Mortality

Risk stratification is important in cardiac surgery and Euroscore is a valuable tool for quantifying operative risk across all types of non-congenital cardiac surgery. Patient, condition, and procedure related factors contribute to a score which predicts 30-day mortality. Predicted operative mortality ranges from < 1% for routine elective procedures to more than 50% for complex emergency operations.

Stroke

Stroke risk varies from 1% to over 10%, and is associated with intracardiac thrombus and severe atheromatous disease of the proximal aorta and carotids. Patients with evidence of peripheral vascular disease have a higher risk of stroke and those with high-grade symptomatic carotid disease may benefit from carotid endarterectomy prior to cardiac surgery (Ch. 21).

Cardiopulmonary bypass (CPB)

Modern cardiac and great vessel surgery became feasible with the development of cardiopulmonary bypass. Venous blood is drained via cannulae inserted into the right atrium or venae cavae and passes to a reservoir. It is then pumped through an oxygenator, which adds O₂ and removes CO₂, through a heat exchanger coil so that its temperature can be varied and finally, the blood is returned to the arterial circulation via a cannula in the ascending aorta or other suitable artery (femoral, axillary) (Figs 22.1, 22.2 and 22.3). Full anticoagulation with intravenous heparin is required to prevent blood clotting in the tubing, oxygenator and pump mechanisms. Roller or centrifugal pumps are used, as these minimize red cell trauma. Semipermeable membranes, or more commonly hollow fibres, form the blood–gas interface within the oxygenator. A trained perfusion technician controls the bypass machine.

Fig. 22.1 Normal cardiac chambers.

(LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle; PA = pulmonary artery).

Fig. 22.2 Schematic of a bypass circuit.

Fig. 22.3 Cannulation for cardiopulmonary bypass.

Upper arrow from right atrium to pump. Lower arrow from pump to aorta.

CPB stimulates a systemic inflammatory response mediated by cytokine release, complement activation and white cell activation. These changes do not generally cause clinical problems but may be implicated in post-bypass pulmonary, renal and cerebral dysfunction. Cerebral damage occurs in about 1% of cases due to intracerebral bleeding, embolization of microbubbles or arterial debris, or inadequate cerebral perfusion. Subtle deterioration in cerebral function, as detected by psychological testing, is more frequent. Coagulopathy and haemolysis are associated with prolonged bypass.

Myocardial preservation

Intensive care

Postoperatively, patients are usually ventilated for a few hours until they are fully rewarmed, and have satisfactory stable haemodynamics, pulmonary gas exchange and acid–base status. Urine output is copious and potassium levels are, therefore, checked frequently so that potassium is administered intravenously to correct urinary losses. Invasive measurement of arterial and central venous pressure is standard. Pulmonary artery catheters may be used to measure pulmonary artery pressure, pulmonary artery capillary wedge pressure and cardiac output.

Complications

Other than death or stroke, established complications include:

Recovery time

Patients undergoing routine elective coronary or valve surgery will usually leave acute hospital care within one week. Those requiring more extensive surgery or emergency procedures may take longer to recover. Most patients will have undergone a median sternotomy (Fig. 22.4). This wound heals quickly and, as the sternal edges are approximated securely by wire or heavy sutures, chest discomfort eases rapidly. Leg vein donor sites may take longer to heal, particularly around the knee. By 2 weeks the patient should be able to walk a few hundred metres, and by 3 months should have returned to full activity, including work.

Fig. 22.4 Surgical approach to the heart.

A Median sternotomy incision. B Right atrium and ascending aorta exposed.

Assessment

Exercise electrocardiography (ECG) is often used as an initial screening test for patients with suspected stable angina. Those with confirmed ischaemia then undergo coronary angiography and assessment of left ventricular function by means of angiography or echocardiography. Contrast medium is injected into the coronary circulation (Fig. 22.5) via a catheter that is usually inserted through the femoral or radial artery (Fig. 22.6). Images are obtained in several different planes so as to minimize the risk of missing eccentric lesions. Intervention is usually only advised for stenoses that exceed a 70% reduction in vessel diameter.

