Surgery for Coronary Artery Disease

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Chapter 9 Surgery for Coronary Artery Disease

Peter Alison, Andrew McKee

Coronary artery bypass graft (CABG) surgery is one of the most commonly performed operations in the United States, and it forms the core of most cardiac surgery programs. CABG surgery provides effective symptom control for angina, and in certain patient groups, it improves survival rates.

Although the basic principle of CABG surgery—of bypassing coronary stenoses with native vascular grafts—has remained unchanged for more than 3 decades, important developments in surgical technique have emerged in the past few years. Also, because of advances in percutaneous coronary intervention (PCI) and changing societal demographics, the types of patients presenting for surgical revascularization have changed. Patients are older, sicker, have more extensive coronary disease, and are more likely to have impaired ventricular function than at any time previously.

In this chapter, the indications, techniques, and postoperative care of patients undergoing CABG surgery are reviewed. Surgery for the mechanical complications of myocardial infarction is also discussed. The first section of this chapter deals with preoperative issues, with an emphasis on high-risk and unstable patients.

INDICATIONS FOR CABG SURGERY

The indications for CABG surgery have recently been reviewed by the American College of Cardiology and the American Heart Association (ACC/AHA) (Table 9-1).1 CABG surgery offers a survival advantage over medical treatment for patients with left main coronary disease (see Fig. 5-4), three-vessel coronary disease, and disease of the proximal left anterior descending (LAD) coronary artery (see Fig. 5-5). This survival advantage is most apparent in patients with impaired left ventricular function. When CABG surgery is compared with PCI, a minimal difference in survival rates is seen2–5—except in diabetic patients, who do better with surgery. Relief from angina and the infrequent need for reintervention are superior with CABG. These trials represent highly selected groups in which patients were considered to be equally treatable by either technique—a feature that may have emphasized the benefits of PCI. The trials were carried out before the introduction of drug-eluting stents, a feature that may have emphasized the benefits of CABG surgery.

Table 9-1 ACC/AHA Indications for CABG Surgery1

Clinical Subset Recommendation
Mild or Asymptomatic Angina  
Left main or left main equivalent CAD (class I) CABG should be performed
3-vessel CAD (class I) CABG is useful
1-2 vessel CAD involving the proximal LAD (class IIa, but becomes class I if there is extensive documented ischemia and/or EF < 50%) CABG can be beneficial
1-2 vessel disease not involving the proximal LAD (class IIb, but becomes class I if there is a large area of viable myocardium and high risk criteria are found on noninvasive testing) CABG may be considered
Stable Angina  
Left main, left main equivalent, or 3-vessel CAD (class I) CABG recommended
2-vessel CAD with proximal LAD stenosis and either EF < 50% or demonstrable ischemia on noninvasive testing (class I) CABG recommended
1-2 vessel CAD without proximal LAD stenosis, but with a large area of viable myocardium and high risk criteria on noninvasive testing (class I) CABG is beneficial
Disabling angina in patients on maximal medical therapy when surgery can be performed with acceptable risk (class I) CABG is beneficial
1-vessel CAD with proximal LAD stenosis (class IIa, but becomes class I if extensive ischemia is documented by noninvasive testing and/or EF is < 50%) CABG is reasonable
1-2 vessel CAD without proximal LAD stenosis, but with a moderate area of viable myocardium and demonstrable ischemia on noninvasive testing CABG may be useful
Unstable Angina/NSTEMI*  
Left main, left main equivalent, or 3-vessel CAD (class I) CABG should be performed
Patients with ongoing ischemia not responsive to maximal non-surgical therapy (class I) CABG is recommended
1-2 vessel CAD with proximal LAD stenosis (class IIa) CABG probably indicated
1-2 vessel CAD without proximal LAD stenosis when PCI is not optimal or possible (class IIa, but becomes class I if large area of viable myocardium and high risk criteria met on noninvasive testing) CABG may be considered
STEMI*  
Indications as for patients with unstable angina/NSTEMI  
Emergency CABG in the following circumstances (class I): CABG recommended
Failed PCI with persistent pain or hemodynamic instability in patients with suitable coronary anatomy  
Persistent or recurrent ischemia refractory to medical therapy in patients who have suitable coronary anatomy, who have a significant area of myocardium at risk, and who are not candidates for PCI  
At the time of surgical repair of postinfarction myocardial rupture or mitral valve regurgitation  
Patients with cardiogenic shock*  
Patients with life-threatening ventricular arrhythmias who have left main or 3-vessel CAD  
Poor Left Ventricular Function  
Left main, left main equivalent CAD (class I) CABG should be performed
2-3 vessel CAD with proximal LAD stenosis (class I) CABG should be performed
Significant viable noncontracting revascularizable myocardium without any of the above anatomic patterns (class IIa) CABG may be performed
Life-Threatening Ventricular Arrhythmias  
Left main, left main equivalent, or 3-vessel CAD (class I) CABG should be performed
1-2 vessel CAD (class IIa, but this becomes class I if the rhythm is resuscitated sudden cardiac death or sustained ventricular tachycardia) CABG is reasonable
Following Failed PCI  
Ongoing ischemia or threatened occlusion with significant myocardium at risk (class I) CABG should be performed
Hemodynamic compromise (class I) CABG should be performed
Removal of foreign body in a crucial anatomic position (class IIa) CABG is reasonable
Hemodynamic compromise in patients with impaired coagulation and without previous sternotomy (class IIa) CABG can be beneficial
Hemodynamic compromise in patients with impaired coagulation and with previous sternotomy (class IIb) CABG can be considered
Patients With Previous CABG  
Disabling angina despite optimal nonsurgical therapy (class I) CABG should be performed
Occluded bypass grafts and class I indications for surgery for native vessel CAD (class I) CABG should be performed
Bypassable distal vessel(s) with a large area of threatened myocardium by noninvasive studies (class IIa) CABG is reasonable
Atherosclerotic vein grafts with > 50% stenosis supplying LAD or large areas of myocardium (class IIa) CABG is reasonable

Criteria for surgery are outlined in text.

CABG, coronary artery bypass graft; CAD, coronary artery disease; EF, ejection fraction; LAD, left anterior descending coronary artery; NSTEMI, non S-T elevation myocardial infarction; PCI, percutaneous coronary intervention; STEMI, S-T elevation myocardial infarction.

* Mortality rates increase for 3 to 7 days following NSTEMI and STEMI. Ideally, the patients should be medically stabilized and surgery delayed beyond this period.

Recent advances in PCI technology, particularly the use of coated stents that elute antiproliferative drugs such as sirolimus, have led to an expanded role for PCI and a modest reduction in the number of patients undergoing CABG surgery. CABG surgery remains the treatment of choice for patients with left main or complex multivessel coronary artery disease, particularly for patients with either diabetes or impaired left ventricular function.

