lschaemic heart disease

Ischaemic heart disease is a major cause of morbidity and mortality in developed countries. The underlying pathology is usually atherosclerosis of the coronary arteries. The coronary anatomy is such that each of the three major arteries (the right, the left anterior descending and the circumflex) supplies a similar proportion of the myocardium (Fig. 48.45). Triple-vessel disease refers to significant stenosis in these three vessels.

Presentation.

Coronary artery disease may be (1) asymptomatic until it presents as sudden death or an acute myocardial infarction as the first manifestation, or (2) symptomatic with angina, typically on exertion and relieved by rest.

Pathophysiology

The starting point in atherosclerosis is believed to be endothelial injury. This may be mechanical or biochemical and the result is platelet aggregation at the site of injury. There is consequent migration of smooth muscle cells into the intima. The risk factors are the following:

· hypercholesterolaemia;

· hypertension;

· cigarette smoking;

· diabetes mellitus;

· advancing age;

· family history of ischaemic heart disease.

An elevated plaque forms within the lumen and, with time, progressive thickening with ulceration, plaque rupture, thrombus formation or calcium deposition will further narrow the lumen. With a narrowing of over 70 per cent, the lumen is critically stenosed (Fig. 48.46).

Slow progression of this process encourages the formation of collateral vessels whereas sudden occlusion results in myocardial infarction. The rate of progression is highly variable and the distribution patchy, but to have only one vessel involved is unusual. Plaques tend to form in the proximal areas of the artery or branches.

Symptomatic patients with ischaemic heart disease can usually be helped by medical treatment in the first instance. Attention is paid to the elimination of risk factors wherever possible.

Pharmacological agents that relieve angina include nitrates, calcium antagonists and n-blockers. These agents reduce the vascular tone and therefore reduce preload and/or afterload of the left ventricular muscle, reduce the work of the heart and therefore reduce the metabolic demand.

Surgical involvement occurs when the symptoms are severe and not adequately controlled on a reasonable trial of medication or when the prognosis is adversely affected by continuing medical treatment.

Investigations

Clinical examination is typically normal (although stigmata of diabetes or hypercholesterolaemia may be evident) and objective evidence of myocardial ischaemia must be sought.

Electrocardiography

The simplest test to demonstrate ischaemia is an exercise ECG. The patient is asked to undergo an increasing amount of exercise on a treadmill according to a carefully described protocol. Every 2 minutes the work rate increases. Full resuscitative equipment is available and the patient is continually monitored by ECG. The test is stopped if the patient experiences chest pain or arrhythmias or becomes dyspnoeic. If there is evidence of ischaemia on the ECG (>2 mm ST depression) then the test is positive.

Radionucleotide studies including thallium scanning also provide objective evidence of reversible ischaemia but the equipment is not always available.

Coronary angiography

This is an invasive test performed under radiographic screening. The arterial circulation is entered via the femoral or brachial artery and a catheter is advanced into the aorta to the coronary sinuses. The coronary ostia are located and iodine-containing dye is infused to outline the coronary anatomy. At least two views of the coronary anatomy are filmed in different planes to give a three-dimensional impression of the arterial system. A left ventriculogram is performed to estimate the ejection fraction, and a measurement of the left ventricular end-diastolic pressure is taken. This test only outlines the coronary anatomy and does not demonstrate ischaemia.

Indications for surgery

Many patients can be managed medically and there is an increasing trend for cardiologists and interventional radiologists to palliate the symptoms of angina by the technique of coronary angioplasty. This involves passing a small balloon- tipped catheter into the feinoral or radial artery and feeding it retrogradely into the aortic root. Soluble dye is injected into the coronary ostia to delineate the coronary anatomy; the catheter is then passed across the stenosis and inflated so as to crush the atheromatous plaque with a 90 per cent initial success rate. If successful, this procedure provides symptomatic relief but restenosis occurs in 30 per cent within 3-6 months. The long-term benefits are unclear and the process may have to be repeated with up to 40 per cent of patients coming to definitive coronary artery bypass grafting within 2.5 years. Coronary artery stenting following angioplasty has improved the medium-term patency rate but the long-term benefits remain unclear. Several trials (RITA, BARI and CABRI) show that the early morbidity for angioplasty is less than that for coronary artery bypass graft (CABG) but the

patients in the angioplasty groups are more likely to have more interventions and require more medication in the short term. A detailed discussion of these points is outside the scope of this chapter.

