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Repair of Postinfarction Ventricular Septal Defects
Repair of Postinfarction Ventricular Septal Defects Joren C. Madsen and Willard M. DaggettJJr Postinfarction ventricular septal defects complicate approximately 1% to 2% of cases of acute myocardial infarction and account for about 5% of early deaths after myocardial infarction. By differentiating the surgical treatment of these acquired lesions from the surgical approaches used to repair congenital ventricular septal defects and realizing the significance of differing anatomic locations of postinfarction ventricular septal defects, techniques have been developed that have improved salvage of patients suffering this catastrophic complication of myocardial infarction. The principles underlying these surgical techniques include (1) expeditious establishment of total cardiopulmonary bypass with moderate hypothermia and meticulous attention to myocardial protection; (2) transinfarct approach to ventricular septal defect with the site of ventriculotomy determined by the location of the transmural infarction; (3) thorough trimming of the left ventricular margins of the infarct back to viable muscle to prevent delayed rupture of the closure; (4) conservative trimming of the right ventricular muscle as required for complete visualization of the margins of the defect; (5) inspection of the left ventricular papillary muscles and concomitant replacement of the mitral valve only if there is frank papillary muscular rupture; (6) closure of the septal defect without tension, which in most instances will require the use of prosthetic material; (7) closure of the infarctectomy without tension with generous use of prosthetic material as indicated, and epicardial placement of the patch to the free wall to avoid strain on the friable endocardial tissue; and (8) buttressing of the suture lines with pledgets or strips of Teflon felt or similar material to prevent sutures from cutting through friable muscle. Copyright © 1998 by W.B. Saunders Company Key words: Postinfarction ventricular septal defect, mechanical complication of myocardial infarction, infarctectomy, patch repair.
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he first step in the evolution of surgical techniques for repair of acute postinfarction ventricular septal rupture involved differentiating the surgical treatment of these acquired lesions from the surgical approaches used to repair congenital ventricular septal defects, which are, for the most part, not applicable. Next, understanding the significance of differing anatomic locations of postinfarction ventricular septal defects led to innovations in terms of the location of the cardiotomy and the type of repair necessary to achieve a successful result in any given patient. Then, the gradual appreciation of different clinical courses pursued by patients after postinfarction ventricular septal rupture, both in terms of location of the defect and the degree of right ventricular functional impairment, led to an increased urgency relative to the timing of surgical repair.' Most From theDivision ofCardiac Surgery, Massachusetts General Hospital, Boston,MA. Address reprint requests toJoren C. Madsen, MD, DPhil,Massachusetts General Hospital, 55 Fruit St, EDR 105,Boston, MA 02114-2696. Copyright © 1998 byWB. Saunders Company 1013-0679/98/1002-0006$08.00/0
recently, the superb results being reported using the technique of endocardial patching with infarct exclusion? may signify yet another milestone in the evolution of the surgical management of postinfarction ventricular septal defects.
Incidence Postinfarction ventricular septal defects complicate approximately I% to 2% of cases of acute myocardial infarctions and account for about 5% of early deaths after myocardial infarction.v' The average time from infarction to rupture has been reported to be between 2 and 4 days, but it may be as short as a few hours or as long as 2 weeks.t-' The age of patients with this complication ranges from 44 to 81 years, with a mean of 62.5 years. However, there is some evidence that the average age is increasing.V The vast majority of patients who experience ventricular septal rupture do so after their initial infarction.t-' The overall incidence of postinfarction ventricular septal rupture may have decreased slightly during the past decade as a result of aggressive pharmacologi-
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cal treatment of ischemi a and thrombolytic th erapy in patients with evolving myocardial infarction, as well as th e prompt control of hypertension in th ese pati ents,"
Anatomy Angiographic evaluation of patients with postinfarction ventricular rupture indicat es that septal rupture is usually associated with complete occlusion , rather than severe stenosis of a corona ry arteryf Postinfarction ventricular septal defects ar e most commonly located in the anteroapical septum as the result of a full-thickness anterior infarction (in approximately 60% of cases). These anter ior septal ruptures are caused by anteroseptal myocard ial infarction following occlusion of the left anterior descending artery. In about 20% to 40% of patients, th e rupture occurs in th e post erior septum following an inferoseptal infarction , which is usually du e to occlusion of a dominant right coronary artery or, less frequ ently, a dominant circumflex artery." Ther e are two types of rupture: simple, consisting of a dir ect through and through defect usually located anteriorly; and complex, consisting of a serpiginous dissection tr act remote from th e primary septal defect th at is usually located inferiorly.l" Multiple defects, which may develop within severa l days of each othe r, occur in 5% to II % of cases , and are probably du e to infarct exte nsion.
Pathophysiology The most important det erminants of early outcome following postinfarction ventricular septal rupture are the development of congestive heart failure and cardiogenic shock which, in turn, depend on the size of th e infarct and the magnitude of the left-to-right shunt. Left ventricular dysfunction du e to extensive necrosis of th e left ventricle is the primary determinant of conge stive heart failur e and cardiogenic shock in patients with ant erior septal rupture, whereas righ t ventricular dysfunction secondary to extensive infarction of th e right ventricle is the principal det erminant of heart failure and cardiogenic shock in pati ents with post erior septal rupture. 2, 11,12 However, the development of conges tive heart failure and cardiogenic shock in patients with postinfarction ventricular septal defects is not explained solely by the extent of damage sustain ed by th e left ventricle. 13 The magnitude of th e left-to-right shunt is the other key variable in th e developm ent of hemodynamic compromise. With th e open ing of a ventricular septal
defect, the heart is cha llenged by an increase in pulmonary blood flow and a decrease in system blood flow as a portion of each stroke volum e is diverted to th e pulmonary circuit. As a consequence of th e sudde n increase in hemodynami c load imposed on a heart already compromised by acute infarction, and possibly by a ventricular ane urysm, mitral valve dysfun ction or a combination of th ese problems, a severe low cardiac output stat e results. The normally compliant right ventricle is especially susceptible to failure in this circumstance.lt-P Pati ents with posterior ventricular septal rupture and right ventricular dysfunction may display shunt reversal during diastole because the end-diastolic pressure in the right ventricle can be higher than in th e left ventricle.l'v'" Ultimately, persistence of a low ca rdiac output state result s in peripheral organ failure.
Diagnosis The typical presentation of a ventricular septal rupture occurs in a patient who has suffered an acute myocardial infarction and who, after convalescing for a few days, develops a new systolic murmur, recurrent chest pain, and an abrupt det erioration in hemodynami cs. The development of a loud systolic murmur, usuall y within th e first week following an acute myocardial infarction, is th e most consistent physical finding of postinfarction ventricular septal rupture (present in more th an 90% of cases). The murmur is usually harsh, pan systolic, and best heard at th e left lower sternal bord er. Th e murmur is often associated with a palpable thrill. Depending on the location of the septal defect, th e murmur may radiate to the left axilla, th er eby mimicking mitral regurgitation.l" Up to half of th ese patients experience post infarction chest pain in association with the appearance of the murmur." Coincident with the onse t of the murmur, there is usuall y an abrupt decline in th e patient's clinical course with congestive failure and often cardiogen ic shock. The findings of cardiac failur e that occur acutely in th ese patients ar e primarily the result of right-sided heart failure, with pulmonary edema being less prominent than that occur ring in pati ents with acute mitral regurgita tion du e to ruptured papill ary mu scle.l? Recent advances in transthoracic and transesophageal echocardiography, especially th e advent of color flow Doppler mapping, have revolut ionized the diagnosis of both the pr esen ce and site of septal rupture. 20.22 Echocardiography can detect the defect, localize its site and size, det ermine right and left
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ventricular fun ction , assess pul monary ar tery and rig ht ven tric ular pressur es, and excl ude coex isti ng m itra l regurgit ati on or free wall rupt ure. Smyllie et al21 reporte d a 100% specificity and 100% sensi tivity when color flow Doppler mapping was use d to differentiate ventricular septal rupture from acute severe mitral regurgita tion following acute myoca rdia l infarction. They also correctly demonstrated th e site of septal rupture in 4 1 of 42 patients. Widespread use of this tec hnology has, for the most part , replaced thermodilu tion catheter insertion, which in outlying hospitals, where patien ts ar e oft en see n first, m ay be time-consuming and difficult to accomplish. Indeed, the trend toward ea rly surgical referral and prompt operative repair is at least pa rtially explained by the more wide spr ead use of color Doppler echocardiogra phy for diagn osis in peri ph eral centers.P T he necessity of preoperative left heart catheterization with coronary angiography has been a matt er of debate. O n the one ha nd, left heart ca theterizatio n pr ovides imp ortant information concerning associated coro nary artery diseas e, left vent ricular wall motion, an d specifics of valvular dysfunct ion, which ar e all importan t in planning operative correction of postin farction septal rupture. In most series 24-26 more than 60% of pat ients 'With se ptal rupture have significant involvem en t of at least one vessel ot he r than the one supplying th e infa rcted area. However, th ere are disadva ntages in performing left heart ca the terization with coronary angiography. It is time -consuming and can contribute to both th e morta lity a nd morbidity of thes e already compromised pat ients. 6,24 Thus, some cente rs do not perform preopera tive left heart cat he te rization; others use it selectively, avoiding invasive studies in patien ts with septal rupture caus ed by ante rior wall infarction, which is associated wit h a much lower inciden ce of mu ltip le vessel disease than septal defec ts res ulting from posterior infarc tions.6,27,2H
Preoperative Management Because the natur al course of the disease in u noperat ed patien ts is so dismal, th e diagnos is of pos tinfarction ventricular septal rupture can be regarde d as its own indicat ion for operat ion." P reoperative man agem en t is directed toward sta biliza tion of th e hem odynamic condit ion so that peri pheral organ perfusion ca n be best maintained while any further diagnostic studies are obtained and whi le dec iding on th e optimal time for surgical interven tion. T he goals of pr eoperative managem ent ar e to ( I) redu ce th e systemic vascula r resistance, and thus, th e left-to-
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right shun t; (2) mai ntain cardiac output and arterial pr essure to ensure peripheral organ perfusion; and (3) mai ntain or im prov e coronary artery blood flow. T hese goals are best accomplish ed by the int ra-aortic balloon pump (IABP) . Alt hough counterpulsation produces an overall improvem ent in th e patient's cond ition, a com plete correction of th e hem odynamic picture cannot be obtained . Pea k improvement occu rs within 24 hour s, and little fur ther benefit has bee n observe d with prolonged balloon pumping.P Ph armacological therapy with inotropic age n ts and diuretics should be inst ituted promptly. It must be stressed th at pharmacological therapy is intended primarily to support th e pa tien t in pr ep aration for operation and should not , in anyway, delay urgent operation in the critically ill pati ent.