CABG SURGERY IN HIGH-RISK PATIENTS

The overall mortality risk for patients undergoing isolated CABG surgery is about 3.5%.6 However, operative risk must be stratified according to the presence or absence of various risk factors. In the absence of risk factors, mortality rates are less than 2%, increasing to more than 50% in patients with multiple risk factors. Independent risk factors for adverse outcome following CABG surgery are summarized in Table 9-2.7 Patients with cardiogenic shock, New York Heart Association class III or IV symptoms, a history of previous cardiac surgery, or the need for urgent (in-hospital) or emergency (within 24 hours) surgery have the greatest perioperative risk. These and other factors are incorporated into the various cardiac risk scoring systems outlined in Chapter 41.

Table 9-2 Risk factors for Mortality in the Short-Term Following CABG Surgery

Variable Odds Ratio for Mortality in the Short Term (95% Confidence Interval)
Age (per 10-year increase) 1.44 (1.37-1.53)
Chronic obstructive pulmonary disease 1.22 (1.11-1.35)
Peripheral vascular disease 1.35 (1.23-1.49)
Cerebral vascular disease 1.37 (1.23-1.51)
Serum creatinine ≥1.5 mg/dl (0.13 mmol/l) 1.72 (1.56-1.90)
Prior heart surgery 2.69 (2.40-3.01)
Canadian cardiovascular society anginal class III or IV 1.27 (1.12-1.44)
Prior myocardial infarction 1.28 (1.16-1.42)
Preoperative ST segment depression on ECG 1.37 (1.24-1.51)
Urgent or emergency surgery 1.83 (1.66-2.02)
New York Heart Association class III or IV 1.77 (1.59-1.96)
Left main coronary stenosis ≥ 50% 1.20 (1.09-1.32)
Left ventricular ejection fraction < 45% 1.26 (1.15-1.39)

Adapted from Gardner SC, Grunwald GK, Rumsfeld JS, et al: Comparison of short-term mortality risk factors for valve replacement versus coronary artery bypass graft surgery. Ann Thorac Surg 77:549-556, 2004.

For a patient at very high perioperative risk (e.g., Euroscore predicted mortality >10% to 20%), a multidisciplinary approach involving the patient’s surgeon and cardiologist, along with input from intensive care and relevant subspecialty physicians, is appropriate. In this way the risks and benefits of surgery and the potential for preoperative optimization can be carefully considered. Further investigations may be indicated (e.g., a myocardial viability scan in patients with low ejection fraction). Alternatives to CABG, such as medical optimization of angina or heart failure symptoms, PCI, or spinal cord stimulation, should also be considered.

Acute Coronary Syndromes

The effectiveness of CABG in patients with severe or unstable angina has been clearly demonstrated. However, mortality rates are substantially increased if CABG surgery is undertaken within 48 hours of an ST segment elevation myocardial infarction (STEMI).8 Increased operative risk is less pronounced following non-ST segment elevation myocardial infarction (NSTEMI).8

In the first few days following a myocardial infarction, myocardial stunning occurs and a systemic inflammatory response develops—the latter characterized by fever, leukocytosis, and increases in inflammatory markers. Myocardial stunning results in a reduced ejection fraction, segmental wall motion abnormalities (SWMAs), and increased left ventricular end-diastolic pressure. Patients may develop acute heart failure or even frank cardiogenic shock. Following STEMI or NSTEMI, CABG surgery should be delayed by 3 to 7 days or until such time as the clinical features of congestive cardiac failure have resolved.1

In patients with critical coronary anatomy, particularly left main or left main equivalent coronary artery disease, the decision regarding the timing of surgery is difficult. Despite a large area of threatened myocardium, it is probably still beneficial to attempt to delay surgery for at least 48 hours following an acute myocardial infarction. Following an anteroseptal STEMI, there may be benefit in waiting several weeks until a scar has developed and then performing CABG surgery in conjunction with a remodeling procedure (see later discussion). Following an inferior myocardial infarction with right ventricular involvement, right ventricular function may take as long as 4 weeks to recover,9 and CABG surgery is best delayed beyond this period.

Despite the advantages of delayed surgery following myocardial infarction, emergency CABG surgery is indicated in a few specific situations:

• Cardiogenic shock. (See Chapter 19.)
• Ongoing ischemia. Emergency CABG surgery should be considered in patients with suitable anatomy if there is ongoing ischemia evidenced by postinfarction angina, new or evolving ECG changes, or life-threatening ventricular arrhythmias.
• Mechanical complications. CABG surgery may be performed at the time of repair of a mechanical complication of myocardial infarction (see Surgery for Complications of Myocardial Infarction later in this chapter).
• Failed PCI. About 0.7% of patients require emergency CABG following PCI.10 The reasons for surgical referral include coronary dissection, stent embolization, coronary rupture (with pericardial tamponade), coronary occlusion, and incomplete revascularization.10 Approximately one quarter of these patients are extremely unwell, experiencing shock, acute ischemia, or arrhythmias. Stabilization in the intensive care unit (ICU) may not be possible, and immediate transfer to the operating room is required. These patients are also likely to have received recent treatment with heparin, aspirin, clopidogrel, and glycoprotein IIb/IIIa inhibitors.

Preoperative Optimization

Prior to urgent CABG surgery, some patients benefit from a short period of aggressive medical optimization in the ICU. While in the ICU, invasive hemodynamic monitoring can be established and, if not already performed, an echocardiogram can be obtained. A pulmonary artery catheter provides important information but is contraindicated in patients with recurrent arrhythmias. Preoperative treatment with an intraaortic balloon pump (IABP) may improve outcome in high-risk patients undergoing CABG surgery11 and should be considered in all patients with acute ischemia, arrhythmias, pulmonary edema, or shock. For patients with profound cardiogenic shock secondary to myocardial infarction, primary treatment with a ventricular assist device may be preferable to CABG surgery (see Chapters 19 and Chapter 22).12

For ongoing myocardial ischemia, intravenous nitroglycerin and a β blocker should be given. For hypotension or pulmonary edema, diuretic and inotropic drugs may be required.

Tight glycemic control has been shown to improve outcome in diabetic patients undergoing cardiac surgery (see Diabetes in subsequent discussion), and in one randomized trial, maintenance of serum glucose between 80 and 110 mg/dl (4.4 and 6.1 mmol/l) improved survival rates in unselected patients (diabetic and nondiabetic; cardiac surgery and noncardiac surgery) admitted to a surgical ICU. Furthermore, treatment with glucose-insulin infusions (as opposed to simply maintaining glycemic control) may improve outcome after CABG surgery in patients with left ventricular failure13 and acute myocardial ischemia.14

Chronic Left Ventricular Dysfunction

Patients with depressed left ventricular function who have demonstrable hibernating myocardium derive substantial benefit from CABG surgery in terms of improved ejection fraction, relief of heart failure symptoms, and enhanced survival rates.15 Hibernating myocardium may be identified by a number of myocardial viability studies, as outlined in Chapter 5. A patient with low ejection fraction (<35%) whose symptoms are predominantly those of heart failure should undergo a myocardial viability study; if hibernating myocardium is demonstrated, and the coronary anatomy is suitable, CABG surgery should be considered. A patient with a low ejection fraction whose symptoms are predominantly those of angina and only minimal heart failure should be offered CABG surgery only if indicated on the basis of their coronary artery disease.1 Patients with extensive anteroseptal scar formation following a STEMI may be suitable for ventricular remodeling surgery (see Surgery to Remodel the Left Ventricle, in subsequent material).

