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Postoperative myocardial
infarction
An article from the e-journal of the ESC Council for
Cardiology Practice
05 Oct 2011
Prof. Nawwar Al-Attar

Biomarker values above five times the 99th percentile of the normal reference
range during the first 72 hrs following coronary artery bypass graft

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surgery (CABG), when associated with the appearance of new pathological


Q-waves or new left bundle branch block (LBBB), angiographically
documented new graft or native coronary artery occlusion, or imaging
evidence of new loss of viable myocardium, should be considered as
diagnostic of CABG-related myocardial infarction.

Table of contents
I - CLINICAL CLASSIFICATION OF MYOCARDIAL INFARCTION
II - DIAGNOSIS
III - MANAGEMENT
REFERENCES

Acute Coronary Syndromes (ACS)

Postoperative MI occurs in 2-15% of patients following cardiac surgery. It leads


to reduced survival - both short and long term, longer hospital stays and results in a
greater burden on hospital finances.
While diagnosis of MI in a non-operative context depends on a triad of 1) clinical
symptoms, 2) a specific cardiac biomarkers increase and 3) ECG changes, the same
cannot be said following cardiac surgery (1, 2, 3).
Even cases of non complicated procedures frequently induce ECG modifications and
generally increased levels of specific cardiac biomarkers well above those which, in
ambulatory patients, are indicative of myocardial infarction.
In 2007, a joint task force of the European Society of Cardiology, American College of
Cardiology, American Heart Association and World Heart Federation for the Redefinition
of MI put forward an expert consensus document entitled Universal definition of
myocardial infarction.
Despite absence of formal proof, the Task Force suggests that biomarker values above
five times the 99th percentile of the normal reference range during the first 72 hrs
following CABG, when associated with the appearance of new pathological Q-waves or

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new LBBB, angiographically documented new graft or native coronary artery occlusion, or
imaging evidence of new loss of viable myocardium, should be considered as diagnostic
of CABG-related myocardial infarction (4).

I - CLINICAL CLASSIFICATION OF MYOCARDIAL INFARCTION


Postoperative MI is classified as type 5 MI (Table 1) (4).
Table 1 - Clinical classification of types of myocardial Infarction
Type 1 : Spontaneous myocardial infarction related to ischemia due to a primary coronary
event such as plaque erosion and/or rupture, fissuring, or dissection
Type 2 : Myocardial infarction secondary to ischemia due to either increased oxygen
demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia,
arrhythmias, hypertension, or hypotension
Type 3 : Sudden unexpected cardiac death, including cardiac arrest, often with symptoms
suggestive of myocardial ischemia, accompanied by presumably new ST elevation, or new
LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at
autopsy, but death occurring before blood samples could be obtained, or at a time before
the appearance of cardiac biomarkers in the blood
Type 4a : Myocardial infarction associated with PCI
Type 4b : Myocardial infarction associated with stent thrombosis as documented by
angiography or at autopsy
Type 5 : Myocardial infarction associated with CABG
Preoperative comorbidities and cardiovascular risk factors are the major determinants of
postoperative complications that follow CABG. Prior to CPB, episodes of preoperative
ischemia especially are particularly associated with higher postoperative incidence of MI.
This is compounded by postoperative tachycardia, hypotension and anemia (5). Indeed
71% of postoperative complications appeared in patients where the perioperative acute
coronary syndrome was not resolved prior to surgical intervention (6). The main
preoperative risk factors are summarised in table 2 (7).
Table 2 -Preoperative risk factors
Age >70 years
Female sex
Renal failure
Diabetes
Peripheral artery disease
Peripheral artery disease
Emergency or redo surgery
Severe LV dysfunction (LVEF<35%) or cardiogenic shock

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Preoperative MI

II - DIAGNOSIS
Establishing a definite diagnosis of postoperative MI can be difficult. A large spectrum of
lesions ranging from transient myocardial ischemia to complete necrosis can occur. The
classical clinical approach using elements such as chest pain, ECG changes and increased
cardiac enzymes (CK-MB, troponin) can be misleading and inadequate, missing numerous
coronary events albeit less severe but frequent enough to call for therapeutic
intervention. Classical signs are often masked by postoperative analgesia that can make
ischemia silent. Q waves are frequently absent and non-specific ECG modifications
following cardiac surgery can blur clinical presentation. Finally, elevation of enzymes
especially post- surgery CK-MB can further complicate the interpretation of biomarkers
in the diagnosis of MI. Current recommendations suggest that biomarker values above
five times the 99th percentile of the normal reference range during the initial 72 hrs
following CABG, when associated with the appears of new pathological Q-waves or new
LBBB, or angiographically documented new graft or native coronary artery occlusion, or
imaging evidence of new loss of viable myocardium, should be considered as diagnostic
of CABG-related myocardial infarction (4).

III - MANAGEMENT
Specific treatment of myocardial ischemia after CABG depends primarily on findings
obtained by imaging techniques, namely, coronary angiography.
In symptomatic patients, early graft occlusion has been identified as the cause of
ischemia in 75% of cases. Perioperative coronary angiography has shown up to 8% of
early occlusions of venous grafts following CABG (8). Emergency PCI with
desobstruction/stenting of the occluded graft is an alternative to emergency surgical
reintervention and is associated with acceptable results and fewer complications. It is
advised that the target for PCI should be the body of the native vessel while freshly
occluded venous grafts or the anastomosis itself should not be targeted due to the risk of
embolisation or perforation. Surgery should be favored if the graft or native artery
appears unsuitable for PCI, or if several important grafts are occluded.
In asymptomatic patients, re-operation or PCI should only be considered if the artery is a
good size, severely narrowed and supplies a large territory of myocardium. Redo CABG or
PCI should be decided by the Heart Team (9).

