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 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.
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 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).
Postoperative MI is classified as type 5 MI (Table 1) (4).
Table 1 - Clinical classification of types of myocardial InfarctionType 1 : Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissectionType 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 hypotensionType 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 bloodType 4a : Myocardial infarction associated with PCIType 4b : Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsyType 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
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).
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).
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