May 29, 2023

Hector Garcia-Garcia, MD, PhD, an attending cardiologist at MedStar Heart & Vascular Institute, Washington, D.C. looks at the results of statin therapy on vessels that do not undergo PCI. This interview was conducted at CRT 2016.

We know that vulnerable plaque identifies high-risk patients who need to be treated aggressively with medication so we’re going to talk here at crt 2016 and look at the final results of ibis 3 and the effects of high-dose reserve a statin in non intervened vessels of a real practice population and to do this i am with dr. hector garcia who is an md at a phd and

An attending cardiologist at medstar heart and vascular institute right here at your hometown let’s remind people about the actual full trial first before we get to the final results thank you rick and now we already kind of inviting me for this interview yeah so first i like to do all this commentary on behalf of my colleagues actually now ex colleagues back in

And the thorak center in rotterdam the netherlands where i was still three months ago and so we did this history study together with a great team over there it is a single center study we did a 300 patient study aiming at imaging the patient at index and then repeating the imaging at 12 months and we wanted to test the effects of rosuvastatin in the coronary of

Those patients by means of using interval scale ultrasound mainly but particularly with the use of the radio frequency analysis which is also commercially called virtual histology and also with another catheter which is the nearest catheter the tvc catheter so we have a multimodality imaging study in these 300 patients and we actually image one of the non culprit

Or non target vessels in this population for a segment a bit longer than four millimeters a what we have is a study population a very broad spectrum of a coronary artery disease basically we included patients from stable angina unstable angina non-stem in stemi population and that was kind of the study design what did you find you’re presented here is your final

Results what we had as primary endpoints is the change in a creek or as evaluated by a radio frequency i was analysis and for that particular point we found no significant change from baseline to follow-up when you would take the necrotic core volume as the primary endpoint and similarly for another key secondary point which was the change in lcbi which is a index

Measuring the amount of lipid in the coronary arteries using this tvc catheter so we also did not observe any significant change in the segments study with we discarded there over the period of 12 months so what you could conclude is two things i believe on one hand is that rosuvastatin did not change the signal coming out of these two different imaging modalities

Which is very hard to accept but that could be a real observation or that that the endpoint that we have picked for this study were particularly not the best that you could take for evaluating the effects of rosuvastatin so there are like two angles i mean the whole concept was that the hydros reserved a statin we kind of dry out the vulnerable plaque and leave it

Less vulnerable correct that’s correct and actually there is actually another element that are like to introduce here it is the time of follow-up so we have only 12 months follow-up when in previous study another progression regression i was studies done in the past the more traditional let’s say follow-up for those is 24 months maybe another compounding factor

Here is that we are real image in those patients very short after the intervention which is only one year and we could have made may be waited another year to see whether we see more effect but indeed our inner hypothesis was that we you would see a decrease in the amount of micro recording the artists of those patients what would make sense and we know that

People respond to statins the the risk drops pretty dramatically fairly soon after starting statin therapy so there is something happening and it’s it’s even before you end up with with ldl changes you get an effect with statins quickly and this was maybe one of the things we were hoping it was going to be that’s correct and and and and you are definitely right

When you look at clinical outcomes and here we were coming more with a mechanistic study trying to to support why you would have such a dramatic effect in reduction of clinical outcomes but we do set up we do know prove that point and we have listed some of the potential confounders for this study now you have a second paper here that’s just taking a look at ibis

For ibis and virtual histology results so just when you when you take a look at that whole package what did you find yeah so that’s very interesting because it is for is another multimodality imaging study in this case the study design is a multicenter study is done in stemi patients so you treat the calpro artery and then what we did is to image the standard the

Newly assented vessel in the other two vessels from the same patient so the full coronary tree was image at baseline with two different imaging modalities virtual histology but also optical coherence tomography and we gave to those patients also rosuvastatin 40 milligrams for a period of 13 months in this case and we repeated in the three coronary vessel of those

Patients oct infertile histology so the observations from that study is as natural curve in the primary endpoint for the radio frequency analysis we did not observe any change similarly to the eb-3 findings in this post stemming population however very interesting and we also discussed it in this meeting where the oct findings so in oct what we were interested in

Was to measure the change in the thickness of the fibrous cap because of the resolution of the imaging modality been about 10 15 microns we were able to capture these small changes occurring over time in that fibrous cap so we observe a thickening of the fibrous cap making or suggesting a less vulnerable those spots and also we observe a reduction in the angle of

Lipid pool as a cells by optical coherence tomography and maybe a unique finding in this setup is the fact that we measure the accumulation of macrophages at index and then repeat that oct an alice is at the follow-up and observe our reduction in the accumulation of macrophages in the vessel wall of those patients so you could say it’s so far taken industry and it

Is for together is that we with one-year treatment of ross was 13 we did not change the amount of necrotic or present in those b cells but when you would use the optical coherence tomography b might be because of the resolution of the imaging modality we observe a significant changes in the thickness of the fibrous cap reduction in the lipid pool and also reduction

In the macrophage accumulation a few years ago some of the great minds of this area seem to suggest that you know don’t concentrate on the vulnerable plaque concentrate on the vulnerable patient your results here seem to argue in support of that exact same thing correct no i i am also strong believer of the vulnerable patient concept although we are focusing our

Imaging results in in the in the serial observations at the black level however you know as a whole while we are interested is in impacting the patient level results and not much just focal changes in the vessel wall that may not have any clinical impact so so yeah so while we use this imaging to in these mechanistic studies to explain some of the observations we

Have ever made in in large clinical outcome trials doesn’t mean that we are obsessed by imaging the the vulnerable back so you think there is still a role to understand better the vulnerable plaque there is a role because when you see these dramatic new you alluded to that when you see these dramatic reduction in cardiovascular events after the the starting with

The treatment without statins so you need to come up with some explanation as why that is happening and a one way to do that is by imaging the actual plots that are being treated and but that’s not the only way so you have some other biomarker assessments and genetics assessment and many others that are now ongoing in in larger trials as well assessing whether

Those changes in all those areas would impact or explain this reduction in cardiovascular outcomes in these statin trials so so is we’re just coming with one piece of the puzzle and trying to contribute to that whole discussion to better understand in which way we are impacting the critical to vascular outcomes of our patients you are you gotta continue looking

At this issue definitely so we we are obsessed about the imaging intravascular imaging and and with newer techniques like optical coherence tomography the level of detail that we are getting out of this vessel walls is getting to the microscopic level so the resolution today is 2m 15 microns but the new developments in that area is as they call it a micro ct is

Getting us to five microns which means what you see on the microscope so you insert the same catheter about what you get out our local sites are dear to the vessel wall flat let’s and in all the beauty of the cholesterol crystals you know with a superb resolution so so we are going to continue if if fans are there and we get sponsorship for for our research where

We believe we are contributing again with one piece of the puzzle right well congratulations it’s fascinating and if you if you look at this some more please come back and talk to us again for sure maybe we should make an appointment for next year coming see our teeth and speaking of crt our coverage of that is online as you can see and it’s also in cardio source

World news interventions please check out there where i have executive editor rick mcguire you

Transcribed from video
Effects of High-dose Rosuvastatin in Non-intervened Vessels: IBIS 3 and 4 By CSWNews