Preoperative Optimization

Chronic left ventricular dysfunction is not an indication for urgent CABG surgery, and patients should be medically optimized prior to surgery to reduce the likelihood of postoperative problems. Systemic and pulmonary congestion should be treated with diuretics. Renal function, volume status, and electrolytes (sodium, potassium, magnesium) should be monitored. Angiotensin-converting enzyme (ACE) inhibitor and β-blocker therapy can inhibit ventricular remodeling and improve ejection fraction, but they may also produce deleterious effects: β blockers initially worsen heart-failure symptoms and can cause symptomatic bradycardia or heart block; ACE inhibitors may cause hypotension, renal impairment, and hyperkalemia. Thus, in patients with severe left ventricular dysfunction, these drugs should not be introduced nor should their doses be increased immediately prior to planned CABG surgery. Oral protein supplements or nasogastric feeding should be considered in patients who are malnourished.

Valvular Heart Disease

In general, any valve pathology graded as moderate or severe should be considered for repair or replacement at the time of CABG surgery. In deciding whether to perform valve surgery, the additive risk of a combined valve-coronary procedure must be weighed against the risk of leaving the patient with an uncorrected valve lesion.

Aortic Stenosis

A patient with moderate or severe aortic stenosis (mean gradient >25 to 30 mmHg) should undergo aortic valve replacement at the time of CABG surgery. The risks involved in aortic valve replacement in a patient with previous CABG surgery are probably greater than those involved in combined CABG and aortic valve surgery, but given the unpredictable natural history of calcific aortic stenosis, aortic valve replacement for mild disease is not justified.

Mitral Regurgitation

The decision to repair or replace a regurgitant mitral valve is difficult and depends on the mechanism of the regurgitation, the likely ease of valve repair, and the degree to which the regurgitation is due to hibernating myocardium. A preoperative transesophageal echocardiogram can help to define the severity and mechanism of the mitral regurgitation. A patient with moderate or severe ischemic mitral regurgitation who undergoes isolated CABG surgery is at risk for important postoperative mitral regurgitation.16 In general, a patient with moderate or severe ischemic mitral regurgitation should undergo mitral valve surgery at the time of CABG surgery. However, combined CABG and mitral valve surgery substantially increases the operative risk,7 particularly in the presence of impaired ventricular function.

Carotid Disease

Carotid disease is common in patients presenting for cardiac surgery. In two studies, the incidence of severe (≥80%) carotid stenosis in unselected patients undergoing cardiac surgery was 8.5% and 12%, with an incidence of postoperative stroke of 18.2% and 5.3%, respectively.17,18 All patients who have carotid bruit or a history of transient ischemic attack, stroke, or previous carotid endarterectomy should undergo ultrasound-flow imaging of the carotid arteries prior to surgery. As age above 65 years, left main coronary disease, smoking, and peripheral vascular disease are all associated with carotid atherosclerosis, routine carotid ultrasonography is justified in these patient groups. Because of the increased risk for postoperative stroke associated with high-grade carotid stenosis in patients undergoing cardiac surgery, carotid endarterectomy is indicated when unilateral or bilateral carotid stenoses are greater than 80%, irrespective of symptoms. The outcomes of staged (with carotid endarterectomy performed first) or combined procedures are similar.19

Chronic Obstructive Pulmonary Disease

Patients with severe chronic obstructive pulmonary disease (COPD), as evidenced by a forced expiratory volume over 1 second (FEV1) <1.25 l, have significantly higher mortality rates following CABG surgery—mainly due to cardiac arrhythmias—than do patients without severe COPD.20 In patients with end-stage COPD (FEV1 <0.5l to 1.0 l), cardiac surgery may be considered to be contraindicated. Patients with moderate to severe COPD are likely to benefit from preoperative optimization, including smoking cessation, incentive spirometry, nutritional support, and effective treatment of the bronchospastic or infective components of their pulmonary diseases.

Diabetes

CABG surgery in patients with diabetes and multivessel coronary disease results in improved long-term survival rates compared to those seen after medical treatment or PCI.21,22 However, diabetic patients suffer a higher rate of perioperative complications, such as renal failure, stroke, and wound infection, and have increased early mortality rates compared to nondiabetic patients.23 Patients with diabetes often have silent myocardial ischemia, diffuse coronary disease, renal dysfunction, and peripheral vascular disease.

In diabetic patients undergoing cardiac surgery, including CABG surgery, perioperative control of serum glucose by means of intravenous insulin improves survival rates and reduces the incidence of various complications such as sternal wound infection.24–26 Management strategies for perioperative glucose control are outlined in Chapter 36.

Renal Dysfunction

A number of factors are associated with developing postoperative renal failure (Chapter 33), the most important of which is preoperative renal dysfunction. A preoperative creatinine level of greater than 2.5 mg/dl (0.22 mmol/l) is strongly associated with the need for long-term dialysis following cardiac surgery.27 Postoperative acute renal failure is associated with a greatly increased mortality rate. In one large series, the mortality rate was 63% in patients who developed dialysis-dependent renal failure following CABG surgery compared to only 0.9% in patients whose renal function remained normal.28

If an elevated creatinine level is discovered prior to cardiac surgery it is essential to know whether it is acute or chronic. An acute deterioration in renal function should be carefully investigated and all potential causes eliminated. In particular, drugs such as spironolactone, nonsteroidal antiinflammatory drugs, and nephrotoxic antibiotics should be discontinued; consideration should also be given to stopping ACE inhibitors and angiotensin receptor blockers. If possible, CABG surgery should be delayed until renal function has returned to baseline following administration of radiocontrast agents.

End-Stage Renal Failure

Patients with dialysis-dependent renal failure have a perioperative mortality rate in excess of 10% following cardiac surgery.29 Such patients frequently have coexisting hypertension, diabetes, anemia, abnormal hemostasis, and electrolyte abnormalities. They are often anuric or oliguric; thus, any fluid that is administered must be removed by dialysis. Immediately following dialysis, patients tend to be hypovolemic and hypokalemic; immediately prior to dialysis, patients tend to be hypervolemic and hyperkalemic. Dialysis should be performed on the day prior to surgery, not on the morning of surgery, to allow postdialysis fluid shifts to equilibrate. Following surgery, dialysis is performed, ideally, on the first postoperative day (see Chapter 33).

Body Mass Index

Underweight patients (body mass index [BMI] <18 kg/m2) undergoing cardiac surgery are at increased risk for adverse outcomes, such as postoperative infection and prolonged ICU stay.30 This finding probably reflects poor nutrition in the context of severe cardiac disease. Such patients may benefit from a period of preoperative supplemental nutrition under the supervision of a dietitian.

