Introduction

Coronary artery disease is one of the major causes of death worldwide, caused by narrowing of the coronary arteries due to the gradual deposition of plaque. The main aim of this chapter is to familiarise the reader with the concepts of ischaemic heart disease and coronary artery disease and the principles of its medical and surgical management.

The reader should gain an understanding of:

• What coronary artery disease is

• The principles of diagnosis and investigation

• How to treat coronary artery disease with medication

• How to treat coronary artery disease with percutaneous intervention (angioplasty or stenting)

• How to treat coronary artery disease with surgery.

The pathophysiology of coronary artery disease

Coronary artery disease (CAD) is caused by the degenerative disease atherosclerosis, which is characterised by plaque formation and fibrosis of the arterial tree. Atheromatous lesions typically develop in three distinct stages (Libby, Ridker & Hansson 2011):

Stage 1, fatty streaks: Initially, blood macrophages migrate into the intima of an artery and mature into lipid-yielding foam cells. Smooth muscle cells start to migrate into the vessel’s endothelial layer and proliferate. These ‘fatty streaks’ appear as a yellow streak running along major arteries, such as the aorta, but do not cause any symptoms.

Stage 2, fibrolipid plaque: More smooth muscle cells migrate into the arterial intima and synthesise extracellular matrix such as collagen and elastin, creating a fibrous cap. Extracellular lipid from dead cells and cholesterol crystals can accumulate in the central region of a plaque, the lipid core. Advancing plaques cause narrowing of the lumen of the blood vessel.

Risk factors

Risk factors for coronary artery disease were established for the first time by the Framingham Heart Study in 1961 (Kannel et al. 1961). Understanding of such factors is critical to prevent cardiovascular morbidity and mortality.

The non-modifiable risk factors for coronary artery disease include:

• Age: Increasing age – over 45 years in men and over 55 years in women

• Gender: Men are generally at greater risk of coronary artery disease, although the risk for women increases after menopause

• Family history: The risk of developing coronary artery disease is highest if the father or brother of the patient was diagnosed with heart disease before the age of 55 or if the mother or a sister developed it before the age of 65

• Race: The cardiovascular death rate for African Americans is reported to be particularly high; Asians and South Asians appear to have a higher independent risk for cardiovascular disease.

Reversible or modifiable risk factors for coronary artery disease include:

• Smoking: Smokers have a significantly increased risk of coronary artery disease (Stallones 2015) but exposure to passive smoking can also increase the risk; cessation of smoking is the most important preventive measure for CAD

• Diabetes

• High blood pressure

• High blood cholesterol levels increase the risk of formation of atherosclerotic plaques.

• High cholesterol can be caused by a high level of low-density lipoprotein, known as the ‘bad’ cholesterol. A low level of high-density lipoprotein, known as the ‘good’ cholesterol, can be a risk factor as well.

• Overweight or obesity, which typically worsens other risk factors. Physical inactivity is also associated with coronary artery disease.

• The Framingham study has revealed other medical conditions that can contribute to coronary artery disease, such as end-stage renal disease, chronic inflammatory diseases affecting connective tissues (e.g. lupus, rheumatoid arthritis) and human immunodeficiency virus infection on highly active antiretroviral therapy (Kannel et al. 1961).

• Researchers are currently examining the role of novel risk factors, including sleep apnoea, high sensitivity C-reactive protein, lipoprotein (a), fibrinogen and homocysteine (Yeboah et al. 2014).

Typical symptoms of ischaemic heart disease are angina, dyspnoea and nausea. Exertional angina is very common and is caused by the reduction of the coronary flow reserve by atherosclerosis.

Angina is graded by severity according to the Canadian Cardiovascular Society Classification (2018):

• Class I – No limitation of physical activity and no symptoms with ordinary activity

• Class II – Slight limitation, with angina only during vigorous physical activity

• Class III – Symptoms with everyday living activities, i.e. moderate limitation

• Class IV – Inability to perform any activity without angina or angina at rest, i.e. severe limitation.

