Between two evils, choose neither; between two goods, choose both.
– Tryon Edwards
Advances in cardiology come via the rapid pace of new clinical findings, each providing a unique lens through which to reassess both our patient-care efforts and historical clinical paradigms.
In many cases, new findings are accompanied by an immediate debate about how to apply the new and what to discard from the old. While these debates are valuable, the pitfalls of myopically overinterpreting, and therefore overapplying, new reports cannot be overstated. For example, withholding revascularization from all stable patients would be a drastic overinterpretation of the ISCHEMIA trial. Although the ISCHEMIA trial does demonstrate stress testing’s failure to guide patient management, substantial data continue to demonstrate the long-term effectiveness of FFR-guided PCI, including lowering the risks of heart attack or death.
Similar debates accompany today’s discussions around the evolving role of coronary plaque quantification and characterization and their potential utility in clinical decision making:
- How does plaque relate to, augment, or replace previously used diagnostic tools?
- What does a coronary artery calcium (CAC) score really tell us?
- Which matters more clinically: total plaque burden or adverse plaque characteristics?
- What quantity of plaque is the norm in patients of a certain age, sex, and in the setting of comorbidities?
- Should information about plaque guide clinical treatment?
A recent State-of-the-Art Review in JACC Cardiovascular Imaging provides much needed perspective in this arena. The world-renowned authors, S. Yang, B. Koo, and J. Narula, argue that powerful plaque insights are interrelated with, and cannot be separated from, their lesion-specific coronary physiology impacts. Rather, the authors state, “there is accumulating evidence that these 2 aspects of coronary artery disease influence each other with significant clinical implications, despite traditionally being considered to have separate effects on significances, treatments, and outcomes.”
This insight informs how we can consider contemporary learnings such as those from the PARADIGM Registry (symptomatic patients with unknown CAD), the Western Denmark Heart Registry (symptomatic patients with known CAD), and the Miami Heart Study (asymptomatic people). Using coronary CTA, these efforts each identified a meaningful proportion of patients with coronary plaque despite a CAC score of 0. Even in the asymptomatic Miami Heart patients, the consistent presence of plaque is striking, but does not immediately inform the clinical utility of having this information.
While studies such as these may provide valuable observations regarding adverse plaque characteristics (APCs), differences in plaque progression, and certain clinical scenarios associated with increased patient risk (e.g., the presence of obstructive CAD caused by noncalcified plaque), it remains clear that plaque insights alone cannot guide clinical treatment decisions. Risk indicators are interesting, but as physicians, we should demand evidence that indicators are tied to outcomes, and that modifying a patient’s management based on these indicators provides clinical benefit. Ultimately, a data-driven and specific treatment decision needs to be made for every patient in the pathway, from those with no or minimal plaque to those with complex disease requiring invasive intervention.
As Yang, et al. spell out, the detailed anatomic understanding of a patient’s plaque cannot be viewed separately from the lesion-specific coronary physiology that results. It is naive and at odds with the very nature of coronary artery disease to consider anatomy at the macroscopic or microscopic level without incorporating information about coronary blood flow, pressure, and forces being applied to individual plaques. These interactions of coronary plaque and blood flow are vital as local hemodynamic realities are central to the probability of a given lesion’s rupture. Consider:
Plaque without physiology? Due to the frequent discordance between anatomic stenosis and physiologic impairment, reported first over 25 years ago, PCI based solely on identification of concerning plaque features would lead to PCI in lesions with preserved FFR (>0.80), an action known to cause, not prevent, MI and death. It also remains purely speculative that withholding revascularization from people with FFR or FFRCT ≤0.80 because of a given plaque’s characteristics is not a dangerous overreach. Clinical outcomes data are required, and rigorous prospective studies should be undertaken to test any such hypothesis before potential utility in patient management is accepted.
As Yang, et al. conclude “a comprehensive understanding of the relationship and integrative assessments of plaque and coronary physiology may better predict future coronary events and better selection of treatment strategies.” To get to the point where the “may” can be removed from this observation will require comprehensive clinical trial programs of utility and outcomes.
Moving forward on that journey, seamless integration of detailed plaque insights with guideline-recognized anatomy and physiology of CTA+FFRCT will ensure that our clinical decisions and our patients benefit from all the precise heart care tools available.
I’ll choose “and” over “or” any day.