Early cardiac complications of coronary artery bypass graft surgery

INTRODUCTION — The treatment of coronary heart disease has evolved significantly over the past several years due in part to improvement in both surgical and percutaneous revascularization techniques. The majority of patients with chronic stable angina are still treated with medical therapy; however, revascularization with either coronary artery bypass graft surgery (CABG) or percutaneous coronary intervention should be considered in several subgroups. (See "Chronic coronary syndrome: Indications for revascularization".)

The early cardiac complications after CABG will be reviewed here. Noncardiac complications and perioperative mortality after CABG are discussed separately. (See "Early noncardiac complications of coronary artery bypass graft surgery" and "Operative mortality after coronary artery bypass graft surgery".)

CARDIAC COMPLICATIONS

Perioperative MI — We recommend obtaining pre- and post-procedural electrocardiographs (ECGs), as well as measurements of troponin at baseline and 8 to 16 hours after the procedure. The diagnosis of perioperative myocardial infarction (MI) may be difficult to make after coronary artery bypass graft surgery (CABG), since cardiac enzyme elevations occur as a result of the surgical procedure and since ECG changes may reflect postoperative pericardial inflammation.

We suggest using the Joint European Society of Cardiology/American College of Cardiology Foundation/American Heart Association/World Health Federation Task Force definition for MI (type 5) after CABG, which requires increases of biomarkers greater than five times the 99^th percentile of the upper reference limit plus either new pathologic Q waves or new left bundle branch block, angiographically documented new graft, native coronary artery occlusion, or imaging evidence of new loss of viable myocardium [1]. (See "Diagnosis of acute myocardial infarction".)

The potential role for ischemic preconditioning to lower the risk of perioperative MI is discussed separately. (See "Myocardial ischemic conditioning: Clinical implications", section on 'Coronary artery bypass graft surgery'.)

Q wave MI — Perioperative MI, as defined by new Q waves on the postoperative ECG, occurs in 4 to 5 percent of patients, with a range among hospitals of 0 to 10 percent [2,3]. Although usually reflecting a new MI, new Q waves after CABG can, in occasional patients, represent unmasking of a previous MI [4].

A new Q wave MI is usually attributed to poor distal perfusion after grafting of the more proximal arteries has been performed. The incidence of MI is less in low-risk patients and higher in those with one or more of the following risk factors:

●Cardiomegaly [2]

●Long time on cardiopulmonary bypass [2]

●Repeat CABG (6.1 percent in one report) [5]

●CABG combined with other cardiac surgery

A new Q wave on the ECG is strongly suggestive of a worse outcome. In a report from the Coronary Artery Surgery Study (CASS), the 62 patients who had a Q wave MI had a higher mortality in-hospital (9.7 versus 1.0 percent in the 1278 patients without a Q wave MI) [2]. Among patients who survived to discharge, there was no significant difference in mortality at three years (6 versus 4 percent).

Worse outcomes were also noted in a report from the BARI trial of patients with stable angina who had multivessel coronary disease and were treated with either CABG or percutaneous transluminal coronary angioplasty [3]. Among 1427 patients who underwent CABG, the five-year mortality rate was higher when a new Q wave developed (8.2 versus 3.7 percent for no new ECG changes, adjusted relative risk 2.6). There was no increase in mortality associated with other new ECG changes (ST segment elevation or depression or T wave abnormalities). In contrast to the above report from CASS, the mortality risk increased with time after discharge from the hospital.

Elevated biochemical markers — We recommend obtaining pre- and post-procedural troponin at baseline and 8 to 16 hours after the procedure. As discussed above (see 'Perioperative MI' above), elevations in serum biomarkers of myocardial necrosis (creatine kinase MB fraction [CK-MB] and troponin) are necessary for the diagnosis of perioperative MI. However, the significance of elevations in these biomarkers is made difficult due to their release as a routine sequela of CABG [6-11]. An increase in serum CK-MB above the upper limit of normal has been noted in 62 to 90 percent of patients [8,9]. (See "Troponin testing: Clinical use", section on 'Coronary artery revascularization'.)

