Education and debate

Grand Rounds - Hammersmith Hospital: Complicated myocardial infarction Ventricular septal rupture is a surgical emergency

Department of Medicine, Hammersmith Hospital, London W12 0NN.

Ventricular septal rupture is a serious complication of acute myocardial infarction that generally produces progressive circulatory failure and rapid deterioration. Prompt diagnosis followed by surgical repair with perioperative circulatory support is often life saving. We present the case of a patient with ventricular septal rupture who experienced recalcitrant attacks of sustained ventricular tachycardia postoperatively and discuss important aspects of management.

Case history

A 64 year old woman was admitted with a three day history of severe retrosternal chest pain followed by progressively worsening dyspnoea at rest. Myocardial infarction was diagnosed, but the delay in admission precluded thrombolysis. Two days later she was transferred to this hospital with breathlessness and oliguria (480 ml over 24 hours) despite having been given intravenous diuretics and low dose dopamine. She had no history of heart disease or hypertension or known coronary risk factors.

On examination she was unwell and mentally obtunded, with cool peripheries and a raised jugular venous pressure. The rhythm was sinus (rate 113 beats/min) and blood pressure 100/65 mm Hg. Her cardiac impulse was laterally displaced, and she had a loud pansystolic murmur, with a palpable thrill, at the lower left sternal border.

Chest radiography showed cardiomegaly, and an electrocardiogram showed evidence of recent extensive anterior myocardial infarction with Q waves in leads V1-6. Her plasma sodium concentration was 123 mmol/l, urea concentration 46.5 mmol/l, and creatinine concentration 209 µmol/l. An echocardiogram showed anteroseptal-apical dyskinesia with infarct expansion, dilated ventricles and impaired biventricular function, and anteroapical septal rupture: colour Doppler ultrasound examination showed shunting and no evidence of mitral regurgitation (fig 1). Swan-Ganz catheterisation showed a pulmonary artery oxygen saturation of 88% and a pressure of 50/23 mm Hg. Ventricular septal rupture with incipient cardiogenic shock was diagnosed, and the circulation was supported with inotropic drugs and intra-aortic balloon counterpulsation pending emergency surgical repair.

View larger version (57K): [in this window] [in a new window]   FIG 1 - Left: modified apical four chamber two dimensional echocardiogram. Centre: schematic drawing showing anteroapical ventricular septal rupture of simple type (arrow). Right: colour flow map showing turbulent flow across defect

At operation a 2 cm² septal defect was found, and rupture of the free wall of the heart seemed imminent. The defect was closed with three heavily pledgeted horizontal mattress sutures, and the ventriculotomy was closed with an aneurysm-type repair with Teflon buttressing. The patient came off the cardiopulmonary bypass uneventfully and was transferred to the intensive care unit receiving 1:1 pump augmentation.

Apart from having a large right haemothorax, which needed drainage, she initially improved and was extubated. On the third postoperative day, however, she developed a sustained monomorphic ventricular tachycardia (rate 200 beats/min), dizziness, and mild hypotension (fig 2). Over the next five days there were 18 similar episodes, all without obvious precipitating myocardial ischaemia or immediate circulatory collapse. They usually responded to a single 100 J or 200 J synchronised direct current countershock given under short acting general anaesthesia. Initially she had hypokalaemia (potassium concentration 3.5 mmol/l) and she received potassium supplements and a magnesium infusion. To prevent tachycardia recurring amiodarone 300 mg was given over 30 minutes followed by 1 g/24 h through a central line; tachycardia recurred, however, despite the infusion rate being increased and lignocaine added. Attacks stopped when oral flecainide (200 mg twice daily) was substituted for the lignocaine.

View larger version (73K): [in this window] [in a new window]   FIG 2 - Electrocardiogram showing sinus rhythm followed by sustained monomorphic ventricular tachycardia (rate 200 beats/min)

She improved progressively, and after flecainide was stopped Holter monitoring showed only occasional ventricular premature beats. Repeat echocardiography two weeks postoperatively showed overall poor left ventricular function and a small residual septal defect. She recovered well, was discharged taking amiodarone and lisinopril, and remained free of arrhythmias. When we last reveiwed her, six months after her discharge, she reported good exercise tolerance and no angina and had normal renal function.

