Stress pharmacological myocardial perfusion scintigraphy (MPS) is a useful diagnostic tool to detect myocardial ischaemia and functional capacity as a preoperative cardiac risk stratification for non-coronary surgery.
Gives risk of perioperative events as ischaemia in three coronary artery territories >20 per cent of myocardium and left ventricular ejection fraction (LVEF) <50 per cent with reversible left ventricular (LV) cavity dilatation indicating higher risk of events.
Total area of ischaemia is more predictive than severity of ischaemia in a given segment.
Guides any further coronary intervention or medical management.
Is relative contraindication within 6 weeks post myocardial infarction.
Should not be used in isolation for pre-surgical risk assessment. It is but one piece of the puzzle to be evaluated, in concert with the more traditional information at the physician’s disposal.
Myocardial Perfusion Scintigraphy and Cardiac Risk Assessment
Single-photon emission computed tomography (SPECT) is a nuclear medicine topographic imaging technique that uses gamma rays. SPECT myocardial perfusion scintigraphy (MPS) is a well-established tool in assessing the perioperative risk of stable patients prior to elective non-cardiac surgery. It is a form of cardiac risk stratification using stress testing. Cardiac stress testing involves exercise ECG or stress imaging using pharmaceutical stress MPS or dobutamine stress echocardiography. Dobutamine stress echocardiography is comparable with MPS stress testing as a preoperative evaluation tool, but it should be avoided in patients with severe hypertension, significant arrhythmias or poor echocardiographic images.
Pathophysiology of Pharmaceutical Myocardial Perfusion Scintigraphy
Stressor agents include adenosine, dipyridamole and dobutamine. Dipyridamole, adenosine and regadenoson all cause coronary vasodilation by increasing endogenous adenosine levels. They cause stress on the heart by a complicated mechanism called the steal phenomenon.
Vertical steal (see Figure 5.B.1) requires the presence of a coronary stenosis. When vasodilation occurs after drug administration, the subepicardium steals blood from the subendocardium due to a fall in post-stenotic pressure. This causes a critical fall in subendocardial perfusion pressure.
At rest, perfusion in the circumflex artery (Cx) is maintained due to vasodilation of the arteriolar bed (larger circles downstream from epicardial vessel), thus using some of the coronary flow reserve (CFR). After dipyridamole-induced vasodilation, flow through the left anterior descending artery (LAD) increases significantly (as it can vasodilate normally since no CFR is used at rest because there is no stenosis). However, the fall in perfusion pressure through the stenosed artery causes a critical drop in perfusion pressure to the capillary bed downstream, resulting in closing or ‘derecruitment’ of the capillaries.
Horizontal steal (see Figure 5.B.2) requires the presence of a collateral circulation. The CFR must be exhausted in the vessel receiving a collateral supply and at least partially preserved in the vessel giving off the collateral supply. In this situation, when arterial vasodilation occurs, the arteriolar bed of the donor vessel now ‘competes’ with that of the receiving vessel. As a result, the vessel with partially preserved CFR receives more blood and the region that was dependent on the collateral circulation is now rendered ischaemic.