Endocrinology Network Editorial Staff 

I’d be interested in what Dr Bhatt says his screening would be in the patient who hasn’t had an event before, who has all their factors controlled, their diabetes, their blood pressure and lipids are controlled by the referring doctor. Some of our doctors do cardiac calcification scores, scares the patient, but they’re already on a statin and their LDL [low-density lipoprotein] is below 70 mg/dL, and I have them on the works of heart-smart drugs and all that. Some of them do stress tests, so I’d be interested in what screening is done. The cardiologists tend to do different things, so I’d be interested in what the guru does.

Dhiren Patel, PharmD, CDCES, BC-ADM, BCACP:

Deepak L. Bhatt, MD, MPH, FACC, FAHA, FSCAI, FESC:

 I think if it’s a tough situation, I just send them to an endocrinologist. That’s what I do. But assuming it’s not too challenging, generally speaking, the guidelines are pretty firm about what things to test for. It’s usually the simple stuff: LDL, cholesterol, blood pressure, glucose, weight. I actually prefer waist circumference, but I think weight or BMI [body mass index] are the more standard ones. Screen for smoking. Beyond that, everything else really is supposed to be symptom-driven. These days, the annual stress test per the guidelines is out, even though that remains a common practice. Any sort of imaging testing or invasive testing, in general, is meant to be driven by the presence of symptoms, such as suspected angina. Though coronary calcium you mentioned; there, that has been promoted in recent years as a way, if there’s really a question to be answered in terms of figuring out if a patient is at high risk. For example, a patient where maybe you think they need to be on a statin but there’s statin hesitancy. There perhaps getting coronary calcium can help tip things over where the patient says, “Oh yeah, I do have plaque in the coronaries. Maybe it’s time to go and start that statin.” I think there’s a role, but I suspect in years to come, there’s going to be a much more prominent role played by imaging tests, even in people who are asymptomatic. But at least per the guidelines, we’re not quite there yet.

 Thank you. Jen, how are you guys classifying this risk and screening?

Jennifer Goldman, RPh, PharmD, CDCES, BC-ADM, FCCP:

 Community pharmacists are highly accessible, and almost every human being goes into a pharmacy at some point. I think that they also get to know their patients, just like in primary care, so they’re in a unique position to be able to say, “Hey, have you seen the doctor? Hey, have you been screened for this? Have you considered this? Have you talked about this?” I think that pharmacists in the community can help answer those questions or at least put it into patients’ minds that, “You need to go see your doctor. Have you had your blood pressure checked? Have you had your cholesterol checked? Have you considered these things?” Even to just make those suggestions, to make sure they’re seeing the appropriate providers. Then clearly the pharmacists who are within primary care or within cardiology and endocrinology are working with the team in terms of drug therapy management, but the community pharmacist is in that unique position.

Videos

Criteria and types of health care professionals who may screen patients at high risk for cardiovascular disease.

Screening for Cardiovascular Disease

 Dr Busch, when you think about some of these risk factors that are associated with what Dr Bhatt just mentioned, how are you talking to your patients about these risk factors? I sometimes think about them as modifiable, nonmodifiable. And then, what are the efforts that you are doing, and we’ll maybe go around, of screening these cardiovascular risks? You’re very involved in clinical trial research. I feel like you’re constantly looking at panels and seeing who could potentially be at risk. So maybe talk to us a little about those risk factors and how your practice takes on the screening of these cardiovascular risks.

 For an endocrinologist, most of our patients have diabetes and mainly type 2 diabetes, but they don’t just come in with a diabetes, as Jen and others have said. They come in with diabetes, hypertension, hyperlipidemia, and obesity; they come in with hypertriglyceridemia. So, which one are we going to tackle first? Say they’ve done the lifestyle stuff, they’ve met with the diabetes educator, and you know they’re going to end up on 6 or 7 drugs down the line. Well, visit 1, you’re not giving them the works. You could, but then the patient will put their shoes and socks on and run away. You have to choose your battles first, and what you’re going to be successful with early. Oftentimes, the LDL [low-density lipoprotein] is the easiest thing to control because the statins work, and if they can tolerate the statin, at least you could show success after the first visit, that you got their LDL at a target, and then try to address the other things.

