Interesting.... we all know someone who has had stents and my thoughts would be like, aren’t they fortunate that stents are available 😁 after this explanation I’ve learned “that all is not what it seems to be”🫣 thanks for the continued education 👍👍
On a not-very-related note: Any chance of doing a piece on coronary collateral circulation? As in: "I have just found out from CTCA that I have 3-vessel heart disease but have no symnptoms,low hsCRP, pulled 12 METs on the exercise stress test etc etc I also have an occluded left SFA but have developed a great leg collateral circulation system which lets me get ~70 Met hours of PA per week. Maybe the same kind of thing has happened with my heart and if so what implications for risk/benefit CABG analysis?"
Obviously I'm talking with cardio about this but would be great to get an independent survey of the evdience base, such as it is.
Hi Eddy - This is a well documented phenomenon we see frequently called collalaterization where smaller vessels develop to make up for obstructed major vessels. It is somewhat of a niche topic and is best described in the CTO literature (Chronic Total Occlusions). The evidence for opening up these blockages (In my view) is limited outside of relieving symptoms.
The engineer in me is thinking there must be a dynamic component to this if structural modifications to arterial wall lumen are comparable to pharmacological interventions? Is it likely that there are a number of biochemical/hormonal etc moderators (identified or not?) influencing the physiology?
I'm sure cleverer people them me have thought that!
You are correct. The engineer in you will know that the maximum resistance is unlikely to be in the main part of a tributary but rather in the multiple small vessels downstream not amenable to mechanical intervention. This is where most of the resistance is and why medical therapy works so well.
Interesting.... we all know someone who has had stents and my thoughts would be like, aren’t they fortunate that stents are available 😁 after this explanation I’ve learned “that all is not what it seems to be”🫣 thanks for the continued education 👍👍
Great!
On a not-very-related note: Any chance of doing a piece on coronary collateral circulation? As in: "I have just found out from CTCA that I have 3-vessel heart disease but have no symnptoms,low hsCRP, pulled 12 METs on the exercise stress test etc etc I also have an occluded left SFA but have developed a great leg collateral circulation system which lets me get ~70 Met hours of PA per week. Maybe the same kind of thing has happened with my heart and if so what implications for risk/benefit CABG analysis?"
Obviously I'm talking with cardio about this but would be great to get an independent survey of the evdience base, such as it is.
Hi Eddy - This is a well documented phenomenon we see frequently called collalaterization where smaller vessels develop to make up for obstructed major vessels. It is somewhat of a niche topic and is best described in the CTO literature (Chronic Total Occlusions). The evidence for opening up these blockages (In my view) is limited outside of relieving symptoms.
The engineer in me is thinking there must be a dynamic component to this if structural modifications to arterial wall lumen are comparable to pharmacological interventions? Is it likely that there are a number of biochemical/hormonal etc moderators (identified or not?) influencing the physiology?
I'm sure cleverer people them me have thought that!
You are correct. The engineer in you will know that the maximum resistance is unlikely to be in the main part of a tributary but rather in the multiple small vessels downstream not amenable to mechanical intervention. This is where most of the resistance is and why medical therapy works so well.
And … as Michael Kane would say “ not a lot of people know that”!