Moderate obesity (BMI 35 to 39.9 kg/m2) is associated with only a slightly increased operative risk compared to normal or mildly obese patients (BMI 18.5 to 34.9 kg/m2) undergoing CABG surgery. In contrast, extreme obesity (BMI >40 kg/m2) is associated with an increased incidence of mediastinitis, renal failure, prolonged hospital stay, and mortality.31

Coexisting diseases, such as diabetes, hypertension, obstructive sleep apnea, and right ventricular dysfunction, are more common in obese patients; they should be investigated and treated prior to elective cardiac surgery. For patients with obstructive sleep apnea, establishment of a continuous positive airway pressure device for home nighttime use prior to surgery may be beneficial. This device can then be used during the postoperative period. A supervised in-hospital weight loss program prior to elective cardiac surgery may be appropriate in extremely obese patients.

Peripheral Vascular Disease

Peripheral arterial disease contributes to poor wound healing, makes vascular access difficult, and can either contraindicate the use of an IABP or make its placement difficult in patients who would benefit from it. Saphenous vein conduits should be taken from the leg with the best arterial perfusion. The presence of varicose veins or a past history of lower limb deep venous thrombosis may preclude the use of the saphenous veins as conduits.

There is controversy about whether coronary revascularization should be undertaken prior to major noncardiac surgery in patients with severe coronary artery disease. Furthermore, it is not certain what form of revascularization should be offered, because patients undergoing PCI are known to have high rates of early stent occlusion if subsequently subjected to major surgery. A recent trial found no difference in outcome between preoperative revascularization and no preoperative revascularization (PCI or CABG surgery) prior to major vascular surgery.32

Other Medical Problems

A patient with a history of adrenocortical disease (including chronic treatment with corticosteroids) or thyroid disease (including chronic treatment with amiodarone) should undergo preoperative testing of adrenal and thyroid function. Guidelines for perioperative treatment with corticosteroids and thyroxine are provided in Chapter 36.

The risk for perioperative gastrointestinal hemorrhage is increased in cardiac surgery patients because of acute stress ulceration and the use of anticoagulant and antiplatelet drugs. Antiulcer therapy should be continued throughout the perioperative period in patients taking it preoperatively. Preoperative suspicion of gastrointestinal hemorrhage (anemia, melena, altered bowel habit) should be investigated by means of upper or lower gastrointestinal endoscopy. Urinary tract, intravenous catheter, or dental infections should be investigated and treated prior to elective surgery.

Reoperation

Up to 10% of patients who undergo CABG surgery present for reoperation.1 The early mortality rate in revision CABG surgery is higher than that in revision valve surgery and in first-time CABG surgery, but long-term survival is good.

A lateral chest radiograph should be obtained preoperatively. Loss of the normal anterior mediastinal air space may indicate an increased risk for damaging a cardiac or vascular structure during sternotomy. Some surgeons also obtain a thoracic computed tomography scan prior to revision cardiac surgery. Additional blood should be cross-matched for transfusion: 4 to 6 units compared to 2 to 4 units prior to first-time surgery. The surgeon must carefully review the coronary angiogram to assess the position and patency of the original coronary grafts.

A range of intraoperative problems may be encountered with revision CABG surgery that are not seen with first-time surgery. Patent grafts may be damaged during resternotomy. A patent mammary graft may allow continued myocardial perfusion during aortic cross-clamp, making effective cardioplegia difficult. Atherosclerosis within diseased saphenous vein grafts can result in coronary emboli during surgical manipulations. Surgery is often prolonged because of the requirement for extensive dissection and division of adhesions. With revision CABG surgery, the entire heart may have to be mobilized. (In contrast, the whole heart does not usually require mobilization for revision valve surgery.) Thus, bleeding, impaired ventricular function, and a pronounced systemic inflammatory response often complicate the postoperative course.

OPERATIVE DECISION MAKING

Only brief accounts of the complexities of the intraoperative period are provided here. The purpose of such a simple overview is to give the reader an appreciation of what takes place in the operating room and how it may have an impact on both the postoperative period and the patient’s long-term outcome.

Coronary Grafts

Different types of conduits are used to bypass blocked or narrowed coronary arteries, including the saphenous vein, internal mammary arteries, radial arteries and, rarely, the gastroepiploic or inferior epigastric arteries. Conduits may be in the form of pedicle grafts, in which the proximal end remains attached at its origin (e.g., the internal mammary arteries), or in the form of free grafts. Most free grafts are aortocoronary grafts; that is, proximally they are sutured to the ascending aorta and distally to the coronary artery. Alternatively, free grafts may be sutured proximally to another graft.

Internal Mammary Arteries

The left and right internal mammary arteries (LIMAs and RIMAs) originate from the left and right subclavian arteries, respectively, and run along the undersurface of the sternum.

The LIMA is typically used as a pedicle graft to the LAD coronary artery. The RIMA is used as a free graft to the posterior descending coronary artery or, alternatively, as a pedicle graft to either the right coronary, left anterior descending, or obtuse marginal artery. When used as a pedicle graft to the left coronary artery, the RIMA crosses behind the sternum and can be at risk for damage during subsequent sternotomy.

The figures for patency vary among studies,33,34 but a LIMA-LAD graft consistently has the highest long-term patency of any graft, typically being greater than 90% at 10 years. Patency rates for the RIMA graft are slightly lower than those for the LIMA-LAD graft.35 There is some evidence of an incremental benefit of using both internal mammary arteries rather than only a LIMA-LAD graft.36

The incidence of sternal dehiscence may be increased by the use of bilateral internal mammary grafts, and some surgeons avoid this technique in diabetic or obese patients. There is a small but appreciable risk for phrenic nerve injury during dissection of an internal mammary artery. Lung trauma causing a postoperative air leak can also occur during dissection of the mammary arteries.

Radial Arteries

The radial artery has recently been reintroduced as a conduit, and it has patency rates superior to those of saphenous vein grafts37 and approaching those of the internal mammary grafts. Because the potential for digital ischemia or hand claudication exists following resection of the radial artery, the graft is usually taken from the nondominant arm. In addition to preoperative clinical examination, a Doppler ultrasound study of the arterial supply to the hand may be carried out prior to surgery. The radial artery should be used only if ulnar arterial supply to the deep and superficial palmar arches is satisfactory. Resection of the radial artery is occasionally associated with radial nerve damage or a brachial plexus injury (due to excessive abduction at the shoulder during positioning).

Saphenous Vein Grafts

Saphenous vein grafts have historically been the most commonly used conduit for CABG surgery, and their use remains widespread today. Reported patency rates of 80% at 3 years are typical.38 However, recently a 5-year patency rate of 95% has been reported,33 possibly related to aggressive use of statin therapy postoperatively.

Graft Placement

Graft placement is determined primarily on the basis of the coronary angiogram (see Chapter 5). In patients with impaired ventricular function, additional information from a myocardial viability study may be sought to help determine optimal graft placement.