Dyspnoea is graded in the same way as angina, according to the New York Heart Association (2017) classification:

• Class I – Cardiac disease, but no symptoms and no limitation of ordinary physical activity

• Class II – Mild symptoms and slight limitation during ordinary physical activity

• Class III – Marked limitation of ordinary activity due to symptoms

• Class IV – Severe limitation of ordinary activity, symptoms with mild activity or even while at rest.

Acute coronary syndrome

Acute coronary syndrome (ACS) is a group of clinical conditions caused by acute myocardial ischaemia. Ischaemia is generally defined as cell damage caused by insufficient oxygen supply. This can progress to infarction, which is defined as cell death caused by a mismatch between oxygen supply and demand.

ACS includes unstable angina (non-ST elevation myocardial infarction or NSTEMI) and (ST elevation myocardial infarction) and is typically caused by a ruptured atherosclerotic plaque causing thrombosis and impairment of the blood flow in a coronary artery.

• Unstable angina is defined as angina occurring with increased frequency or severity, occurring at rest or at night and is not quickly relieved with glyceryl trinitrate. There can be transient electro cardiogram changes, but troponin is normal.

• Non-ST segment elevation MI is closely related to unstable angina but with infarction of myocardium as indicated by elevated troponin levels. The ECG can be normal or demonstrate transient ST changes.

• ST segment elevation MI is caused by acute vessel occlusion causing ST elevation or Q waves in the ECG in association with elevated troponin levels and chest pain lasting longer than 20 minutes.

The acute medical management of patients with unstable angina (NSTEMI) aims to stabilise the plaque, restore coronary blood flow and alleviate symptoms. It consists of administering oxygen, nitrates or other antianginals, analgesia, low-molecular weight heparin and dual antiplatelet therapy.

The definitive treatment depends on individual angiographic findings and symptoms. The required treatment may include:

• Percutaneous coronary intervention (PCI) – if there are lesions that are considered culprits and amenable to PCI

• Urgent coronary artery bypass grafting (CABG) surgery – in multivessel disease or left main stem disease, patient may be referred for urgent in-house CABG.

In addition to the medical management, patients with STEMI may receive primary PCI (or sometimes thrombolysis if PCI is not available) to restore coronary blood flow. Multidisciplinary team discussion in a heart team may be needed to decide the best option.

Investigations for CAD

Patients with coronary artery disease referred for coronary artery bypass graft surgery are seen either in elective preoperative assessment clinics or they have their preoperative work-up carried out as inpatients if their procedure is performed urgently after admission with myocardial infarction. The first steps in patient assessment are taking a thorough history and carrying out a physical examination. Important points to elicit in the patient’s history are the onset and severity of their symptoms, their cardiovascular risk factors, any previous cardiac events or surgical procedures as well as major comorbidities such as chronic obstructive pulmonary disease, chronic kidney disease, peripheral vascular disease or previous cerebrovascular accident events. Important points to establish when considering conduit suitability are a history of varicose veins, previous deep vein thrombosis, peripheral vascular diseases, Raynaud’s disease and whether the patient is left- or right-handed.

A general examination will focus on the presence of any cardiorespiratory problems as well as possible conduit problems (such as varicose veins, chest wall procedures or radiation, previous vein harvesting for other surgical procedures). Patients will undergo a standard panel of blood tests consisting of full blood count, urea and electrolytes, lung function tests, complete coagulation screen, fasting glucose, lipid screen, and group and save. A chest radiograph is taken to screen for pulmonary pathology as well heart failure features or aortic abnormalities. Pulmonary function testing is indicated for high-risk patients (such as smokers and those with known respiratory disease) and patients at risk of carotid stenosis (e.g. previous CVA, carotid bruit, left main stem disease or peripheral vascular disease) will require preoperative carotid duplex scanning. A recent echocardiogram is required to assess for heart valve disease and establish the ventricular systolic and diastolic function.