Comment

Mechanical complications of acute myocardial infarction include ventricular septal rupture, papillary muscle rupture, left ventricular aneurysm, pseudoaneurysm, and rupture of the free wall; and these lesions may occur in combination.¹ Septal rupture reflects transmural necrosis and occurs in about 1% of patients admitted because of infarcts, usually between day 2 and day 6. The site of the infarct and location of the defect are anteroapical in 60% of cases and inferior in 40%.² Although there is a range of severity, most patients are gravely ill with cardiogenic shock or a low output, and even the small minority with stable haemodynamics may deteriorate rapidly and unexpectedly. When patients are managed conservatively the mortality is 50% one week after septal rupture and nearly 90% two months after.³

Echocardiography has revolutionised diagnosis and allows septal ruptures to be classified as simple or complex.¹ A complex rupture pursues an oblique course through the septum and is most commonly located inferiorly.¹ Smyllie et al found that two dimensional echocardiography identified 35% of defects whereas colour Doppler ultrasound examination detected 100%, a fifth of which had multiple jets.⁴ Transoesophageal echocardiography is reserved for patients who are poorly echogenic.⁵ Right heart oximetry shows a stepped increase in saturation in the right ventricle and so allows distinction from acute mitral regurgitation, the main differential diagnosis. Centres with echocardiographs no longer use left ventriculography to diagnose septal ruptures.

Coronary angiography was not done in our patient because her condition was deteriorating rapidly and the risks and delay to surgery that would result were too great.⁶ Skehan et al found single vessel disease in 45% of cases and fewer collateral vessles than in a comparison group.⁷ One centre advocated coronary angiography only for patients with inferior defects after finding that multivessel disease was significantly more common in such patients.⁶ Coronary angiography is perhaps best reserved, however, for those patients with small infarcts and shunts who are haemodynamically stable (about 10%), thereby permitting a delayed repair with bypass grafting as necessary. Though clearly of secondary importance, the place of concomitant revascularisation remains contentious. Pooled data from three large surgical series showed no differences in early or late survival between patients who had and had not received grafts.^2,6,8

Delayed operation for ventricular septal rupture, to allow tissue fibrosis and a better repair, used to be advised; but the advantages of early surgery for the majority of patients with worsening haemodynamics have become so clear that this complication of myocardial infarction is now considered to be a surgical emergency.^2,6 Operative mortality is higher for inferior defects⁶; they are harder to close and commonly associated with right ventricular dysfunction, and occasionally the mitral valve has to be replaced or repaired.⁹ The choice of surgical technique depends on the size and location of the defect and how long it has been present. Direct suture may suffice for small lesions or late repairs whereas large inferior defects commonly require a Dacron patch.¹⁰ Closure with a double umbrella device¹¹ or with a balloon catheter¹³ has been described.

The mechanism underlying a sustained monomorphic ventricular tachycardia is usually re-entry, and our patient's repeated attacks posed a major problem with regard to her management (box). (Beta) Blockers were not used because of the poor left ventricular function and absence of precipitating ischaemia. Additionally, ventricular pacing was not used because of concerns that the lead might disrupt the repair or perforate the necrotic free wall of the heart. Intravenous amiodarone is effective for terminating and suppressing recurrent ventricular tachycardia; most patients who respond do so within two hours.¹³ Side effects include hypotension, bradycardia that necessitates pacing, sinus arrest after cardioversion, and, rarely, degeneration to polymorphic ventricular tachycardia.^13,14 Proarrhythmia is more likely to occur when more than one drug is used, and in these cases the electrocardiographic trace, particularly the QT interval, must be carefully monitored.¹⁵ The need for maintenance treatment with amiodarone in our patient is debatable because there is no evidence that it improves the prognosis. If maintenance treatment is prescribed, however, the lowest dose capable of suppressing the arrhythmia should be used to minimise the hazards of long term treatment.¹⁶