If they come in with an A1C [glycated hemoglobin] over 7.5%, you’re going to give them 2 drugs for diabetes and heart-smart drugs. You give them a statin, or a statin plus something else to get their LDL down. Now we have the REDUCE-IT trial that Dr Bhatt is famous for. You’re going to look at the triglycerides and do something about that as an additional marker. And then of course, their blood pressure. And even if their blood pressure is good, congratulations, you have good blood pressure, here’s your ACE [angiotensin-converting enzyme inhibitor] or ARB [angiotensin receptor blocker] based on the HOPE trial. Congratulations, your LDL is 92 mg/dL, here’s your statin based on the CARDS study, that statins should be in the drinking water of diabetes.

You have to roll out the regimen for the patient, and most of our patients, if you ask them what did they have for breakfast? Their answer is pills, because after a year, they’re on 6 or 7 medications and some injectables as well. So, each thing has to be addressed, because these are risk multipliers, and you want to address each thing. But it takes about 6 months to a year to roll out the full regimen that the patient is going to be on. But you’re not telling them day 1, especially if they come in saying, “I don’t want medications, I want to treat things the natural way,” and you know what you have cooking down the line.

 Absolutely. It’s a lot, especially as some of these medications start blurring and have cardiac benefits, you have different specialties that normally didn’t use them that are now using them. And we’re going to get to that. Joyce, when we started, you mentioned you spent a lot of time on both preventive cardiology and secondary prevention. From where you sit in the specialty arena, where you get to interact with endocrinologists and pharmacists and cardiologists, how do you go about what Dr Busch just mentioned, with primary prevention and secondary prevention? How do you tackle each of those?

Joyce Ross, MSN, RNC, CRNP, CS, FNLA, FPCNA:

 Well, I think the first thing I want to say is, I totally agree with Dr Busch that we really can’t just throw everything at the patient the first time we see them. They will run and they won’t come back. And the idea of multiple medications all at one time is something that me is a nurse practitioner, a person who sees the patient on a regular basis, even more than perhaps the physicians in the various settings, I’m kind of a gatekeeper in a lot of ways. At least for our practice, I would be able to make sure that everybody was getting the information. I think communication between the health care providers is critically important, because this is a team. And of course, the most important part of the team is that patient. So, for me, every time a patient is seen by any of a group, and it’s wonderful if you’re all in the same health system, and you can just pick up where you where you want to, but that’s not always ideal. But what happens, what is very important, is for you, as a provider, no matter what your entity is, to communicate with the others about what you saw, what you did, how the patient is doing.

And you know what? The most important thing to me is that patient gets that same letter, because they need the congratulations, they need that idea that, “look what we did.” Again, to go back to what Dr Busch was saying, we’re helping them and supporting them in the decision that they have to make to take a lot of medication. I think that the most important thing is to depend on all the team, communicate, but communicate first with the patient. My opportunities have always been to develop long-term relationships with the patients, because dyslipidemia is not something that’s going to go away. And I’ve taken care of patients from the time they’ve been 6 years old until out of college, married and have children. This long relationship that you have with them is critically important. As a nurse practitioner, I’ve been fortunate to do that, where many specialists don’t have that opportunity. When others communicate with me, I have a great chance of weaving their thoughts and plan into the overall plan. That’s how the team works.

Recommendations for establishing relationships and talking with patients about primary and secondary prevention against cardiovascular events.

Counseling Patients on CVD Risk Factors

Dhiren Patel, PharmD, CDE, BC-ADM, BCACP:

 Excellent. Thank you for that. Like I said, we have a lot of different tools in our toolbox. It’s always nice to understand and help our primary care colleagues. They have a lot on their plate. They have a lot that they need to do within a 15-, 20-, 30-minute visit, and it’s also nice to be able to share some of these best practices in clinical pearls as they sort through some of their options and as they talk to their patients.

I’d love to talk about a real-life case and how we’re using some of this hot-off-the-presses, so to speak, information, and how we’re incorporating that into practice. We have a patient case. This is a 64-year-old woman with a history of hypertension, peripheral artery disease, and chronic kidney disease, that is newly hospitalized for heart failure. Dr. Vaduganathan, if you could walk us through your approach and what you were thinking as you saw this patient.

