Fig. 5.3b. Apical post-infarction VSD repaired by resection of the entire apex of the heart, including the VSD and portions of the left and right ventricles.

with severe mitral regurgitation and poor left ventricular ejection fraction, again mitral valve replacement may be done but one is less likely to take a chance with a mitral valve repair.


This is a complex and controversial topic. Several guidelines must be drawn up for indications for coronary artery bypass alone, compared to carotid endarterec-

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Fig. 5.4. Repair of posteriorly located post-infarction VSD requiring excision of nonviable tissue, plication of the interven-tricular septum to the free ventricular wall and closure of the right ventricle as a patch repair.

tomy alone. Combined carotid and coronary artery disease is common, particularly in patients with left main coronary artery disease. The chance of left main coronary artery disease in a patient who has combined carotid and coronary artery disease is one in three whereas patients without carotid disease but who do have coronary artery disease have a 14% chance of having left main disease. Conversely, if a patient has left main coronary artery disease, the chance of carotid disease is 30-50%; this is compared to a 20% incidence of carotid disease in patients with coronary artery disease without left main disease. The point is that carotid artery disease must always be suspected in patients with coronary artery disease and in particular in patients who have left main coronary artery disease since one-third to half of these people will have concomitant, significant carotid disease. If there is a neck bruit, whether or not it is symptomatic, a noninvasive evaluation, i.e. carotid duplex, is mandatory. In asymptomatic patients who have greater than 80% carotid stenosis, the chance of developing symptoms or developing more significant carotid lesions within 2 years is about 50%. It is therefore felt by most surgeons that carotid lesions greater than 80%, even if they are asymptomatic, should be treated by carotid endarterectomy. In general, the rule when deciding on the operation for combined carotid and coronary artery disease is that one operates first on the more compelling lesion; if both lesions are compelling then a combined procedure is done, i.e. a carotid endarterectomy is performed while the saphenous vein for coronary bypass is being harvested; the patient is then placed on cardiopulmonary bypass and the coronary artery bypass graft is done with the neck open. Then both wounds are closed after Protamine is given to prevent excess bleeding from the neck wound.

Fig. 5.5. Ischemic ruptured papillary muscle attached to resected mitral valve leaflet. Courtesy of Dr. Lawrence Burr, University of British Columbia.

Fig. 5.5. Ischemic ruptured papillary muscle attached to resected mitral valve leaflet. Courtesy of Dr. Lawrence Burr, University of British Columbia.

Here are some examples. 1) The first is a patient with unstable angina, left main coronary artery disease and an asymptomatic 80% carotid stenosis. In this situation, coronary artery bypass is clearly the more compelling of the operations. This should be performed with the patient systemically cooled to protect the brain. The perfusion pressure is kept high. Later, after the patient has recovered from his coronary revascularization, a carotid endarterectomy should be performed because the chance of him developing a stroke, TIA or worsening carotid pathology within 2 years is about 50%. 2) The patient with stable angina, who has TIAs and a critical carotid lesion should clearly undergo a carotid endarterectomy first. After the patient has recovered, a coronary artery bypass graft is performed. Obviously, during the carotid endarterectomy, appropriate hemodynamic monitoring including a Swan-Ganz and arterial line may be critical. 3) In a patient who has unstable angina from left main coronary artery disease, as well as a critical carotid lesion with TIAs, a simultaneous procedure is performed in the fashion described above with the carotid endarterectomy done off bypass. For patients with unstable angina with critical coronary artery disease and a bilateral critical carotid lesion, then the surgeon can fix one carotid while off bypass, then perform coronary artery bypass grafting at the same sitting. Later, after the patient has recovered from his combined carotid-CABG, surgery, the surgeon can fix the other carotid, i.e. the less critical side. These examples serve as acceptable methods for approaching combined carotid and coronary artery disease; yet other approaches may work as well.


The treatment of ventricular tachycardia (VT) during or after myocardial infarction varies depending upon the interval since the event. If the tachycardia occurs 24-48 h of myocardial infarction, it is considered less malignant, especially if not sustained (less than 30 sec in duration). This often is caused by reperfusion of infarcted tissue and is not considered a malignant rhythm.

Runs of VT less than 30 sec that impair hemodynamics enough to cause symptoms of reduc ed blood flow are considered the equivalent of a sustained VT. These are generally considered to be included among the life-threatening cardiac arrhythmias. In the patient with prior myocardial infarction and a defined ventricular aneurysm, sustained VT occurs at rates from 140-200/min, and this arrhythmia may be relatively well-tolerated. In contrast, patients with transient myocardial ischemia often have more rapid ventricular tachyarrhythmias (>200/ min) that may be polymorphic causing hemodynamic instability. When the hemodynamic status is stable and there is no evidence of myocardial ischemia, acute infarction or poor central nervous system perfusion, electrical cardioversion can await a therapeutic trial of intravenous drug. With acute myocardial infarction, falling blood pressure or evidence of ischemia, immediate cardioversion is indicated. If acute ischemia is not thought to be the cause, long-term therapy, with an automatic internal defibrillator or antiarrhythmic therapy depends upon the result of an electrophysiologic study as well as the severity of the clinicla presnetation. If ischemia is found to be the underlying cause of VT, vascularization is indicated with continued observation.