Fig. 22.5 Coronary circulation.

Fig. 22.6 Coronary angiography.

A Left coronary angiogram demonstrating severe left main stem stenosis. B Right coronary angiogram demonstrating multiple stenoses.

Indications

Elective surgery is indicated primarily for the control of angina that is refractory to medical treatment and is unsuitable for percutaneous intervention (PCI) usually with stent insertion. Historically, patients with three-vessel disease or left main stem disease have exhibited a high (c. 8% per year) risk of death from MI with medical therapy alone. Surgery improves long-term survival for such patients, particularly when LV function is also impaired. PCI has an important role in the management of patients with acute coronary syndrome ranging from ST elevation myocardial infarction to unstable angina.

Some patients requiring other cardiac procedures may be shown to have significant coronary disease during cardiological assessment. In these cases, coronary surgery may be added to the primary procedure to improve perioperative survival and prevent future ischaemic problems. Emergency coronary surgery is rare and patients with incipient or established MI fare better with PCI and supportive medical therapy, as the mortality of surgery in this setting is much increased.

Coronary bypass

A coronary artery bypass graft (CABG) delivers blood to the distal coronary artery beyond a stenosis. If the distal artery is obliterated by atheroma, an endarterectomy procedure may be performed to restore the lumen. Originally, nearly all grafts comprised reversed segments of the long saphenous vein anastomosed proximally to the ascending aorta and distally to the coronary artery. Such grafts have patency rates of around 70% at 5 years and 40% at 10 years. Venous graft failure occurs as a result of intimal hyperplasia, which is thought to be, in part at least, a response to arterial pressure. The relatively high rate of vein graft failure stimulated interest in arterial grafts and led to the almost universal use of the internal thoracic artery (ITA). This is usually employed as a pedicled graft when it is left attached to the subclavian artery proximally, but can also be used as a free graft in the same manner as vein. ITA graft patency exceeds 90% at 5 years and 70% at 10 years. A common combination is to use the left ITA for the left anterior descending artery and vein grafts for the other vessels (Fig. 22.7).

Fig. 22.7 Completed coronary bypass procedure with venous and left internal thoracic artery grafts in situ.

The radial artery is a possible option as a free graft for use in people with poor-quality saphenous vein and critical proximal occlusion of more than 70% in the target vessel, and may be used together with ITA grafts to achieve ‘total arterial revascularization’. Occasionally, when there is a shortage of good conduit (e.g. in a ‘redo’ operation), the surgeon may consider using the right gastroepiploic artery, the short saphenous vein and the cephalic vein. Prosthetic grafts occlude early and are not used.

Results

Uncomplicated coronary surgery should carry a 2–3% risk of mortality and a 1–2% risk of stroke. Angina is relieved completely in about 70% of cases, is significantly improved in the remainder, and recurs with a frequency of about 10% per year. Successful revascularization may also improve breathlessness if it is related to myocardial ischaemia, and survival is probably enhanced in patients with left main stem and triple vessel disease. The use of arterial conduits is associated with better graft patency and improved survival. Although there is a trend in that direction for patients with multiple arterial grafts followed up beyond 10 years, the added benefit over one ITA graft placed to the left anterior descending coronary is small. This may reflect the progression of native coronary disease. Secondary prevention is mandatory in all patients with CAD and includes antiplatelet medication (aspirin) and cholesterol reduction (statin) (EBM 22.1).