In general, every coronary stenosis of more than 50% occurring in a vessel larger than 1 mm internal diameter should be bypassed. For stenoses of less than 50%, competition for flow between the native vessel and the graft results in early graft occlusion. Complete revascularization is defined as at least one bypass or patent native vessel to each of the anterior, lateral, and inferior left ventricular walls. However, this may not be possible; certain patients, particularly small women and diabetics, have very narrow vessels or diffuse coronary disease that may precludes graft placement.

Patency rates are better for grafts to the left coronary artery than to the right coronary artery and are better when larger (>2 mm internal diameter) vessels are grafted, irrespective of the conduit used.34 The ACC/AHA guidelines recommend that a LIMA-LAD graft be considered in all patients undergoing CABG surgery. Although arterial conduits are associated with high long-term patency, they are more prone to postoperative spasm than are saphenous vein grafts—particularly the radial artery.39 Also, there is an increased risk for early occlusion when arterial grafts are used to bypass coronary stenoses of less than 70%. Thus, arterial conduits tend to be favored in younger patients with high-grade, discrete stenoses, whereas saphenous vein grafts are more likely to be used in older patients with lower grade (50% to 70%) stenoses or diffuse disease.

Common sites for graft placement are the LAD coronary artery, the large diagonal or intermediate branches of the left system, the OM branch of the circumflex coronary artery, and the posterior descending artery (PDA) branch of the right coronary artery. The circumflex coronary artery is buried in the atrioventricular groove and therefore is an unsuitable site for anastomosis. Distal atherosclerosis within the right coronary artery is common, so the PDA is the preferred site for graft placement in the right coronary system. However, a graft to the PDA precludes the use of a pedicle RIMA graft because of insufficient length.

Techniques of Coronary Artery Surgery

The ideal conditions in which to perform CABG surgery is a still, bloodless operative field. The conventional way of achieving these conditions has been by the use of cardiopulmonary bypass (CPB) and a full sternotomy. Over the past decade, techniques have been developed that allow CABG surgery to be performed without CPB (off-pump coronary artery bypass; OPCAB surgery) or via minimally invasive incisions.

On-Pump CABG Surgery

In addition to CPB, on-pump CABG surgery usually involves cross-clamping the aorta and the administration of cardioplegia solution to protect the ischemic myocardium.

The circuit for the CPB machine is shown in Fig. 9-1. Deoxygenated blood is drained by gravity to the venous reservoir via a large-bore cannula placed in the patient’s right atrium. For CABG surgery, this is usually a single venous cannula that drains both the superior and inferior vena cavae. This is distinct from tricuspid and mitral valve surgery in which selective cannulation of the vena cavae (i.e., bicaval cannulation) is usually performed to allow the right atrium to be opened (in tricuspid valve surgery) or to improve surgical access (in mitral valve surgery). From the reservoir, blood is pumped, typically using a roller or constrained vortex pump, through a heat exchanger to allow precise temperature control, and through a hollow-fiber membrane oxygenator where gas exchange takes place. Oxygenated blood then passes through a 20- to 40-μm filter and is returned to the patient via a cannula (usually) placed in the proximal ascending aorta. In this way the heart and lungs are “bypassed,” allowing the heart to be stopped to facilitate surgery.

image

Figure 9.1 Diagram of a standard cardiopulmonary bypass circuit. Venous blood drains via the right atrial (RA) cannula into the venous reservoir; then, via roller pump A, it passes through a heat exchanger and oxygenator. From the oxygenator, arterial blood passes through a filter into (in this case) the ascending aorta. The vent returns blood from the left heart to roller pump B and then back to the venous reservoir. The vent is usually inserted through the right upper pulmonary vein, but it may be inserted into the pulmonary artery or the aortic root proximal to the aortic cross-clamp. The surgical suction (“pump sucker”) returns blood from the operative field to the venous reservoir via roller pump C. Based on the diameter of the tubing, roller pump D draws a fixed ratio of fluid from the cardioplegia solution and blood from the venous reservoir to form blood cardioplegia. This solution passes via the cardioplegia cannula to the aortic root (antegrade cardioplegia). The cardioplegia cannula may also be inserted into the coronary sinus (retrograde cardioplegia) through a cannula placed into the right atrium. Notice that the aortic cross-clamp is placed between the cardioplegia cannula and the systemic perfusion (aortic) cannula.

To provide a still, bloodless surgical field, a clamp is placed on the ascending aorta proximal to the arterial cannula, and the heart is arrested in diastole by its isolated perfusion with cardioplegia solution. By inducing cardiac arrest in diastole, cardioplegia facilitates surgery and helps protect the heart against ischemia during aortic cross-clamping—hence the term myocardial protection. Cardioplegia may be administered antegrade into the coronary arteries (via a cannula placed in the aortic root proximal to the aortic cross-clamp) or retrograde into the coronary sinus. Cardioplegia may be perfused into coronary grafts once the distal anastomoses have been completed. Various types of cardioplegia solution are used, but usually cardiac arrest is achieved by administering a cold, potassium-rich solution. To enhance myocardial protection, the cardioplegia solution is usually mixed with blood from the bypass circuit (blood cardioplegia). Cardioplegia may be administered continuously or, more commonly, intermittently every 10 to 20 minutes throughout the period of aortic cross-clamping. Various metabolic substrates such as aspartate may be added to the cardioplegia solution. Because most of the reduction in myocardial oxygen consumption achieved with cardioplegia comes from cardiac arrest rather than from hypothermia, sometimes techniques of warm cardioplegia are employed in an attempt to better preserve myocardial metabolic function. In particular, the last dose of cardioplegia, given just before removal of the cross-clamp, is commonly warm (“hotshot”). To limit the duration of aortic cross-clamping and to enable a longer period of time for myocardial recovery prior to separation from cardiopulmonary bypass, many surgeons perform the proximal aortic anastomoses with a partially occluding “side-biting” aortic clamp.

The techniques described provide ideal operating conditions, including a still, relatively bloodless surgical field. However, a number of potential problems exist, including the following:

• CPB involves blood contact with nonbiologic surfaces, blood-gas interfaces, and nonpulsatile flow, all of which contribute to the development of coagulopathy, platelet dysfunction, neurocognitive impairment, and the systemic inflammatory response syndrome.
• Prolonged aortic cross-clamping and difficulties with myocardial protection can result in postoperative myocardial dysfunction due to stunning or infarction, particularly in patients with tight coronary stenoses, ventricular hypertrophy, or preoperative acute myocardial ischemia.
• Manipulation of the aorta (cross-clamping and placement of proximal grafts) may result in systemic embolization, with the potential for neurologic, mesenteric, and renal dysfunction.

The fluid load associated with the CPB prime and the cardioplegia solution (along with the use of mannitol in the prime fluid, as occurs in some centers) can result in marked polyuria during the early postoperative period.

