Drs. Michael Koren and Dennis Leahy, cardiovascular specialists, continue with part 2 in a 4 part series of MedEvidence exploring Lipoprotein A, also know as Lp(a). Dr. Leahy shares his personal experience with Lp(a), and the duo delve into cutting-edge strategies for managing this risk factor for cardiovascular disease. So, tune in to learn more about this lesser known condition and possible treatment options.
Dr. Dennis Leahy is a retired interventional cardiologist living in San Diego. He received his education from Princeton University and Columbia University and his residency at the University of California. In addition to enjoying the opportunity to surf and golf, he has maintained a personal and professional interest in Lipoprotein A research and treatment.
Michael J. Koren, MD, is a practicing cardiologist and Chief Executive Officer at Jacksonville Center for Clinical Research, which conducts clinical trials at 7 locations in Florida. He received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine and fellowship in cardiology at New York Hospital/Memorial Sloan-Kettering Cancer Center/Cornell Medical Center.
He is a fellow of the American College of Cardiology, fellow and two-time president of the Academy of Physicians in Clinical Research, and the regional chapter of the American Heart Association.
Dr. Koren has served as an Investigator in over 2,000 trials and as the international lead investigator for many multi-centered trials including ALLIANCE, ROLE, TREAT to TARGET, OSLER, and MENDEL studies. He has written and co-authored over
Drs. Michael Koren and Dennis Leahy, cardiovascular specialists, continue with part 2 in a 4 part series of MedEvidence exploring Lipoprotein A, also know as Lp(a). Dr. Leahy shares his personal experience with Lp(a), and the duo delve into cutting-edge strategies for managing this risk factor for cardiovascular disease. So, tune in to learn more about this lesser known condition and possible treatment options.
Dr. Dennis Leahy is a retired interventional cardiologist living in San Diego. He received his education from Princeton University and Columbia University and his residency at the University of California. In addition to enjoying the opportunity to surf and golf, he has maintained a personal and professional interest in Lipoprotein A research and treatment.
Michael J. Koren, MD, is a practicing cardiologist and Chief Executive Officer at Jacksonville Center for Clinical Research, which conducts clinical trials at 7 locations in Florida. He received his medical degree cum laude at Harvard Medical School and completed his residency in internal medicine and fellowship in cardiology at New York Hospital/Memorial Sloan-Kettering Cancer Center/Cornell Medical Center.
He is a fellow of the American College of Cardiology, fellow and two-time president of the Academy of Physicians in Clinical Research, and the regional chapter of the American Heart Association.
Dr. Koren has served as an Investigator in over 2,000 trials and as the international lead investigator for many multi-centered trials including ALLIANCE, ROLE, TREAT to TARGET, OSLER, and MENDEL studies. He has written and co-authored over
Welcome to MedEvidence, where we help you navigate the truth behind medical research with unbiased, evidence-proven facts powered by Encore Research Group and hosted by cardiologist and top medical researcher, Dr Michael Koren.
Speaker 2:
My name is Dr Michael Koren and I'm delighted to be part of another episode of MedEvidence with my colleague, dr Dennis Leahy, who's talking about his own experience with lipoprotein little a, and this is a lipid particle that we call the really really, really really bad cholesterol, because people that have this particle tend to have serious complications, and these complications tend to run in families. And so Dr Leahy and I were just discussing this, and he was telling us this fascinating history of a very strong family history of premature cardiovascular disease, going back to when he was 10 years old and a relative had some carotid surgery, and then he personally learned that he had the same genetic marker. He did not have coronary calcium, but maybe that was a false indicator of what his true risk is. So, dennis, is that a reasonable summary of what we talked about in the first session? Yeah, I think so. Okay, so get back to your story a little bit more. And so you learned that you didn't have any coronary calcium, but you had a high LPA level.
Speaker 2:
And, just for the audience, lpa is measured in different ways. In fact, there's kind of a debate of the best way to measure it, but the two major ways of measuring it are either by mass, and the typical measurement there is milligrams per deciliter, or by concentration, and then the typical measurement would be nanomoles per liter and then the typical measurement would be in nanomoles per liter. And they are related to each other. But because lipoprotein little a is a heterogeneous molecule, more and more of us think that the concentration is a better way to describe it, because each particle can actually have a different mass and it's hard to know your risk based on quote the size of your particles. So just looking at the overall concentration of particles is probably the way most of us are going in the lipid field.
