Cardiovascular risk can be significantly impacted by the presence of diabetes.
Yehuda Handelsman, MD, FACP, FNLA, FASPC, MACE:We’ve got the individuals that Jennifer called low risk.
Eugene E. Wright Jr, MD: Relatively.
Yehuda Handelsman, MD, FACP, FNLA, FASPC, MACE: That’s my point. What’s low risk? A person who has type 2 diabetes but 0 to 1 other risk factors? I don’t know those patients. My patients have at least 2 or 3, if not 4 other risk factors. My way to deal with it is to differentiate. I’ll do a cardiovascular ultrasound. I’ll do a calcium scoring. Sometimes, with claudication, I’ll look at that because peripheral vascular disease—an area we don’t put a lot of attention on—is as much a high risk for the next death as established cardiovascular disease. We have to look at our patients. If by age 36 they have type 1 [diabetes],they, they may already have atherosclerosis in their vascular sclerosis. How do you differentiate lower risk from the higher risk?
Jennifer B. Green, MD: In my endocrinology clinic, I rarely see anyone I’d consider low risk. If you look hard enough, you’re going to find some kind of an abnormality, at least in patients in the endocrinology clinic. That will cause you to consider that person to be at an even higher risk than might be associated with type 2 diabetes. That category of risk is probably shrinking all the time. For example, even clinically evident cardiovascular disease, like a peripheral vascular disease, is often present in our patients. But because we don’t check their pulses or do an ABI [ankle brachial index test], we aren’t aware of it. It takes a bit of extra time to do these assessments. Perhaps team-based approach, in which a nurse or someone who’s trained to do an ABI has done that alongside your clinic visit, might help integrate and touch on all these aspects of risk identification and reduction that we need to incorporate into the care of individuals with diabetes.
Eugene E. Wright Jr, MD: In primary care, we have certain tools that are questionnaires that patients can go through, and they can fill out and identify individuals. They look at family history, smoking history, hypertension, obesity, the medication you’re on for hypertension, etc. You can get a pretty good idea, but very few individuals don’t hit the threshold for increased risk. Therefore, it doesn’t make the diagnosis, but it gets you to do further testing.
Yehuda Handelsman, MD, FACP, FNLA, FASPC, MACE: You’re much more percussive and you know the data, and you have the knowledge that a lot of your colleagues in primary care don’t know everything and don’t always know the guidelines that they should follow. Is that where the IT [information technology], which you talked about, comes in? Suppose we live in Utopia. Six to 8 years ago, I was in Colombia lecturing. For them, Lantus insulin was $10 a month, and that’s all there was. Suppose we get a long-acting GLP1 receptor agonist with proven efficacy for $22 a month and an SGTL2 inhibitor for $5 a month. We have it. We have the drugs. We have the availability. Would it be executed by your primary care colleagues?
Eugene E. Wright Jr, MD: Not many. Some would—maybe those who know the evidence. But there’s another way to change behavior. IT as you mentioned, Jaime, is a great tool. If we could use that to risk-stratify patients who are at risk, we send an appropriate flag and say, “Here’s a patient who should be on these therapies—this therapy should be considered.” If you don’t want to use them, fine. Just tell me why you don’t want to use them. That starts to change behavior very quickly, and then individuals will become aware of why we do things like that. We’ve used that for vaccination rates. We do that to get individual rates up. We do that with chronic diseases like diabetes, hypertension, and hyperlipidemia.
Yehuda Handelsman, MD, FACP, FNLA, FASPC, MACE: We did not use metformin in primary care for a bunch of years. They primarily used insulin and sulfonylureas, until it all of a sudden became the darling of every prescriber. Maybe SGLT2 inhibitors will go that way. But the data do exist. The earlier we start, the more points we’ll hit early on and the better the outcomes will be. Look at the kidney. The kidney was a lost organ for a while. I’ve admitted many times that I don’t like it—not in medical school or residency either. There are 2 areas: the kidney and GI [gastrointestinal]. For the past 15 years, all I do is [work with] kidney and GI. That’s what we are. But I recognize that the kidney is a bit of a condition. About 10 or 12 years ago, 1 of the drug companies had an analog vitamin D1, and then it became all [companies]. They started to see if we could get it into the population. They looked into who needed that. This was around the time the nephrologist decided to go with CKD [chronic kidney disease] 1, 2, 3, 4, and 5. It was a whole spectrum. Something caught my eye. This was 10 to 12 years ago. The numbers have changed. For CKD3, there were 6.5 million individuals. For CKD4, they were 400,000. [These 2 were] 90% of the patients. That’s when I recognized how bad CKD is. We started to look at that. In our lipid guidelines, we introduced CKD as a major cardiovascular risk factor. We have to look at that. If we stop it early, we don’t let it get to CKD4. This is my point. We shouldn’t let it go. The earlier we can start, the more chance we have to go forward with that.
Transcript edited for clarity.
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