Patients with elevations in serum biomarkers after CABG have a worse prognosis than those without [7-10,12]. However, the threshold of elevated troponin that identifies patients who have had a perioperative MI or other periprocedural myocardial injury has been uncertain. Based on earlier studies, current guidelines propose a threshold of elevated troponin that is 10 times or greater than the troponin upper reference limit [12-14]. However, a more recent study [15] found troponin I ratio levels that predict clinically important periprocedural myocardial injury were markedly higher than prior studies had demonstrated [12]. In this prospective investigation of 13,862 cardiac surgery patients in a multicenter international registry, the association between postoperative day 1 troponin I levels and 30-day mortality was studied (2.1 percent of patients died within 30 days after surgery) [15]. Among patients who underwent isolated CABG for coronary artery disease or for aortic valve replacement or repair, the threshold troponin level associated with hazard ratio of more than 1 for death within 30 days was 5670 ng per liter (this level was 218 times the troponin upper reference limit). Among patients who underwent other cardiac surgeries, the corresponding threshold troponin level was 12,981 ng per liter (a level 499 times the upper reference limit).

These results are in contrast to the prior study, which investigated the relationship between myocardial enzyme elevation and survival following CABG in nearly 19,000 patients enrolled in seven randomized trials or registries [12]. The 30-day mortality increased significantly as the ratio of the value of troponin to the upper limit of normal increased; the relative risk of death was 1.00, 1.89, 2.22, 3.61, and 10.91 for troponin ratios of 6 to <10, 10 to <20, 20 to <40, 40 to <100, and ≥100, respectively. A potential reason for the marked difference in association between troponin ratio and thresholds for mortality as compared with the more recent study is that the specific troponin assays were different in the two studies.

These marked elevations in serum biomarkers of myocardial necrosis are thought to result from early graft failure, inadequate myocardial protection during bypass, and/or distal embolization of plaque material [9].

Elevated serum troponins appear to be more specific and sensitive markers than CK-MB of a new MI after CABG, and may be more predictive of early complications [11,16]. This issue was addressed in a report of 224 patients in whom serum troponin T and CK-MB were measured every eight hours after cardiac surgery [11]. In a multivariable analysis, serum troponin T concentrations ≥1.58 ng/mL (which represented the upper quintile) were the strongest predictor of postoperative death or shock immediately postoperatively or at 18 to 24 hours. Serum CK-MB did not have independent prognostic importance when troponin T was measured. Long-term data were not provided.

Early graft occlusion — Early (within the first 30 days after surgery) occlusion occurs in approximately 5 to 10 percent of saphenous vein grafts. These occlusions are usually thrombotic and are generally related to technical problems at the anastomosis; injury related to manipulation during harvesting may also be important [17]. The risk of early graft occlusion appears to be reduced by aspirin therapy, which is typically restarted within six hours after surgery. (See "Coronary artery bypass surgery: Perioperative medical management", section on 'Aspirin'.)

Approximately 3 to 6 percent of patients develop clinically apparent postoperative ischemia as manifested by ischemic symptoms, significant ischemic ECG abnormalities, hemodynamic instability, and/or ventricular arrhythmias [18-20].

In two series of patients undergoing urgent postoperative angiography for recurrent ischemia, SVG occlusion or stenosis occurred in 37 to 56 percent and internal mammary graft occlusion or stenosis in 12 to 29 percent [18,19]. In one of these studies, 131 of 2052 patients (6.4 percent) undergoing CABG met one or more of the criteria for ischemia at a median of 12 hours (range 0.5 to 96 hours) after CABG [18]. Angiography was performed in 108, while 23 went immediately to surgery because of severe hemodynamic compromise. Angiography revealed normal grafts in 45, saphenous vein or internal mammary artery graft occlusion in 41, incorrect anastomosis in 29, graft stenosis in 14, graft spasm or a displaced graft in six each, poor distal runoff in five, and incomplete revascularization in two.

Revascularization is generally attempted if the anatomy is appropriate. In a study in which repeat CABG was evaluated, 16 of 43 patients who underwent acute angiography were not revascularized because it was not necessary or not feasible due to poor vessel quality or nonavailability of graft material [19].

The optimal revascularization strategy for early graft occlusion is not known. Repeat CABG is one approach [18,19], while balloon angioplasty with and without stenting has been performed immediately after surgery and for treatment of fresh anastomoses [20-22]. Both procedures are associated with risk:

●Repeat CABG has been associated with 30-day mortality rates of 7 to 9 percent in clinically stable patients and as high as 39 to 50 percent in patients with severe hemodynamic compromise or severe sustained ventricular tachyarrhythmias who underwent immediate surgery [18,19].