Speaker 2:
But for those of you out there that may be wondering what we're saying, a typical, normal level of LPA meaning that you're not at high risk using the milligrams per deciliter is typically thought of as 30 milligrams per deciliter or below, and when you get up to about 100 milligrams per deciliter is typically thought of as 30 milligrams per deciliter or below, and when you get up to about 100 milligrams per deciliter, then we're talking about some serious issues. Similarly, for the concentration measurement in nanomoles, that would typically be something less than 75, is considered low risk, and then when you get up in that 150, 200 range. We're talking about something that's of great concern. So just to clarify that for the audience. And, dennis, why don't you jump in and keep on telling us this fascinating story?
Speaker 1:
Yeah. So again, I think we left off in 2002, at which time there was very little clarity about LP, little a's role and actually there are very inconsistent ways of measuring it. But from that point I felt well, a negative calcium scan was going to be real positive and I think I went on a low dose statin just because I did want to get my LDL down below 100. But, you know, felt pretty good about things. Did the statin change your LPA at all? I didn't really repeat it, but that's a whole other discussion. As you know, the relationship between statins and LPL delay is a complex one.
Speaker 2:
Yeah, the general point of view being that statins do very little or nothing for LPA, or increase it in some cases.
Speaker 1:
Yeah, potentially, yes, so anyway, I was doing my usual thing. So, anyway, I was doing my usual thing. And then a very important moment in life was New Year's morning in 2007. So this is about four years after I had my negative calcium scan. I was surfing, it was a cold, windy morning for San Diego and kind of an arduous paddle out and I had my first episode of chest pain when I was paddling out and I knew exactly what it was, having been in this position with thousands of patients over the years, kind of backed off and got into the beach. The pain was gone, but I was quite certain I was now living out my, my legacy here as a lahey um, and indeed so. Then I I did get a cardiac workup, uh and uh had some stents placed shortly thereafter um, what was your anatomy?
Speaker 2:
uh, describe, if you're willing.
Speaker 1:
Yeah, it was mostly two vessel disease. My right coronary looked pretty good. I had um lad disease that was fairly significant and circumflex disease that was moderate.
Speaker 2:
So for the non-cardiologists out there, you have three major coronary arteries and you have a left main coronary artery which bifurcates by and large into an LAD, left anterior, descending in a circumflex system and depending on the location of blockages and the extent of atherosclerosis, we make decisions about intervention and prognosis et cetera. So in Dennis's case he had two vessels that were blocked in disease that I assume were treated with stents?
Speaker 1:
They were, and so that's when the story gets even more interesting, particularly for me as an interventional cardiologist. I'd placed thousands of stents. At this point, three months after my stent procedure, I was surfing same beach. Same situation had chest pain again.
Speaker 2:
Is that standard cardiac rehab in san diego?
Speaker 2:
is surfing me and so, sure enough, uh, I had restenosis in in one of the stents um the other one didn't look too bad at that time and we decided to stent within the stent with a different, uh, a different coating, with these were drug eluding stents, um so so just again for clarification, for for the the lay folks out there not the lay, he's the lay folks but um, uh, when you have restenosis, what's happening is that there is a biological phenomenon where the stent, which is usually a little piece of plastic that gets expanded in the artery, becomes blocked up. Uh, typically through this proliferative process that we now control better with certain types of stents and with using certain drugs after stents are placed. But one of the questions is if you have this milieu of LP little a, are you more prone to have this phenomenon where your stents actually get clogged up very quickly after the initial procedure?
Speaker 1:
Well, you might guess where the story goes from here Three months later where your stents actually get clogged up very quickly after the initial procedure. Well, you might guess where the story goes from here. Three months later, surfing chest pain again, and at this point really, not only was there some stent re-stimulosis, there was progression of Zs on either end of the stents and actually kind of encroaching the left main.
Speaker 2:
Now were you on high doses of statins at this point end of the stents and actually kind of encroaching the left main. Now were you on high doses of statins at this point.
Speaker 1:
Yeah, I was on high doses of statins and you know dual antiplatelet therapy.
Speaker 2:
So that would be just for the audience. Again, that would probably be aspirin and Plavix or clopidogrel.
Speaker 1:
So now this is really getting concerning to me.