Operative Techniques Exp eri ence with a variety of techniques for closure of postinfarctio n ventricula r septal rupture has led us to th e evolution of eight basic principles (Table I). Adh erence to these principles in the closure of sep tal defects in differe nt location s has led to the evolut ion of individualized approaches to apical, anterior, and inferoposterior septal defects,7,3o,31
Table 1. Principles of Repair of Postinfarction Ventricular Septal Defects
I) Expeditious establishment of total cardiopulmonary bypasswith moderate hypothermia and meticulous attention to myocardial protection. 2) Transinfarct approach to ventricular septal defect with the site of ventriculotomy determined by the location of the transm ural infarction. 3) Thorough trimming of the left ventricular margins of the infarct back to viable muscle to prevent delayed rupture of the closure. 4) Conservative trimming of the right ventricular muscle as required for complete visualization of the margins of the defect. 5) Inspection of the left ventricular papillary musclesand concomitant replacement of the mitral valve onlyif there is frank papillary muscular ruptur e. 6) Closure of the septal defect wi thout tension, which in most instances will require the use of prosthetic mat erial. 7) Closure of the infarctectomy without tension with generous use of prosthetic material as indicated and epicardial placement of the patch to the free wall to avoidstrain on the friable endocardial tissue. 8) Buttressing of the suture lines with pledgets or strips of Teflon felt or similar material to prevent sutures from cutting through friable muscle.
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Apical Septal Rupture The technique of apical amputation was described by Daggett et al in 1970.30 An incision is made through the infarcted apex of the left ventricle. Excision ofthe necrotic myocardium back to healthy muscle results in amputation of the apical portion of the left ventricle, right ventricle, and septum (Figs lA and B). The remaining apical portions of the left and right ventricle free walls are then approximated to the apical septum. This is accomplished by means of a row of interrupted mattress sutures of 0 Tevdek that are passed sequentially through a buttressing strip of Teflon felt, the left ventricular wall, a second strip of felt, the interventricular septum, a third strip of felt, the right ventricular wall, and a fourth strip of felt (Figs 2A and B). After all sutures have been tied, the closure is reinforced with an additional over-andover suture, as in ventricular aneurysm repair, to
Figure 2. (A) Necrotic infarct and apical septum have been debrided back to healthy muscle. (B) All sutures are placed before any are tied. A second running over and over suture (not shown) is used, as in left ventricular aneurysm repair, to insure a secure hemostatic ventriculotomy closure. Abbreviations: A, aorta; LAD, left anterior descending coronary artery; RV, right ventricle; LV, left ventricle. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgery in the Adult. New York, NY, McGraw-Hill, 1997.)
insure hemostasis of the ventriculotomy closure (not shown).
Anterior Septal Rupture
Figure 1. (A) Apical postinfarction ventricular septal defect. (B) View of the apical septal rupture, which is exposed by amputating apex of left and right ventricles. Stippled region, infarcted myocardium; A, aorta; LAD, left anterior descending coronary artery; RV, right ventricle; LV, left ventricle. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgery in the Adult. New York, NY, McGraw-Hill, 1997.)
The approach to these defects is by a left ventricular transinfarct incision with infarctectomy (Figs 3A and B). Small defects beneath anterior infarcts can be closed by the technique of plication as suggested by Shumaker.V This involves approximation of the free anterior edge of the septum to the right ventricular free wall using mattress sutures of 0 Tevdek over strips of felt (Fig 4A). The transinfarct incision is then closed with a second row of mattress sutures buttressed with strips of felt (Fig 4B and C). An over-and-over running suture completes the ventriculotomy closure (not shown). Most anterior defects require closure with a prosthetic patch (DeBakey Elastic Dacron fabric made by U.S.C.I., Division ofC.R. Bard, Inc., Billerica, MA) to avoid tension that could lead to disruption of the
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are then approximated by a two-layer closure consisting of interrupted mattress sutures passed through buttressing strips of Teflon felt and a final over-andover running suture (not shown).
Posterior Septal Rupture
LAD
Infarct
Figure 3. (A) Transinfarct left ventricular incision to
exposean anterior septal rupture. An incision(dashed line) is made parallel to anterior descending branch of left coronary artery (LAD) through center of infarct (stippled area) in anterior left ventricle (LV). (B) View of septal defect following infarctectomy. Abbreviations: A, aorta; RV, right ventricle; PA,pulmonary artery. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgeryin the Adult. NewYork, NY,McGraw-Hill, 1997.) repair (Fig 5). After debridement of necrotic septum and left ventricular muscle, a series of pledgeted interrupted mattress sutures are placed around the perimeter of the defect (Fig 5A). Along the posterior aspect of the defect, sutures are passed through the septum from right side to left. Along the anterior edge of the defect, sutures are passed from the epicardial surface ofthe right ventricle to the endocardial surface. All sutures are placed before the patch is inserted. All sutures are then passed through the edge of a synthetic patch, which is seated on the left side of the septum (Fig 5B). Each suture is then passed through an additional pledget and then all are tied. We use additional pledgets on the left ventricular side overlying the patch (Fig 5C) to cushion each suture as it is tied down to prevent cutting through the friable muscle. The edges of the ventriculotomy
Closure ofinferoposterior septal defects, which result from transmural infarction in the distribution of the posterior descending artery, has posed the greatest technical challenge.P Early attempts at primary closure of these defects by simple plication techniques similar to those used in the repair of anterior defects was frequently unsuccessful because of the sutures tearing out of soft, friable myocardium that had been closed under tension. This resulted in either reopening of the defect or catastrophic disruption of the infarctectomy closure. It was, in large part the analysis of such early failures that led to the evolution of the operative principles enumerated in Table 1. Use of the following techniques have been associated with improved operative survival. After the establishment of bypass with bicaval cannulation, the left side of the heart is vented via the right superior pulmonary vein. The heart is retracted out of the pericardial well as for bypass to the posterior descending coronary artery. The margins of the defect may involve the inferior aspects of both ventricles, or of the left ventricle only (Fig 6A). A transinfarct incision is made in the left ventricle to the left of and parallel to the posterior descending artery, and the left ventricular portion of the infarct is excised (Fig 6B), exposing the septal defect. The left ventricular papillary muscles are inspected. Only if there is frank papillary muscle rupture or infarction is mitral valve replacement performed. When it is indicated, we prefer to perform mitral valve replacement through a separate conventional left atrial incision, to avoid trauma to the friable ventricular muscle. After all infarcted left ventricular muscle has been excised, a less aggressive debridement of the right ventricle is accomplished, with the goal of ressecting only as much muscle as is necessary to afford complete visualization of the defect. Using this technique, delayed rupture of the right ventricle has not been a problem. If the posterior septum has cracked or split from the adjacent ventricular free wall without loss of a great deal of septal tissue, then the septal rim of the posterior defect may be approximated to the edge of the diaphragmatic right ventricular free wall using mattress sutures buttressed with stripsof Teflon felt (Figs 6C, D).