Angina can be relieved by surgical revascularisation in most patients and symptomatic improvement can be expected for over 10 years. Patients with lesions in one or two vessels may benefit from balloon angioplasty, but triple-vessel disease or left main stem stenosis is an indication for surgery.

Data from prospective, randomised trials demonstrate that patients with angina and left main stem stenosis or triple-vessel disease have a poor natural history which is significantly improved by surgery. Survival in patients with single-vessel disease is equally good when medical and surgical treatment are compared. Survival is further increased if an internal mammary artery is used to bypass a proximal stenosis of the left anterior descending (LAD) artery. Acute unstable angina usually settles with medical treatment but continuing pain in spite of adequate therapy is an indication for surgery. Surgery should be considered for chronic stable angina when a reasonable trial of medication has failed to control symptoms.

The history of surgical revascularisation

The earliest surgical proposal for the relief of angina was in 1899 by Franck when he suggested cervical sympathectomy to divide the cardiac afferents and cause coronary vasodilatanon. It was not until the 71930s that augmentation of coronary blood flow was suggested as a treatment for angina.

Various attempts to provide additional blood to the myocardium were tried (omentopexy and induced pericardial adhesions) but were of little benefit. Vineberg pioneered an operation in which the internal mammary artery was dissected from its bed and the distal end implanted in the myocardium. This procedure was successful in some cases but gave inconsistent results and it is no longer performed. Cardiopulmonary bypass meant that it was possible to operate directly on the coronary arteries. The development of coronary angiography by Mason Somes led to the first CABG performed by Favorolo at the Cleveland Clinic in 1967. This was found to be an effective and reliable way to revasculanise the myocardium. The long saphenous vein is the most commonly used conduit, but the internal mammary artery is now used for the left anterior descending graft in over 60 per cent of cases.

Vessels with 70 per cent stenosis or more require bypassing. Stenoses of less than 50 per cent may not progress and there is no evidence that grafting is beneficial. The usual procedure is three to four grafts.

Choice of conduit

The patient's own saphenous vein and internal mammary artery are the conduits of choice but there is a small trend towards using other arterial conduits such as the gastroepiploic artery and the inferior epigastric artery. Other conduits such as human umbilical vein, bovine internal mammary artery and prosthetic grafts (Dacron and polytetrafluoroethylene) have disappointing patency rates of less than 50 per cent at 1 year.

The long saphenous vein graft (Fig. 48.47)

Although this graft has been used for over 25 years, there is a significant occlusion rate of 10-15 per cent at 1 year. Thereafter there is an occlusion rate of 2-3 per cent per annum. Low-dose aspirin from the time of operation reduces the graft occlusion rate.

The internal mammary graft (Fig. 48.48)

This graft has been accepted as the conduit of choice in terms of reliability, low occlusion rate and long-term patency. It can be adapted to the demands placed on it and provides excellent symptomatic relief.

The operation is usually performed with cardiopulmonary bypass (Fig. 48.49). The distal anastomosis is performed beyond the narrowing in the coronary vessel. Application of the aortic cross-clamp facilitates this by preventing blood flow down the coronary arteries. This renders the myocardiurn ischaernic but there are ways of minimising this which are discussed in the Myocardial protection section. Once the final distal anastomosis is completed, the cross-clamp is removed and the heart is reperfused with oxygenated blood. Rewarming is commenced and the final proximal anastomosis is completed. The patient is returned to the intensive care unit at the completion of the operation. There is a trend to try and avoid cardiopulmonary bypass in coronary artery surgery altogether. Coronary anastomoses are possible on the beating heart with the aid of appropriate stabilising devices. The advantage is that the patient avoids the potential damaging effects of cardiopulmonary bypass and therefore

has a shortened hospital stay. There is concern that the quality of the anastomosis may not be as good as those done on a completely still heart in a bloodless field. An extension of this principle is the development of port access surgery, where the operation is carried out through a small incision. The early results appear encouraging but the techniques have yet to gain widespread acceptance.

