Author + information
- Ivo M. van Dongen, MD,
- Joëlle Elias, MD,
- Gert van Houwelingen, MD, PhD,
- Pierfrancesco Agostoni, MD, PhD,
- Loes P. Hoebers, MD, PhD,
- Dagmar M. Ouweneel, MD, PhD,
- Ronak Delewi, MD, PhD,
- Bimmer E.P.M. Claessen, MD, PhD,
- René J. van der Schaaf, MD, PhD,
- José P.S. Henriques, MD, PhD∗ (, )
- on behalf of the EXPLORE investigators
- ↵∗Department of Cardiology, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, the Netherlands
In patients with ST-segment elevation myocardial infarction (STEMI), presence of a chronic total coronary occlusion (CTO) is associated with a worse prognosis. The presence of well-developed collateral vessels towards a concomitant CTO has been associated with improved outcomes (1). In the EXPLORE (Evaluating Xience and left ventricular function in PCI on occLusiOns afteR STEMI) trial (2), an independent angiographic core lab evaluated all angiograms and percutaneous coronary interventions (PCIs). An interesting finding, a decrease in collateral quality to the CTO several days after primary PCI (pPCI), was noted. The aim of this work was to describe this phenomenon and to assess its impact on functional and clinical outcomes.
In the EXPLORE trial, patients with STEMI and a concomitant CTO were randomized after pPCI to either early CTO PCI (within 7 days) (n = 148) or to no-CTO PCI within 4 months (n = 154). One patient refused CTO PCI, leaving 147 patients in the CTO PCI arm. Well-developed collateral vessels were defined as Rentrop grade 2 to 3, and poorly developed collateral vessels as Rentrop grade 0 to 1. The primary endpoint consisted of left ventricular ejection fraction (LVEF) and left ventricular end-diastolic volume (LVEDV), assessed by cardiac magnetic resonance imaging at 4-month follow-up. SYNTAX scores were calculated by Cardialysis BV, Rotterdam, the Netherlands, using the pre-defined SYNTAX score calculation definitions. Clinical follow-up was collected and adjudicated up to 5 years after randomization.
In the CTO PCI group, we found that the percentage of patients with well-developed collateral vessels to the CTO had decreased significantly several days after the index STEMI, compared with collateral vessels visualized on the angiogram immediately before pPCI (Figure 1). This decay in well-developed collateral vessels was mainly a result of a decrease from Rentrop grade 2 collateral vessels during pPCI to Rentrop grade 0 and 1 collateral vessels pre-CTO PCI (Figure 1).
A decay in collateralization was observed in 34 of the 147 patients (23%); and in 109 patients (74%), the collateral quality remained unchanged. Neither Thrombolysis In Myocardial Infarction flow grade over the culprit lesion nor location of the culprit lesion differed significantly between these patient groups. In 4 patients (3%), an increase in collateral quality was seen. Successful CTO PCI was achieved in 24 (74%) of patients with collateral quality decay, and in 81 (74%) of patients without any collateral quality change.
In patients showing collateral quality decay, the LVEF had increased significantly (from 41.1% [29.8% to 47.3%] to 45.5% [35.3% to 55.0%]; p = 0.022) and the LVEDV had decreased slightly (from 232.4 ml [189 to 265 ml] to 208 ml [171 to 252 ml]; p = 0.845). In patients without any collateral quality change, the LVEF increased (from 43.4% [32.6% to 51.1%] to 45.1% [37.6% to 52.3%]; p = 0.006), and there was a trend for an increased LVEDV (from 190 ml [166 to 247 ml] to 205 ml [169 to 245 ml]; p = 0.063). Adjusted for baseline LVEF, the LVEF at 4-month follow-up was statistically not different between patients with or without collateral quality decay (p = 0.284). The same observation was made for LVEDV at 4-month follow-up (p = 0.086), adjusted for baseline LVEDV. Therefore, the occurrence of collateral quality decay within the first week was not associated with an adverse impact on LVEF and LVEDV. Clinical follow-up did not differ between patients with or without collateral quality decay. On multivariable analysis, only the SYNTAX score pre-pPCI was found to be a negative predictor for the occurrence of a decay in collateral quality in this small population (odds ratio: 0.944; 95% confidence interval: 0.899 to 0.991; p = 0.021).
In conclusion, we describe for the first time that a quality decay of collateralization to a CTO within 1 week after pPCI occurs in 23% of patients with STEMI and a concurrent CTO. This pseudo-coronary steal phenomenon is likely to involve several mechanisms. The acute ischemia may elicit higher blood pressure and extreme vasodilation of the CTO territory; both likely leading to better angiographically visible collateral vessels before pPCI, compared with several days later. This contradicts previous observations by Rentrop et al. (3), describing that 10 to 14 days post-infarction, a significant increase in the prevalence of visible collateral vessels to an infarct-related artery occurs. However, Rentrop et al. (3) described this observation in a small (N = 42) cohort of patients with persistently occluded infarct-related arteries, whereas our observation was made in CTOs in STEMI patients. Primary PCI reduces ischemia, intracoronary pressure, and the adrenergic state, which combined could explain the decay in collateral quality several days after the index event.
Interestingly, this pseudo-coronary steal appears to be associated with a modest improvement in cardiac function (LVEF and LVEDV) compared with patients without any change in collateral quality. This could suggest that the capability to improve the quality of collateral vessels to a CTO during a STEMI episode may have a protective role. Therefore, we believe that the quality of collateral vessels on the pPCI angiogram should not be a part of clinical decision making with regard to a CTO in STEMI patients, because this quality can be dynamic, and the consequence is unknown.
Please note: The EXPLORE trial is an investigator-initiated study and was funded by the Academic Medical Center (Amsterdam, the Netherlands) in combination with an unrestricted research grant from Abbott Vascular (Santa Clara, California). Dr. Agostoni has received institutional honoraria from Aquilant, Meril, Neovasc, Genae, and Angiodynamics outside of the submitted work. Dr. van der Schaaf has received grants from Abbott Vascular, Biotronik, and Biosensors; has received personal fees from Biotronik and Boston Scientific; has been a consultant for Biotronik; and has received speaker fees from OrbusNeich, Boston Scientific, and Asahi Intecc outside the submitted work. Dr. Henriques has received grants from Abbott Vascular during the conduct of the study and has received grants from B. Braun, Abiomed, and Biotronik outside the submitted work. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. (Multicenter, randomized trial to study the impact of percutaneous coronary intervention on left ventricular function in patients with a non-infarct related chronic total occlusion after ST-elevation myocardial infarction: PCI vs. conservative approach in CTO patients after STEMI [EXPLORE]; NTR1108).
- 2018 American College of Cardiology Foundation
- Elias J.,
- Hoebers L.P.C.,
- van Dongen I.M.,
- Claessen B.,
- Henriques J.P.S.
- Henriques J.P.,
- Hoebers L.P.,
- Ramunddal T.,
- et al.
- Rentrop K.P.,
- Feit F.,
- Sherman W.,
- Thornton J.C.