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Figure 4. (A) Repai r of an anterior septal rupture by placating the free anterior edge of septum to right ventricular free wall with interrupted 0 Tevdek mattress sutures buttressed with strips of T eflon felt. (B, C, and D) Th e left ventriculotom y is th en closed as a separa te suture line, again with int errupted mattress suture s of a Tevdek buttressed with felt strips . A second running suture (not shown) is used to ensure a secure left ventriculotomy closure. Abbreviations: A, aorta; lAD, left anter ior descending coronary artery; PA, pulmonary art ery; LV, left ventricl e. (Reprinted with permission from Edmunds LH (ed): Cardiac Sur gery in the Adult. New York, NY, McGraw-Hill, 1997.)
Larger posterior defects require patch closur e (Fig 7). Pledgeted mattress sutures are placed from the right side of th e septum and from the epicardial side of th e right ventricular free wall (Fig 7B). All sutures ar e pass ed through th e perimeter of th e pat ch and then through additional pledgets , and ar e th en tied (Fig 7C). Thus, as in closure of larg e anterior defects, th e patch is secured on th e left ventricular side of th e septum. Dir ect closure of th e remaining infarctectomy is rarely possible because of tension required to pull together the edges of th e gaping defect. A prosthetic pat ch is generally required. Originally, we cut an oval patch from a Cooley low porosity woven Dacron tube graft (Meadox Medicals , Inc. Oakland, 1\;)). Currently, we cut thi s pat ch from a I-Iemashield woven Dacron collagen impregnated graft (Meadox Medicals, Inc). Pledget ed mattress sutures are passed out through th e
margin of the infarctectomy (endocardium to epicardium) a nd th en through th e patch (Fig 7D), which is seated on the epicardial surface of th e heart. After each suture is passed through an add itional pledget , all sutures ar e tied (Fig 7E). The cross-sectional view of th e completed repair (Fig 8) illustrates th e restoration of relati vely normal ventricular geomet ry, which is accomplished by th e use of appropriately sized prosthetic patches.
Weaning from Cardiopulmonary Bypass Intraoperative transesoph ageal echocardiography is essenti al to assess ventricular function, ventricular volum e, residual shunt, and mitral regurgitation when weaning from bypass. The two most common problem s encountered in separating from bypass following repair of a postinfarction ventricular septal
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Figure 5. (A) Larger anterior septal defects require a patch (DeBakey Dacron, United States Cath eter and Instrum ent Corporation, Billerica, MA), which is sewn to the left side of the ventricular septum with interrupt ed matt ress sutures, each of which is buttressed with a pledget of Teflon felt on the right ventricular side of the septum and anteriorly on the epicardial surface of the right ventricular free wall. (B and C) We use additional pledgets on the left ventricular side overlying the patch to cushion each sutur e as it is tied down to prevent cutt ing through the friable muscle. Abbreviations: ~ aorta; lAD, left ant erior descending coronary art ery; PA, pulmonary artery; LV,left ventricle. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgery in the Adult. NewYork, NY,McGraw-Hill, 1997.) d efect are low cardiac output and bleeding. Although th e tr eatment of low cardiac output following ca rdiac surgery is beyond th e scope of thi s discussion , a few age nts and principles are worth mentioning. Fir st, most of th ese patients will have had an intra-aortic ball oon pump (IABP) inserted befor e surgery. If not , on e should be ins erted in th e ope ra ting room, especially if th e low output state is seco ndary to left ven tri cular dysfunction. Also, IABP may benefit patients with right ventricular failure by improving right coro nary artery blood flow du e to diastolic au gm entation. W e have found intravenous milrinone, a phosphodiest erase inhibitor, to be very effective in reversing low output states secondary to left ven tr icular dysfun ction . Milrinon e possesses a balan ce of inotropic and vasodilatory properties which, together, produce an increase in cardiac output and reduct ion in right and left filling pressures a nd
systemic vascular resi stance. It is less arrhythmogenic than dobutamine, causes less hypot ension th an amrinone, a nd is not associated with thrombocytopenia." Post eri or defects are com monly associated with mitral regurgitation and right heart dysfun ction secondary to extensive right ventricular infarction.P Managem ent of right heart failure is aimed at reducing right ventricular aft erload whil e maintaining systemic pressure.t" Initial steps to manage right ventricular dysfunction include volume loading, inotropic support, and corr ection of acidosis, hypoxemia, and hypercarbia. If pati ents remain unresponsive to th ese measures, we have successfully treated right ventricul ar failure with a prostaglandin E ] infusion (0.5 to 2.0 lLg/min) int o th e right h eart, counterbalanced with a norepinephrine infusion ti trated into the left a triu m.F Inhaled nitric oxid e (20 to 80 ppm),
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which selectively dilat es the pulmonary circuit, has also proven efficacious in th e treatment of right heart failure.38 More recently, it has been shown that intravenous aden osine (50 J-Lglkglmin) is as effective as nitric oxide in diminishin g pulmonary vascular resistance and increasin g cardiac output without diminishing syste mic hemodynamics.P In our experience, inability to separate from bypass has not been not ed if th e re pair has been successful. H owever, if a pati en t could not be weaned from bypass using conventiona l therapy and was younger than 70 years old with no residual hemodynamically significant lesion, we would consider a
ventricular assist device. Indi cati ons for a left ventricular assist device are a cardiac ind ex less than 1.8 Umin per m'', a left atrial pr essur e mor e than 18 to 25 mm H g, a right atrial pr essur e less than 15 mm H g, and an aortic pressure less th an 90 mm Hg peak systolic. Indications for a right ventricular assist device are a cardiac ind ex less th an 1.8 Umin per m 2, a n aortic pressure less th an 90 m m Hg peak systolic, a nd a left atrial pressure less th an 15 mm Hg despite volum e loading to a right atrial pr essure of 25 mm H g with a competent tri cuspid valve. Four important points to remember when insti tuting ventricular assistance are that (1) right ventricular failur e m ay not become evident until left ventricular assistance is instituted, (2) once refractory ventricular failur e has been identified, delay in initi ating support is associated with increased morbidity and mortality, (3) closure of a patent foram en ovale is mandatory before left ventricular support, and (4) postoperative bleeding should be tr eated aggr essively and com plet ely controlled.i" T o prevent post-pump coag ulopathy, we begin antifibrinolyt ic therapy with eithe r aprotinin or Eam inocaproic acid (Amicar) before com mencing cardiopulmonary bypass . Half-dose aprotinin is administer ed by first giving an intraven ous test dose of 10,000 KIU over 10 minutes (before adm inistering blocker s), th en loading pati ents with I million KIU over 20 minutes before bypass. Another 1 million KID is given in the pump prime, th en 250,000 KIUIh is administered for th e durati on of the surgery. H eparin is managed in th e usual fashion with acti -
Figure 6. (A) View of an inferior infar ct (stippled area) associated with posterior septal ruptu re. Apex of the heart is to the right . (B) The inferop osterior infar ct is excised to expose the posterior septal defect. Co mplete excision of the left ventricular port ion of the infarct is important to prevent dela yed rupture of the ventriculoto my repair. (C a nd D) Repair of th e posterior septal rupture by approximat ing the edge of th e post erior septum to th e free wall of th e diaphragmatic right ventricle with felt-buttressed mattr ess sutures . The repair is possible when the septum has cracked or split off from th e posterior ventricular wall ..vithout necrosis of a gr eat deal of septal mu scle. The left vent riculotomy is th en closed as a separa te suture line, again with int errupted mat tr ess suture s of 0 Tevd ek buttressed with felt strips. A second running suture (not shown) is used to ensure a secure left ventriculotomy closur e (not shown) . Abbr eviati ons: RV, diaphragmatic surface of right ventricle; LV, posteri or left ventricle; PDA, post erior descending arte ry. (Reprinted with permission from Edmunds LH (ed): Cardi ac Surgery in th e Adult. New York, NY, McGraw-Hill, 1997.)
