Surgical strategies have evolved which address the full range of ischaemic heart disease from angina pectoris to end-stage congestive heart failure. This chapter describes methods of acute surgical intervention in the more common complications which result from ischaemic heart disease, including acute coronary thrombosis, mitral regurgitation of ischaemic aetiology, post-infarction ventricular septal and left ventricular rupture, ventricular aneurysms and pseudoaneurysms, and end-stage dilated myopathy secondary to coronary artery disease.

Rapid revascularization of the myocardium following acute coronary occlusion dramatically improves survival. Studies showing that contractile dysfunction and ultrastructural alterations caused by brief periods of ischaemia are completely reversible following reperfusion have resulted in vigorous searches for prompt and effective methods of restoring perfusion to ischaemic myocardium. The clinical success of this approach hinges on the presence of myocardium which can potentially be salvaged with revascularization.

The reperfusion phenomenon, despite intensive study, is not completely understood. Potentially deleterious effects from restoration of flow to ischaemic tissue have been observed both clinically and experimentally. It is likely that at least some of this effect is mediated by the generation of superoxide radicals, which cause cellular oedema, disrupting the integrity of cellular membranes, and increase vascular permeability. The net result appears to be myocardial injury and interstitial haemorrhage, which causes both systolic and diastolic cardiac dysfunction. These effects can potentially be mitigated by so-called scavenger agents which can be introduced in the reperfusate solution. The optimal composition of the reperfusion milieu, however, has not yet been determined.

The success of methods which can reliably re-establish perfusion to ischaemic myocardium is time dependent. Reperfusion must be established within 4 to 6 h following the onset of ischaemia to avoid irreversible tissue injury. In this regard, the advent of thrombolytic agents has made non-surgical intervention in acute coronary thrombosis a more attractive option than coronary bypass, although there is some evidence that they may exacerbate reperfusion injury. During the past 15 years, refinement of non-surgical methods of revascularization have markedly reduced the frequency with which emergency coronary artery bypass is performed as primary treatment for acute thrombosis. In the acute setting, coronary bypass has generally been relegated to the protection of an area of myocardium at risk following successful reperfusion and to the management of complications following coronary angioplasty. Nevertheless, unsuccessful thrombolysis, refractory symptoms representing active ischaemia, and cardiogenic shock are occasional indications for immediate surgery. In these circumstances, it is preferable to stabilize haemodynamic parameters by pharmacological means and to perform surgery on an urgent rather than an emergency basis.

The success of thrombolytic therapy in averting the loss of myocardium following coronary thrombosis has improved the survival of patients with coronary artery disease. Pharmacological thrombolysis effects the conversion of the glycoprotein, plasminogen, into plasmin. Agents such as streptokinase and the more potent tissue plasminogen activator are effective in lysing established thrombus in nearly 75 per cent of patients. Indications for immediate surgical revascularization include failure to obtain adequate thrombolysis or ongoing ischaemia despite dissolution of the offending thrombus. The latter situation is caused by increased myocardial demands in the presence of a pre-existing, fixed stenosis. Patients with residual lesions which supply a significant area at risk for infarction may also require urgent surgery if the lesion is not suitable for angioplasty.

Once the decision to proceed to surgery has been made infusion of the thrombolytic agent is discontinued. Surgery need not be delayed until the activity of the agent in the circulation is eliminated. Although such activity may result in increased bleeding during surgical intervention, the relatively short half-lives of these agents usually allow satisfactory surgical haemostasis by the time the procedure is carried out. Prompt revascularization is of paramount important. Surgical bleeding can be controlled with the administration of homologous plasma and plasma fraction as well as the antagonist of fibrinolysis, &egr;-aminocaproic acid.

The most common indication for immediate coronary bypass arises from complications following percutaneous transluminal coronary angioplasty. In most centres a full surgical team and operating theatre is available during the performance of coronary angioplasty: urgent surgery following coronary angioplasty is currently required in 4 to 6 per cent of patients. Under these circumstances, surgery can be performed with few risks. Indications for surgical intervention depend on the condition of the patient and not on a given angiographic pattern: such indications include persistent angina, life-threatening arrhythmias, or haemodynamic instability despite adequate pharmacotherapy. The overall risk of death after surgery following a failed angioplasty is in the range of 5 to 6 per cent. Evidence of myocardial infarction is demonstrated in 30 to 50 per cent of patients postoperatively.

