LETTER TO THE EDITOR
Prognostic significance of coronary blood flow velocity patterns in patients with reperfused acute myocardial infarction and TIMI-2 flow: Reply
Hiroshi Ito, MD and
Koichi Yamamoto, MD
Sakurabashi Watanabe Hospital, Cardiology Department, 2-4-32 Umeda, Kita-ku, Osaka-shi Osaka 530-0001, Osaka, Japan
itomd{at}osk4.3web.ne.jp
We thank Dr. Garot for his interest in our work (1) and his thorough comments. We previously documented that systolic flow reversal (SFR) measured immediately after reopening of culprit coronary artery is the specific finding of TIMI-2 (Thrombolysis In Myocardial Infarction trial) flow as well as of the no-reflow phenomenon in patients with anterior myocardial infarction (MI) (2). Using a microcirculation model, we theoretically explained that capillary obstruction could be a main cause of SFR. Recently, a possibility of distal embolization has been addressed as another cause of TIMI-2 flow in the patients treated with catheter-based intervention. Microemboli of thrombus and plaque gruels are believed to be showered downstream of the microcirculation after catheter-based intervention, causing obstruction of small arteries and arterioles. Therefore, we hypothesized there should be at least two mechanisms of TIMI-2 flow in acute MI patients treated with percutaneous coronary intervention (PCI), and coronary blood flow velocity (CBFV) patterns would be different depending on the mechanisms.
Location of MI was different between the patients with and without SFR among acute MI subjects with TIMI-2 flow after PCI. Thirteen of 14 patients with SFR had anterior MI, whereas 9 of 11 patients without SFR had inferior MI. As we previously reported, SFR is associated with large size of MI, and such large MI is often observed in patients with anterior MI. Our recent studies demonstrated that size of risk area and anterior MI location are determinants of the no-reflow phenomenon (3). Because of the relatively small perfusion territory of right coronary artery, MI size is usually not so large, and this is the reason why frequency of no-reflow is much less in patients with inferior MI. Even in patients with inferior MI, however, TIMI-2 flow is found, but it is not necessarily associated with SFR but with reduced flow velocity.
Recently, several studies reported other determinants of sluggish coronary flow, which appears just after PCI procedure (4,5). These factors are related to amount of intracoronary thrombus, intravascular ultrasound plaque morphology, and contents of the thrombus. Among them, large vessel size and a great deal of thrombus are frequent findings in patients with inferior MI. Our report also showed that the site of MI is not necessarily a determinant of SFR and MI size (1). In our study, one patient with SFR had inferior MI with large MI size, and two patients without SFR had anterior MI with angiographically visible thrombus. Multivariate analysis also did not determine the type of infarct-related artery as an independent predictor of TIMI-2 without SFR.
As Dr. Garot pointed out, the CBFV pattern of the right coronary artery is different from that of the left coronary artery and is characterized by the relative dominance of systolic flow. Heller et al. (6) examined CBFV pattern in the right coronary artery in noninfarct heart. The systolic predominant flow is found in the proximal right coronary artery, whereas diastolic predominant CBFV is observed in the posterior descending and artrioventricular arteries. Therefore, we measured CBFV in the atrioventricular branch. The systolic average peak velocity/diastolic average peak velocity (SAPV/DAPV) ratio was compatible between those with TIMI-3 inferior MI and those with TIMI-3 noninferior MI. Therefore, a bias of difference in type of coronary arteries could be minimized by this approach. We also compared CBFV variables between patients with TIMI-2/SFR(–) and those with TIMI-3 flow among patients with inferior MI. The SAPV/DAPV ratio was also higher and diastolic peak velocity was lower in patients with TIMI-2/SFR(–) than in those with TIMI-3 flow. In the clinical setting, we believe TIMI-2 flow is caused by both capillary damage and microthrombi, and the contribution of these factors may vary among patients. Analysis of CBFV pattern with Doppler flow wire is helpful to differentiate which factor is more prominent in each patient, and this examination should help to shape therapeutic strategies in the emergency setting.
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References
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1. Yamamoto K, Ito H, Iwakura K, et al. Two different coronary blood flow velocity patterns in thrombolysis in myocardial infarction flow grade 2 in acute myocardial infarction. Insight into mechanisms of microvascular dysfunction. J Am Coll Cardiol. 2002;40:1755–1760[Abstract/Free Full Text]
2. Iwakura K, Ito H, Takiuchi S, et al. Alteration in the coronary blood flow velocity pattern in patients with no reflow and reperfused acute myocardial infarction. Circulation. 1996;94:1269–1275[Abstract/Free Full Text]
3. Iwakura K, Ito H, Ikushima M, Kawano S, et al. Association between hyperglycemia and the no-reflow phenomenon in patients with acute myocardial infarction. J Am Coll Cardiol. 2003;41:1–7[Abstract/Free Full Text]
4. Yip HK, Chen MC, Chang HW, et al. Angiographic morphologic features of infarct-related arteries and timely reperfusion in acute myocardial infarction: predictors of slow-flow and no-reflow phenomenon. Chest. 2002;122:1322–1332[Abstract/Free Full Text]
5. Tanaka A, Kawarabayashi T, Nishibori Y, et al. No-reflow phenomenon and lesion morphology in patients with acute myocardial infarction. Circulation. 2002;105:2148–2152[Abstract/Free Full Text]
6. Heller LI, Silver KH, Villegas BJ, et al. Blood flow velocity in the right coronary artery: assessment before and after angioplasty. J Am Coll Cardiol. 1994;24:1012–1017[Abstract]
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