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Raval et al. Vessel Plus 2024;8:5 https://dx.doi.org/10.20517/2574-1209.2023.99 Page 5 of 11

hyperemic coronary blood flow increased significantly post-TAVI, and FFR was noted to decrease
[27]
significantly post-TAVI . Thus, FFR may underestimate the significance of CAD pre-TAVI. However,
another prospective observational study of 133 lesions in 54 patients with severe aortic stenosis assessed FFR
[28]
pre- and post-TAVI . This study showed that even though there were significant variations pre- and post-
TAVI in positive and negative pre-TAVI FFR values, overall, the variations were minor, and changed the
indication to treat coronary stenosis with PCI in only a small number of patients (6%) post-TAVI when PCI
was not indicated pre-TAVI.

In the study by Ahmed et al., during diastole, wave-free period flow did not show any significant change
post-TAVI, and thus, iFR did not change pre- and post-TAVI, suggesting that it may be more accurate for
assessing CAD severity in patients with severe AS . iFR does not require the administration of adenosine,
[27]
[16]
so it may be the better modality for physiologic assessment of CAD in severe AS patient . However, the
conventional iFR threshold of < 0.89 to determine significant lesion severity might not be accurate in these
patients . In a prospective observational study, Scarsini et al. report an iFR value of > 0.93 to have a NPV
[29]
of 98.4% to exclude FFR non-significant stenosis and a value of < 0.83 to have a PPV of 91.3% to diagnose
FFR significant stenosis . They recommended the use of FFR only when iFR ranges between 0.83-0.93.
[30]
This allowed 63% of patients to avoid FFR with adenosine, and still reproduced results which had 97%
overall agreement with FFR. Although further research is needed to validate the cut-offs of FFR and iFR for
physiologically significant CAD in the severe AS subset, based on current data, it is reasonable to continue
with traditional cut-offs of ≤ 0.80 for FFR and ≤ 0.89 for iFR to guide revascularization.

Revascularization of stable CAD in patients undergoing TAVI
Patients with acute coronary syndrome and unstable angina or NSTEMI who are candidates for TAVI
should undergo PCI pre-TAVI. However, robust, conclusive, and randomized clinical evidence for the
management of stable ischemia and CAD pre-TAVI is lacking . Current guidelines recommend PCI in
[16]
patients with stable CAD with > 70% stenosis in the proximal coronary segments as a part of the pre-TAVI
work-up [24,31] . However, these recommendations are based on single-center observational studies,
[32]
retrospective studies, and meta-analyses . These studies have limitations, with the majority being
observational with no defined criteria for revascularization, and with complete vs. incomplete
revascularization decided at the discretion of the proceduralist.

The benefits of PCI pre-TAVI for stable ischemia remain uncertain. A meta-analysis of 9 studies comprising
3,858 patients studied the outcomes of patients who underwent TAVI with and without PCI . Patients who
[33]
underwent TAVI after PCI had a higher rate of major vascular complications with an odds ratio of 1.86 and
a higher 30-day mortality with an odds ratio of 1.42. No differences were noted between the groups in other
outcomes, including myocardial infarction, acute kidney injury, stroke, and 1-year mortality. The increased
bleeding and vascular complications and probably the higher preoperative risk in the PCI cohort
contributed to the higher early 30-day mortality which was not seen at 1 year. However, another meta-
analysis of 11 studies with 5,580 patients noted no difference in 30-day or 1-year all-cause mortality in the
[34]
patients who underwent TAVI with or without PCI prior .
These results in patients with severe aortic stenosis and stable CAD mirror the ISCHEMIA trial in 5,179
patients with stable CAD and moderate or severe ischemia on stress testing (but no aortic stenosis)
randomized to ICA and PCI vs. medical therapy. For stable CAD in ISCHEMIA, there was no difference in
the composite outcome of death from cardiovascular causes, myocardial infarction, or hospitalization for
unstable angina, heart failure, or resuscitated cardiac arrest in patients randomized to invasive vs. initial
conservative strategy .
[35]