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Cangemi et al. Mini-invasive Surg 2022;6:3 https://dx.doi.org/10.20517/2574-1225.2021.99 Page 3 of 13

Figure 1. Rate of coronary revascularization in patients undergoing aortic valve treatment.

[23]
primary endpoints of death and re-hospitalization at one-year follow-up between the two groups.
Moreover, at one year follow-up, there was no evidence of a difference in the rates of stroke, myocardial
infarction, or acute kidney injury, but there was a higher rate of any bleed in the PCI arm . The SURTAVI
[23]
[24]
trial was the only randomized study to compare both percutaneous (TAVI + PCI) and surgical (SAVR +
CABG) treatment strategies in patients with severe AS and no-complex CAD. At two-year follow-up, there
was no significant difference in the primary endpoint (all-cause mortality or stroke). Similar results were
obtained by the Observant study (an Italian registry 2010-2012). In addition, a recent meta-analysis
[25]
showed that a percutaneous strategy was comparable to a surgical one in patients with severe AS and
CAD .
[26]
FUNCTIONAL GUIDED REVASCULARIZATION OF CONCOMITANT CORONARY ARTERY
DISEASE IN PATIENTS WITH SEVERE AORTIC STENOSIS
Functional guided revascularization with FFR has been shown to have numerous advantages compared to
angiography-guided revascularization [27,28] and medical therapy alone . However, even though the
[29]
European Society of Cardiology guidelines on chronic coronary syndrome recommend the use of
[30]
functional assessment in patients with intermediate coronary artery stenosis, the European guidelines for
[20]
the management of valvular heart disease only recommend angiographic evaluation. The American
guidelines on valvulopathies consider the use of invasive coronary physiology in patients who are
[21]
candidates for TAVI safe. The discordance between European and American guidelines is related to the
[20]
absence of randomized controlled trials on clinical outcome and the low reliability of physiological indices
in severe aortic stenosis. In patients with severe aortic stenosis, there is a significant increase in resting
coronary flow due to the hypertrophy of the left ventricle [31-35] . The augmented resting coronary flow cannot