 Yeah, exactly. This is kind of the prototypical person we’re meeting now, who is newly diagnosed with heart failure, in this case with reduced ejection fraction. She was diuresed in the hospital with loop diuretics. She’s now clinically improved. She actually feels quite well. Her transthoracic echocardiogram showed an ejection fraction of 30% and she had moderate mitral regurgitation. She has preexisting kidney disease. Her estimated glomerular [filtration rate] is 45 and she has a nonischemic picture with nonobstructive coronary disease on angiography.

So now we’re meeting her and we’re engaging more closely in her care as we approach discharge, and the clinical question comes up, what do we do next? Her blood pressure is 95 to 100 mmHg, her systolic blood pressure, her heart rate is 85 BPM, and she’s otherwise fairly euvolemic. At present, she’s on low doses of 3 pillars. She’s on metoprolol succinate, 25 milligrams [mg]; lisinopril, 2.5 mg; and spironolactone, 25 mg, and she’s also on a modest dose of a loop diuretic as well as aspirin and a statin. The question becomes in heart failure management today, we now have multiple options. We can up-titrate this patient to target doses of her existing therapies, we can switch her from lisinopril to sacubitril/valsartan, which has been shown to have incremental potential in improving survival, or we can initiate an SGLT-2 [sodium-glucose cotransporter-2] inhibitor.

I think this is becoming increasingly common in terms of multiple potential decisions that can still benefit patients. In this case, we chose to start dapagliflozin, 10 mg once daily. And I think the primary reason that supported that decision was that her blood pressure was borderline. She was already on low doses of other therapies, and we know that probably touching on each of these pillars, each of these components, is important in modifying pathophysiology. So that was the decision we made. Since she was clinically euvolemic, we didn’t alter her diuretic dose. And, importantly, in both DAPA-Heart Failure and EMPEROR-Reduced, there were really minimal diuretic changes during the course of the trial for most patients. A minimal subset, 10% to 15%, required dose de-escalation, down-titration, during the trials. She was closely followed, and otherwise has done well and she’s awaiting follow-up with repeat echocardiography.

 Excellent, that’s really helpful. I have a follow-up question for you there. In a lot of the heart failure trials, we saw these target doses that we were always aiming for, and you mentioned the 3 pillars, now we have a 4th pillar. Is it more important now to making sure there is 4 pillars on board versus the initial approach that we had of getting everyone to target? How are you now thinking about this 4th pillar? For those of us that don’t do heart failure on a daily basis, but now we are because the same way diabetes is becoming a disease that you guys now have to be more attuned to, we’re seeing concurrent heart failure in our patients with diabetes. What would your thoughts be there?

 Unfortunately, we don’t have direct clinical trials comparing, for instance, high doses of 2 therapies, 2 pillars, versus low doses of 4 pillars. That said, indirect evidence does suggest that a more comprehensive approach of low doses of multiple therapies is the path forward. That indirect evidence comes in a few lines. First is that there have been direct dose comparison trials for ACE [angiotensin-converting enzyme] inhibitors and ARBs [angiotensin receptor blockers], where low doses and high doses were compared, and on average there were no survival benefits of higher doses. But at higher doses, people did appear to have a hospitalization benefit. People remained out of the hospital to a greater extent. For beta blockers, probably the therapy with the clearest dose response, higher doses do appear to provide incremental advantage. For the MRAs [mineralocorticoid-receptor antagonists] and of course SGLT-2 inhibitors in heart failure and CKD is fixed dosing, that question is less relevant.

So, in general, based on that and extrapolating from that, touching on multiple therapies especially since all these therapies work on distinct mechanistic pathways and targets, we would anticipate that their benefits in practice would also be additive when combined. So that has been our approach and that’s been also supported in more expert consensus pathways. But unfortunately, I don’t think that there will be, at least in the near term, a planned clinical trial investigating combination versus various combinations.

 That’s really helpful. One thing that we all heard today, and we can all agree on, that we’re never just managing one condition. If it’s diabetes, we’re also dealing with other comorbidities, and if it’s heart failure, we’re dealing with CKD and a long list of other things. This has been an excellent discussion and we hope you found this information to be useful. Thank you all for watching this Medical Economics Around the Practice program. Thank you all for joining us today.