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Figure 7. (A) Repair of posterior sept al rupture when there has been necrosis of a substantial portion of th e posterior septum requires use of pat ches. (B) Int err upted ma ttr ess sutures of 2-0 T evdek ar e placed circum fer entially around th e defect. T hese sutu res are buttressed with felt pledgets on th e right ventricular side of the septum and on th e epicardial surfac e of the diaph ragmati c right ventricle. (C) All sutures are placed and then th e pa tch (DeBakey elas tic Dacron fabric) is slid into place on the left ventricular side of th e septu m. Th e patch sutur es are tied down with an additiona l felt pledget placed on top of th e pat ch (left vent ricular side), as each suture is tied, to cushion th e tie and prevent cutt ing through th e friabl e muscle. Th ese maneuvers are viewed by th e a uthors as essential to the success of ea rly repair of the poster ior sep ta l rupture. (D) Rem aining to be repaired is the posterior left ventricular free wall defe ct created by infarctectomy. Mattress sutures of 2-0 Tevdek are placed circumfer entially around the mar gins of th e posterior left ventricular free wall defect. Each suture is buttressed with a T eflon felt pledget on the endocar dial side of th e left ven tricle. With all sutures in place, a circular pat ch, fashioned from a H em ash ield woven doubl e velour Dacron collagen-impregnated gra ft (Meadox Medicals Inc., Oakland, i'{J), is slid down onto th e epicardial surface of the left ventricle. (E) Co mpleted repair. (Repri nte d with permission from Edm unds LH (ed): Cardiac Surg ery in the Adult. New York, NY, McGraw-Hill, 1997.)
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gradient induced by the increased extravascular pulmonary water associated with cardiopulmonary bypass. Once the patient has warmed, we commonly use an intravenous infusion of Lasix combined with mannitol (1 g of Lasix in 400 mL of20% mannitol) at a rate of 1 to 20 mI)h to maintain the urine output greater than 100 mlzh, If renal function has been compromised preoperatively, continuous veno-venous hemofiltration (CVVH) is employed postoperativelyand managed by our ICU nurses. Intractable postoperative ventricular arrhythmias secondary to reperfusion injury are sometimes difficult to control using standard therapy. We have been impressed with the efficacy of intravenous amiodarone in these situations (10 to 20 mg/kg over 24 hours).45
Figure 8. Cross-sectional view of the completed repair of
posterior septal rupture with prosthetic patch placement of the posterior left ventricular free wall defect created by infarctectomy. RV, right ventricular cavity;LV,left ventricular cavity. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgery in the Adult. New York, NY, McGrawHill, 1997.)
vated clotting times (ACT), but koalin, not Celite, is used as the ACT activator. Because controversy surrounds the issue of increased renal dysfunction and perioperative thrombotic events in patients receiving aprotinin,"! we prefer to use Amicar in patients who (1) require aortocoronary bypasses, (2) are diabetic, or (3) have known renal dysfunction. Amicar is administered by loading patients with 10 g before commencing bypass and then adding another 10 g to the pump prime. During the procedure Amicar is continuously infused at 1 g/h for the duration of surgery. We avoid giving more than 30 g of Amicar. Postpump suture line bleeding may be reduced by application of a fibrin sealant to the ventricular septum around the septal defect before formal repair.f Biological glue 43 may be effective in controlling bleeding suture lines following repair, but we have had limited experience with these compounds. As a last resort, Baldwin and Cooley'? have suggested insertion of a left ventricular assist device solely as an adjunct to the repair of friable or damaged myocardium to reduce left ventricular distension and, thus, control bleeding.
Highlights of Postoperative Care Early postoperative diuresis and positive end-expiratory pressure ventilation are used to decrease the A-a
Conclusion The incorporation of specific anatomical concepts of surgical repair and a better understanding of the physiological consequences of the disease has led to an integrated approach to the patient which has improved salvage of patients suffering this catastrophic complication of acute myocardial infarction.
References I. Daggett WM: Postinfarction ventricular septal defect repair: Retrospective thoughts and historical perspectives. Ann Thora Surg 50:1006-1009,1990 2. David TE, Dale L, Sun Z: Postinfarction ventricular septal rupture: repair by endocardial patch with infarct exclusion.] ThoracCardiovascSurg 110:1315-1322, 1995 3. Lundberg S, Sodestrom J Perforation of the interventricular septum in myocardial infarction: A study based on autopsy material. Acta Med Scand 172:413A20, 1962 4. Hutchins GM: Rupture of the interventricular septum complicating myocardial infarction: Pathological analysis of 10 patients with clinically diagnosed perforation. Am Heart ] 97:165-\70,1979 5. Mann ]M, Robert WC: Acquired ventricular septal defect during acute myocardial infarction: Analysis of 38 unoperated necropsy patients and comparison with 50 unoperated necropsy patients without rupture. Am] CardioI62:8-19, 1988 6. Skillington PD, Davies RH, Luff A], et al: Surgical treatment for infarct-related ventricular septal defects.] Thorac Cardiovasc Surg 99:798-808, 1990 7. Daggett WM, Buckley M], Akins CW, et al: Improved results of surgical management of postinfarction ventricular septal rupture.AnnSurg 196:269-277,1982 8. SkehanjD, Carey C, Norrell MS, et al: Patterns of coronary artery disease in post-infarction ventricular septal rupture. Br Heart] 62:268-276, 1989 9. SwithingbankJM: Perforation of the interventricular septum in myocardial infarction. Br Heart] 21:562-567,1959 10. Edwards BS, Edwards WD, Edwards]E: Ventricular septal rupture complicating acute myocardial infarction: Identifica-
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tion of simple and complex types in 53 autopsied hearts. AmJ CardioI54:1201-1205,1984 II. Deville C, Fontan F, Chevalier JM, et al: Surgery of postinfarction ventricular defect: Risk factors for hospital death and long-term results. Eur J Cardiothorac Surg 5:167-175, 1991 12. Fanapazir L, Bray CL, DarkJF: Right ventricular dysfunction and surgical outcome in postinfarction ventricular septal defect. EurJ Cardiothorac Surg 4:155-167, 1983 13. Radford MJ, Johnson RA, Daggett WM, et aI: Ventricular septal defect following myocardial infarction: Factors affecting survival. Clin Res 26:262A, 1978 14. Moore CA, Nygaard TW, Kaiser DL, et aI: Postinfarction ventricular septal rupture: The importance of location of infarction and right ventricular function in determining survival. Circulation 74:45-55,1986 15. Zehender M, Kasper W, Kauder E: Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 328:981-988, 1993 16. David TE: Surgery for postinfarction ventricular septal defects, in David TE (ed): Mechanical Complications of Myocardial Infarction, 1st ed. Austin, TX, R.G. Landes Company, 1993,pp 175-191 17. Anderson DR, Adams S, Bhat A, Pepper JR: Postinfarction ventricular septal defect: The importance of site of infarction and cardiogenic shock on outcome. Eur J Cardiothorac Surg 3:554-557, 1989 18. Selzer A, Gerbode F, Keith V\C[: Clinical, hemodynamic and surgical considerations of rupture of the ventricular septum after myocardial infarction. Am HeartJ 78:598-604, 1969 19. Campion BL, Harrison CE, Guiliani ER, et al: Ventricular septal defect after myocardial infarction. Ann Intern Med 70:251-261,1969 20. Harrison MR, MacPhail B, Gurley JC, et al: Usefulness of color doppler flow imaging to distinguish ventricular septal defect from acute mitral regurgitation complicating acute myocardial infarction. AmJ CardioI64:697-701, 1989 21. SmyllieJH, Sutherland GR, Geuskens R, et aI: Doppler color flow mapping in the diagnosis of ventricular septal rupture and acute mitral regurgitation after myocardial infarction. J Am Coli Cardiol 15:1455, 1990 22. Fortin DF, Sheikh KH, KissloJ: The utility of echocardiography in the diagnostic strategy of postinfarction ventricular septal rupture: A comparison of two-dimensional versus Doppler color flow imaging. Am HeartJ 121:25-32,1991 23. Silver MD, ButanyJ, Chiasson DA: The pathology of myocardial infarction and its mechanical complications, in David TE (ed): Mechanical Complications of Myocardial Infarction, 1st ed. Austin, TX, R.G. Landes Company, 1993,pp 4-43 24. Blanche C, Khan SS, MatloffJM, et al: Results of early repair of ventricular septal defect after an acute myocardial infarction.J Thorac Cardiovasc Surg 104:961-965, 1992 25. Jones MT, Schofield PM, DarkJF: Surgical repair of acquired ventricular septal defect: Determinants of early and late outcome.J Thorac Cardiovasc Surg 93:680-686, 1987 26. Muehrcke DD, Daggett WM, Buckley MJ, et al: Postinfarct ventricular septal defect repair: Effect of coronary artery bypass grafting. Ann Thorac Surg 54:876-883, 1992 27. Matsui K, Kay JH, Mendez M, et al: Ventricular septal rupture secondary to myocardial infarction: Clinical approach and surgical results.JAMA245:1537-1539, 1981
