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NEW ORLEANS -- The concept of using myocardial viability to guide revascularization in severe ischemic cardiomyopathy was laid to rest following the REVIVED-BCIS2 trial.

Going back decades, the idea was that intervention may be warranted to save viable myocardial cells that have not died despite being subject to myocardial ischemia -- perhaps supplied by collateral channels and newly formed vessels in the coronary circulation -- which may eventually recover upon revascularization. Imaging for myocardial viability is therefore thought to identify patients who have potential for improvement in contractility due to angioplasty.

However, an analysis now shows that the extent of such dysfunctional-yet-viable segments in the heart did not predict event-free survival nor tilt outcomes to favor those had received percutaneous coronary intervention (PCI) over optimal medical therapy (OMT) alone, according to Divaka Perera, MD, of King's College London.

This challenges the whole theory of hibernating myocardium, Perera told the audience at the American College of Cardiology annual meeting.

"We have come to use viability as a prospective marker of hibernation and that's predicated on assumptions that we can pick the parts of the ventricle that can recover," he said. "We need to challenge the paradigm, and hibernation as we've known and used it doesn't seem to be useful in clinical practice anymore."

The main report of REVIVED, released in the summer of 2022, had been noteworthy for showing that multivessel PCI did not reduce death from any cause or hospitalization for heart failure in a population of people with left ventricular (LV) ejection fractions no higher than 35% and extensive coronary artery disease (CAD).

The study required people with ischemic cardiomyopathy to have viable myocardium confirmed and quantified on imaging. The degree of viable myocardium was based on normal wall motion and potential for recovery if dysfunctional. Viability was characterized through a blinded cardiac MRI core laboratory and a blinded stress echocardiography core laboratory.

Session discussant Sunil Rao, MD, of NYU Langone in New York City, agreed that the analysis of REVIVED-BCIS2 "challenges long-held beliefs in our profession." He raised questions about whether viability tests should continue to be performed in people with severe ischemic cardiomyopathy and who should be the ones to receive revascularization going forward.

"Should we throw out myocardial [viability] testing altogether? I don't think so," Perera replied, citing its possible uses such as a source information of scarring and the possibility that viable myocardium may help identify candidates for implantable cardioverter-defibrillator therapy.

Altogether, there were 700 people randomized to multivessel PCI or OMT in REVIVED-BCIS2. After excluding people whose imaging tests produced poor quality, investigators were left with 610 people (median age 69.3, 12.3% women). PCI and OMT treatment groups shared fairly balanced baseline characteristics.

Unlike myocardial viability at baseline, the metric of scar burden, assessed in a subgroup of 478 individuals, did predict fewer deaths and heart failure hospitalizations (HR 1.18, 95% CI 1.04-1.33)

All-viable myocardium and lower scar burden were both associated with a greater likelihood of LV recovery independent of baseline ejection fraction or extent of CAD. Greater recuperation of ejection fraction, not assignment to PCI versus OMT, was tied to subsequently fewer clinical events (HR 0.62, 95% CI 0.41-0.95).

REVIVED participants seemed to have fairly modest CAD given that about half of individuals had two-vessel disease and the median number of lesions and vessels treated was two per patient.

A limitation of the study, therefore, was that patients with the most severe CAD could have been referred for coronary artery bypass grafting (CABG) surgery instead of being enrolled in the trial, potentially diluting any treatment effect for PCI.

Indeed, the had found a link between CABG and improved survival among patients with LV systolic dysfunction and the most extensive and severe CAD.

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