Coronary steal is conventionally de...

Coronary steal is conventionally defined as a fall in absolute coronary perfusion (ml/min/g) of collateralized myocardium after coronary arteriolar vasodilation, usually after IV administration of dipyridamole. It has been studied experimentally,[1-5] patterned theoretically,[6] demonstrated in humans,[7] and come into one's heads in 10 to 30 percent of patients with coronary artery disease undergoing dipyridamole perfusion imaging, as evidenced on chest pain, ECG changes, and abnormal perfusion scans.[8,9] The mechanism is a fall in perfusion compressing at the origin of collateral sailing crafts due to proximal stenoses or to proximal viscous friction developing at high pour rates even in normal arteries from which the collaterals arise. press outed in terms of circuit examples decreased collateral flow (steal) is suitable to proportionately greater increase in conductance of the normal vascular bed in parallel with the relatively subdued fixed conductance of the collateral bed, which cannot compensate further for the fall in hurry at their origin.[6]

In view of these mechanisms, the boundary "steal" is a misnomer, since house is not "stolen" from the collateralized bed by way of backward flow through collateral channels to the normal vascular bed. It purely reflects a fall in collateral deliquesce during arteriolar vasodilation below resting repress levels, thereby producing ischemia. While developing solitary in the presence of bitter coronary artery stenosis, collaterals in humans harbor the myocardium from necrosis and deteriorating contractile function if sufficiently bring outed over prolonged periods before occlusion occurs[1011] Although the extent of stenosis and the extent of time it is near prior to occlusion are recognized factors in collateral disclosure genetically mediated angioneogenesis may also be important.[12]

Coronary subendocardial steal is defined as a fall in absolute subendocardial perfusion with a rise or no change in subepicardial perfusion after coronary arteriolar vasodilation following IV dipyridamole. As nicely demonstrated in the article on Meerdink et al in this issue of Chest (see p 400) subendocardial steal present itselfs with severe coronary artery stenosis in the absence of collaterals. Although the drifts of low perfusion pressure in succession transmural flow distribution have been described,[1-5,13] this reflection definitively documents the occurrence and conditions for subendocardial steal associated with rigid stenoses in which collaterals play no part The mechanisms are the same as outlined previously. At normal resting conditions with strict stenosis, resting flow and/or distal coronary constraining force are reduced enough to stimulate compensatory subendocardial vasodilation, thereby using up its limited be derived reserve. Subendocardial conductance is therefore relatively fixed. In these circumstances, IV dipyridamole then causes subepicardial arterioles to vasodilate proportionately more than subendocardial arterioles. Consequently absolute perfusion falls in the subendocardium appropriate to greater increase in conductance of subepicardial ducts that are in parallel with relatively fixed conductance utensils of the subendocardium, which cannot compensate for the fall in distal crushing The necessary conditions for subendocardial steal are a bitter stenosis, which produces maximally vasodilated, fixed conductance, subendocardial arterioles, and a fall in distal constraining force after dipyridamole administration, which causes lower subendocardial perfusion. Thus, the mechanisms for coronary collateral steal and subendocardial steal are the same, yet the anatomy producing them is different.

Clinically, coronary steal, as manifested by means of chest pain and ST depression after IV dipyridamole, is usually a sign of unrelenting coronary artery disease with viable myocardium. In my experience, steal in the absence of collaterals, ie, subendocardial steal, is not commonly seen clinically, since these patients frequently have severe or unstable angina at cessation and are therefore likely to be exclud from dipyridamole stres Consequently in the majority of patients undergoing appropriate dipyridamole perfusion imaging, coronary steal is a sign of collaterals providing significant resting spring rather than subendocardial steal without collaterals. Figure 1 illustrates a clinical example of coronary steal demonstrated from positron emission tomography (PET) as a fall in stres activity below resting horizontals PET also provides the percent of the heart outside of 25 SD from normal which, for the polar map display of the ratio of absolute considers stress/rest, indicates the percent of the heart that is collateralized (Fig 2)

A rare patient with the hyperadrenergic syndrome of mitral valve prolapse may have angina and ST depression after IV dipyridamole relieved with aminophylline nevertheless no regional perfusion defect in succession PET scanning. These patients may have a form of sympathetically driven "fixed" subendocardial conductance producing subendocardial steal without coronary artery atherosclerosis. However, they are identifiable by dint of the absence of regional perfusion defects