OPCAB Graft Surgery

During OPCAB graft surgery, coronary grafting is performed on a beating heart. Various stabilizing devices are used to keep the heart still during the coronary anastomoses (Fig. 9-2), and temporary intracoronary shunts may be used to provide a relatively bloodless surgical field and distal vessel perfusion. To place grafts to the obtuse marginal and posterior descending arteries, the heart must be partially lifted out of the chest and rotated, with the possibility of hemodynamic instability and, occasionally, cardiovascular collapse. Proximal aortic anastomoses are performed by using a partial occlusion side-biting aortic clamp. Alternatively, proximal anastomoses may be attached to a pedicle LIMA graft. Some surgeons perform most or all of their coronary surgery off-pump; others limit the technique to grafts to the LAD coronary artery and its branches; and other surgeons do not use the technique at all.

image

Figure 9.2 The Medtronic Octopus® system II for stabilizing the heart during off-pump coronary artery bypass surgery. The Medtronic Starfish™ 2 heart positioner allows the surgeon to position the heart so as to allow maximum access to the blocked coronary artery. The Medtronic Octopus® 4 suction pods are placed so that they straddle the artery to be bypassed and thereby hold the suturing site steady. Both the Starfish 2 and the Octopus 4 attach to the sternal retractor and use suction to hold the heart.

(Image courtesy of Medtronic Inc., Minneapolis, MN.) Ao, aorta; MPA, main pulmonary artery.

The main advantage of OPCAB surgery is the avoidance of CPB and its deleterious effects. A disadvantage of OPCAB is that concomitant intracardiac surgery (e.g., valve or ventricular remodeling surgery) cannot be performed without the use of CPB. OPCAB graft surgery has been the subject of an enormous amount of research and debate over the past 10 years. For surgeons and institutions experienced in off-pump surgery, reduced perioperative morbidity and mortality rates can be achieved.40,41 A recent metaanalysis of randomized controlled trials demonstrated a nonsignificant trend toward improved outcome with OPCAB,42 but a subsequent large randomized trial demonstrated almost identical short-term outcomes with the two techniques.43 There is some evidence that early graft patency may be reduced with OPCAB surgery.44

OPCAB surgery in which all of the proximal anastomoses are attached to the LIMA pedicle graft provides a technique in which there is no manipulation of the proximal aorta. This approach may be used in patients with severe atheromatous disease of the ascending aorta so as to reduce the likelihood of postoperative stroke.

A 2003 survey of Canadian practice found that 16% of all coronary revascularizations were performed off-pump, with only 23% of respondents indicating that their use of the technique would increase over the next 5 years.45

The ICU management of patients having OPCAB surgery is essentially the same as that for patients undergoing on-pump revascularization. One difference is that the polyuria seen following on-pump CABG surgery does not usually occur following OPCAB graft surgery.

Minimally Invasive Surgery

Minimally invasive surgery encompasses a range of techniques. Standard on-pump or off-pump coronary revascularization can be performed through a small incision, such as a lower two-thirds sternotomy or an anterolateral thoracotomy. One technique, minimally invasive direct coronary artery bypass, involves an off-pump LIMA-LAD anastomosis via a small anterior thoracotomy incision. Although this technique is potentially appealing, it is of limited use because of the very low percentage of patients who require only a single graft to the LAD coronary artery. Minimally invasive direct coronary artery bypass surgery has been combined with PCI in a hybrid approach to revascularization. In this way, complete revascularization may be achieved, including the benefits of a LIMA-LAD graft but without the need for CPB or sternotomy. In a few centers, coronary revascularization (and also mitral valve repair) is performed with the assistance of robotics. A range of techniques has been described, from robotic assistance of LIMA harvesting to totally endoscopic surgery with computer-controlled port-access telemanipulators.

Minimally invasive surgery reduces the surgical scar and potentially reduces postoperative pain, thereby shortening the recovery period. However, unless combined with off-pump surgery, the disadvantages of CPB are not avoided.

POSTOPERATIVE CARE FOLLOWING CABG SURGERY

In most respects, the care of patients following CABG surgery is the same as that of any patient undergoing heart surgery, as outlined in Chapter 17. However, two issues specific to patients undergoing CABG surgery warrant special mention here: (1) pharmacotherapy following CABG surgery; and (2) the diagnosis and treatment of postoperative myocardial ischemia.

PHARMACOTHERAPY FOLLOWING CABG SURGERY

The pharmacology and use of the drugs listed subsequently are discussed in Chapter 3.

Drugs to Prevent Coronary Graft Spasm

Vasodilators are widely used after CABG surgery to prevent spasm within coronary grafts. Both nitrates and calcium channel blockers are effective for this purpose.46 In the early postoperative period, an intravenous agent such as nitroglycerin or nicardipine may be used. Milrinone is also a potent dilator of arterial vessels and, in patients with impaired ventricular function, has been reported to reduce myocardial injury more than nifedipine.47

The radial artery has a greater propensity for spasm than other grafts.39 Consequently, in most centers, a dihydropyridine calcium channel blocker (e.g., felodopine, 2.5 to 5 mg daily) or a long-acting nitrate is continued for 3 to 6 months following surgery if a radial artery conduit has been used. The use of calcium channel blockers has been associated with improved in-hospital survival following CABG surgery,48 but there is no benefit in continuing treatment beyond 1 year.49

Drugs to Prevent Coronary Graft Thrombosis or Atherosclerosis

All patients should receive aspirin (100 mg/daily) indefinitely because it has been shown to improve the patency of saphenous vein grafts.50 Unless the patient is bleeding excessively, aspirin should be given within 7 hours of surgery; if it is started at 48 hours after surgery, the beneficial effect on saphenous vein patency may not occur.51 If aspirin is contraindicated because of allergy, clopidogrel can be used as an alternative.52 Clopidogrel and aspirin are sometimes used in combination following OPCAB surgery.

Aggressive treatment with statins improves the long-term patency of saphenous vein grafts and reduces the need for revascularization.53 Additionally, preoperative statin therapy has been associated with a reduction in early postoperative mortality following CABG surgery.54 Statins should be commenced in all patients following CABG surgery, aiming for a low-density lipoprotein cholesterol less than 100 mg/dl or less than 70 mg/dl in high-risk patients.1

Other Drugs

In patients undergoing CABG surgery, preoperative use of β blockers is associated with reduced mortality rates.55 β Blockers reduce the incidence of postoperative atrial fibrillation and other arrhythmias and are useful as antihypertensive agents. In patients with left ventricular dysfunction, β blockers help prevent ventricular remodeling and, over time, improve ejection fraction. Acute cessation of therapy at the time of surgery in patients chronically treated with β blockers may precipitate arrhythmias or, in patients who are incompletely revascularized, myocardial ischemia. Thus, β blockers should be continued up until the morning of surgery and reinstituted on the first postoperative day. In the absence of contraindications, routine treatment with β blockers should be considered in all patients after CABG surgery. However, in patients with impaired ventricular function or histories of congestive cardiac failure, β blockers should be introduced cautiously.

ACE inhibitors improve survival rates in patients with impaired left ventricular function and in patients with normal left ventricular function at risk for ischemic cardiac events.56 Thus, in the absence of contraindications, routine treatment with ACE inhibitors should be considered in all patients after CABG surgery. ACE inhibitors should be introduced cautiously in patients with recent renal dysfunction (see Chapter 3).

