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Eventual Recovery of Regional Perfusion After Acute Myocardial Infarction

Ishihara et al’ evaluated the time course of impaired coronary flow reserve after reperfusion in 12 patients with acute myocardial infarction (AMI) who underwent successful percutaneous translu- minal coronary angioplasty (PTCA) of the anterior descend- ing artery. They measured coro- nary flow reserve at rest and after dipyridamole by coronary Dopp- ler velocimeter, measurements were repeated at predischarge and, in 9 patients, also 2 to 12 (mean 6 t 3) months later. An improved coronary flow reserve in the in- farcted zone was found 2 weeks after AMI, although some impair- ment persisted at 6 months.

There is already substantial ev- idence that the recovery of both perfusion and contraction in the infarcted area may continue after the acute setting in many patients with AMI, suggesting myocardial hibernation and/or repetitive stun- ning.2-5 In 13 patients with AM1 and l-vessel coronary disease who were treated with thrombo- lytic therapy, Uren et al3 measured coronary flow reserve by rest-di- pyridamole positron tomography with oxygen- 15 water. The severe vasodilator abnormality docu- mented 1 week after AM1 (and in- volving not only the resistive in- farct-related vessels, but also those in remote areas supplied by normal coronaries) had improved at 6 months, both in the infarcted and in the remote region.3 In 45 patients with anterior AM1 who achieved successful coronary re- flow by intracoronary thrombol- ysis and/or PTCA, Ito et al5 as- sessed the temporal changes in perfusion of the infarcted area

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0 1997 by Excerpto Medica, Inc. All rights reserved.

with myocardial contrast echocar- diography. Shortly after reflow, the peak contrast intensity was significantly reduced in the in- farcted area. However, a sponta- neous recovery of resting hypo- perfusion was found 1 month later, in association with improve- ment in regional contractile func- tion. We recently reported that re- covery of resting perfusion and contraction after AM1 may occur even later.4 In 71 consecutive pa- tients with anterior AM1 in whom resting regional perfusion and contraction were quantitatively assessed at 5 weeks after AM1 and then 6 months later by serial ses- tamibi tomography and 2-dimen- sional echocardiography, we doc- umented a delayed increase in the tracer distribution in the infarct area in two thirds of our patients, suggesting an improved perfusion to the infarcted area. Ejection fraction and regional wall motion had improved significantly after 6 months only in patients who had reduced resting hyoperfusion. In our study, which was not limited to patients with a reperfused in- farct vessel, no significant relation was found between vessel patency or collaterals and, on the other hand, improved perfusion.4 In agreement with Ishihara et al,’ we were unable to find a significant correlation between changes in resting hypoperfusion and in wall motion abnormalities.

Brief periods of ischemia caus a prolonged impairment of coro- nary vasodilation (“microvascu- lar stunning”).6 Consistent with the phenomenon of microvascular stunning described in experimen- tal models of reversible ischemic injury,2,6 microvascular injury could explain the fact that resting coronary flow reserve is impaired shortly after reperfusion.5 More- over, recurrent bouts of ischemia in the infarct-related artery could cause a persistent contractile dys- function and/or a persistent reduc- tion in resting blood flow with consequent hibernation. Ishihara et al raise the issue of whether an

impaired coronary flow reserve could contribute to residual isch- emia. In fact, we found that the delayed reduction in resting hy- poperfusion in the infarct area is associated with a reduced isch- emit burden at serial stress test- ing.7

An important clinical implica- tion of all of these data is that in patients with AMI, the eventual recovery of regional function and perfusion cannot be accurately es- timated by measurements ob- tained in the subacute phase or even later, due to the fact that postreperfusion myocardial flow abnormalities can be reversible.

Michele Galli, MD

Claudia Marcassa, MD

Pontalea Giannuzzi, MD

Veruno, Italy 26 January 1997

1. Ishihara M, Sato H, Tateishi H, Kawagoe T, Shi- matani Y, Kurisu S, Sakai K. Time course of im- paired coronary flow reserve after reperfusion in pa- tients with acute myocardial infarction. Am .I Cardiol 1996;78: 1103-l 108. 2. Bolli R. Myocardial stunning in man. Circulation 1992;86:1671-1691, 3. Uren N, Crake T, Lefroy DC, De Silva R, Davies GJ, Maseri A. Reduced coronary vasodilator func- tion in infarcted and normal myocardium after myo- cardial infarction. NEngl .lMed 1994;331:222-227. 4. Galli M, Marcassa C, Bolli R, Giannuzzi P, Tem- porelli PL, Imparato A, Silva P, Giubbini R, Gior- dano A, Tavazzi L. Spontaneous delayed recovery of perfusion and contraction after the first five weeks following anterior infarction: evidence for the presence of hibernating myocardium in the in- farcted area. Circulation 1994;90: 1386-1397. 5. Ito H, Iwakura K, Oh H, Masuyama T, Hori M, Hoigashino Y, Fujii K, Minamino T. Temporal changes in myocardial perfusion patterns in patients with reperfused anterior wall myocardial infarction. Circulation 1995;91:65&662. 6. Bolli R, Triana F, Jeroudi M. Prolonged impair- ment of coronary vasodilation after reversible isch- emia. Evidence for microvascular stunning. Circ Res 1990:67:332-343. 7. Marcassa C, Galli M, Temporelli PL, Campini R, Silva P, Zoccarato 0, Giordano A, Giannuzzi P. Evaluation of residual ischemia after anterior myo- cardial infarction by wmTc-sestamibi tomography. J Am Co!/ Cardiol 1995;25:590-596,

Dipyridamole-Induced Myocardial ischemia

Dr. Gliozheni et al’ confirmed that the presence of epicardial cor- onary collaterals increases the vulnerability to myocardial isch- emia during intravenous dipyri-

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