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28. Kaplan MA, Harris CN, Kay]H, et al: Postinfarctional septal rupture: Clinical approach and surgical results. Chest 69:734738, 1976 29. Loisance DY, CacheraJP, Poulain H, et al: Ventricular septal defect after acute myocardial infarcion. J Thorac Cardiovasc Surg 80:61-67,1980 30. Daggett WM, Burwell LR, Lawson DW, Austen WG: Resection of acute ventricular aneurysm and ruptured interventricular septum after myocardial infarction. N EnglJ Med 283:15071514,1970 31. Daggett WM: Surgical management of ventricular septal defects complicating myocardial infarction. World J Surg 2:753-758,1978 32. Shumaker H: Suggestions concerning operative management of postinfarction ventricular septal defects. J Thorac Cardiovase Surg 64:452-457,1972 33. Daggett WM, Mundth ED, Gold HK, et al: Early repair of ventricular septal defects complicating inferior myocardial infarction. Circulation 50:112-119, 1974 (SuppI3) 34. Marchetti A, Wechsler AS: Pharmocologic intervention for acute low cardiac output. Adv Cardiac Surg 7:31-64, 1996 (abstr) 35. Cummings RG, Reimer KA, Catliff R, et aI: Quantitative analysis of right and left ventricular infarction in the presence of postinfarction ventricular septal defect. Circulation 77:3342, 1988 36. V1ahakes Gj: Management of pulmonary hypertension and right ventricular failure: Another step forward. Ann Thorac Surg61:1051-1052,1996 37. D'Ambra MN, LaRaia PJ, Philbin DM, et aI: Prostaglandin E]: A new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement. J Thorac Cardiovasc Surg 89:567-572,1985 38. Rich GF, Murphy GD,Jr., Roos CM,Johns RA: Inhaled nitric oxide: Selective pulmonary vasodilatation in cardiac surgical patients. Anesthesiology 78:1028-1035, 1993 39. Fullerton DA,Jones SD, Grover FL, McIntyre RC,Jr: Adenosine effectively controls pulmonary hypertension following cardiac surgery. Ann Thorac Surg 61:1118-1124, 1996 40. Pae WE, Jr., Pierce WS, Sapirstein JS: Intra-aortic balloon counterpulsation, ventricular assist pumping, and the artificial heart, in Baue AE, Geha AS, Hammond GL, et al (eds): Glenn's Thoracic and Cardiovascular Surgery, 6th ed. Stamford, CT, Appleton & Lange, 1996,pp 1825-1855. 41. Sundt TM, III, Kouchoukos NT, Saffitz JE, et aI: Renal dysfunction and intravascular coagulation with aprotinin and hypothermic circulatory arrest. Ann Thorac Surg 55:14181424,1993 42. SeguinJR, Frapier JM, Colson P, Chaptal PA: Fibrin sealant for early repair of acquired ventricular septal defect. J Thorac Cardiovasc Surg 104:748-751, 1992 43. FabianiJ-N,Jebara VA, Deloche A, et al: Use of surgical glue without replacement in the treatment of type A aortic dissection. Circulation 80:264-268, 1989 44. Baldwin RT, Cooley DA: Mechanical support for intraventricular decompression in repair of left ventricular disruption. Ann Thorac Surg 54:176, 1992 45. Saksena S, Rothbart ST, Shah Y: Clinical efficacy and electropharmacology of continuous intravenous amiodarone infusion and chronic oral amiodarone in refractory ventricular tachycardia. AmJ CardioI54:347-352, 1984
T
he first step in the evolution of surgical techniques for repair of acute postinfarction ventricular septal rupture involved differentiating the surgical treatment of these acquired lesions from the surgical approaches used to repair congenital ventricular septal defects, which are, for the most part, not applicable. Next, understanding the significance of differing anatomic locations of postinfarction ventricular septal defects led to innovations in terms of the location of the cardiotomy and the type of repair necessary to achieve a successful result in any given patient. Then, the gradual appreciation of different clinical courses pursued by patients after postinfarction ventricular septal rupture, both in terms of location of the defect and the degree of right ventricular functional impairment, led to an increased urgency relative to the timing of surgical repair.' Most From theDivision ofCardiac Surgery, Massachusetts General Hospital, Boston,MA. Address reprint requests toJoren C. Madsen, MD, DPhil,Massachusetts General Hospital, 55 Fruit St, EDR 105,Boston, MA 02114-2696. Copyright © 1998 byWB. Saunders Company 1013-0679/98/1002-0006$08.00/0
recently, the superb results being reported using the technique of endocardial patching with infarct exclusion? may signify yet another milestone in the evolution of the surgical management of postinfarction ventricular septal defects.
Incidence Postinfarction ventricular septal defects complicate approximately I% to 2% of cases of acute myocardial infarctions and account for about 5% of early deaths after myocardial infarction.v' The average time from infarction to rupture has been reported to be between 2 and 4 days, but it may be as short as a few hours or as long as 2 weeks.t-' The age of patients with this complication ranges from 44 to 81 years, with a mean of 62.5 years. However, there is some evidence that the average age is increasing.V The vast majority of patients who experience ventricular septal rupture do so after their initial infarction.t-' The overall incidence of postinfarction ventricular septal rupture may have decreased slightly during the past decade as a result of aggressive pharmacologi-
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cal treatment of ischemi a and thrombolytic th erapy in patients with evolving myocardial infarction, as well as th e prompt control of hypertension in th ese pati ents,"
Anatomy Angiographic evaluation of patients with postinfarction ventricular rupture indicat es that septal rupture is usually associated with complete occlusion , rather than severe stenosis of a corona ry arteryf Postinfarction ventricular septal defects ar e most commonly located in the anteroapical septum as the result of a full-thickness anterior infarction (in approximately 60% of cases). These anter ior septal ruptures are caused by anteroseptal myocard ial infarction following occlusion of the left anterior descending artery. In about 20% to 40% of patients, th e rupture occurs in th e post erior septum following an inferoseptal infarction , which is usually du e to occlusion of a dominant right coronary artery or, less frequ ently, a dominant circumflex artery." Ther e are two types of rupture: simple, consisting of a dir ect through and through defect usually located anteriorly; and complex, consisting of a serpiginous dissection tr act remote from th e primary septal defect th at is usually located inferiorly.l" Multiple defects, which may develop within severa l days of each othe r, occur in 5% to II % of cases , and are probably du e to infarct exte nsion.
Pathophysiology The most important det erminants of early outcome following postinfarction ventricular septal rupture are the development of congestive heart failure and cardiogenic shock which, in turn, depend on the size of th e infarct and the magnitude of the left-to-right shunt. Left ventricular dysfunction du e to extensive necrosis of th e left ventricle is the primary determinant of conge stive heart failur e and cardiogenic shock in patients with ant erior septal rupture, whereas righ t ventricular dysfunction secondary to extensive infarction of th e right ventricle is the principal det erminant of heart failure and cardiogenic shock in pati ents with post erior septal rupture. 2, 11,12 However, the development of conges tive heart failure and cardiogenic shock in patients with postinfarction ventricular septal defects is not explained solely by the extent of damage sustain ed by th e left ventricle. 13 The magnitude of th e left-to-right shunt is the other key variable in th e developm ent of hemodynamic compromise. With th e open ing of a ventricular septal
defect, the heart is cha llenged by an increase in pulmonary blood flow and a decrease in system blood flow as a portion of each stroke volum e is diverted to th e pulmonary circuit. As a consequence of th e sudde n increase in hemodynami c load imposed on a heart already compromised by acute infarction, and possibly by a ventricular ane urysm, mitral valve dysfun ction or a combination of th ese problems, a severe low cardiac output stat e results. The normally compliant right ventricle is especially susceptible to failure in this circumstance.lt-P Pati ents with posterior ventricular septal rupture and right ventricular dysfunction may display shunt reversal during diastole because the end-diastolic pressure in the right ventricle can be higher than in th e left ventricle.l'v'" Ultimately, persistence of a low ca rdiac output state result s in peripheral organ failure.
