الفهرس 
ANATOMY AND PHYSIOLOGY OF CORONARY CIRCULATIONOnly 14 pages are availabe for public view
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Abstract
The etiology of PMI is multifactorial. The perioperative period induces large, unpredictable and unphysiological changes in sympathetic tone, cardiovascular performance, coagulation and inflammatory response. These changes induce, in turn, unpredictable alterations in plaque morphology, function and progression. Simultaneous perioperative alterations in homeostasis and coronary plaque characteristics may trigger a mismatch of myocardial oxygen supply and demand by numerous mechanisms. If not alleviated in time, it will ultimately result in MI, irrespective of its aetiology.
So the aim is shifting from an emphasis on extensive non-invasive preoperative risk stratification to an emphasis on a combination of selective non-invasive testing, and aggressive perioperative pharmacological therapy.
The mechanism(s) and trigger(s) of perioperative myocardial ischaemia and infarction remain poorly understood. Existing data are inconclusive and do not allow us to decide definitively whether long-duration subendocardial myocardial ischaemia, or acute coronary occlusion due to plaque disruption or thrombosis, is the primary mechanism of perioperative myocardial injury in the individual patient.
In many patients with unstable coronary artery disease, numerous mechanisms are responsible for the unstable nature of the disease. These include coronary artery thrombosis, platelet aggregation and emboli, progression of coronary artery disease, coronary artery vasospasm and vasoconstriction, systemic and local inflammation and infection, and increased myocardial oxygen demand in the presence of a fixed stenosis.
Sudden rupture of a vulnerable plaque may occur spontaneously without apparent reason, or it may follow a particular event, such as extreme cardiovascular demand, exposure to cold or acute infection.
If the plaque disruption is major, with extensive exposure of thrombogenic core material to the blood stream, acute total coronary occlusion with subsequent myocardial infarction or sudden death may develop. If the disruption is minor, the forming thrombus can be non-occlusive and the patient may stay asymptomatic or develop unstable angina or a non-Q-wave infarction. A concomitant increase in coagulability and coronary vasoconstriction (as is common in the perioperative setting) may, however, transform a non-occlusive thrombus to an occlusive thrombus. Ultimately, the balance of thrombosis vs thrombolysis is the decisive factor in determining whether the clinical outcome will be myocardial ischaemia or myocardial infarction.
The best strategy for management of PMI is one that emphasizes prevention. Preventive strategies should be based on preoperative utilization and optimization of ß-blockers, 2-agonists if ß-blockers cannot be used, and HMG-CoA reductase inhibitors (statins). If MI does occur, a multidisciplinary approach involving the operating surgeon, cardiologist, and intensivist should be followed. The decision to get interventional or medical treatment should be individualized based on the category and severity of infarction (STEMI vs NSTEMI), type of surgery, and the need for hemostasis. Anticoagulant use is often needed. Particular vigilance will be required regarding the recognition and treatment of occult and overt bleeding and related complications.
Perioperative plaque stabilization by pharmacological means (statins, aspirin, ß-blockers) may be as important in the prevention of PMI as an increase in myocardial oxygen supply (by coronary revascularization), or a reduction in myocardial oxygen demand by ß-blockers or alpha2-agonists.
The use of surgical intervention (PTCA, PCI, etc...) is still a subject of controverse in patient with IHD under going non cardiac surgery.