Coronary angiography

In special circumstances, the viability of the affected myocardium is assessed with dobutamine stress-echo or cardiac MRI to guide revascularisation. On cardiac MRI, a scar involving >50% thickness of the LV wall, is unlikely to recover useful contractile function with revascularisation while <50% scarring indicates recoverable contractile function by revascularisation. Perfusion scanning with technetium-99m sestamibi and thallium-201 or single-photon emission computed tomography may be used to assess ischaemic muscle mass (Carrascosa & Capunay 2017). LV muscle mass ischaemia of >10% is used as indication for surgery if there is no angina (e.g. diabetes) or in redo CABG. In patients with a previous history of cardiac surgery, who will undergo redo sternotomy, a CT scan with contrast should be performed to identify the position of previous grafts and the anatomical relation of the right ventricle to the sternum.

Medical management of CAD

The mainstay of coronary artery disease treatment is the use of drugs to reduce plaque formation and stabilise the atherosclerotic plaques.

Antiplatelet medications

1. Aspirin: Aspirin blocks the platelet adhesion irreversibly by inhibiting the enzyme cyclooxygenase. It should be given to all patients with known coronary disease or angina. When used for secondary prevention, ‘Aspirin reduces all-cause mortality by 18%, reduces the number of strokes by 20%, myocardial infarctions by 30%, and other vascular events by 30%’ (Aronson 2015, p. 27).

2. Clopidogrel and ticagrelor: Clopidogrel and ticagrelor act by inhibiting the adenosine diphosphate receptor on platelet cell membranes. Clopidogrel is a prodrug, which requires CYP2C19 in liver for its activation, while ticagrelor does not need activation. Clopidogrel specifically and irreversibly inhibits the P2Y12 subtype of adenosine diphosphate receptor, which is important in activating platelets and eventual cross-linking by the protein fibrin (Wijeyeratne & Heptinstall 2011).

Ticagrelor binds reversibly as it is an allosteric antagonist and therefore acts for a shorter time. Both ticagrelor and clopidogrel are used to prevent heart attack and stroke in people with a history of myocardial infarction, acute coronary syndrome, stroke and peripheral artery disease. They are also recommended for 12 months following implantation of drug-eluting stents, along with aspirin. Side effects include GI bleeding. The Platelet Inhibition and Patient Outcomes Trial found that ticagrelor had better mortality rates than clopidogrel (9.8% vs 11.7%, p<0.001) in treating patients with acute coronary syndrome (Cannon et al. 2010).

4. Beta blockers: These reduce the cardiac work by reducing heart rate and myocardial oxygen demand. They are also proven to reduce morbidity and mortality in acute MI (Kezerashvili, Marzo & De Leon 2012).

5. Nitrates: These drugs cause veno-dilatation and reduce cardiac preload. They are also useful for immediate relief in an acute angina attack. They can be given sublingually, via a spray or tablet or in sustained-release formulations for longer effect. Their usefulness is limited by development of tolerance due to tachyphylaxis (Soman & Vijayaraghavan 2017).

6. Calcium channel blockers: These interfere with the inward displacement of calcium ions through the slow channels of active cell membranes. They influence the myocardial cells, the cells within the specialised conducting system of the heart, and the cells of vascular smooth muscle. Thus, myocardial contractility may be reduced; the formation and propagation of electrical impulses within the heart may be depressed; and coronary or systemic vascular tone may be reduced. Calcium channel blocker brands include: Verapamil, Nifedipine, Lacidipine, Diltiazem (Godfraind 2017). These are the vasodilators that are commonly used in chronic stable angina.

7. Angiotensin-converting enzyme inhibitors: These cause relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart. They inhibit the angiotensin-converting enzyme, an important component of the renin–angiotensin system. These drugs are especially useful for patients with low ejection fraction, and those with heart failure and diabetes.

8. Angiotensin II receptor blockers: Their main uses are in the treatment of hypertension (high blood pressure), diabetic nephropathy (kidney damage due to diabetes) and congestive heart failure. They block the activation of AT1 receptors, preventing the binding of angiotensin II. They can be used when the patient is intolerant of ACE inhibitor therapy. They do not inhibit the breakdown of bradykinin or other kinins and are thus only rarely associated with the persistent dry cough and/or angioedema that limit ACE inhibitor therapy.

