Portal de Periódicos da CAPES

Coronary Steal

1989; Elsevier BV; Volume: 96; Issue: 2 Linguagem: Inglês

10.1378/chest.96.2.227

1931-3543

K. Lance Gould,

Ultrasound and Hyperthermia Applications

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,1Schaper W Gunter G Winkler B Schaper J. The collateral circulation of the heart.Prog Cardiovasc Dis. 1988; 31: 57-77Abstract Full Text PDF PubMed Scopus (160) Google Scholar, 2Flameng W Wusten B Schaper W. On the distribution of myocardial blood flow: II.Effects of arterial stenosis and vasodilation. Basic Res Cardiol. 1974; 69: 435-446Crossref PubMed Scopus (69) Google Scholar, 3Flameng W Wusten B Winkler B Pasyk S Schaper W. Influence of perfusion pressure and heart rate on local myocardial flow in the collateralized heart with chronic coronary occlusion.Am Heart J. 1975; 89: 51-59Abstract Full Text PDF PubMed Scopus (49) Google Scholar, 4Becker LC. Conditions for vasodilator-induced coronary steal in experimental myocardial ischemia.Circulation. 1978; 57: 1103-1110Crossref PubMed Scopus (276) Google Scholar, 5Patterson RE Kirk ES. Coronary steal mechanisms in dogs with one-vessel occlusion and other arteries normal.Circulation. 1983; 67: 1009-1015Crossref PubMed Scopus (74) Google Scholar modeled theoretically,6Demer L Gould KL Kirkeeide R. Assessing stenosis severity: coronary flow reserve, collateral function, quantitative coronary arteriography, positron imaging, and digital subtraction angiography: a review and analysis.Prog Cardiovasc Dis. 1988; 30: 307-322Abstract Full Text PDF PubMed Scopus (71) Google Scholar demonstrated in humans,7Demer LL Goldstein R Mullani N Kirkeeide R Smalling R Nishikawa A et al.Coronary steal by noninvasive PET identifies collateralized myocardium.J Nucl Med. 1986; 27: 977Google Scholar and occurs in 10 to 30 percent of patients with coronary artery disease undergoing dipyridamole perfusion imaging, as evidenced by chest pain, ECG changes, and abnormal perfusion scans.8Albro PC Gould KL Westcott RJ Hamilton GW Ritchie JW Williams DL. Noninvasive assessment of coronary stenoses by myocardial imaging during pharmacologic coronary vasodilation: III.Clinical trial. Am J Cardiol. 1978; 42: 751-760Abstract Full Text PDF PubMed Scopus (308) Google Scholar,9Chambers CE Brown KA. Dipyridamole-induced ST segment depression during thallium-201 imaging in patients with coronary artery disease: angiographic and hemodynamic determinants.J Am Coll Cardiol. 1988; 12: 37-41Abstract Full Text PDF PubMed Scopus (80) Google Scholar The mechanism is a fall in perfusion pressure at the origin of collateral vessels due to proximal stenoses or to proximal viscous friction developing at high flow rates even in normal arteries from which the collaterals arise. Expressed in terms of circuit models, decreased collateral flow (steal) is due to proportionately greater increase in conductance of the normal vascular bed in parallel with the relatively low, fixed conductance of the collateral bed, which cannot compensate further for the fall in pressure at their origin.6Demer L Gould KL Kirkeeide R. Assessing stenosis severity: coronary flow reserve, collateral function, quantitative coronary arteriography, positron imaging, and digital subtraction angiography: a review and analysis.Prog Cardiovasc Dis. 1988; 30: 307-322Abstract Full Text PDF PubMed Scopus (71) Google Scholar In view of these mechanisms, the term "steal" is a misnomer, since blood is not "stolen" from the collateralized bed by backward flow through collateral channels to the normal vascular bed. It merely reflects a fall in collateral flow during arteriolar vasodilation below resting control levels, thereby producing ischemia. While developing only in the presence of severe coronary artery stenosis, collaterals in humans protect the myocardium from necrosis and deteriorating contractile function if sufficiently developed over prolonged periods before occlusion occurs.10Rentrop KP Thornton JC Feit F Van Buskirk M. Determinants and protective potential of coronary arterial collateral as assessed by an angioplasty model.Am J Cardiol. 1988; 61: 677-684Abstract Full Text PDF PubMed Scopus (200) Google Scholar,11Mizuno K Horiuchi K Matui H Miyamoto A Arakawa K Shibuya T et al.Role of coronary collateral vessels during transient coronary occlusion during angioplasty assessed by hemodynamic, electrocardiographic and metabolic changes.J Am Coll Cardiol. 1988; 12: 624-628Abstract Full Text PDF PubMed Scopus (33) Google Scholar Although the degree of stenosis and the length of time it is present prior to occlusion are recognized factors in collateral development, genetically mediated angio-neogenesis may also be important.12Kurachi K Davie EW Strydom DJ Riordan JF Vallee BL. Sequence of the cDNA and gene for angiogenin, a human angiogenesis factor.Biochemistry. 