Muthiah Vaduganathan, MD, MPH, presents a case study for a patient hospitalized with heart failure whose therapy was optimized with an SGLT-2 inhibitor.

Case Study: Optimization of Heart Failure Therapy with an SGLT-2 Inhibitor

 I think you would all agree that many of you are embedded in specialty clinics. Overall, and the last numbers I looked at, and I’d probably bet that they’re still kind of there, I saw GLP [glucagon-like peptide] usage of around 7%, SGLT-2s [sodium-glucose cotransporter-2], 4%. Nonetheless they’re probably both less than 10%. What message do you have for those that are on the front lines, our primary care providers, as they think about the impact of some of these CV [cardiovascular] medications? But obviously we’re not conferring to our patients because they’re not, maybe they’re on an SU, maybe they’re on a DPP-4 [dipeptidyl peptidase 4] inhibitor. What would your message to that group of folks be? They’ve adopted DPP-4 maybe too well. Now we need them to adopt a different oral pill. Dr. Isaacs, maybe we’ll start with you. I know you get a lot of your referrals from that community.

Diana Isaacs, PharmD, BCPS, BCACP, BC-ADM, CDCES:

 Yeah, I’m glad you went to me because I have a message, yes. I would be avoiding therapeutic inertia. We see these guidelines and we see, oh, yeah, person has cardiovascular risk, we should be considering these agents. But a lot of the patients that come to me have had diabetes for so many years, they are already on some established regimen, sometimes it’s a basal insulin, it could be with a DPP-4 inhibitor, or they’re already on MDI. I always tell my students and my residents training with me, we must think big, right? If they are not on these agents, they’re not on an SGLT-2 inhibitor, they’re not on a GLP-1 agonist, even if they’re not on metformin, we have to ask why. Sometimes it was just something like they were in the hospital, and they just got rid of all these agents and decided to put them on MDI. Some people mistakenly think once someone is on insulin, they cannot continue their other agents. There’s all these people out there that could be benefitting from these agents, so we really need to think big, don’t just continue. Yes, while it may seem like, oh, it is easier to just increase the insulin by 2 units, no. We need to be thinking about the benefits of these agents.

 If they want to get the hugs, they should initiate it. Remember, these drugs also induce weight loss. You have someone who hasn’t lost weight for many years and put on an SGLT-2 and/or GLP-1, they will lose weight and they don’t get hypoglycemic on it, and if they’re on insulin or a sulf, you can taper it down, maybe come off of it down the line. I think that’s what alienates some of our cardiologists. If the patient is on an insulin, they don’t want to go into the insulin titration business, they leave it to someone else. They might be a little gun shy to start those. But amongst our cardiologists, if you’re not on insulin or sulf or a drug that causes hypoglycemia, feel comfortable to use these classes because hypoglycemia is a non-issue. The patient doesn’t have to monitor their sugar in those cases. But not only the A1C lowering, but these other benefits plus the weight loss.

Just to cap this off, if I told my chief of endocrine years ago that you had a drug that could lower weight, blood pressure, and A1C without hypoglycemia, prevent heart failure, pre-heart failure, and treat kidney disease in diabetics and nondiabetics, he would fire me for hallucinating. Here you have a class of drug that does that in a pill. It’s pretty incredible.

 Yeah. As we hear from the cardiology perspective, I would love some color around, you know, obviously in the diabetes, you kind of heard it, but also now in heart failure, you’re seeing a lot of referrals coming into you for heart failure. What’s your message to the primary care folks because they’ve been managing heart failure to a certain extent, and this is all so new? What would your message to them also be there?

 Yeah. This is increasingly becoming a dialogue we’re having. As Dr. Busch said, the SGLT-2 inhibitors have formed this latest pillar in the management of heart failure with reduced EF [ejection fraction] alongside 3 other core therapies that prolong survival in these patients. Of those other components, the SGLT-2 inhibitors are some of the easiest to use in practice. I think reinforcing that message to all clinicians who care for people with heart failure is going to be increasingly important.

A panel of experts provide clinical pearls for primary care providers who manage patients with diabetes and cardiovascular comorbidities.  