Coronary angioplasty and stenting

Sometimes, when the plaque is particularly hard, or the artery is so narrow that the balloon can’t pass through it, rotablation may be used. Again, a very fine wire is guided through the narrowing. After this, a special catheter is inserted along the wire with a tiny drill at its tip, powered by compressed air.

PCI may be appropriate for patients with stable coronary artery disease if they meet certain criteria, such as having any coronary stenosis greater than 50% or having angina symptoms that are unresponsive to medical therapy, with low SYNTAX scores (Singh 2010). Although, for patients with stable coronary artery disease, PCI may not provide any greater help in preventing death or myocardial infarction than oral medication, it probably provides better relief for angina.

In ST-segment elevation myocardial infarction, using primary PCI to open the culprit-occluded vessel can be critical for survival, as it reduces deaths, myocardial infarctions and angina (compared with oral medication).

Surgical management of CAD

Coronary artery bypass grafting surgery

Coronary artery bypass grafting is usually done for multiple stenoses in coronary artery disease which cannot be treated with stents – for example, calcified vessels or long segments of stenosis or where surgery provides better survival/symptom relief than PCI (e.g. CAD with impaired LV function, diabetics, high SYNTAX score or left main stem disease).

The Surgery or Stent trial was a randomised controlled trial that compared CABG to PCI with bare-metal stents. The Surgery or Stent trial demonstrated that CABG was superior to PCI in multivessel coronary disease (Hirshfeld & Fiorilli 2016).

The Synergy between PCI with Taxus and Cardiac Surgery (SYNTAX) trial was a randomised controlled trial of 1800 patients with multivessel coronary disease, comparing CABG versus PCI (in a 1:1 ratio) using drug-eluting stents. The study found that rates of major adverse cardiac or cerebrovascular events at 12 months were significantly higher in the drug-eluting stents group (17.8% vs 12.4% for CABG; P = 0.002). This difference was primarily driven by the higher need for repeat revascularisation procedures in the PCI group with no difference in repeat infarctions or survival. Higher rates of strokes were seen in the CABG group (Serruys et al. 2009).

The FREEDOM (Future Revascularisation Evaluation in Patients with Diabetes Mellitus—Optimal Management of Multivessel Disease) trial showed CABG was superior to drug-eluting stents in patients with diabetes with multivessel disease (Farkouh et al. 2012).

Indications for surgery

1. Class I recommendations (Hillis et al. 2011):

• Significant (>50% diameter stenosis) left main coronary artery stenosis (level of evidence: B)

• Significant (>70% diameter) stenosis in 3 major coronary arteries (level of evidence: B)

• In survivors of sudden cardiac death with presumed ischaemia-mediated ventricular tachycardia caused by significant (>70% diameter) stenosis in a major coronary artery (level of evidence: B).

2. Class IIA recommendations (Hillis et al. 2011):

• Significant (>70% diameter) stenosis in 2 major coronary arteries with severe myocardial ischaemia (e.g. on stress testing, abnormal intracoronary haemodynamic evaluation, or >20% perfusion defect by myocardial perfusion stress imaging) or target vessels supplying a large area of viable myocardium (level of evidence: B)

• In patients with mild to moderate LV systolic dysfunction (EF 35–50%) and significant (>70% diameter stenosis) multivessel CAD or proximal LAD coronary artery stenosis, when viable myocardium is present in the region of intended revascularisation

• CABG with a LIMA graft is reasonable in patients with significant (>70% diameter) stenosis in the proximal LAD artery and evidence of extensive ischaemia (level of evidence: B)

• Patients with complex 3-vessel CAD (e.g. SYNTAX score >22), with or without involvement of the proximal LAD artery, who are good candidates for CABG (level of evidence: B)

• Patients with multivessel CAD and diabetes mellitus, particularly if a LIMA graft can be anastomosed to the LAD artery (level of evidence: B).

