Critical review · Apr 9, 2026
Doma et al.: chronic total occlusion PCI in acute MI with cardiogenic shock
Doma M, Ramadan A, Cogar B, McEntegart MB, Mashayekhi K, Alaswad K, et al. Percutaneous Coronary Intervention for Chronic Total Occlusion in Acute Myocardial Infarction Complicated by Cardiogenic Shock. Can J Cardiol. 2026;42(7):1513-5.
doi:10.1016/j.cjca.2026.03.047 · Retrospective single-arm cohort from an administrative database (research letter), n = 617
Summary
Research letter on chronic total occlusion (CTO) PCI in patients with acute MI complicated by cardiogenic shock. CTO-PCI was identified by CPT/HCPCS billing codes. The time criterion required a shock diagnosis on the day before or the same day as the CTO-PCI.
The cohort had 617 patients. 81.9% also had PCI of another vessel, described as preceding the CTO-PCI (culprit-vessel treatment). More than 60% received mechanical support (intra-aortic balloon pump, Impella or ECMO).
| Outcome | Value |
|---|---|
| 30-day mortality | about 27% |
| 5-year mortality | 40.4% |
| Mean follow-up | 1.68 ± 1.97 years |
The authors compared 30-day mortality with the roughly 50% reported in large all-comer AMI-shock registries (Karami et al., Goyal et al.).
Strengths
- The first dedicated study of CTO-PCI in AMI with shock that I know of.
- A sample of 617 patients in a scenario with little data.
Methodological issues
- CTO not confirmed. The consensus definition requires a documented occlusion of at least 3 months. With no core lab, adjudication or angiographic confirmation of chronicity, classification depends on the operator’s code. The cohort likely includes acute occlusions coded as CTO. Treating an acute non-culprit occlusion in shock is a different scenario from opening a chronic, collateralized one.
- When the CTO was identified. The CTO did not have to be found during the index admission. A patient with a known right coronary CTO who presents with anterior MI and shock meets the criteria. The cohort mixes at least three groups: CTO found at the index angiogram, known CTO treated because of the shock (for example, difficulty weaning support after culprit PCI) and acute occlusion coded as CTO. No supplementary material allows separating them.
- No timing data. The time criterion is coarse. The actual interval and whether patients were stabilized before CTO-PCI are unknown. The roughly 18% without culprit PCI are the least clear subgroup: possibly NSTEMI with multiple CTOs or a vein graft culprit.
- No comparator. The study is single-arm. The cited registries include SCAI C to E, out-of-hospital arrest, mechanical complications and patients who never reached the cath lab. Without SCAI staging or hemodynamic data, it is unknown whether CTO-PCI was done in stable patients or as a last attempt.
- Selection bias. To undergo CTO-PCI in shock, a patient must survive the acute event, have culprit PCI (81.9%), stabilize on mechanical support (more than 60%) and be judged fit for a complex procedure. No one does a retrograde CTO in SCAI E. These are the survivors judged salvageable.
- Immortal time bias. The interval from shock diagnosis to CTO-PCI is immortal: the exposed group cannot die before the procedure. The comparison registries accumulate deaths from time zero. This alone can produce an apparent survival advantage.
- Descriptive analysis only. No multivariable adjustment, propensity matching or regression. With a mean follow-up of 1.68 ± 1.97 years, the 5-year mortality of 40.4% rests on few patients at risk after 3 years. There are no confidence intervals for cumulative incidence. There are no subgroups (staged versus same-sitting PCI, balloon pump versus Impella, culprit plus CTO versus CTO only).
Opinion
CULPRIT-SHOCK (Thiele et al., NEJM 2017) showed that immediate multivessel PCI in AMI with shock increased 30-day mortality compared with culprit-only PCI. The mechanism is procedure time, contrast and hemodynamic stress in a decompensating patient. CTO-PCI is the longest and most complex form of PCI: retrograde approach, high-support guides, long fluoroscopy, dissection and re-entry. If treating non-occluded non-culprit lesions caused harm in a randomized trial, I see no reason a CTO would be better tolerated.
Until recently, even angina benefit in stable patients was not established: DECISION-CTO was neutral and EURO-CTO was underpowered. Plausibility of benefit in shock runs the other way, and the risk of death in this setting is too high for a PCI effect to show.
The study shows that presumed CTO-PCIs performed during AMI-shock admissions had high mechanical support use and about 27% 30-day mortality. By design, it cannot show that CTO-PCI improves outcomes. Lower mortality than historical registries is better explained by selection and immortal time, in a cohort with uncertain and heterogeneous CTO status.
The next step would be a target trial emulation, with time zero at the index angiogram showing a non-culprit CTO, assignment to CTO-PCI or not, and cloning or weighting for immortal time. Stratification by SCAI stage, CTO territory and mechanical support use would be needed. In practice, close to impossible.
ACC/AHA guidelines recommend culprit-only PCI in AMI with shock (class I). In my view, this study provides no evidence against that recommendation, but it points to a population that deserves more rigorous study.