The goal of surgical revascularization whether undertaken following failure of thrombolysis, rethrombosis, or complications of coronary angioplasty, is to identify major target vessels and bypass offending lesions with saphenous vein grafts. In more stable patients, in whom reperfusion has been successful and surgery is performed to protect an area of myocardium at risk, arterial conduits, whenever feasible, are desirable. Most patients require insertion of an intra-aortic balloon for counterpulsation: this may stabilize haemodynamics and allow for a less urgent operation. Some patients gradually improve with counterpulsation alone over a period of days. Those who do not benefit from counterpulsation initially, however, usually have a poor outcome regardless of the method of revascularization employed. Of patients initially evaluated in cardiogenic shock following acute coronary thrombosis, 2-year survival does not exceed 40 per cent, regardless of whether surgical or non-surgical therapy is used. In patients with balloon-dependent cardiogenic shock those treated medically have a mortality of nearly 100 per cent while mortality in those treated surgically is 50 per cent. Factors which affect survival following emergency coronary bypass are the period of time elapsed from onset of ischaemia to reperfusion, the prompt institution of aortic counterpulsation, the patient's age, and the pre-existing level of ventricular function.

Mitral regurgitation secondary to coronary ischaemia is relatively common, occurring in approximately 20 per cent of patients with ischaemic heart disease. Fortunately, less than one in 20 patients with mitral regurgitation after myocardial infarction have haemodynamically significant valvar dysfunction. Management and prognosis depends mostly on the anatomical derangement, as well as the chronicity of presentation.

Regurgitation results from severe ischaemia or infarction, generally in the left coronary artery distribution, rendering the papillary muscle mechanism incompetent. In addition, dyskinesis of segments of the ventricular wall may result in a lack of synchrony of contraction with distortion of the mitral valve annulus. This inhibits coaptation of the mitral valve leaflets and allows regurgitation of blood, especially in the presence of elevated left ventricular end-diastolic pressures. In patients with chronic mitral regurgitation, the onset of symptoms and the occurrence of a new murmur can often be traced to the myocardial infarction. Some patients may have episodic insufficiency as a result of intermittent ischaemia.

Surgery should be reserved for those patients in whom moderate to severe mitral regurgitation results in haemodynamic compromise. In all cases, revascularization is the salient feature of surgery for ischaemic mitral regurgitation. A significant number of patients show substantial improvement following revascularization alone. Clinical judgement is imperative in determining whether revascularization is likely to result in an appreciable restoration of mitral function or whether valve repair or replacement is justified.

One of the most dramatic complications of ischaemic heart disease leading to acute mitral regurgitation is the rupture of a papillary muscle. This occurs in approximately 1 to 2 per cent of patients following myocardial infarction, usually between 1 and 10 days following infarction. The posteromedial muscle, which is supplied solely by the posterior descending coronary artery, is most commonly involved. The anterolateral papillary muscle has a dual blood supply from branches of the anterior descending and the circumflex coronary arteries. Symptoms arise almost immediately following rupture, although some patients may not manifest symptoms for up to 2 weeks. Patients usually develop pulmonary oedema and, not uncommonly, progress to cardiogenic shock. Although echocardiography is usually sufficient to establish the diagnosis, papillary muscle rupture must occasionally be differentiated from ventricular septal rupture. Septal rupture can often be excluded by the absence of a step-up in oxygen saturation in the pulmonary artery. Moreover, pulmonary arterial pressure tracings usually manifest striking V waves in papillary rupture. Coronary angiography will identify vessels for bypass grafting preoperatively but may delay surgery unnecessarily in patients suffering profound haemodynamic deterioration.