Grafts required for surgery

Grafts, such as internal mammary artery, radial artery, greater saphenous vein and short saphenous vein, can be harvested during the surgery. The number of grafts required for the surgery will depend on the number of significant blocked coronary arteries needing revascularisation.

Saphenous vein harvesting

The greater saphenous vein (GSV) is routinely harvested for CABG surgery due to its anatomical location and the length readily available. The vein can be harvested either using traditional open vein harvesting or endoscopic vein harvesting.

Open vein harvesting

The surgical care practitioner or the operating surgeon will assess the donor leg preoperatively for any contraindications for harvesting the greater saphenous vein. The number of grafts will be confirmed with the surgical team during the World Health Organisation checklist team briefing before surgery (WHO 2016).

The skin should be incised over the whole length of the vein to the required length and careful dissection is required to isolate the vein in situ. Attention should be given to avoid any unnecessary trauma to the vein or its tributaries. It is particularly important not to traumatise the saphenous nerve which runs along the saphenous vein as far as the knee area. Side branches should be ligated and clipped with 4/0 Vicryl ties on the vein side and mosquito clips on the patient side. All the branches on the patient side should be ligated with 4–0 Vicryl ties and haemostasis carefully completed.

Precautions needed while tying the GSV branches:

• The branches of GSV should be left approximately 1cm long

• Remember to tie the branches at least 1–2mm away from the main GSV.

Closure of the leg:

• After careful haemostasis, the subcutaneous fat layer needs to be closed with 2-0 Vicryl absorbable suture

• The tissue should be caught in the same quantity on both sides of the leg incision site to approximate the edges properly and to eliminate dead space, which could lead to postoperative complications, such as infection

• The skin needs to be closed with 3-0 Monocryl suture

• The wound and surrounding area needs to be cleaned with the wet, clean swab

• The incision should dry, ensuring no collection of blood in the wound by pressing the site from thigh to ankle

• Check the instruments/needles/swabs according to the local hospital policy.

Note: If leg haemostasis is questionable or in doubt, use leg drains. Tie all the vein branches in the leg (rather than using metal clips for haemostasis) because the sutures will get absorbed, thus reducing the risk of infection.

Common complications of the donor leg after surgery:

• Postoperative pain

• Delayed rehabilitation

• Haematoma

• Bleeding, dehiscence of the wound

• Infection

• Cellulitis/necrosis/abscess/neuropathies.

Important points to bear in mind during open vein harvesting:

• Dissection of tissues should be minimal

• Carry out meticulous haemostasis and close the leg before full heparinisation of the patient

• The skin should be closed with minimal tension

• Minimally invasive vein harvesting, such as bridging, is preferable; endoscopic should be considered for all patients unless it is contraindicated due to severe varicose veins or if there is no other conduit available for the patient except GSV.

Radial artery harvesting

Allen test

It is very important to perform the Allen test to confirm the patency of the ulnar artery. If there is no collateral flow through the ulnar artery, radial artery puncture is contraindicated, since it can result in a gangrenous finger or loss of the hand from spasm or clotting of the radial artery. The Allen test is performed with the patient sitting with their hands supinated on their knees.

Stand at the patient’s side with your fingers around their wrist; and compress the tissue over both radial and ulnar arteries. Allow a few minutes for the blood to drain from the hand while the patient opens and closes their hands several times. Release the pressure on the ulnar artery while keeping the radial artery occluded. Normal skin colour should return to the ulnar side of the palm in seconds, followed by quick restoration of normal colour to the entire palm. A hand that remains white indicates either absence or occlusion of the ulnar artery, and radial artery puncture is contraindicated (Duke 2011).

• Positive modified Allen test – if the hand flushes within 5–15 seconds, it indicates that the ulnar artery has good blood flow; this normal flushing of the hand is a positive test.