Suggested Reading

1. Karp RB. Special considerations in mitral valve and coronary artery disease. Adv Card Surg 1990; 1:71-92.

2. Lytle BW, Cosgrove DM, Gill CC et al. Mitral valve replacement combined with myocardial revascularization. Early and late results for 300 patients. Circulation 1985; 71:1179-1190.

3. Disesa VJ, Cohn LH, Collins JJ et al. Determinations of operative survival following combined mitral valve replacement and coronary revascularization. Ann Thorac Surg 1982, 34:482-489.

4. Minami K, Sagoo KS, Breymann J et al. Operative strategy in combined coronary and carotid artery disease. J Thorac Cardiovasc Surg 1988; 95:303-309.

5. Newman DC, Hicks RG. Combined carotid and coronary artery surgery: a review of the literature. Ann Thorac Surg 1988; 45:574-581.

6. Foster AH, Salter DR. Cerebral pathophysiologic considerations in patients with co-existing carotid and coronary artery disease. Adv Card Surg 1991; 2:203-225.

7. Coulden R, Lipton MJ. Noninvasive therapy for the diagnosis and management of myocardial ischemia. Adv Card Surg 1993; 4:173-205.

8. Elefferiades JA, Biblo LA, Batsford WP et al. Evolving patterns in the surgical treatment of malignant ventricular tachyarrhytmias. Ann Thorac Surg 1990; 49:94-100.

9. Klein H, Trappe HJ. Implantable cardioverter-defibrillator therapy. Indications and decision making in patients with coronary artery disease. PACE 1992; 15:610-615.

10. Dagget WM, Buckley MJ, Akins CW et al. Improved results of surgical management of post-infarction ventricular septal rupture. Ann Surg 1981; 196:269.

11. Heitmiller R, Jacobs ML, Daggett WM. Surgical management of post-infarction ventricular septal rupture. Ann Thorac Surg 1986; 41:683.

12. Silva JP, Cascudo MM, Baumgratz JF et al. Post-infarction ventricular septal defect: An efficacious technique for early surgical repair. J Thorac Cardiovasc Surg 1989; 97:86.

Piwrica A, Menasche P, Beaufils P, Julliard JM. Long-term results of emergency surgery for post-infarction ventricular septal defect. Ann Thorac Surg 1987; 44:274.

European Coronary Surgery Study Group. Long-term results of prospective randomized study of coronary artery bypass surgery in stable angina pectoris. Lancet 1982; 2:1173-1180.

CASS Principal Investigators and Their Associates. Coronary artery surgery study (CASS): a randomized trial of coronary artery bypass surgery. Survival data. Circulation 1981; 68:939-950.

The Veterans Administration Coronary Artery Bypass Cooperative Study Group, 1984. Eleven year survival in the Veterans Administration Randomized Trial of Coronary Bypass Surgery for stable angina. N Engl J Med 1984; 311:133-139. Passamani E, Davis KB, Gillespie MJ et al. A randomized trial of coronary artery bypass surgery. Survival of patients with a low ejection fraction. N Engl J Med 1985; 312:1665-1671.

Kouchoukos NJ, Ksrp RB, Oberman A et al. Long-term patency of saphenous veins for coronary bypass grafting. Circulation 1978; 58 (Suppl I):96. Lytle BW, Loop FD, Cosgrove DM et al. Long-term serial studies of internal mammary artery and saphenous vein coronary bypass grafts. J Thorac Cardiovasc Surg 1985; 89:248.

Loop FD, Lytle BW, Cosgrove et al. Influences of the internal mammary artery graft on 10-year survival and other cardiac events. N Engl J Med 1986; 314:1-6. Cameron A, Kemp HG, Green GE. Bypass surgery with the internal mammary artery graft: 15 year follow-up. Circulation 1986; 74 (Suppl III); 30-36. Jatene AD. Left ventricular aneurysmectomy. Resection of reconstruction. J Thorac Cardiovasc Surg 1985; 89:331.

Barratt-Boyes BG, White HD, Agnew JM et al. The results of surgical treatment of left ventricular aneurysms. An assessment of the risk factors affecting early and late mortality. J Thorac Cardiovasc Surg 1984; 87:87. Olearchyk AS, Leomole GM, Spagna PM. Left ventricular aneurysm. Ten years experience in surgical treatment of244 cases. Improved clinical status, hemodynamics, and long-term longevity. J Thorac Cardiovasc Surg 1984; 88:544.

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