Treatment of acute mitral regurgitation requires replacement of the valve, unless a discrete anatomical lesion involving the posterior leaflet can easily be repaired. Some clinicians have argued that repair with simultaneous revascularization may produce the lowest mortality rate in these patients. The feasibility of repair may be jeopardized by the presence of ischaemic or necrotic tissue at the base of the papillary muscle or in myocardium when reimplantation of chordae is contemplated (Fig. 1) 1788. Ischaemic regurgitation associated with annular dilatation may be adequately treated by insertion of a mitral annular ring. However, it is not clear that repair is superior to replacement in combination with myocardial revascularization. The inherent uncertainty of restoration of function in valve repair and the possibility of subsequent replacement tend to support mitral valve replacement as a more prudent primary option in these very ill patients. Mitral valve repair is probably best reserved for the stable patient with established, chronic mitral valve dysfunction.

The choice of prosthesis is relatively unimportant, although the possibility of strut perforation of the posterior wall warrants the use of a low profile device, especially if infarction has occurred in that region. Following valve replacement for mitral regurgitation, improved valve function has been noted when the posterior leaflet is left intact. This appears to preserve the co-ordination of ventricular contraction in order to achieve a maximal cardiac output. Preservation of the posterior papillary muscle and chordae should, therefore, be standard practice.

Since the dysfunctional ventricle has accommodated to the artificial reduction in afterload provided by a regurgitant mitral valve, systemic adminstration of vasodilators for the first 3 to 5 days after surgery is standard practice. Ordinarily, intravenous vasodilators are replaced with oral agents, in the form of nitrates or calcium antagonists combined with angiotensin converting enzyme inhibitors.

The mortality rate in patients undergoing combined revascularization and mitral valve replacement in the acute setting has remained in the range of 20 to 40 per cent. As expected, the mortality rate is higher when mitral regurgitation is associated with cardiogenic shock. In patients with long-standing ischaemic mitral regurgitation, prognosis is usually associated with the degree of ventricular dysfunction, as well as the presence of accompanying complications such as a left ventricular aneurysm. As in the case of coronary surgery, maximizing medical therapy prior to surgery is important: administration of afterload reducing agents is particularly crucial in patients with acute mitral regurgitation. Sodium nitroprusside reduces peripheral as well as pulmonary vascular resistance through its direct actions on vascular smooth muscle. Afterload reduction can be further enhanced by preoperative insertion of an intra-aortic balloon pump, especially in patients with profound clinical deterioration such as those with frank papillary muscle rupture. There is no substitute, however, for prompt surgical intervention, despite the operative mortality rate of approximately 50 per cent. Starr's group has reported a 5-year survival rate of 43 per cent in patients undergoing coronary artery bypass grafting and mitral valve replacement for ischaemic mitral regurgitation. Survival is dramatically lower than that in patients with mitral regurgitation resulting from other causes.

Rupture of the septal wall is a catastrophic complication of myocardial infarction which occurs in 1 to 2 per cent of patients usually within 2 weeks of the infarct. These patients often have coronary artery disease of limited extent and develop necrosis of the septum as a result of the relative lack of collateral vessels, compared to patients with more severe forms of coronary artery disease. The most common location is the muscular anteroapical septum. This lesion is occasionally associated with ischaemic mitral regurgitation, and is associated with a ventricular aneurysm in 30 to 60 per cent of patients.

Symptoms are generally related to poor peripheral perfusion and to right-sided heart failure, in contradistinction to ischaemic mitral regurgitation in which pulmonary oedema predominates. A harsh murmur can be heard in most patients. The diagnosis is established by placement of a pulmonary artery catheter and demonstration of an oxygen saturation step-up from central venous to pulmonary arterial blood. Left ventriculography and coronary angiography is helpful in localizing the lesion and appraising the coronary anatomy, and should be performed promptly.

Patients with ventricular septal rupture should undergo surgery shortly after the diagnosis is made. Prompt placement of an intra-aortic balloon allows diagnostic studies such as cardiac catheterization to be performed. As in patients with acute mitral regurgitation, afterload reduction is a fundamental strategy. However, profound deficits in peripheral perfusion may limit the use of vasodilating agents. The optimal combination of afterload reduction and cardiotonic agents varies among patients and, in a given patient, changes as the severity of pump failure evolves. Delay in surgery achieves nothing other than selection of patients more likely to survive.