• Negative modified Allen test – if the hand does not flush within 5–15 seconds, it indicates that ulnar circulation is inadequate or non-existent; in this situation, the radial artery supplying arterial blood to that hand should not be punctured.

Harvesting

Before harvesting the radial artery, make sure the patient has a satisfactory Allen’s test and make sure the anaesthetist is clear about which radial artery is to be harvested. A radial arterial line must be placed on the contralateral site. To expose the radial artery, an incision is made from approximately 2cm below the brachial pulse in the antecubital crease, to the radial pulse at the wrist crease, parallel to the medial edge of the brachioradialis muscle. The subcutaneous tissue is divided with diathermy down to the fascia of the flexor carpi radialis muscle. The fascial sheath is divided between the brachioradialis muscle and the flexor carpi radialis. Care must be taken to prevent injury to the lateral cutaneous nerve of the forearm nerve by displacing the nerve laterally (Blitz, Osterday & Brodman 2013).

Left internal mammary artery harvesting

Surgical technique

Median sternotomy incision is carried out using a sternal saw and thymic fat is divided to ensure good haemostasis of the thymic veins. An asymmetric left internal mammary artery (LIMA) sternal retractor is used to elevate the left hemisternum. Various retractors can be used for this purpose, most commonly the Delacroix-chevalier retractor. Another useful one is the Rultract^® Skyhook Retractor which does not depress the right hemisternum.

The operating table is usually turned away from the surgeon and elevated to the appropriate height to take pressure off the surgeon’s neck and back. The operating light is adjusted or, preferably, a headlight is routinely worn by the surgeon.

The pleural reflection is bluntly dissected from the anterior chest wall using a swab. Some surgeons like to leave the pleura intact by simply pushing it away from the endothoracic fascia. This keeps the lung away from the operative field and helps reduce the incidence of postoperative pleural effusion and left lower lobe atelectasis. Most surgeons open the left pleural space fully for good exposure and the lung can be pushed down with a swab while harvesting the LIMA. This helps to avoid postoperative pericardial effusions and kinking of the LIMA once it is anastomosed into the heart.

The landmarks for harvesting are the subclavian vein near the apex and the LIMA bifurcation near the xiphisternum. The phrenic nerve is very close to the apex and should therefore be protected. The LIMA can be harvested using electric diathermy or a harmonic scalpel which uses ultrasonic vibrations.

A large mediastinal branch of the LIMA may be found running towards the precardial fat tissue and this should be secured with clips to avoid excessive bleeding. Pulsation of the artery may be visualised or manually palpated during harvesting.

The LIMA runs approximately 1.5cm lateral to the sternal edge, between the two veins, in the extra-pleural space behind the transversus thoracic muscle. Towards the apex, the LIMA can sometimes come off the chest wall and should be watched carefully to avoid inadvertent injury. The medial aspect of the endothoracic fascia is then incised at the most accessible portion of the LIMA, usually level with the middle third, and two tram lines are made on either side of the LIMA.

The dissection may be started at any point along the LIMA, which is easily visible. The artery should not be handled directly (to avoid vasospasm). The fascia or the vein is usually used for retraction, with a DeBakey forceps. The first intercostal artery should be ligated to avoid the so-called ‘steal phenomenon’. The LIMA can be harvested using either the skeletonised or pedicle harvesting techniques.

The skeletonised LIMA is harvested on its own without any of the accompanying veins or fat/tissues. The main advantages of this technique include longer length, ease of doing jump grafts/T grafts and doppler assessment of grafts by transit time flow measurement (TTFM). The disadvantages include longer time needed for harvesting and a higher chance of injury due to the close proximity of dissection to the LIMA.

Downward traction is applied on the fascia, and the artery is gently separated from the veins using blunt dissection with cold diathermy spatula. The LIMA branches are ligaclipped on both sides (chest wall and on the artery) and divided with a fine straight Pott’s scissors. Diathermy is sparingly used, away from the artery. The diathermy setting can vary from 20 to 25, according to the surgeon’s preference. The medial branches are divided first, followed by superior and then lateral branches from the chest wall. Dissection is carried out along the entire course of the artery.