Postoperative complications are not uncommon following cardiac surgery. Many patients are ex-smokers or diabetic so respiratory infections and basal collapse are common after surgery, and should be treated aggressively with antibiotics and physiotherapy. Minor wound infections may need little attention, but major wound infections leading to sternal dehiscence and mediastinitis may be very difficult to treat. The risk of serious sternal infection increases in elderly and diabetic patients and in those undergoing bilateral internal mammary artery grafting.

Results of treatment

Relief of symptoms and functional capacity are significantly improved following surgery when compared with medical therapy alone. Patients with impaired left ventricular function have a poor natural history, and it is this group that benefits most from surgical revascularisation. The hospital mortality rate has increased slightly to 3-4 per cent as a result of operating on older patients and those with impaired ventricular function. There is no doubt that the internal mammary artery improves patient survival and has a superior long-term patency over other conduits.

Up to 80 per cent of patients have complete relief of symptoms and require no further medication. Unfortunately, angina may return as a result of the following:

· graft thrombosis;

· anastomotic stenosis;

· conduit atherosclerosis;

· progression of native disease.

Attention is paid to secondary prevention of progressive disease and return of symptoms requires careful evaluation. There is clear evidence that cholesterol lowering (even in those who have a normal cholesterol) significantly reduces the progression of atherosclerosis in saphenous vein grafts. Developments in cardiology and therapeutics mean that patients have a wide range of options before reoperation is considered. Many patients respond to medical treatment but some require redo surgery. This is associated with an increased operative mortality and is only recommended for patients with severe symptoms. It is hoped that the use of arterial conduits will reduce the need for redo surgery, although this remains to be seen.

Surgery for the complications of myocardial infarction

Myocardial infarction leads to myocyte necrosis which may heal to form scar tissue or rupture if the ventricular wall gives

way. Free rupture of the ventricle is usually fatal in spite of treatment, but intramyocardial rupture gives rise to a number of mechanical problems that have a very high mortality without surgery. The myocardial rupture rate is less than 2 per cent with the distribution in proportion to the relative risk. Free wall rupture is the most common, followed by ventricular septal rupture and then papillary muscle rupture.

Ventricular septal rupture (Fig. 48.50)

This occurs following an anterior or inferior infarct affecting the ventricular septum. The patient typically presents with an infarction and 3-7 days later develops pulmonary oedema with a pansystolic murmur and hypotension. The prognosis is dismal without surgery but operation carries a mortality rate of up to 40 per cent. The diagnosis is confirmed by transoesophageal echocardiography or Swan-Ganz cathetenisation (the degree of left-to-right shunting can be calculated using this technique). The patient requires stabilisation and myocardial support (inotropes, renal dopamine and intraaortic balloon pump counterpulsanion) before surgical repair if this is indicated. The repair is undertaken with the aid of cardiopulmonary bypass and a penicardial patch or an artificial graft may be used to facilitate repair.

Papillary muscle necrosis (Fig. 48.51)

This occurs with full-thickness myocardial papillary muscle necrosis. The patient develops a pansystolic murmur and pulmonary oedema. Unlike chronic mitral regurgitation, where the left ventricle has time to adapt to the increased

volume load, the left ventricle is acutely overloaded and failure results. Diagnosis is made by echocardiography and right heart catheterisation (showing large V waves). Mitral valve replacement is usually necessary, but the mortality is higher than in valve replacement for rheumatic heart disease as a result of the associated coronary artery disease.

Ventricular aneurysm (Fig. 48.52)

Partial-thickness necrosis of the ventricular wall may result in the development of a ventricular aneurysm if the free wall is replaced by noncontractile fibrous tissue. Left ventricular function is affected because the fibrous wall balloons out during systole and reduces the actual stroke volume. Repair is undertaken using cardiopulmonary bypass and CABG is undertaken at the same time if necessary.

Some patients develop refractory cardiac failure from a variety of causes that are not amenable to surgery because of poor left ventricular function. These patients should be considered for heart transplantation.