Surgery for this condition has been improved dramatically in recent years. Basic tenets in surgical technique include a transinfarct approach and radical infarctectomy with adequate exposure of the septal rupture through the left ventricle. The incision is made without reference to the position of involved coronary arteries. In addition, it is important to debride all of the friable, necrotic tissue in order to avoid postoperative patch dehiscence. This can generally be accomplished using large Russian forceps. The debridement of necrotic tissue must be continued even if it involves the entire interventricular septum (Fig. 2) 1789. The defect which remains following aggressive debridement should be closed with a prosthetic patch, preferably elastic Dacron, without any tension. The sutures should be pledgetted and should be placed from the right ventricular aspect (Fig. 3) 1790. It is also useful to place pledgets on the side of the patch in order to cushion the tissue as the knots are tied down. Any associated mitral valve dysfunction can also be corrected through the ventriculotomy. For anterior defects, it is often possible to reapproximate the free edge of the left ventricle to the right ventricle where the anterior patch has been anchored (Fig. 4) 1791. This is done using interrupted mattress sutures of 2–0 non-absorbable braided suture along with parallel strips of Teflon felt. After closure is completed, it should be reinforced with heavy continuous polypropylene suture.

It is usually difficult to reapproximate the ventricular edges of posterior septal defects without significantly altering the configuration of both ventricular cavities. A free-wall patch of low porosity Dacron is usually required in order to re-establish the integrity of the ventricular wall (Fig. 5) 1792. The patch is attached with interrupted, pledgetted mattress sutures of 3–0 non-absorbable material. In general, repair of posterior defects is considerably more demanding technically, as a result of its location as well as the usual requirements for a patch.

Although its importance to survival is not as well established as it is in the case of ischaemic mitral regurgitation, coronary revascularization is an important feature of the procedure, and distal anastomoses can be constructed immediately following debridement of the ischaemic septum. Myocardial preservation during diastolic arrest is of the utmost importance. Intracavitary topical cooling is used during construction of distal anastomoses, and cardioplegia can be administered via the grafts while repair of the defect is accomplished.

The mortality rate associated with this operation is high, particularly in elderly patients, exceeding 50 per cent after the first week without surgical intervention. The surgical mortality rate approaches 25 per cent and depends on the patient's haemodynamic status preoperatively. Long-term survival depends upon extent of coronary disease as well as the residual left ventricular function.

Left ventricular rupture is a usually fatal complication of myocardial infarction, most commonly occurring approximately 1 week after the infarct. The patient ordinarily develops sudden hypotension as a result of cardiac tamponade. Occasionally, the rupture may be contained by haematoma, allowing time for resuscitative measures and emergency surgery. The surgical approach involves excision of the infarction and primary approximation of the viable edges of the ventricular myocardium using interrupted, non-absorbable sutures with Teflon buttresses. The repair should be performed with monofilament suture. When left ventricular rupture is contained, scar develops, bridging the defect and creating a pseudoaneurysm. Generally speaking, this defect, also called a ‘subepicardial aneurysm’, is clinically indistinguishable from a left ventricular aneurysm.

Left ventricular aneurysm complicates 10 to 35 per cent of transmural myocardial infarctions and generally occurs after 2 to 8 weeks. In 85 per cent of patients, the presenting symptoms are angina, congestive heart failure, or both. Ventricular arrhythmias and embolic phenomena are less common initial presentations. The presence of any of these in association with a left ventricular aneurysm is an indication for surgery.

Although the distinction between a discrete aneurysm and an area of markedly diminished contractility is often difficult, aneurysms are generally characterized by ‘paradoxical’ expansion of the segment in response to the increased intracavitary pressures generated during systole. The aneurysmal wall is composed of fibrous tissue which has replaced necrotic myocardium. The resulting structural weakness results in an inability to resist the high wall stress imparted. With time, an increase in the size of the aneurysm leads to elevated surface tension, resulting in further stretching of the wall. These lesions may attain considerable size causing further reduction in cardiac output. Congestive heart failure ensues as a result of physiological alterations during both systole and diastole. The stasis of blood in the aneurysmal sac in combination with an abnormal and thrombogenic endocardium increases the propensity for thrombus formation and embolization.