●Percutaneous coronary intervention (PCI) may be associated with high rates of angiographic and bleeding complications, particularly in patients treated very soon after cardiac surgery. In a series of 10 patients undergoing urgent PCI (mostly saphenous vein graft [SVG] lesions, six fixed with a drug-eluting stent), significant periprocedural complications occurred in four [20]. There were three perforations (one during stenting of a distal vein graft anastomosis, one during high-pressure balloon angioplasty of an internal mammary graft distal anastomosis, and one during PCI of a native artery total occlusion). Acute thrombosis of a sirolimus stent occurred in a fourth patient, who was not loaded with clopidogrel. Major bleeding complications occurred in four patients, including two with cardiac tamponade, one with gastrointestinal bleeding, and one with excessive chest tube drainage.

The authors concluded that the safety of drug-eluting stents was uncertain in such patients [20]. This is a particular concern in patients at high risk for perioperative bleeding, since the need to discontinue antiplatelet therapy increases the risk of stent thrombosis. The balance between stent thrombosis and major bleeding is especially critical in the early postoperative period. (See "Coronary artery stent thrombosis: Incidence and risk factors".)

Recommendations for therapy — The 2005 American College of Cardiology/American Heart Association/Society for Cardiovascular Angiography and Interventions (ACC/AHA/SCAI) guideline update for PCI concluded that there was general agreement that, if feasible, PCI should be performed in patients with early ischemia (usually within 30 days) after CABG [23]. When the lesion is in an SVG, use of a distal embolic protection device was recommended, if feasible. This approach was not changed in the 2011 American College of Cardiology Foundation/AHA/SCAI focused update [24,25].

It is our practice to recommend emergent cardiac catheterization for patients developing acute ischemia soon after CABG. Percutaneous revascularization is performed when feasible and if at least a moderate amount of myocardium is jeopardized. We believe this offers advantages over early reoperation in many patients. Caution is required during treatment of fresh anastomoses and the operator should be prepared to treat possible perforations, including the placement of covered stents if needed.

We generally attempt low pressure balloon angioplasty for early treatment of distal anastomoses with stenting used only if the result is suboptimal. In comparison, for severely thrombotic grafts, we frequently attempt revascularization of the native vessel with drug-eluting stents. If stents are to be employed, we proceed with usual measures for the prevention of thrombosis, including glycoprotein IIb/IIIa inhibitors and clopidogrel loading, and are prepared to treat bleeding complications if needed. (See "Early noncardiac complications of coronary artery bypass graft surgery", section on 'Bleeding' and "Antithrombotic therapy for elective percutaneous coronary intervention: General use".)

Issues related to the management of late recurrent angina after CABG are discussed separately. In this setting, angina may be due to graft problems or progression of native vessel disease. (See "Late recurrent angina pectoris after coronary artery bypass graft surgery".)

Low cardiac output — A frequent complication of CABG is a low cardiac output, primarily due to left ventricular dysfunction. In a prospective observational study of over 8600 patients undergoing CABG between 1992 and 1997, the incidence of low output syndrome varied from 6 percent with a left ventricular ejection fraction (LVEF) >40 percent to 12 percent with an LVEF between 20 and 40 percent to 23 percent with an LVEF <20 percent [26].

The impairment in left ventricular function can result from a variety of factors, including:

●Cardioplegic arrest and ischemic injury, which can lead to myocardial stunning and diastolic dysfunction [27].

●Reduced preload, which, in the immediate postoperative period, can be induced by loss of vasomotor tone, intraoperative and postoperative blood loss, increased capillary permeability, and a high urine output due to hypothermia.

●Excessive afterload due to hypertension [28,29]

●Arrhythmias

●Perioperative MI

●Mechanical complications

The low cardiac output is often transient and responds to fluid replacement and/or a brief period of inotropic support or, in patients with marked hypertension, nitroprusside. However, cardiogenic shock can occur and, not surprisingly, is an adverse predictor of outcome [30].

When pharmacologic therapy is ineffective, mechanical support with an intraaortic balloon pump or left ventricular assist device is necessary. Occasional patients need to return to the operating room for treatment of a mechanical problem such as acute graft failure or tamponade. (See "Intraaortic balloon pump counterpulsation" and "Short-term mechanical circulatory assist devices" and "Acute myocardial infarction: Mechanical complications".)

