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Royse et al. Vessel Plus 2020;4:5 I http://dx.doi.org/10.20517/2574-1209.2019.34 Page 5 of 22

Equivalence of arterial conduits?
There is considerable theoretical or in vitro evidence to suggest that the LIMA has properties that renders
it “superior”. These are claimed to include increased synthesis of nitric oxide, resistance of smooth muscle
cells to proliferation, tight endothelial junctions, decreased expression of adhesion molecules and other
theoretical correlations between histological structure and long-term function [26-29] . The discussion,
however, has mainly been confined to the comparison with SVG, where the RA is considered to have a
thicker muscular layer and in vitro and in vivo experimentation suggests that it is prone to spasm and
theoretically more likely to develop atherosclerosis [30-36] .

However, direct observation suggests otherwise. Consider the following propositions:
1. If a 75-year-old patient had a LIMA, RA and GEA harvested, and all were normal - why should they
be so (given that the popular belief that only the LIMA is especially resistant to the development of
atherosclerosis)? Specifically, all conduits have been exposed to the arterial blood pressure and flow for
75 years prior to harvest - and are normal - suggesting that all three behave similarly.
2. Angiograms of patent arterial conduits more than 10 or 20 years postoperative reveal a “binary” outcome.
Either the conduit is Patent + Normal or Occluded/String sign. These findings are the same for all arterial
conduits. Specifically, all conduits are exposed to the arterial blood pressure and flow postoperatively - and
remain normal - suggesting that all three behave similarly.
3. If a length of artery remains normal whilst in the arterial circulation for decades prior to surgery -
why should it suddenly develop atherosclerosis within a few years of being transplanted into the arterial
circulation of the heart (when it is exposed to the same blood pressure and flow as pre-harvest)?
Specifically, the haemodynamics of the coronary circulation are essentially the same as for the chest wall,
forearm or stomach and there is no credible reason to expect that an arterial conduit will alter its behaviour
merely upon use as a coronary graft.

How should the many theoretically- or laboratory experiment-based predictions as to the short- and long-
term behaviour of various arterial conduits which conflict with direct observations be interpreted? In the
view of the authors, direct observation overrides theoretical- or laboratory-based conclusions, and suggest
that further refinement of both theory and interpretation of experimentation is required.

It is suggested that there is a striking similarity for all arterial conduits used in coronary surgery, and, if
they do not fail early due to competitive flow, they may be expected to remain patent. All behave differently
to SVG, giving rise to the saying, “arteries are arteries - and veins are not”. Should all arterial conduits be
considered as interchangeable - would it be acceptable to use RA or GEA to graft the LAD? This is the
position that the authors now accept as valid. Please refer to Part 2 for why widespread adoption of this
concept is not likely to be rapid.

Complete revascularisation
The consideration of incomplete revascularisation relates primarily to a difference in strategy between PCI,
where treatment of the “culprit lesion” is preferred (at least in the acute setting), and the usual surgical
strategy of full revascularisation with CABG. Within CABG, off pump CABG has been associated with few
grafts, suggesting that incomplete revascularisation is more common, which may impact on outcome. This
is beyond the scope of this paper and for the remainder of this paper it is assumed that all patients received
full revascularisation.

Could RAY and TAR achieved by any other reconstruction technique be similar?
In a large institutional cohort, we demonstrated that the survival of RAY and TAR by other techniques was
[37]
not different (P = 1.000 , Figure 3).