Pedicled harvesting

A longitudinal tram track – fascial incision – is made approximately 1cm lateral and medial to the artery. The artery is harvested as a pedicle, including the fascia, muscle, connective tissue and both veins. The dissection is started on the cartilage, as there are no branches of the artery. The entire pedicle is detached from the chest wall. Sternal perforating arteries are cauterised or clipped, depending on the size of the branches. Downward traction is applied on the fascia of the pedicle with Debakey forceps and ligaclips are applied to the branches towards the LIMA. Electrocautery is then used towards the chest wall side for securing haemostasis. Once the dissection is completed across the pedicle, a closed forceps or finger may be used to provide downward traction and facilitate the exposure. Dissection is carried out along the entire course of the artery.

Final steps

Once the dissection is completed and haemostasis from the chest wall has been checked, heparin is given by the anaesthetist and the distal end of the LIMA is clamped with a Roberts surgical clamp or right-angled surgical clamp and divided proximally to assess the flow. A non-crushing bulldog vascular clamp is applied, and the LIMA is wrapped in a soaked swab (with or without papaverine) to help minimise any vasospasm. The use of vasodilators depends upon the surgeon’s preference. Some surgeons like to use papaverine or nitroglycerine or nothing. The distal end of the artery in the Roberts clamp is then ligated or transfixed with No 1 Vicryl^® or secured with a ligaclip. Note: The right internal mammary artery (RIMA) can be harvested using the same technique with minor alterations with anatomical adjustments.

Coronary artery bypass grafting

Incision

The xiphisternum is freed from pericardio-sternal ligament and cut longitudinally with straight Mayo scissors. The sternum is then divided with the sternal saw, starting at the xiphisternum, gently lifting the saw as it is moved forwards. Sometimes the saw gets stuck in the soft tissues and it helps to move it back a centimetre to free it from the tissues before moving forward again. The cranial end of the incision can be retracted with a Langenbeck retractor to aid the division of the manubrium. Once the bone is divided, place a large swab under the bone edges and ensure haemostasis by diathermising the periosteal edges and sealing the bone marrow surfaces with bone wax. Following sternotomy, the left internal mammary artery can be harvested if required.

Exposure of heart

Once the thymus is divided and the pericardium is opened, the heart can be inspected. Note the size of the heart (hypertrophied, dilated) and the rhythm. Look for patchy areas of scarring from previous myocardial infarctions and check the coronary targets. It is also important to palpate the aorta to check for calcification prior to cannulation (to avoid risks of athero-embolisation, which can cause stroke, and avoid aortic dissection). Before commencing cardiopulmonary bypass, the conduits must be checked.

Central cannulation and initiation of cardiopulmonary bypass

After systemic heparinisation and insertion of purse strings, the aorta is cannulated, allowing enough space for cross-clamp, cardioplegia cannula and all proximal anastomoses. The right atrium is cannulated with a 2-stage venous wire-reinforced cannula; and an additional retrograde cardioplegia cannula can be inserted into the coronary sinus through the right atrium in patients with tight proximal stenosis to maximise myocardial protection. Please note that retrograde cannula usage is not routine practice in all cardiac centres. A DLP™ cannula is placed into the aorta, allowing the administration of antegrade cardioplegia as well as venting of the aortic root. Once bypass is established, the cross-clamp is applied and the heart arrested with antegrade and/or retrograde cardioplegia. It can be useful to mark the targets by incising the epicardium over the relevant segments of the coronary arteries prior to giving cardioplegia in order to aid identification once the heart is arrested.

Distal anastomoses

As a general principle, the distal anastomoses are performed starting with the right coronary artery, posterior descending artery, then obtuse marginal branches of left circumflex artery, followed by intermediate vessels, diagonals and left anterior artery. Most surgeons use double ended 7-0 or 8-0 Prolene with a Castroviejo needle holder and fine forceps (e.g. ring-tipped or Gerald’s forceps).