Diagnosis The typical presentation of a ventricular septal rupture occurs in a patient who has suffered an acute myocardial infarction and who, after convalescing for a few days, develops a new systolic murmur, recurrent chest pain, and an abrupt det erioration in hemodynami cs. The development of a loud systolic murmur, usuall y within th e first week following an acute myocardial infarction, is th e most consistent physical finding of postinfarction ventricular septal rupture (present in more th an 90% of cases). The murmur is usually harsh, pan systolic, and best heard at th e left lower sternal bord er. Th e murmur is often associated with a palpable thrill. Depending on the location of the septal defect, th e murmur may radiate to the left axilla, th er eby mimicking mitral regurgitation.l" Up to half of th ese patients experience post infarction chest pain in association with the appearance of the murmur." Coincident with the onse t of the murmur, there is usuall y an abrupt decline in th e patient's clinical course with congestive failure and often cardiogen ic shock. The findings of cardiac failur e that occur acutely in th ese patients ar e primarily the result of right-sided heart failure, with pulmonary edema being less prominent than that occur ring in pati ents with acute mitral regurgita tion du e to ruptured papill ary mu scle.l? Recent advances in transthoracic and transesophageal echocardiography, especially th e advent of color flow Doppler mapping, have revolut ionized the diagnosis of both the pr esen ce and site of septal rupture. 20.22 Echocardiography can detect the defect, localize its site and size, det ermine right and left
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ventricular fun ction , assess pul monary ar tery and rig ht ven tric ular pressur es, and excl ude coex isti ng m itra l regurgit ati on or free wall rupt ure. Smyllie et al21 reporte d a 100% specificity and 100% sensi tivity when color flow Doppler mapping was use d to differentiate ventricular septal rupture from acute severe mitral regurgita tion following acute myoca rdia l infarction. They also correctly demonstrated th e site of septal rupture in 4 1 of 42 patients. Widespread use of this tec hnology has, for the most part , replaced thermodilu tion catheter insertion, which in outlying hospitals, where patien ts ar e oft en see n first, m ay be time-consuming and difficult to accomplish. Indeed, the trend toward ea rly surgical referral and prompt operative repair is at least pa rtially explained by the more wide spr ead use of color Doppler echocardiogra phy for diagn osis in peri ph eral centers.P T he necessity of preoperative left heart catheterization with coronary angiography has been a matt er of debate. O n the one ha nd, left heart ca theterizatio n pr ovides imp ortant information concerning associated coro nary artery diseas e, left vent ricular wall motion, an d specifics of valvular dysfunct ion, which ar e all importan t in planning operative correction of postin farction septal rupture. In most series 24-26 more than 60% of pat ients 'With se ptal rupture have significant involvem en t of at least one vessel ot he r than the one supplying th e infa rcted area. However, th ere are disadva ntages in performing left heart ca the terization with coronary angiography. It is time -consuming and can contribute to both th e morta lity a nd morbidity of thes e already compromised pat ients. 6,24 Thus, some cente rs do not perform preopera tive left heart cat he te rization; others use it selectively, avoiding invasive studies in patien ts with septal rupture caus ed by ante rior wall infarction, which is associated wit h a much lower inciden ce of mu ltip le vessel disease than septal defec ts res ulting from posterior infarc tions.6,27,2H
Preoperative Management Because the natur al course of the disease in u noperat ed patien ts is so dismal, th e diagnos is of pos tinfarction ventricular septal rupture can be regarde d as its own indicat ion for operat ion." P reoperative man agem en t is directed toward sta biliza tion of th e hem odynamic condit ion so that peri pheral organ perfusion ca n be best maintained while any further diagnostic studies are obtained and whi le dec iding on th e optimal time for surgical interven tion. T he goals of pr eoperative managem ent ar e to ( I) redu ce th e systemic vascula r resistance, and thus, th e left-to-
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right shun t; (2) mai ntain cardiac output and arterial pr essure to ensure peripheral organ perfusion; and (3) mai ntain or im prov e coronary artery blood flow. T hese goals are best accomplish ed by the int ra-aortic balloon pump (IABP) . Alt hough counterpulsation produces an overall improvem ent in th e patient's cond ition, a com plete correction of th e hem odynamic picture cannot be obtained . Pea k improvement occu rs within 24 hour s, and little fur ther benefit has bee n observe d with prolonged balloon pumping.P Ph armacological therapy with inotropic age n ts and diuretics should be inst ituted promptly. It must be stressed th at pharmacological therapy is intended primarily to support th e pa tien t in pr ep aration for operation and should not , in anyway, delay urgent operation in the critically ill pati ent.
Operative Techniques Exp eri ence with a variety of techniques for closure of postinfarctio n ventricula r septal rupture has led us to th e evolution of eight basic principles (Table I). Adh erence to these principles in the closure of sep tal defects in differe nt location s has led to the evolut ion of individualized approaches to apical, anterior, and inferoposterior septal defects,7,3o,31
Table 1. Principles of Repair of Postinfarction Ventricular Septal Defects
I) Expeditious establishment of total cardiopulmonary bypasswith moderate hypothermia and meticulous attention to myocardial protection. 2) Transinfarct approach to ventricular septal defect with the site of ventriculotomy determined by the location of the transm ural infarction. 3) Thorough trimming of the left ventricular margins of the infarct back to viable muscle to prevent delayed rupture of the closure. 4) Conservative trimming of the right ventricular muscle as required for complete visualization of the margins of the defect. 5) Inspection of the left ventricular papillary musclesand concomitant replacement of the mitral valve onlyif there is frank papillary muscular ruptur e. 6) Closure of the septal defect wi thout tension, which in most instances will require the use of prosthetic mat erial. 7) Closure of the infarctectomy without tension with generous use of prosthetic material as indicated and epicardial placement of the patch to the free wall to avoidstrain on the friable endocardial tissue. 8) Buttressing of the suture lines with pledgets or strips of Teflon felt or similar material to prevent sutures from cutting through friable muscle.
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Apical Septal Rupture The technique of apical amputation was described by Daggett et al in 1970.30 An incision is made through the infarcted apex of the left ventricle. Excision ofthe necrotic myocardium back to healthy muscle results in amputation of the apical portion of the left ventricle, right ventricle, and septum (Figs lA and B). The remaining apical portions of the left and right ventricle free walls are then approximated to the apical septum. This is accomplished by means of a row of interrupted mattress sutures of 0 Tevdek that are passed sequentially through a buttressing strip of Teflon felt, the left ventricular wall, a second strip of felt, the interventricular septum, a third strip of felt, the right ventricular wall, and a fourth strip of felt (Figs 2A and B). After all sutures have been tied, the closure is reinforced with an additional over-andover suture, as in ventricular aneurysm repair, to
Figure 2. (A) Necrotic infarct and apical septum have been debrided back to healthy muscle. (B) All sutures are placed before any are tied. A second running over and over suture (not shown) is used, as in left ventricular aneurysm repair, to insure a secure hemostatic ventriculotomy closure. Abbreviations: A, aorta; LAD, left anterior descending coronary artery; RV, right ventricle; LV, left ventricle. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgery in the Adult. New York, NY, McGraw-Hill, 1997.)
insure hemostasis of the ventriculotomy closure (not shown).
Anterior Septal Rupture
Figure 1. (A) Apical postinfarction ventricular septal defect. (B) View of the apical septal rupture, which is exposed by amputating apex of left and right ventricles. Stippled region, infarcted myocardium; A, aorta; LAD, left anterior descending coronary artery; RV, right ventricle; LV, left ventricle. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgery in the Adult. New York, NY, McGraw-Hill, 1997.)
The approach to these defects is by a left ventricular transinfarct incision with infarctectomy (Figs 3A and B). Small defects beneath anterior infarcts can be closed by the technique of plication as suggested by Shumaker.V This involves approximation of the free anterior edge of the septum to the right ventricular free wall using mattress sutures of 0 Tevdek over strips of felt (Fig 4A). The transinfarct incision is then closed with a second row of mattress sutures buttressed with strips of felt (Fig 4B and C). An over-and-over running suture completes the ventriculotomy closure (not shown). Most anterior defects require closure with a prosthetic patch (DeBakey Elastic Dacron fabric made by U.S.C.I., Division ofC.R. Bard, Inc., Billerica, MA) to avoid tension that could lead to disruption of the
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are then approximated by a two-layer closure consisting of interrupted mattress sutures passed through buttressing strips of Teflon felt and a final over-andover running suture (not shown).
