I’ll take you up on the bypass statement. :) This is an 80 yo woman, that alone would probably make me not want to put her under for bypass. Also, she had a history of paroxysmal afib and prior pulmonary embolism (they don’t state if it wad provoked or not) but is not on anticoagulation. By CHADS2-Vasc criteria she should have been on AC alone, but isn’t. She’s clearly intelligent and has no issues with access to care (engineer, has an Apple Watch) which further makes me think that her underlying health warrants a more conservative approach.
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".
Eh, I think the data is controversial and case-dependent in two-vessel disease. If this were three vessel disease, the data is far more in favor of CABG. The fluoroscopy doesn't look convincing to me of major stenosis, so a PCI/stent could certainly be placed for symptomatic relief without a CABG.
Additionally, the patient definitely did not need emergency CABG. My understanding is that CABG could be completed after stenting, and may very well have happened for this patient without our knowledge.
Herodotus38|5 years ago
op03|5 years ago
azalemeth|5 years ago
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|5 years ago
epmaybe|5 years ago
Additionally, the patient definitely did not need emergency CABG. My understanding is that CABG could be completed after stenting, and may very well have happened for this patient without our knowledge.
unsrsly|5 years ago
ashtonkem|5 years ago