Surgery involves excision of the aneurysm and repair with restoration of near-normal left ventricular configuration (Fig. 6) 1793. It is especially important to avoid embolization of laminated thrombus within the aneurysm. Application of the aortic cross-clamp prior to manipulation of the heart is an essential feature of the technique. Aneurysmectomy should not interfere with the function of the papillary muscles or the mitral valve apparatus, but resection should be complete, leaving only a 1 cm rim of scar for suture placement. Concomitant revascularization, in most cases, lowers operative mortality. As in ventricular septal rupture, the initial step of excising the aneurysm affords the possibility of intracavitary cooling. In addition, early construction of the distal anastomoses allows the administration of cardioplegia via the grafts during aneurysm repair.

Overall, the mortality rate associated with left ventricular aneurysm resection and coronary bypass grafting remains at 10 to 15 per cent. Among 268 patients with left ventricular aneurysm in the Coronary Artery Surgery Study (CASS), there was a 9 per cent operative mortality for revascularization and aneurysm resection. In general, hospital mortality has been correlated with degree of congestive heart failure and the extent of coronary artery disease. Moreover, the long-term outlook has been somewhat discouraging in all centres, with Barrett-Boyes' group reporting a 30 per cent incidence of late death in an average follow-up of 39 months. The patients are, however, consistently improved in terms of symptoms, and improvement is more likely in patients with angina than in those with congestive heart failure. The Oslo group has shown that significant right ventricular dysfunction is common in patients with left ventricular aneurysm (89 per cent of patients). They have also shown that repair of the aneurysm does not generally result in early improvement in right ventricular function.

Ultimately, when congestive heart failure results from coronary artery disease, consideration must be given to replacement of the heart. At the present time, so called ‘ischaemic cardiomyopathy’ is the most common indication for cardiac transplantation. The decision for transplantation rather than revascularization is multifactorial: consideration is given to the relative prominence of failure symptoms as opposed to angina, availability of target vessels, and candidacy for mechanical ‘bridging’ to transplantation, should revascularization be unsuccessful. In the current era of revascularization with advanced methods of myocardial preservation, it is possible to perform coronary bypass grafting in many patients who would formerly have undergone transplantation. In one group of patients who were candidates for transplantation but who instead underwent reparative procedures, survival was comparable to that of a cohort of transplanted patients. In general, patients with angina pectoris are likely to benefit from revascularization. The decision for cardiac transplantation is based upon the presence of markedly reduced ventricular function and the lack of feasibility of conventional surgery. Occasionally, cardiac transplantation is undertaken in patients with angina or arrhythmias, but congestive heart failure is far more common as an indication.

The technique of cardiac transplantation is described elsewhere in this volume. The 1-year survival rate of patients receiving a cardiac transplant for ischaemic heart disease is in the range of 80 to 85 per cent; 5-year survival is about 65 per cent (Fig. 7) 1794. Attention is being increasingly focused on the potential use of vascularized muscle flaps for augmentation of ventricular function and for diastolic counterpulsation in patients with long-standing coronary artery disease. This experience thus far is small, and while physiological effects can be shown, significant clinical improvement remains an elusive goal.

Considerable attention has been focused on the use of mechanical devices for replacement of the heart. While a number of devices had been employed, none has proved to be a reliable alternative to transplantation. At present, implantable devices, such as the Novacor left ventricular assist device, are available for use as a ‘bridge’ for patients who are awaiting transplantation and for those who cannot be weaned from cardiopulmonary bypass after conventional cardiac surgery (Fig. 8) 1795. Undoubtedly, mechanical devices will gain greater currency as they are improved and as they move through the requisite clinical trials. At the same time, results with allograft transplantation are improving, and the possibility of xenograft transplantation as another and possibly preferable biological alternative is being pursued. At some point in the future, there may well be a division of opinion with respect to cardiac replacement separating advocates of mechanical and biological hearts, similar to the current considerations with respect to valve replacement. As with mechanical valves, mechanical hearts may have the advantage of durability and the disadvantage of requirement for anticoagulation, while biological hearts will have fewer implant-related complications but will have the potential for ‘wearing out’ due to the effects of chronic rejection.

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