Posterior Septal Rupture
LAD
Infarct
Figure 3. (A) Transinfarct left ventricular incision to
exposean anterior septal rupture. An incision(dashed line) is made parallel to anterior descending branch of left coronary artery (LAD) through center of infarct (stippled area) in anterior left ventricle (LV). (B) View of septal defect following infarctectomy. Abbreviations: A, aorta; RV, right ventricle; PA,pulmonary artery. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgeryin the Adult. NewYork, NY,McGraw-Hill, 1997.) repair (Fig 5). After debridement of necrotic septum and left ventricular muscle, a series of pledgeted interrupted mattress sutures are placed around the perimeter of the defect (Fig 5A). Along the posterior aspect of the defect, sutures are passed through the septum from right side to left. Along the anterior edge of the defect, sutures are passed from the epicardial surface ofthe right ventricle to the endocardial surface. All sutures are placed before the patch is inserted. All sutures are then passed through the edge of a synthetic patch, which is seated on the left side of the septum (Fig 5B). Each suture is then passed through an additional pledget and then all are tied. We use additional pledgets on the left ventricular side overlying the patch (Fig 5C) to cushion each suture as it is tied down to prevent cutting through the friable muscle. The edges of the ventriculotomy
Closure ofinferoposterior septal defects, which result from transmural infarction in the distribution of the posterior descending artery, has posed the greatest technical challenge.P Early attempts at primary closure of these defects by simple plication techniques similar to those used in the repair of anterior defects was frequently unsuccessful because of the sutures tearing out of soft, friable myocardium that had been closed under tension. This resulted in either reopening of the defect or catastrophic disruption of the infarctectomy closure. It was, in large part the analysis of such early failures that led to the evolution of the operative principles enumerated in Table 1. Use of the following techniques have been associated with improved operative survival. After the establishment of bypass with bicaval cannulation, the left side of the heart is vented via the right superior pulmonary vein. The heart is retracted out of the pericardial well as for bypass to the posterior descending coronary artery. The margins of the defect may involve the inferior aspects of both ventricles, or of the left ventricle only (Fig 6A). A transinfarct incision is made in the left ventricle to the left of and parallel to the posterior descending artery, and the left ventricular portion of the infarct is excised (Fig 6B), exposing the septal defect. The left ventricular papillary muscles are inspected. Only if there is frank papillary muscle rupture or infarction is mitral valve replacement performed. When it is indicated, we prefer to perform mitral valve replacement through a separate conventional left atrial incision, to avoid trauma to the friable ventricular muscle. After all infarcted left ventricular muscle has been excised, a less aggressive debridement of the right ventricle is accomplished, with the goal of ressecting only as much muscle as is necessary to afford complete visualization of the defect. Using this technique, delayed rupture of the right ventricle has not been a problem. If the posterior septum has cracked or split from the adjacent ventricular free wall without loss of a great deal of septal tissue, then the septal rim of the posterior defect may be approximated to the edge of the diaphragmatic right ventricular free wall using mattress sutures buttressed with stripsof Teflon felt (Figs 6C, D).
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Figure 4. (A) Repai r of an anterior septal rupture by placating the free anterior edge of septum to right ventricular free wall with interrupted 0 Tevdek mattress sutures buttressed with strips of T eflon felt. (B, C, and D) Th e left ventriculotom y is th en closed as a separa te suture line, again with int errupted mattress suture s of a Tevdek buttressed with felt strips . A second running suture (not shown) is used to ensure a secure left ventriculotomy closure. Abbreviations: A, aorta; lAD, left anter ior descending coronary artery; PA, pulmonary art ery; LV, left ventricl e. (Reprinted with permission from Edmunds LH (ed): Cardiac Sur gery in the Adult. New York, NY, McGraw-Hill, 1997.)
Larger posterior defects require patch closur e (Fig 7). Pledgeted mattress sutures are placed from the right side of th e septum and from the epicardial side of th e right ventricular free wall (Fig 7B). All sutures ar e pass ed through th e perimeter of th e pat ch and then through additional pledgets , and ar e th en tied (Fig 7C). Thus, as in closure of larg e anterior defects, th e patch is secured on th e left ventricular side of th e septum. Dir ect closure of th e remaining infarctectomy is rarely possible because of tension required to pull together the edges of th e gaping defect. A prosthetic pat ch is generally required. Originally, we cut an oval patch from a Cooley low porosity woven Dacron tube graft (Meadox Medicals , Inc. Oakland, 1\;)). Currently, we cut thi s pat ch from a I-Iemashield woven Dacron collagen impregnated graft (Meadox Medicals, Inc). Pledget ed mattress sutures are passed out through th e
margin of the infarctectomy (endocardium to epicardium) a nd th en through th e patch (Fig 7D), which is seated on the epicardial surface of th e heart. After each suture is passed through an add itional pledget , all sutures ar e tied (Fig 7E). The cross-sectional view of th e completed repair (Fig 8) illustrates th e restoration of relati vely normal ventricular geomet ry, which is accomplished by th e use of appropriately sized prosthetic patches.
Weaning from Cardiopulmonary Bypass Intraoperative transesoph ageal echocardiography is essenti al to assess ventricular function, ventricular volum e, residual shunt, and mitral regurgitation when weaning from bypass. The two most common problem s encountered in separating from bypass following repair of a postinfarction ventricular septal
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Figure 5. (A) Larger anterior septal defects require a patch (DeBakey Dacron, United States Cath eter and Instrum ent Corporation, Billerica, MA), which is sewn to the left side of the ventricular septum with interrupt ed matt ress sutures, each of which is buttressed with a pledget of Teflon felt on the right ventricular side of the septum and anteriorly on the epicardial surface of the right ventricular free wall. (B and C) We use additional pledgets on the left ventricular side overlying the patch to cushion each sutur e as it is tied down to prevent cutt ing through the friable muscle. Abbreviations: ~ aorta; lAD, left ant erior descending coronary art ery; PA, pulmonary artery; LV,left ventricle. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgery in the Adult. NewYork, NY,McGraw-Hill, 1997.) d efect are low cardiac output and bleeding. Although th e tr eatment of low cardiac output following ca rdiac surgery is beyond th e scope of thi s discussion , a few age nts and principles are worth mentioning. Fir st, most of th ese patients will have had an intra-aortic ball oon pump (IABP) inserted befor e surgery. If not , on e should be ins erted in th e ope ra ting room, especially if th e low output state is seco ndary to left ven tri cular dysfunction. Also, IABP may benefit patients with right ventricular failure by improving right coro nary artery blood flow du e to diastolic au gm entation. W e have found intravenous milrinone, a phosphodiest erase inhibitor, to be very effective in reversing low output states secondary to left ven tr icular dysfun ction . Milrinon e possesses a balan ce of inotropic and vasodilatory properties which, together, produce an increase in cardiac output and reduct ion in right and left filling pressures a nd
systemic vascular resi stance. It is less arrhythmogenic than dobutamine, causes less hypot ension th an amrinone, a nd is not associated with thrombocytopenia." Post eri or defects are com monly associated with mitral regurgitation and right heart dysfun ction secondary to extensive right ventricular infarction.P Managem ent of right heart failure is aimed at reducing right ventricular aft erload whil e maintaining systemic pressure.t" Initial steps to manage right ventricular dysfunction include volume loading, inotropic support, and corr ection of acidosis, hypoxemia, and hypercarbia. If pati ents remain unresponsive to th ese measures, we have successfully treated right ventricul ar failure with a prostaglandin E ] infusion (0.5 to 2.0 lLg/min) int o th e right h eart, counterbalanced with a norepinephrine infusion ti trated into the left a triu m.F Inhaled nitric oxid e (20 to 80 ppm),
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which selectively dilat es the pulmonary circuit, has also proven efficacious in th e treatment of right heart failure.38 More recently, it has been shown that intravenous aden osine (50 J-Lglkglmin) is as effective as nitric oxide in diminishin g pulmonary vascular resistance and increasin g cardiac output without diminishing syste mic hemodynamics.P In our experience, inability to separate from bypass has not been not ed if th e re pair has been successful. H owever, if a pati en t could not be weaned from bypass using conventiona l therapy and was younger than 70 years old with no residual hemodynamically significant lesion, we would consider a
ventricular assist device. Indi cati ons for a left ventricular assist device are a cardiac ind ex less than 1.8 Umin per m'', a left atrial pr essur e mor e than 18 to 25 mm H g, a right atrial pr essur e less than 15 mm H g, and an aortic pressure less th an 90 mm Hg peak systolic. Indications for a right ventricular assist device are a cardiac ind ex less th an 1.8 Umin per m 2, a n aortic pressure less th an 90 m m Hg peak systolic, a nd a left atrial pressure less th an 15 mm Hg despite volum e loading to a right atrial pr essure of 25 mm H g with a competent tri cuspid valve. Four important points to remember when insti tuting ventricular assistance are that (1) right ventricular failur e m ay not become evident until left ventricular assistance is instituted, (2) once refractory ventricular failur e has been identified, delay in initi ating support is associated with increased morbidity and mortality, (3) closure of a patent foram en ovale is mandatory before left ventricular support, and (4) postoperative bleeding should be tr eated aggr essively and com plet ely controlled.i" T o prevent post-pump coag ulopathy, we begin antifibrinolyt ic therapy with eithe r aprotinin or Eam inocaproic acid (Amicar) before com mencing cardiopulmonary bypass . Half-dose aprotinin is administer ed by first giving an intraven ous test dose of 10,000 KIU over 10 minutes (before adm inistering blocker s), th en loading pati ents with I million KIU over 20 minutes before bypass. Another 1 million KID is given in the pump prime, th en 250,000 KIUIh is administered for th e durati on of the surgery. H eparin is managed in th e usual fashion with acti -
Figure 6. (A) View of an inferior infar ct (stippled area) associated with posterior septal ruptu re. Apex of the heart is to the right . (B) The inferop osterior infar ct is excised to expose the posterior septal defect. Co mplete excision of the left ventricular port ion of the infarct is important to prevent dela yed rupture of the ventriculoto my repair. (C a nd D) Repair of th e posterior septal rupture by approximat ing the edge of th e post erior septum to th e free wall of th e diaphragmatic right ventricle with felt-buttressed mattr ess sutures . The repair is possible when the septum has cracked or split off from th e posterior ventricular wall ..vithout necrosis of a gr eat deal of septal mu scle. The left vent riculotomy is th en closed as a separa te suture line, again with int errupted mat tr ess suture s of 0 Tevd ek buttressed with felt strips. A second running suture (not shown) is used to ensure a secure left ventriculotomy closur e (not shown) . Abbr eviati ons: RV, diaphragmatic surface of right ventricle; LV, posteri or left ventricle; PDA, post erior descending arte ry. (Reprinted with permission from Edmunds LH (ed): Cardi ac Surgery in th e Adult. New York, NY, McGraw-Hill, 1997.)