Vasodilatory shock — Cardiopulmonary bypass, not limited to bypass surgery, can be complicated by vasodilatory (or distributive) hypotension or shock, which is characterized by a primary and marked reduction in systemic vascular resistance with a well-preserved or increased cardiac output. (See "Definition, classification, etiology, and pathophysiology of shock in adults".)

The usual treatment for vasodilatory shock in the setting of cardiac surgery is low-dose intravenous norepinephrine. At least some patients have inappropriately low serum arginine vasopressin concentrations and, in those who do not respond to norepinephrine, intravenous vasopressin may be effective. Increased production of nitric oxide has also been implicated, and treatment with methylene blue, which inhibits the production of nitric oxide, has been reported to be beneficial. (See "Postoperative complications among patients undergoing cardiac surgery", section on 'Vasodilatory shock'.)

Arrhythmias — Arrhythmias, most often tachyarrhythmias, are common after CABG. Although it is difficult to predict patients at risk for perioperative arrhythmia, preoperative hypokalemia may be important. In a review of 2402 patients undergoing elective CABG, preoperative serum potassium concentrations below 3.5 meq/L increased the risk for serious perioperative arrhythmias (odds ratio 2.2), the need for resuscitation, and the incidence of atrial fibrillation (AF) and flutter (odds ratio 1.7) [31].

Atrial fibrillation — AF occurring after CABG is described in detail elsewhere. (See "Atrial fibrillation and flutter after cardiac surgery".)

Summarized briefly, AF occurs in 15 to 40 percent of patients undergoing CABG and up to 60 percent of those who undergo combined CABG with valve replacement. Beta blockers, sotalol, and amiodarone reduce the frequency of postoperative AF by 52 to 65 percent [32]. The beta blocker should be given before or as soon as possible after cardiac surgery [33,34].

The optimal duration of therapy for prevention of postoperative atrial arrhythmias is uncertain, but the beta blocker is often continued until the first postoperative visit. However, many patients who undergo CABG have a clear indication for the continued use of beta blocker therapy (eg, previous MI, heart failure, or hypertension).

AF that develops after CABG is usually self-limited in patients without a prior history of AF. The arrhythmia reverts spontaneously to sinus rhythm within 24 hours in 80 percent and by six to eight weeks in over 90 percent. (See "Atrial fibrillation and flutter after cardiac surgery".)

Ventricular tachyarrhythmias — Ventricular tachyarrhythmias associated with CABG have a variable effect on prognosis. Nonsustained ventricular tachycardia (VT) occurs in 17 to 97 percent of patients and is thought to be reperfusion-induced; it is typically benign, although some patients may be at increased risk of future life-threatening arrhythmias [35-37].

Sustained monomorphic or polymorphic VT or ventricular fibrillation (VF) occur in approximately 1 to 3 percent of patients, usually within the first week after surgery [35,37-41]. In two reports including a total of 9159 patients, 114 (1.2 percent) with VT or VF, predictors of perioperative ventricular arrhythmias included [38,41]:

●Age <65 years

●Female sex

●Body mass index <25 kg/m²

●Unstable angina

●Ejection fraction ≤50 percent

●Pulmonary or systemic hypertension

●Prolonged cardiopulmonary bypass time

●Requirement for inotropes and/or an intraaortic balloon pump

Patients with perioperative VT or VF, compared to those without these arrhythmias, had a significant increase in postoperative mortality (24.6 versus 1.5 percent). In one of the reports, intraoperative VT or VF had a greater impact on mortality than postoperative arrhythmia (42 versus 18 percent) [38].

Polymorphic VT is typically associated with perioperative MI, combined with multiple risk factors that are present in the perioperative period such as hemodynamic instability, increased sympathetic activity, and metabolic abnormalities. In comparison, sustained monomorphic VT is most likely in patients with a history of a prior MI, heart failure, and depressed left ventricular function [39,40]. When all three of these factors are present, the risk of VT in one report was 30 percent, a 14-fold increase compared to the absence of all three risk factors [39]. An additional factor may be the placement of grafts across a noncollateralized occlusion in a vessel supplying an infarct zone [39], suggesting that reperfusion may restore electrical function, creating reentrant circuits, in a previously quiescent region of myocardium.

Magnesium supplementation may reduce the incidence of postoperative ventricular arrhythmias. In a meta-analysis, 10 trials including 1195 patients were identified that evaluated the use of magnesium for this purpose [42]. Ventricular arrhythmias occurred significantly less often in patients treated with magnesium compared to controls (6 versus 13 percent; relative risk 0.52). There was no effect on length of hospital stay, frequency of perioperative MI, or mortality.