REFERENCES

1. Chen JC, Kaul P, Levy JH, Haverich A, Menasche P, Smith PK, Carrier M, Verrier ED, Van de Werf F, Burge R,

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Finnegan P, Mark DB, Shernan SK. Myocardial infarction following (http://www.ncbi.nlm.nih.gov/pubmed


/17414091)coronary artery bypass graft surgery increases healthcare resource utilization. Crit Care Med
2007;35:1296-1301
2. NALYSNYK L, FAHRBACH K, REYNOLDS MW, ZHAO SZ, ROSS S. Adverse events in coronary artery bypass
graft (CABG) trials: a systematic review (http://www.ncbi.nlm.nih.gov/pubmed/12807853)and analysis. Heart
2003; 89:767-72
3. Ramsay J, Shernan S, Fitch J, Finnegan P, Todaro T, Filloon T, Nussmeier NA. Increased creatine kinase MB
(http://www.ncbi.nlm.nih.gov/pubmed/15678039) level predicts postoperative mortality after cardiac surgery
independent of new Q waves. J Thorac Cardiovasc Surg 2005;129:300-306
4. Thygesen K, Alpert JS, White HD; Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial
Infarction. Universal definition (http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&
pmid=17951287)of myocardial infarction. Eur Heart J. 2007 Oct;28(20):2525-38.
5. LEUNG JM, OKELLY BF, MANGANO DT. Relationship of regional wall motion abnormalities to
hemodynamic indices (http://www.ncbi.nlm.nih.gov/pubmed/2240670)of myocardial supply and demand in
patients undergoing CABG surgery. Anesthesiology 1990; 73:802-9
6. MOISES VA, MESQUITA CB, CAMPOS O, et al. Importance of intraoperative transesophageal
echocardiography during coronary artery surgery without cardiopulmonary bypass
(http://www.ncbi.nlm.nih.gov/pubmed?term=MESQUITA CB 1998). J Am Soc Echocardiogr 1998; 11:1139-44
7. NASHEF SAM, ROQUES F, MICHEL P, et al. European system for cardiac operative risk evaluation
(EuroSCORE (http://www.ncbi.nlm.nih.gov/pubmed/10456395)). Eur J Cardiothorac Surg 1999; 16:9-13
8. Zhao DX, Leacche M, Balaguer JM, Boudoulas KD, Damp JA, Greelish JP, Byrne JG, Ahmad RM, Ball SK,
Cleator JH, Deegan RJ, Eagle SS, Fong PP, Fredi JL, Hoff SJ, Jennings HS III, McPherson JA, Piana RN, Pretorius
M, Robbins MA, Slosky DA, Thompson A. Routine intraoperative completion angiography after coronary
artery bypass grafting and 1-stop hybrid revascularization results from a fully integrated hybrid
catheterization laboratory/operating room (http://www.ncbi.nlm.nih.gov/pubmed/19147039). J Am Coll
Cardiol 2009;53:232241.
9. European Association for Percutaneous Cardiovascular Interventions, Wijns W,Kolh P, Danchin N, Di Mario C,
Falk V, Folliguet T, Garg S, Huber K, James S, Knuuti J, Lopez-Sendon J, Marco J, Menicanti L, Ostojic M, Piepoli
MF, Pirlet C, Pomar JL, Reifart N, Ribichini FL, Schalij MJ, Sergeant P, Serruys PW, Silber S, Sousa Uva M,
Taggart D; ESC Committee for Practice Guidelines, Vahanian A, Auricchio A, Bax J, Ceconi C, Dean V, Filippatos
G, Funck-Brentano C, Hobbs R, Kearney P, McDonagh T, Popescu BA, Reiner Z, Sechtem U, Sirnes PA, Tendera
M, Vardas PE, Widimsky P; EACTS Clinical Guidelines Committee, Kolh P, Alfieri O, Dunning J, Elia S, Kappetein
P, Lockowandt U, Sarris G, Vouhe P, Kearney P, von Segesser L, Agewall S, Aladashvili A, Alexopoulos D,
Antunes MJ, Atalar E, Brutel de la Riviere A, Doganov A, Eha J, Fajadet J, Ferreira R, Garot J, Halcox J, Hasin Y,
Janssens S, Kervinen K, Laufer G, Legrand V, Nashef SA, Neumann FJ,Niemela K, Nihoyannopoulos P, Noc M,
Piek JJ, Pirk J, Rozenman Y, Sabate M, Starc R, Thielmann M, Wheatley DJ, Windecker S, Zembala M. Guidelines
on myocardial revascularization (http://eurheartj.oxfordjournals.org/content/31/20/2501.extract): The Task
Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European
Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J. 2010 Oct;31(20):2501-55.
VolumeNumber:
Vol10 N4

The content of this article reflects the personal opinion of the author/s and is
not necessarily the official position of the European Society of Cardiology.

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