65 years, an increase to 43.4% of patients with congestive heart failure, and a decrease to 42.8% of patients with angina. In the most recent interval, 30.7% of patients had mammary grafts, 81.1% had associated grafts, and 47.2% of patients were completely revascularized. Mortality rate, however, increased to 8%. Deaths were attributed to cardiac causes in 59.7% of cases. Multivariate analysis identified emergent procedures, advancing age, left main trunk disease, and history of congestive heart failure as risk factors. We conclude that the incidence of aneurysm resection is decreasing and operative risk has been constant despite advancing patient age and more extensive operative procedure.
Magovern GJ, Sakert T, Simpson K, et al.
Surgical therapy for left ventricular aneurysms: a 10 year experience.
Circulation 1989;79(Suppl):I-102-7.
Circulation. 1989 Jun;79(6 Pt 2):I102-7.
Surgical therapy for left ventricular aneurysms. A ten-year experience.
Magovern GJ, Sakert T, Simpson K, Laub GW, Park SB, Liebler G, Burkholder J, Maher T, Benckart D, Magovern GJ Jr.
Department of Surgery, Allegheny General Hospital, Pittsburgh, Pennsylvania 15212.
We reviewed retrospectively the surgical results of left ventricular aneurysm reduction in 197 consecutive patients operated on in 1977-1987. There were 19 hospital deaths (9.6%) and 38 late deaths. The cumulative 5- and 10-year survival probabilities were 79% and 67%. Of the 140 late survivors, 130 underwent follow-up study in 1988 (mean, 5 years postsurgery). We analyzed preoperative, perioperative, and postoperative variables to evaluate the efficacy of surgical therapy. The risk of early mortality was increased by worsening preoperative New York Heart Association class, operation within 30 days of myocardial infarction, combinations of ventricular arrhythmia and congestive heart failure, renal failure, and preoperative cardiogenic shock. There was a trend toward increased early mortality with multivessel coronary artery disease. Late mortality and length of survival were not predicted by any variable examined.
Stephenson LW, Hargrove WC, Ratcliffe MB, Edmunds LH.
Surgery for left ventricular aneurysm: early survival with and without endocardial resection.
Circulation 1989;79(Suppl):I-108-11.
Circulation. 1989 Jun;79(6 Pt 2):I108-11.
Surgery for left ventricular aneurysm. Early survival with and without endocardial resection.
Stephenson LW, Hargrove WC 3rd, Ratcliffe MB, Edmunds LH Jr.
Department of Surgery, School of Medicine, University of Pennsylvania, Philadelphia 19104.
In the past 3 years, 86 patients had left ventricular aneurysms resected or plicated. Sixty-eight had recurrent sustained ventricular tachycardia as the indication for surgery and had preoperative and intraoperative electrophysiologic mapping. There were 14 hospital deaths (16%). Eight preoperative potential risk factors for early hospital mortality were analyzed by multivariate analysis. Only acute myocardial infarction within 30 days before surgery correlated with hospital death at the p less than 0.05 level. History of previous heart surgery and advanced New York Heart Association functional class were important risk factors at the p less than 0.1 level. Hospital mortality was 17.6% for patients who had intraoperative mapping and endocardial resection and 11.1% for the others. Patients who had aneurysm repair for ventricular tachycardia had a significantly higher incidence of low cardiac output early after surgery (p less than 0.025).
McKay RG, Pfeffer MA, Pasternak RC, et al.
Left ventricular remodelling after myocardial infarction: a corollary to infarct expansion.
Circulation 1986;74:693-702.
Circulation. 1986 Oct;74(4):693-702.
Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion.
McKay RG, Pfeffer MA, Pasternak RC, Markis JE, Come PC, Nakao S, Alderman JD, Ferguson JJ, Safian RD, Grossman W.
Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p less than .01), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p less than .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p less than .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p less than .05) and significant increases in angiographic cardiac index (p less than .01) and LVESV index (p less than .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akinetic-dyskinetic segments and volume-overload hypertrophy of noninfarcted segments.
Jatene AD.
Left ventricular aneurysmectomy.
J Thorac Cardiovasc Surg 1985;89:321-31.
Cooley DA, Collins HA, Morris GC, Chapman DW.
Ventricular aneurysm after myocardial infarction: surgical excision with use of temporary cardiopulmonary bypass.
JAMA 1958;167:557-60.
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