Acute iFR evaluation may be a valid approach for ruling out non-culprit lesions in STEMI patients

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Troels Thim

The iSTEMI study, published in JACC: Cardiovascular Interventions, suggests that instantaneous wave-free ratio (iFR) in the acute setting—ie. immediately after successful primary percutaneous coronary intervention (PCI)—is a valid method for assessing the functional significance of non-culprit lesions in patients with ST-segment elevation myocardial infarction (STEMI) and multivessel disease.

Cardiovascular News spoke to study investigator Troels Thim (Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark) about the study and the use of iFR in STEMI patients with multivessel disease

What data are available for complete revascularisation?

Meta‐analyses1,2 and recent randomised trials3–6 support complete revascularisation, as compared with culprit lesion only revascularisation, after STEMI to reduce major adverse cardiac events (death, myocardial infarction and repeat revascularisation). This finding is mainly driven by a reduction in repeat revascularisation.

What is the available evidence for the physiological assessment of non‐culprit lesions in patients with multivessel disease?

There is evidence for physiological assessment to guide revascularisation in patients with stable coronary artery disease and non‐STEMI (NSTEMI).7,8 Also, data show that in patients with STEMI, complete revascularisation guided by both angiography and by fractional flow reserve (FFR) is better than incomplete revascularisation.3–6

If physiological assessment is to be used in this context, when should it be performed—at the index procedure or afterwards?

There are physiological disarrangements that affect both iFR and FFR and that exist during STEMI; these could, therefore, support physiological assessment at a later time point. However, there are currently no trials comparing acute complete revascularisation guided by physiology with staged complete revascularisation guided by physiology; therefore, it is uncertain how the classification disagreement between acute physiological assessment and staged physiological assessment may impact outcomes. When staged physiological assessment is elected, our data suggest that re‐evaluation more than two weeks after STEMI may yield a physiological assessment comparable to stable conditions.

What are the potential advantages and disadvantages of iFR vs. FFR in this context?

In the acute STEMI setting, iFR may be attractive as the side effects of adenosine are avoided and time may be saved as compared with FFR. However, iFR tends to overestimate stenosis severity in the acute setting whereas FFR tends to underestimate stenosis severity in the acute setting.

What were the key findings of your study?

The study showed that when iFR is used the acute setting and indicates that a non‐culprit stenosis is not haemodynamically significant, the need for revascularisation will be unlikely. Furthermore, it found that if iFR in this setting suggests that a non-culprit lesions is haemodynamically significant, only approximately two of three such lesions will be hemodynamically significant when re‐evaluation is performed at a later time point.

What further evidence in this area is needed?

Currently, we have no trials comparing acute complete revascularisation guided by physiology with staged complete revascularisation guided by physiology. Fortunately, such trials are underway and it will be very interesting to see whether or not acute complete revascularisation guided by physiology is favourable when compared with staged complete revascularisation overall or in specific subsets of patients.

References

  1. Bainey et al. Am Heart J 2014; 167: 1
  2. Elgendy et al. JACC Cardiovasc Interv 2017; 10: 315–24.
  3. Wald et al. N Engl J Med 2013; 369: 1115–23.
  4. Gershlick et al. J Am Coll Cardiol 2015; 65: 963–72.
  5. Engstrom et al. Lancet 2015; 386: 665–71.
  6. Smits et al. N Engl J Med 2017; 376: 1234–44.
  7. Tonino et al. N Engl J Med 2009; 360: 213–24.
  8. De Bruyne et al. N Engl J Med 2012; 367: 991–1001.
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