The clinical challenge. What we're going to discuss today is actually something we see every day in our clinical practice.
A patient comes into our room, for instance, this one, 59 years old, hypertension, smoking, type 2 diabetes, dyslipidemia, he has PCI in 2021, relatively recent, medication, as you can expect, and recent lab actually is still way from being optimal. If we calculate risk-- We don't need to calculate risk. PCI and diabetes, it's very high risk.
If we look at the individual numbers, we can actually see that there's a lot of abnormalities, and if we look at the recent data which have offered us new modalities to treat these patients and further reduce residual risk, we can see that dual antiplatelet therapy, GLP-1, fish oil, PCSK9, we have a lot of tools to actually reduce the risk. Where shall we start?
We all know that atherogenic dyslipidemia is a major risk factor, so maybe we should start with atherogenic dyslipidemia. Further lowering of LDL, maybe even triglycerides, data are complicated. Lp(a) data are emerging.
The other hand, we can also say, "No, it's predominantly blood pressure and kidney protection and metabolic risk factors." Also, there, we have a plethora of different choices to actually address suboptimal risk factor control,
But also more recent data, this is data from the CANTOS, but it's also the colchicine data, show if CRP was high, maybe we should address the residual inflammatory risk, which gives you a cardiovascular risk reduction independent of any lipid change. Wow. Lot of choices.
What's even more complicated is that we've learned, if I take the example of the lipid axis, that it's highly unlikely that we get optimal control of an individual risk factor as one single agent. Hypertension treatment already showed that we nearly always give dual or triple therapy, while the same is going to hold true with constantly lowering of, for instance, the LDL-C target that will have to go for double or even triple therapy to completely eradicate lipid risk. But the problem is atherogenesis is a multifactorial disease. You can recognize lipids, blood pressure, it's inflammation, it's coagulation. If you look at these pillars contributing to the disease process of atherogenesis, you might need one, two, or even three drugs in each of these pillars, and if you only take these five, this will already result in at least 9 or 10 pills per day. That's a lot of choices, and that's a lot of medication.
Then there's the elephant in the room. When we look at statin use, we know that after one and a half years, approximately 50% of patients, which is still a moderate estimate, has discontinued their statin therapy. If you look predominantly at the study in the elderly, we've also learned that if you use more than three or four or five, whatever study you read, actually, the chance of medication discontinuation is huge. Polypharmacy is a major risk factor for loss of adherence. In the back of our mind, we then go back to adding medication helps, but in fact, it's a relative risk reduction. What's the absolute risk reduction? At what cost should we start medication stacking, and what's the return of the investment, which is a complicated question.
The overall question which comes to mind in a clinician seeing a very high-risk patient is actually, how can we make choices which are optimal, affordable, and sustainable in the long run? We see all these different risk factors which can be controlled. We are so happy that we have positive studies supporting that we do something good, beneficial for the patient, but what would we actually have to choose to give the optimal choice, the best risk reduction, keep total healthcare spending affordable, and make sure that the medication we prescribe is actually also being used in a sustainable way? That's what we're going to learn from the next presentations
This lecture by Prof. Erik Stroes was part of the EBAC-accredited symposium "The challenge of choosing in cardiovascular risk management" held during the ESC congress 2022.
Prof. Erik Stroes, MD, PhD is professor of Vascular Medicine at Amsterdam University Medical Center in Amsterdam, The Netherlands.
This recording was independently developed under auspices of PACE-cme. The views expressed in this recording are those of the individual presenter and do not necessarily reflect the views of PACE-cme.
Funding for this educational program was provided by unrestricted educational grants from Amgen & Novo Nordisk A/S.
The information and data provided in this program were updated and correct at the time of the program development, but may be subject to change.
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