Management of recurrent sustained ventricular tachycardia

General measures (for suppression): Correct hypokalaemia Give magnesium infusion (especially if hypokalaemia is present) Correct acid-base disturbances and hypoxaemia Treat myocardial ischaemia ((Beta) blockers) Treat heart failure Stop arrhythmogenic drugs Electrical treatments (for termination or suppression): Direct current cardioversion Ventricular burst pacing (termination) Atrial pacing (suppression) Ventricular pacing (suppression) Antiarrhythmic drugs (for termination or suppression, or both): Lignocaine Amiodarone Flecainide Other drugs (for example, disopyramide, (Beta) blockers) Drug combinations (for example, amiodarone, and flecainide)

Skillington et al⁶ reported postoperative residual or recurrent ventricular septal rupture in 22 of 101 patients, and a repeat operation was necessary in eight cases. As a rule, defects with large shunts causing heart failure should be closed whereas small, asymptomatic defects are best left alone.⁶ Angiotensin converting enzyme inhibitors should be given long term to patients with appreciable left ventricular dysfunction after infarction because of the clear benefits.¹⁷

Discussion

KMT: This case is a typical example of ventricular septal rupture. The surgical problem with these patients is that you have to operate while an acute myocardial infarction is evolving, when the myocardium is soft and friable. Certainly the best surgical results are obtained in patients who are haemodynamically stable and who can be managed conservatively until some myocardial fibrosis has occurred. This woman's operation had to be done immediately, though, because her clinical condition was deteriorating rapidly. The overall operative mortality associated with repair of a septal rupture after infarction in the United Kingdom is around 40-45%.

AJR: How often can surgery be delayed in these patients?

CMO: Very rarely, and in those cases the surgeon can repair the defect relatively easily and safely. A combination of amiodarone (class 3) and flecainide (class 1 c) is effective for really recalcitrant ventricular tachycardia. I have seen it work in this sort of patient on several occasions.

AJR: What clinical features differentiate ventricular septal rupture from acute mitral regurgitation due to papillary muscle rupture?

CMO: Patients with acute mitral regurgitation are usually more breathless and have pulmonary oedema. They may also have a normal jugular venous pressure whereas septal rupture is often associated with a greatly raised jugular venous pressure, as in this woman. Both conditions produce a pansystolic murmur at the left sternal edge. A high pulmonary artery oxygen saturation in a patient with a low cardiac output gives the diagnosis when echocardiography is not available.

AJR: Is there ever any confusion between acquired and congenital ventricular septal defects when someone presents with an infarct?

CMO: Patients with a congenital condition usually know their diagnosis and also would have a murmur at the outset, unlike people with an acquired ventricular septal defect. Most congenital ventricular septal defects in adults are perimembranous and have a different location in the echocardiogram.

AJR: What causes ventricular septal rupture?

CMO: The underlying pathological finding is transmural infarction. Coronary angiographic studies show that about 40-50% of patients have single vessel disease and seem to have fewer collateral vessels to the septum. This may explain the full thickness necrosis.⁷

PKM: Whether treatment with streptokinase affects the incidence of septal rupture is unclear,¹⁸ but rupture seems to occur earlier, at around 24 hours, in patients who have been given thrombolysis.¹⁹

GJD: Elderly people, women, and those with hypertension seem to be at greatest risk. Many patients who die of myocardial infarction do so because of cardiac rupture; this just happens to be an internal rupture. The fact that mortality from infarction is higher in elderly people might be explained by the frailty of their tissues or the more advanced state of their coronary disease as they do not seem to have larger infarcts.

