Page 57 - Coronary hemodynamics in acute myocardial infarction - Matthijs Bax

Microvascular resistance of infarct and noninfarct coronary arteries
Table 3 Angiographic variables after reperfusion
TIMI flow grade 1
2
3
Corrected TIMI frame count Myocardial blush grade
13 2 32 (44%) 12 (16%)
IRA
1 (1%) 16 (22%) 56 (77%) 44 ± 22 3 (4%)
Non-IRA
0
1 (1%) 72 (99%) 29 ± 15 0
3 38 (52%) 61 (84%)
Values are numbers of patients (percentages) or mean ± SD. TIMI = Thrombolysis In Myocardial Infarction.
Discussion
This study demonstrates, in a homogenous cohort of patients with a first anterior wall AMI, increased levels of minimal microvascular resistance and decreased values of CFVR in IRAs and non-IRAs. Further, this study shows that microvascular function improved during 6-month follow-up in the 2 territories. Our study confirms previous observations that CFVR in IRA is decreased after reperfusion in the early phase of AMI secondary to a low hyperemic flow velocity.2, 3 Impairment of hyperemic flow velocity was due to increased microvascular resistance because the epicardial conduit was treated with angioplasty and stented, if necessary. Several mechanisms may contribute to a low hyperemic flow velocity in the IRA, including peripheral embolization, neurohumoral activation that leads to microvascular vasoconstriction due to vasoactive agents that are released from a thrombus, ongoing ischemia,16, 17 and angioplasty-mediated α-receptor activation.18 Minimal microvascular resistance in infarcted and noninfarcted territories decreased over time, resulting in similar resistances at 6-month follow-up. In accord to other studies, we demonstrated that CFVR was decreased7, 8 and corrected Thrombolysis In Myocardial Infarction frame count was increased19 in non-IRAs in the early phase of AMI. In our study, baseline flow velocity in non-IRAs after correction for the rate–pressure product was highest during the acute phase of AMI. In response to severe dyskinesia in the infarcted area, a compensatory increase in the thickening fraction in remote nonischemic regions was reported in the isovolumetric phase of systole, resulting in an increased baseline flow velocity and thus decreasing CFVR.10 It is unlikely that this mechanism fully
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