1985; 24: 5494-5499Crossref PubMed Scopus (238) Google Scholar 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 by Meerdink et al in this issue of Chest (see p 400), subendocardial steal occurs with severe coronary artery stenosis in the absence of collaterals. Although the effects of low perfusion pressure on transmural flow distribution have been described,1Schaper W Gunter G Winkler B Schaper J. The collateral circulation of the heart.Prog Cardiovasc Dis. 1988; 31: 57-77Abstract Full Text PDF PubMed Scopus (160) Google Scholar, 2Flameng W Wusten B Schaper W. On the distribution of myocardial blood flow: II.Effects of arterial stenosis and vasodilation. Basic Res Cardiol. 1974; 69: 435-446Crossref PubMed Scopus (69) Google Scholar, 3Flameng W Wusten B Winkler B Pasyk S Schaper W. Influence of perfusion pressure and heart rate on local myocardial flow in the collateralized heart with chronic coronary occlusion.Am Heart J. 1975; 89: 51-59Abstract Full Text PDF PubMed Scopus (49) Google Scholar, 4Becker LC. Conditions for vasodilator-induced coronary steal in experimental myocardial ischemia.Circulation. 1978; 57: 1103-1110Crossref PubMed Scopus (276) Google Scholar, 5Patterson RE Kirk ES. Coronary steal mechanisms in dogs with one-vessel occlusion and other arteries normal.Circulation. 1983; 67: 1009-1015Crossref PubMed Scopus (74) Google Scholar,13Bache RJ Schwartz JS. Effect of perfusion pressure distal to coronary stenosis on transmural myocardial blood flow.Circulation. 1982; 65: 928-932Crossref PubMed Scopus (122) Google Scholar this study definitively documents the occurrence and conditions for subendocardial steal associated with severe stenoses in which collaterals play no role. The mechanisms are the same as outlined previously. At normal resting conditions with severe stenosis, resting flow and/or distal coronary pressure are reduced enough to stimulate compensatory subendocardial vasodilation, thereby using up its limited flow 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 due to greater increase in conductance of subepicardial vessels that are in parallel with relatively fixed conductance vessels of the subendocardium, which cannot compensate for the fall in distal pressure. The necessary conditions for subendocardial steal are a severe stenosis, which produces maximally vasodilated, fixed conductance, subendocardial arterioles, and a fall in distal pressure after dipyridamole administration, which causes lower subendocardial perfusion. Thus, the mechanisms for coronary collateral steal and subendocardial steal are the same, but the anatomy producing them is different. Clinically, coronary steal, as manifested by chest pain and ST depression after IV dipyridamole, is usually a sign of severe 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 often have severe or unstable angina at rest and are therefore likely to be excluded from dipyridamole stress. Consequently, in the majority of patients undergoing appropriate dipyridamole perfusion imaging, coronary steal is a sign of collaterals providing significant resting flow rather than subendocardial steal without collaterals. Figure 1 illustrates a clinical example of coronary steal demonstrated by positron emission tomography (PET) as a fall in stress activity below resting levels. PET also provides the percent of the heart outside of 2.5 SD from normal which, for the polar map display of the ratio of absolute counts stress/rest, indicates the percent of the heart that is collateralized (Fig 2).FIGURE 2Shows activity outside 2.5 SD compared with normal subjects as blacked out areas. The numbers beside the polar map indicate the percent of the heart outside 2.5 SD. Thus, polar maps demonstrate a small inferior apical resting defect (Study 1) and a severe large stress defect of anterior, apical, and apical lateral myocardium (Study 2) involving 45 percent of the heart. Of this large area of viable myocardium, 31 percent shows collateralized myocardium associated with myocardial steal as seen in the polar display of S2/S1 absolute ratios (upper right). PET imaging therefore correctly demonstrated the extent and severity of coronary artery disease with collaterals, confirmed at arteriography.(PET scan courtesy of Don Gordon, M.D., Jacksonville Cardiovascular Clinic and Memorial PET Center.)View Large Image Figure ViewerDownload (PPT) A rare patient with the hyperadrenergic syndrome of mitral valve prolapse may have angina and ST depression after IV dipyridamole relieved with aminophylline but no regional perfusion defect on 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 the absence of regional perfusion defects. Thus, clinical steal is an important, useful diagnostic sign seen during dipyridamole perfusion imaging that indicates severe coronary artery disease and viable myocardium, most commonly associated with significant collateral supply, occasionally without collaterals, and with abnormal perfusion images; it may occur rarely with subendocardial small vessel dysautonomia in the absence of coronary artery disease.