Anticoagulation with warfarin is indicated in patients with recent anteroapical myocardial infarction and a persistent wall motion abnormality after CABG surgery. Treatment should be continued for 3 to 6 months.1 Warfarin is also indicated for atrial fibrillation that lasts longer than 24 to 48 hours. Other routine postoperative drug therapy, not specific for CABG surgery, is discussed in Chapter 17.

POSTOPERATIVE MYOCARDIAL ISCHEMIA AND INFARCTION

Perioperative myocardial infarction, as identified by new Q waves on the ECG, occurs in 2% to 4% of patients after CABG surgery and is predictive of increased likelihood of mortality.57,58 However, the diagnoses of postoperative myocardial ischemia and infarction are not straightforward. In the early period, the critical issue is whether there is acute ischemia secondary to a problem with a coronary graft or native coronary vessel that warrants urgent intervention.

Diagnosis of Myocardial Ischemia and Infarction

Some degree of myocardial injury virtually always occurs after CABG surgery. At one end of the spectrum, this myocardial injury is manifested as a small troponin release with no clinical sequelae. Troponin release occurs for a variety of reasons, including direct myocardial trauma resulting from surgical incisions, occlusion or resection of small coronary vessels, and imperfect intraoperative myocardial protection, a particular problem in patients with hypertrophied ventricles and tight proximal coronary stenoses. At the other end of the spectrum is severe myocardial ischemia or infarction that is associated with hypotension, low cardiac output, and ventricular arrhythmias. This latter situation demands urgent investigation because it may represent an acute obstruction (spasm, kinking, or thrombosis) of a coronary graft or native coronary vessel. Timely intervention may be lifesaving.

Clinical Assessment

If awake, patients may complain of angina-type pain. However, pain caused by myocardial ischemia is very difficult to distinguish from wound pain. Most patients are sedated and ventilated during their early postoperative period and cannot report their symptoms. Hemodynamic instability has many causes, but one of the most important to consider in patients after CABG surgery is myocardial ischemia. Acute ischemia of severity sufficient to cause hypotension or low cardiac output implies a large region of threatened myocardium and warrants urgent intervention and treatment. If a pulmonary artery catheter is in place, there may be elevations in the pulmonary artery and pulmonary artery wedge pressures, but these findings are nonspecific. A systematic approach to hemodynamic instability is outlined in Chapter 20.

ECG Diagnosis

New significant Q waves on an ECG (≥ 0.04 second duration in any two leads except III and aVR) may be indicative of full-thickness myocardial infarction, but they take 24 to 48 hours to develop and are therefore not useful in the assessment of suspected ischemia (see also Chapters 8 and Chapter 18). In contrast, ST segment deviation (≥ 1 mm, measured 0.06 sec after the J point), if it occurs, develops concurrently with myocardial ischemia. ST segment deviation, particularly elevation, is associated with the subsequent development of new Q waves after CABG surgery59 and therefore may provide a useful marker of acute ischemia. However, ST segment and T-wave abnormalities, particularly the “pericarditic” pattern of upsloping ST segment elevation across multiple leads, are common following cardiac surgery and do not necessarily imply ischemia. New left bundle branch or atrioventricular block may indicate acute ischemia, but they too are common following cardiac surgery. However, ventricular arrhythmias, particularly recurrent ventricular tachycardia or fibrillation, are strongly suggestive of severe acute ischemia. Despite the limitations of ECG analysis, the finding of ST segment depression or elevation that is limited to a specific coronary territory, particularly if associated with hemodynamic instability or ventricular arrhythmias, is strongly suggestive of acute ischemia.

Echocardiography

All patients with suspected myocardial ischemia after CABG surgery should undergo urgent echocardiograms—preferably a transesophageal echocardiogram examination— looking for segmental wall motion abnormalities (SWMAs). SWMAs are more sensitive and specific for myocardial ischemia than ECG changes, but they can be difficult to interpret in postoperative patients. In addition to acute ischemia, SWMAs may be caused by myocardial infarction, stunning, hibernation, and the effects of pacing. Any SWMAs identified should be compared with findings in the preoperative or intraoperative echocardiograms and with previously known patterns of myocardial ischemia and infarction. The characteristics of SWMAs that are suggestive of acute ischemia are outlined in Chapter 7.

Biochemical Markers

As noted earlier, a small rise in serum troponin is a normal finding after CABG surgery. However, large increases are indicative of perioperative myocardial infarction and are associated with adverse outcome. For troponin I, a value greater than 20 μg/l is associated with prolonged hospital stay60 and indicative of early graft failure.61 For troponin T, a value above 1.58 μg/l at 18 to 24 hours after surgery is predictive of adverse outcome, including death.62

A limitation of making judgments based on troponins is that peak levels occur at about 24 hours after an ischemic event; troponin T peaks a little later than troponin I (see Fig. 18-11). Thus, these markers are not ideal for the evaluation of acute ischemia soon after surgery.

Elevation of the creatine kinase (CK) muscle and brain subunits (MB) fraction is also associated with adverse outcome following CABG surgery63 but is less sensitive and specific than the troponins.61 CKMB takes nearly 24 hours to reach peak levels. Myoglobin levels peak within 6 to 12 hours of ischemic injury but are poorly predictive of outcome.61

Interventions for Suspected Postoperative Myocardial Ischemia

If myocardial ischemia is suspected on the basis of hemodynamic instability or ECG changes, an urgent transesophageal echocardiogram should be performed and a serum troponin level obtained. The ECG and echocardiographic findings must be integrated into the surgical findings. For instance, an anterior SWMA may fit with surgical concern regarding the LAD graft. If SWMAs consistent with acute myocardial ischemia are confirmed by echocardiography, aggressive treatment for presumed graft spasm should be commenced. If the patient is hypertensive, an intravenous vasodilator such as nitroglycerin or nicardipine should be commenced, and the dose should be increased to the maximum level tolerated, while avoiding hypotension. In the hypotensive patient, hypovolemia should be corrected and, if necessary, a vasopressor such as norepinephrine used to support blood pressure. The reduction in blood flow through arterial conduits due to hypotension greatly exceeds the adverse effects of α1-receptor-mediated vasoconstriction of the conduit.46 An IABP should be considered in patients refractory to pharmacologic therapy or in cardiogenic shock.

If a patient fails to respond to vasodilator and fluid therapy, with normalization of the ECG and echocardiogram, a mechanical obstruction of a coronary graft should be considered. In the presence of ongoing myocardial ischemia, particularly if accompanied by hemodynamic instability or arrhythmias, urgent coronary angiography or return to the operating theater should be considered. If the patient is critically unwell and shows evidence of ongoing ischemia, arrhythmias, and hypotension, the delay and inherent risks involved in transporting the patient to the angiography suite are not justified, and immediate return to the operating room to revise the coronary grafts is indicated.

