[azalemeth]

In three vessel disease, PCI is decidedly worse than CABG [1], but the latest evidence is, AFAIK, equivocal for CABG over PCI in one and two vessel disease [2].

I've personally often thought that this is due to the degree of collatoralisation that goes on in the ischaemic myocardium, even when we are convinced that the reduced FFR is all the story: stenosis does not happen overnight and metabolic adaption to, e.g., decreased O2 starts to begin. In three vessel disease you've burnt your reserves and are desperate for O2. In two vessel disease you're (mal)adapted.

Incidentally, this is why my scientific research is focused on using a slightly crazy CMR technique to directly image glycolysis and beta-oxidation in the ischaemic myocardium. We can make PCI kill fewer people if the interventionalists can be told "This region is ischaemic and has shifted towards anaerobic glycolysis due to this branch of (LCx/whatever) artery. Go revascularise".

[1] https://academic.oup.com/eurheartj/article/35/40/2821/229322... [2] https://openheart.bmj.com/content/3/2/e000489?utm_term=usage...

[unsrsly]

Hyperpolarized 13C MR?

[azalemeth]

Are you in the field -- and if so, where do you work? UCSF? (I'm in Oxford :-)

[azalemeth]

Yep :-)