1. Edwards BS, Edwards WD, Edwards JE. Ventricular septal rupture complicating acute myocardial infarction: identification of simple and complex types in 53 autopsied hearts. Am J Cardiol 1984;54:1201-5. [Medline]
2. Jones MT, Schofield PM, Dark JF, Moussalli H, Deiraniya AK, Lawson RAM, et al. Surgical repair of acquired ventricular septal defect. Determinants of early and late outcome. J Thorac Cardiovasc Surg 1987;93:680 -6. [Abstract]
3. Sanders RJ, Kern WH, Blount SG. Perforation of the interventricular septum complicating myocardial infarction. Am Heart J 1956;51:736-48. [Medline]
4. Smyllie J, Dawkins K, Conway N, Sutherland GR. Diagnosis of ventricular septal rupture after myocardial infarction: value of colour flow mapping. Br Heart J 1989;62:260-7. [Abstract/Free Full Text]
5. Ballal RS, Sanyal RS, Nanda NC, Mahan EF. Usefulness of transesophageal echocardiography in the diagnosis of ventricular septal rupture secondary to acute myocardial infarction. Am J Cardiol 1993;71:367- 70. [Medline]
6. Skillington PD, Davies RH, Luff AJ, Williams JD, Dawkins KD, Conway N, et al. Surgical treatment for infarct-related ventricular septal defects. Improved early results combined with analysis of late functional status. J Thorac Cardiovasc Surg 1990;99:798-808. [Abstract]
7. Skehan JD, Carey C, Norrell MS, de Belder M, Balcon R, Mills PG. Patterns of coronary artery disease in post-infarction ventricular septal rupture. Br Heart J 1989;62:268-72. [Abstract/Free Full Text]
8. Radford MJ, Johnson RA, Daggett WM, Fallon JT, Buckley MJ, Gold HK, et al. Ventricular septal rupture: a review of clinical and physiologic features and an analysis of survival. Circulation 1981;64:545-53. [Abstract/Free Full Text]
9. Daggett WM, Buckley MJ, Akins CW, Leinback RC, Gold HK, Block PC, et al. Improved results of surgical management of postinfarction ventricular septal rupture. Ann Surg 1982;196:269-77. [Medline]
10. Daggett WM. Surgical technique for early repair of posterior ventricular septal rupture. J Thorac Cardiovasc Surg 1982;84:306-12. [Medline]
11. Lock JE, Block PC, McKay RG, Baim DS, Keane JF. Transcatheter closure of ventricular septal defects. Circulation 1988;78:361-8. [Abstract/Free Full Text]
12. Hachida M, Nakano H, Hirai M, Shi CY. Percutaneous transaortic closure of postinfarctional ventricular septal rupture. Ann Thorac Surg 1991;51:655-7. [Abstract]
13. Helmy I, Herre JM, Gee G, Sharkey H, Malone P, Sauve MJ, et al. Use of intravenous amiodarone for emergency treatment of life-threatening ventricular arrhythmias. J Am Coll Cardiol 1988;12:1015-22. [Abstract]
14. Schutzenberger W, Leisch F, Kerschner K, Harringer W, Herbinger W. Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation. Br Heart J 1989;62:367-71. [Abstract/Free Full Text]
15. Griffith MJ, Linker NJ, Garratt CJ, Ward DE, Camm AJ. Relative efficacy and safety of intravenous drugs for termination of sustained ventricular tachcardia. Lancet 1990;336:670-3. [Medline]
16. Herre JM, Sauve MJ, Malone P, Griffin JC, Helmy I, Langberg JJ, et al. Longterm results of amiodarone therapy in patients with recurrent sustained ventricular tachycardia or ventricular fibrillation. J Am Coll Cardiol 1989;13:442-9. [Abstract]
17. Pfeffer MA, Braunwald E, Moye LA, Basta L, Brown EJ, Cuddy TE, et al. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. N Engl J Med 1992;327:669-77. [Abstract]
18. Massel DR. How sound is the evidence that thrombolysis increases the risk of cardiac rupture? Br Heart J 1993;69:284-7.
19. Westaby S, Parry A, Ormerod O, Gooneratne P, Pillai R. Thrombolysis and postinfarction ventricular septal rupture. J Thorac Cardiovasc Surg 1992;104:1506-9. [Abstract]