Interventions for Postoperative Myocardial Infarction

A proportion of patients, many of whom will have had uneventful postoperative courses, demonstrate either ECG or biochemical evidence of myocardial infarction on routine postoperative tests. Such patients are at increased risk for adverse events and should be kept in a highly monitored environment (ICU or high-dependency unit) during their early postoperative periods. Prior to discharge to the ward, such patients should be medically optimized with β blockers, ACE inhibitors, antiplatelet agents (aspirin ± clopidogrel), and statins.1

SURGERY FOR THE COMPLICATIONS OF MYOCARDIAL INFARCTION

Surgery may be required for acute or chronic complications of myocardial infarction. Acute complications include ventricular septal rupture, free wall rupture, and acute mitral regurgitation. Patients are typically critically unwell and have cardiogenic shock. Mortality rates are very high. The major chronic complications of myocardial infarction are congestive cardiac failure and mitral regurgitation. A number of procedures to remodel the left ventricle and therefore improve the outcome of congestive cardiac failure have been developed. The causes and treatment of chronic ischemic mitral regurgitation are discussed in Chapter 10.

Acute Mitral Regurgitation

Acute mitral regurgitation64 causing shock is usually caused by rupture of the posteromedial papillary muscle and is associated with inferior myocardial infarction. The posteromedial papillary muscle is prone to infarction because it is supplied entirely by branches of the right coronary artery. In contrast, the anterolateral papillary muscle has dual blood supply from branches of the LAD and circumflex coronary arteries. The abrupt onset of shock and pulmonary edema 2 to 7 days following a myocardial infarction is the most useful diagnostic clue. The precipitating myocardial infarction may be clinically insignificant. The murmur of mitral regurgitation may be soft and limited to early systole; in the presence of shock, it may be inaudible. The diagnosis is best confirmed by echocardiography. A pulmonary artery catheter typically demonstrates pulmonary hypertension and elevated pulmonary artery wedge pressure by revealing large V waves.

Treatment involves stabilizing the patient with an IABP, inotropes, and diuretic therapy followed by urgent mitral valve (±CABG) surgery.

Acute mitral regurgitation may also occur after a myocardial infarction in the absence of papillary muscle rupture. This mitral regurgitation is usually not severe and may either settle with the resolution of myocardial stunning or progressively worsen due to left ventricular remodeling.

Ventricular Free Wall Rupture

Ventricular free wall rupture65 occurs in 0.8% to 6.2% of patients after myocardial infarction. Risk factors include female sex, increased age, and large, full-thickness infarction with persisting ST segment elevation. Late thrombolysis (>11 hr) increases the risk, whereas early thrombolysis (<7 hr) and PCI diminish the risk.

The majority of ruptures occur within 24 hours of infarction. The classic presentation is an abrupt onset of pulseless electrical activity or asystole in association with distended neck veins in a patient not previously shocked. Complete rupture is rapidly fatal, but in about 30% of patients, the presentation is subacute, showing signs of hypotension, syncope, recurrent chest pain, and arrhythmias. Pulsus paradoxus and distended neck veins are classic signs of tamponade but are absent in a significant proportion of cases of subacute rupture. Evidence of pericardial fluid and signs of tamponade should be sought by means of echocardiography. However, of the 20 patients who developed cardiac rupture in the SHOCK trial registry, only 15 had evidence of a pericardial collection on echocardiography.66 Furthermore, pericardial fluid can be identified echocardiographically in 25% of patients following myocardial infarction without evidence of rupture.

Following subacute rupture, a small proportion of patients will survive and go on to develop a contained rupture (ventricular pseudoaneurysm),67 but for the majority of patients, early surgery is the only hope for survival. Pericardiocentesis (see Chapter 40) may be performed as a temporizing measure prior to surgery. Mortality rates are very high.

Ventricular Septal Rupture

Ventricular septal rupture68 occurs in less than 2% of patients after myocardial infarction. It may occur within a few hours following a myocardial infarction but more commonly presents within a few days to a week. The condition is associated with the sudden onset of pulmonary edema, hypotension, a harsh pansystolic murmur best heard over the left sternal edge and, possibly, recurrence of angina. The ECG may show a new rightward axis and conduction defects such as right bundle branch or atrioventricular block.

With echocardiography, the condition can be distinguished from ventricular free wall rupture and papillary muscle rupture. Most defects are located in the anteroapical region of the septum and are best identified by demonstrating left-to-right flow across the septum by means of color-flow Doppler echocardiography. In many cases the actual defect itself is not visible through two-dimensional echocardiographic imaging. With a pulmonary artery catheter, a step-up in oxygen saturation of greater than 10% may be demonstrated between the right atrium and pulmonary artery. Pulmonary hypertension is usual. Functional mitral regurgitation is common, causing V waves on the pulmonary artery wedge pressure trace.

If the patient is sufficiently stable, coronary angiography should be performed prior to surgery to facilitate appropriate revascularization. If the patient’s clinical condition precludes angiography, the surgeon may consider “blind” revascularization based on the appearances of the heart and the site of the defect. Mortality rates are very high.

Surgery to Remodel the Left Ventricle

STEMI may be associated with significant scar formation and ventricular remodeling within the surrounding (noninfarcted) myocardium. Ventricular remodeling results in the loss of the normal cylindrical shape of the left ventricle and the development of a more spherical conformation. Left ventricular dilatation, specifically a left ventricular end-systolic volume index greater than 40 ml/m2 is an independent predictor of mortality following myocardial infarction.69

These observations have led to the development of a number of operations to remodel the left ventricle, of which the most widely employed is the Dor operation (Fig. 9-3). CABG surgery, mitral repair, or resection of endocardium and cryotherapy for ventricular arrhythmias may be performed at the same time. The aim of the surgery is to return the ventricle to a more physiologic shape and to reduce the left ventricular end-systolic volume index >60 ml/min/m2. The ideal candidate for this type of operation has a dilated left ventricle (endsystolic volume index >60 ml/min/m2), an anteroseptal scar with evidence of remote viability, graftable coronary disease, and minimal mitral regurgitation.

image

Figure 9.3 Dor procedure to remodel the left ventricle. An oblique pursestring suture (Jatene) is placed around the edges of the anteroapical scar. When the suture is tightened, the ventricular volume is reduced and the scar is excluded from the pumping chamber. A Dacron patch is used to close the remaining defect. End-diastolic sizing devices maybe used to avoid excessive ventricular volume reduction.

(Image reproduced with permission from O’Neill JO, Starling RC: Curr Treatment Options Cardiovasc Med 5:311-319, 2003.)

Dor has demonstrated an average increase in ejection fraction from 20% to 40% at 1 year following surgery and a perioperative mortality of 12% with this procedure.70 Despite the fact that the procedure involves a ventriculotomy and concomitant CABG surgery (and possibly also mitral valve surgery), patients do not usually have stormy postoperative courses. A period of support with inotropic therapy and possibly an IABP may be required. A feared complication of this procedure is an excessive reduction in ventricular volume, resulting in persisting postoperative congestive cardiac failure due to diastolic dysfunction.

Surgery of the left ventricle may also be indicated for resection of a true (dyskinetic) aneurysm or a chronic walled-off pseudoaneurysm.

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