Speaker 1:
I really felt I mean there's objective black and white evidence on the angiogram that this process is really kind of taking off, and my own suspicions were that the stents were really, you know, an itis for an inflammatory response and my LP little a level was really really making me extremely vulnerable to that.
Speaker 1:
I had one more go around with stents three months later, surfing chest pain again, and so at this point I had a more go around with stents Three months later, surfing chest pain again, and so at this point I had a fair amount of metal in my arteries and actually there was a little progression disease in my right coronary, which was pretty much clean a year before. And so I remember having that angiogram and going over it with my interventionalists and I said, well, it's time to go to surgery. For sure, I was going to be handcuffing my surgeons if I put any more stents in. And fortunately I had a very good friend who is an extremely good and creative surgeon, and so I had a six-vessel bypass in 2008. Really, wow, that went well. He actually used mammary graft, left mammary for my LID and did some really crafty free grafting using my right mammary and I had one vein graft placed.
Speaker 2:
So again for the audience, the mammaries are arterial grafts and they tend to last longer than the venous grafts that are used for bypass surgery. So using two arterial grafts requires a great deal of skill on the part of the surgeon, and it sounds like in your case, dennis, you found the right person to perform the operation.
Speaker 1:
Yeah, he did me well that day and he did me well later as well. We'll get into that. So things went well. After bypass surgery I continued my practice, maybe cut back a little bit on the really arduous night call stuff, but didn't stop surfing? No, that's to this day Good for you.
Speaker 2:
I love it.
Speaker 1:
So yeah, I've been really fortunate in that regard. So things went along reasonably well. Went along reasonably well and in 2016,. Now I had another dramatic episode and this time it was cerebrovascular symptoms. I was home one evening, sat down on my computer, suddenly developed a left-sided headache, looked at my computer screen nothing looked quite right. Tried to describe to my wife what was going on and missed a couple words. And I had known at the time of my bypass surgery they'd studied my carotids and I had 40 or 50% carotid lesions in both right and left internal carotids. I had them checked periodically and the left had progressed to about 60 or 70% a year. Before this night, and the first thing as soon as I had trouble speaking with my wife, I knew that my left carotid was in trouble and went to the ER was a stroke coat and I had a really large lesion in my left carotid that had already embolized a couple of places. Yeah, so TPA in the ER that night, which?
Speaker 2:
is a clot buster. That's a clot buster that can be used for an acute stroke.
Speaker 1:
And, after the longest night of my life, was transferred over to the hospital where my good friend who'd done my bypass surgery did a carotid endarterectomy on me the next day.
Speaker 2:
Wow, wow. And that's an operation to clean up the carotid artery and establish full blood flow. So tremendous, right? Wow, quite a Wow, quite a story.
Speaker 1:
Yeah, and you know obviously one that again, at that point we didn't have a lot of options about what we're going to do, about LP little a and and this is certainly the culprit in my situation I really didn't.
Speaker 2:
What were other risk factors managed? Your blood pressure was pretty good.
Speaker 1:
I never had any issues with blood pressure Always at ideal weight, no diabetes, never a smoker. It was pretty much LP delay and then perhaps not perfectly ideal LDL, as I said with my 2002 readings.
Speaker 2:
And you mentioned something about inflammatory parameters. What was your CRP? Do you recall that, or was there any evidence of ongoing inflammation I had that checked, as I said, first time in 2002.
Speaker 1:
And again, we had no idea what it meant. I don't remember how elevated it was. I really don't recall rechecking it because I didn't know what I would do about it.
Speaker 2:
anyway, Sure, yeah, there's some controversy about that, but just curious if there was any other trackable parameter to show that the inflammation was really an important factor for you.
Speaker 1:
So anyway, after the CVA, I think you probably know Sam Samikis, who is at UCSD, and I Very well known, extremely well known LPA researcher, brilliant guy Very fortunate to cross paths with him. So I saw him in 2017, the year after the CVA, to see what, if anything, he was on the horizon that might kind of get in the way of this momentum that I had. That was pretty worrisome.
Speaker 2:
Yeah, In the next chapter we'll talk about the therapies for LPA, including the therapy that you chose.
Speaker 1:
Thank you for listening to MedEvidence the truth behind the data. Please hit the subscribe button to stay up to date on our weekly releases.