Percutaneous intervention for concurrent chronic total occlusions in patients with STEMI: the EXPLORE trial
Selected in Journal of the American College of Cardiology by D. Milasinovic
Henriques JP, Hoebers LP, Råmunddal T, Laanmets P, Eriksen E, Bax M, Ioanes D, Suttorp MJ, Strauss BH, Barbato E, Nijveldt R, van Rossum AC, Marques KM, Elias J, van Dongen IM, Claessen BE, Tijssen JG, van der Schaaf RJ; EXPLORE Trial Investigators
J Am Coll Cardiol. 2016 Oct 11;68(15):1622-1632
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What is know
While multivessel disease has been associated with increased morbidity and mortality in patients with ST-segment myocardial infarction (STEMI), the presence of a concurrent non-culprit artery chronic total occlusion (CTO) carries the greatest risk. However, percutaneous coronary intervention (PCI) for CTO has been burdened by the lack of evidence of clinical benefit from randomized trials.
Is routine PCI of a concurrent non-culprit artery CTO within 7 days of primary PCI for STEMI associated with improved left ventricular (LV) function, as compared to conservative treatment?
- 304 STEMI patients with a non-culprit artery CTO were randomized at 14 sites, 150 to non-culprit CTO PCI and 154 to medical therapy.
- Co-primary endpoints were LV ejection fraction (LVEF) and LV end-diastolic volume (LVEDV) at 4 months on cardiac magnetic resonance imaging (CMR).
- In patients undergoing CTO PCI vs. no CTO PCI, LVEF was similar at 4 months (44.1 ± 12.2% vs. 44.8 ± 11.9%, respectively; p=0.6), as was LVEDV (215.6 ± 62.5 ml vs. 212.8 ± 60.3 ml, respectively; p=0.7).
- In the subgroup of patients with non-culprit CTO located in the LAD, conservative treatment was inferior to CTO PCI, in terms of LVEF (40.4 ± 11.9% vs. 47.2 ± 12.3%, respectively; p for interaction 0.002) and LVEDV (p for interaction 0.039).
- 4-month MACE rate was similar in both study groups (5.4% in CTO PCI vs. 2.6% in no-CTO PCI, p=0.35).
Although the scope of the EXPLORE trial is well defined, it nevertheless appears to partially conflate two distinct questions, namely the value of complete revascularization in STEMI and impact of CTO PCI by itself on LV function. Therefore, at least three confounding factors need to be taken into account when interpreting the trial’s results.
First, as optimal timing of non-culprit PCI in STEMI patients has so far not been clearly defined, performing CTO PCI within 7 days of primary PCI may have biased the results. While previous large registries had favored staging of a non-culprit PCI, during or after index hospitalization, three recent, moderately-sized randomized trials indicated potential benefit of non-culprit PCI in the same sitting or shortly after primary PCI, albeit with the caveat of largely excluding patients with non-culprit artery CTO.
Secondly, although the effects of CTO recanalization may be dependent on the presence of viable myocardium, viability of myocardium subtended by the occluded non-culprit artery was not assessed in all patients prior to inclusion in the study.
Thirdly, differences in LV functional improvement in STEMI patients cannot be attributed only to non-culprit artery CTO revascularization or lack thereof, but also to a great extent to the success of primary PCI. However, predictors of LV recovery that go beyond postprocedural TIMI flow in the infarct-related artery, such as microvascular obstruction, have not been accounted for.
In summary, there still appears to be no definite evidence of benefit of routine CTO PCI, even in a high-risk population such as STEMI patients with non-culprit artery CTO. Instead, a selective approach to CTO PCI may seem warranted, e.g. in primary PCI-treated STEMI patients with a bystander CTO in the LAD.
What is your preferred strategy in STEMI patients with a remaining non-culprit artery CTO after successful primary PCI, who are not surgical candidates?