Ischemic preconditioning reduces ischemia-reperfusion injury and appears to reduce sustained VT/VF after CABG. This was illustrated in a trial of 86 patients who were randomly assigned to two periods of two minutes of ischemia followed by three minutes of reperfusion or to no ischemic preconditioning [37]. On continuous ECG monitoring, ischemic preconditioning was associated with significant reductions in VF after declamping (49 versus 79 percent) and VT during early reperfusion (0.7 versus 3.7 percent) and 24 hours after reperfusion (0.1 versus 2.1 percent). (See "Myocardial ischemic conditioning: Clinical implications".)

Bradyarrhythmias — Postoperative bradyarrhythmias requiring permanent pacemaker implantation occur in 0.8 to 4 percent of patients [43-45]. The most common abnormalities are complete atrioventricular block with a narrow or wide complex escape rhythm, sinus node dysfunction, and a nodal rhythm. (See "Postoperative complications among patients undergoing cardiac surgery", section on 'Dysrhythmias'.)

Pericarditis, pericardial effusion, and tamponade — The presentation and clinical course of pericarditis after CABG, which is due to pericardial injury and known as a postpericardiotomy syndrome, is comparable to that of the post-MI syndrome. The most frequent complaint is chest pain, occurring a few days to several weeks after surgery. (See "Post-cardiac injury syndromes" and "Pericardial complications of myocardial infarction", section on 'Post-cardiac injury syndrome'.)

Serial echocardiography shows that postoperative pericardial effusion is considerably more common than clinically apparent disease, occurring in as many as 85 percent of patients [46]. The effusion is usually present by the second postoperative day, but may not occur until day 10. In one report, effusion was present in 22 percent of patients at 20 days and 8 percent at 30 days [47].

In most cases, the effusion is small and clinically insignificant; however, the effusion may be large, resulting in tamponade and hemodynamic instability and requiring urgent therapy with pericardiocentesis or reoperation. Postoperative anticoagulation may increase the risk of tamponade in patients who develop an effusion [47,48]. In some patients, continuing pericardial inflammation over months leads to a thickened, fibrous pericardium and the signs and symptoms of constrictive pericarditis. (See "Constrictive pericarditis: Diagnostic evaluation" and "Cardiac tamponade".)

EARLY NONCARDIAC SURGERY — A related question is how soon after cardiac surgery can a patient proceed with elective noncardiac surgery. There are three major concerns:

●Incomplete sternal healing. We suggest waiting at least six weeks prior to any procedure in which intubation/mechanical ventilation may be necessary.

●Bacteremia in patients who have received prosthetic valves and are undergoing bowel or urological procedures. We suggest waiting two to three months for surgery on the bowel or genitourinary tract in these patients.

●Thromboembolic risk early after valve surgery. Despite routine anticoagulation, thromboembolic risk is elevated early after mechanical or bioprosthetic valve replacement or mitral valve annuloplasty. Interruption of anticoagulation for surgery or complications of surgery may exacerbate this risk. We suggest waiting at least three months following valve surgery prior to elective noncardiac surgery. (See "Antithrombotic therapy for mechanical heart valves".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Coronary artery bypass graft surgery".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on “patient info” and the keyword(s) of interest.)

●Beyond the Basics topics (see "Patient education: Coronary artery bypass graft surgery (Beyond the Basics)" and "Patient education: Recovery after coronary artery bypass graft surgery (CABG) (Beyond the Basics)")

●Basics topic (see "Patient education: Coronary artery bypass graft surgery (The Basics)")

SUMMARY — The major early cardiac complications of coronary artery bypass graft surgery include:

●Myocardial infarction (MI) (see 'Perioperative MI' above)

●Graft occlusion (with or without MI) (see 'Early graft occlusion' above)

●Low cardiac output due to ventricular dysfunction (see 'Low cardiac output' above)

●Vasodilatory shock (see 'Vasodilatory shock' above)

●Atrial and ventricular arrhythmias (see 'Arrhythmias' above)

●Pericarditis (see 'Pericarditis, pericardial effusion, and tamponade' above)

ACKNOWLEDGMENT — The UpToDate editorial staff thank Dr. Julian M. Aroesty for his past contributions as an author to prior versions of this topic review.