Repair cfPostirfa rct Venticular SeptalDefects
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\ \
I
I ./
/
/
A
•
c
E
Figure 7. (A) Repair of posterior sept al rupture when there has been necrosis of a substantial portion of th e posterior septum requires use of pat ches. (B) Int err upted ma ttr ess sutures of 2-0 T evdek ar e placed circum fer entially around th e defect. T hese sutu res are buttressed with felt pledgets on th e right ventricular side of the septum and on th e epicardial surfac e of the diaph ragmati c right ventricle. (C) All sutures are placed and then th e pa tch (DeBakey elas tic Dacron fabric) is slid into place on the left ventricular side of th e septu m. Th e patch sutur es are tied down with an additiona l felt pledget placed on top of th e pat ch (left vent ricular side), as each suture is tied, to cushion th e tie and prevent cutt ing through th e friabl e muscle. Th ese maneuvers are viewed by th e a uthors as essential to the success of ea rly repair of the poster ior sep ta l rupture. (D) Rem aining to be repaired is the posterior left ventricular free wall defe ct created by infarctectomy. Mattress sutures of 2-0 Tevdek are placed circumfer entially around the mar gins of th e posterior left ventricular free wall defect. Each suture is buttressed with a T eflon felt pledget on the endocar dial side of th e left ven tricle. With all sutures in place, a circular pat ch, fashioned from a H em ash ield woven doubl e velour Dacron collagen-impregnated gra ft (Meadox Medicals Inc., Oakland, i'{J), is slid down onto th e epicardial surface of the left ventricle. (E) Co mpleted repair. (Repri nte d with permission from Edm unds LH (ed): Cardiac Surg ery in the Adult. New York, NY, McGraw-Hill, 1997.)
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Madsen andDaggett
gradient induced by the increased extravascular pulmonary water associated with cardiopulmonary bypass. Once the patient has warmed, we commonly use an intravenous infusion of Lasix combined with mannitol (1 g of Lasix in 400 mL of20% mannitol) at a rate of 1 to 20 mI)h to maintain the urine output greater than 100 mlzh, If renal function has been compromised preoperatively, continuous veno-venous hemofiltration (CVVH) is employed postoperativelyand managed by our ICU nurses. Intractable postoperative ventricular arrhythmias secondary to reperfusion injury are sometimes difficult to control using standard therapy. We have been impressed with the efficacy of intravenous amiodarone in these situations (10 to 20 mg/kg over 24 hours).45
Figure 8. Cross-sectional view of the completed repair of
posterior septal rupture with prosthetic patch placement of the posterior left ventricular free wall defect created by infarctectomy. RV, right ventricular cavity;LV,left ventricular cavity. (Reprinted with permission from Edmunds LH (ed): Cardiac Surgery in the Adult. New York, NY, McGrawHill, 1997.)
vated clotting times (ACT), but koalin, not Celite, is used as the ACT activator. Because controversy surrounds the issue of increased renal dysfunction and perioperative thrombotic events in patients receiving aprotinin,"! we prefer to use Amicar in patients who (1) require aortocoronary bypasses, (2) are diabetic, or (3) have known renal dysfunction. Amicar is administered by loading patients with 10 g before commencing bypass and then adding another 10 g to the pump prime. During the procedure Amicar is continuously infused at 1 g/h for the duration of surgery. We avoid giving more than 30 g of Amicar. Postpump suture line bleeding may be reduced by application of a fibrin sealant to the ventricular septum around the septal defect before formal repair.f Biological glue 43 may be effective in controlling bleeding suture lines following repair, but we have had limited experience with these compounds. As a last resort, Baldwin and Cooley'? have suggested insertion of a left ventricular assist device solely as an adjunct to the repair of friable or damaged myocardium to reduce left ventricular distension and, thus, control bleeding.
Highlights of Postoperative Care Early postoperative diuresis and positive end-expiratory pressure ventilation are used to decrease the A-a
Conclusion The incorporation of specific anatomical concepts of surgical repair and a better understanding of the physiological consequences of the disease has led to an integrated approach to the patient which has improved salvage of patients suffering this catastrophic complication of acute myocardial infarction.
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28. Kaplan MA, Harris CN, Kay]H, et al: Postinfarctional septal rupture: Clinical approach and surgical results. Chest 69:734738, 1976 29. Loisance DY, CacheraJP, Poulain H, et al: Ventricular septal defect after acute myocardial infarcion. J Thorac Cardiovasc Surg 80:61-67,1980 30. Daggett WM, Burwell LR, Lawson DW, Austen WG: Resection of acute ventricular aneurysm and ruptured interventricular septum after myocardial infarction. N EnglJ Med 283:15071514,1970 31. Daggett WM: Surgical management of ventricular septal defects complicating myocardial infarction. World J Surg 2:753-758,1978 32. Shumaker H: Suggestions concerning operative management of postinfarction ventricular septal defects. J Thorac Cardiovase Surg 64:452-457,1972 33. Daggett WM, Mundth ED, Gold HK, et al: Early repair of ventricular septal defects complicating inferior myocardial infarction. Circulation 50:112-119, 1974 (SuppI3) 34. Marchetti A, Wechsler AS: Pharmocologic intervention for acute low cardiac output. Adv Cardiac Surg 7:31-64, 1996 (abstr) 35. Cummings RG, Reimer KA, Catliff R, et aI: Quantitative analysis of right and left ventricular infarction in the presence of postinfarction ventricular septal defect. Circulation 77:3342, 1988 36. V1ahakes Gj: Management of pulmonary hypertension and right ventricular failure: Another step forward. Ann Thorac Surg61:1051-1052,1996 37. D'Ambra MN, LaRaia PJ, Philbin DM, et aI: Prostaglandin E]: A new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement. J Thorac Cardiovasc Surg 89:567-572,1985 38. Rich GF, Murphy GD,Jr., Roos CM,Johns RA: Inhaled nitric oxide: Selective pulmonary vasodilatation in cardiac surgical patients. Anesthesiology 78:1028-1035, 1993 39. Fullerton DA,Jones SD, Grover FL, McIntyre RC,Jr: Adenosine effectively controls pulmonary hypertension following cardiac surgery. Ann Thorac Surg 61:1118-1124, 1996 40. Pae WE, Jr., Pierce WS, Sapirstein JS: Intra-aortic balloon counterpulsation, ventricular assist pumping, and the artificial heart, in Baue AE, Geha AS, Hammond GL, et al (eds): Glenn's Thoracic and Cardiovascular Surgery, 6th ed. Stamford, CT, Appleton & Lange, 1996,pp 1825-1855. 41. Sundt TM, III, Kouchoukos NT, Saffitz JE, et aI: Renal dysfunction and intravascular coagulation with aprotinin and hypothermic circulatory arrest. Ann Thorac Surg 55:14181424,1993 42. SeguinJR, Frapier JM, Colson P, Chaptal PA: Fibrin sealant for early repair of acquired ventricular septal defect. J Thorac Cardiovasc Surg 104:748-751, 1992 43. FabianiJ-N,Jebara VA, Deloche A, et al: Use of surgical glue without replacement in the treatment of type A aortic dissection. Circulation 80:264-268, 1989 44. Baldwin RT, Cooley DA: Mechanical support for intraventricular decompression in repair of left ventricular disruption. Ann Thorac Surg 54:176, 1992 45. Saksena S, Rothbart ST, Shah Y: Clinical efficacy and electropharmacology of continuous intravenous amiodarone infusion and chronic oral amiodarone in refractory ventricular tachycardia. AmJ CardioI54:347-352, 1984