Mitral valve regurgitation (MR)

Postmyocardial infarction ventricular septal defect

Necrosis of the intraventricular septum due to MI may lead to a ventricular septal defect. Blood flows from the high-pressure left to the low-pressure right ventricle (left-to-right ‘shunt’). This increases right ventricular work and pulmonary blood flow and decreases cardiac output. Typically, the patient complains of sudden, severe breathlessness 3–8 days after an MI and is noted to have developed a pansystolic murmur. The diagnosis is confirmed by echocardiography and coronary angiography is performed. Emergency repair is technically difficult due to the poor quality of the recently infarcted muscle to which the patch is attached. In addition, these patients have impaired cardiac function in the aftermath of an acute MI. Typically, such patients will require mechanical support of their ventricle with an intra-aortic balloon pump. Surgical mortality ranges from 20–50%. Patients with minor shunts are managed medically and may be considered for surgery some weeks later to allow cardiac function to stabilize. The margins of the defect will have healed by fibrosis, making patch repair relatively straightforward with more acceptable operative mortality (< 10%).

Left ventricular aneurysm

LV aneurysm complicates about 8% of MIs and occurs when a large left ventricular free-wall MI scar becomes aneurysmal as a result of intraventricular pressure. A large aneurysm impairs cardiac contraction and increases myocardial work. Complications include clot formation within the aneurysm, which may embolize, and arrhythmias generated within the zone of ischaemic myocardium around the periphery of the aneurysm.

At operation, the aneurysm is excised, the clot removed and the resulting defect usually closed by direct suture, reinforced by buttressing strips of Teflon felt or vascular graft. Occasionally, a small patch repair is performed to preserve the shape of the left ventricle. Surgery performed electively has a mortality of 6–10% and an increased risk of stroke.

Stenosis

Aortic stenosis is the commonest indication for valve surgery in the UK. Although rheumatic disease remains a common problem in underdeveloped countries, the most frequent aetiology in the Western world is calcific aortic stenosis which develops in the older population usually over 70 years. The normal aortic valve has three cusps but a congenital bicuspid valve usually calcifies from the sixth decade onwards (Fig. 22.10). Aortic stenosis causes left ventricular hypertrophy, effort angina, episodes of arrhythmia with syncope or even sudden death, and left ventricular failure.

Fig. 22.10 Calcified aortic valve.

Clinically, the patient has a slow rising pulse, a forceful apex beat and an ejection systolic murmur in the right upper parasternal area that may radiate to the root of the neck. Echocardiography will confirm a valvular gradient, which is considered severe aortic stenosis when this exceeds 60 mmHg. However, measurement of orifice area is independent of cardiac output and may be a more reliable measure. The onset of symptoms should initiate referral for surgery. Patients with cardiac failure have a low cardiac output and consequently a low gradient. In these cases, the decision to operate may be a difficult judgement, based on the absence of any other likely cause of poor left ventricular function and echocardiographic evidence of severe aortic valve disease.

In high risk patients e.g. the very elderly, those with patent ITA grafts or significant other co-morbidities, percutaneous replacement of the aortic valve may be considered (TAVI – transcatheter aortic valve insertion) where a biological valve on a holder is introduced percutaneously via the femoral artery or left ventricular apex.

Regurgitation

Native aortic regurgitation may be due to primary valve pathology (rheumatic fever, endocarditic valve destruction or, rarely, a bicuspid valve) or secondary to aortic root pathology with annular dilatation (see below). Prosthetic valve regurgitation can occur as a result of deterioration of a biological prosthesis, partial obstruction of a mechanical device, or paraprosthetic leakage. Chronic aortic regurgitation causes progressive left ventricular dilatation and hypertrophy.

Clinically, there is a wide pulse pressure – collapsing pulse, lateral displacement of the apex beat and a diastolic murmur in the left parasternal area. Chronic aortic regurgitation is well tolerated and often asymptomatic. In severe cases, the patient may complain of dyspnoea and angina, and may exhibit features of congestive cardiac failure. Surgery is advised to forestall the onset of cardiac failure due to irreversible myocardial damage. The timing of surgery is determined by serial echocardiography measurements demonstrating left ventricular dilatation.

Acute aortic regurgitation produces severe dyspnoea, with rapid onset of left ventricular failure and pulmonary oedema. The patient may require emergency ventilation and urgent surgery.