Clinical Insights for Primary Care Providers in Type 2 Diabetes and Cardiovascular Disease

 OK. That’s helpful. Dr. Busch, I can’t think of a clinical trial that you probably have not been an investigator in, but maybe help us walk through some of these larger trials as they pertain to GLP-1 and SGLT-2 [sodium-glucose cotransporter-2] inhibitors. You’ve seen the progression over the years where, you know, first it was secondary prevention, now we’re seeing primary prevention, as well as some of these additional indications.

 OK. The DPP-4 [dipeptidyl peptidase 4] is still very commonly used, no cardiac benefit, they’re safe in the heart. Some increase the risk of heart failure a little bit, but certainly at least safe. Then the SGLT-2s, EMPA-REG started the ball rolling. And then EMPA-REG in the purely cardiac patients who had any kind of ASCVD [atherosclerotic cardiovascular disease] with diabetes, lowered MI/stroke death 14% and cardiac death 38%. It also lowered heart failure, but that wasn’t an end point. It was a secondary end point and not in the label for it at that time. Canagliflozin also lowered MI/stroke death in sort of a mixed population, two-thirds cardiac, one-third not cardiac, but unfortunately that got outshadowed by the amputation fear. But then eventually it did get into their label to lower MI/stroke death.

Then dapagliflozin was very creative because they studied primary prevention as well. Knowing the results of EMPA-REG, that it lowered heart failure and death, they had 2 primary end points. One was MI/stroke death, which it was safe for that, but interestingly, dapagliflozin has the primary prevention indication to prevent heart failure hospitalization.

Then we have the GLPs [glucagon-like peptides]. Long acting exenatide is safe for the heart. Unfortunately, in that study, the placebo group had too much SGLT-2, so it benefitted the placebo group. It probably would have been beneficial if there wasn’t so much SGLT-2 in the placebo group. But, as we know, SGLT-2s benefit the heart, so the placebo was more likely to be on an SGLT-2 because their A1C wasn’t as good.

Then the LEADER trial with liraglutide lowered MI/stroke death as well as cardiac death, has that indication. And then semaglutide, the weekly GLP, lowered MI/stroke death. Interestingly, oral semaglutide, the study was not long enough. Even though it showed beneficial trends, the FDA [Food and Drug Administration] said, no, you must do a bigger study. Fortunately for us, we are in that study. That is the SOUL trial. So maybe for our cardiologists, there will be a pill of GLP-1 that has that indication. Right now, that pill is only safe. Interestingly, 2.4 semaglutide for weight loss is doing a cardiac outcome study in the nondiabetics, so nondiabetics, obese patients with heart disease. So that may get that indication. I wouldn’t be surprised if it did because it worked in 1.0 in diabetics, but we shall see. So that is the SGLT-2 and GLP studies.

The only one that was not a positive study was ertugliflozin, was safe for the heart, but it also lowered heart failure. All of them lowered heart failure. Then, of course, we have the heart failure studies as was mentioned, you had DAPA-Heart Failure with reduced ejection fraction and you have EMPEROR[-Reduced] with reduced ejection fraction, with very similar results in those two. I guess the pillars of therapy that you’ll talk about are ARNI [angiotensin receptor neprilysin inhibitor], beta blocker, aldosterone inhibitor, and now SGLT-2 as well.

 That is excellent. I think the body of evidence has continued to grow. Recently I saw that there are a few HFrEF [heart failure with reduced ejection fraction] studies with the GLP-1s. I think it’s going to be great to continue to see what comes out of it.

Robert Busch, MD, provides an overview of the clinical trials supporting improved cardiovascular disease outcomes in patients with and without diabetes.

Cardiovascular Outcome Trials for Diabetes Medications

 Absolutely. That segues nice into our next section. What I heard from all of you is like it doesn’t really matter which guidelines we look at; we see that these medications are elevated within those guidelines. They tend to have a lot of pleiotropic effects, some of which we’ll talk about more, where you’re seeing 3-point MACE, renal heart failure, all of these additional benefits in addition to original use cases of some of these drugs. I really think that these drugs, for the first time, have brought together a lot of disciplines. For the first time we’re talking to the heart failure team, we’re talking to preventive cardiology, we’re talking to the renal team, we have a multidisciplinary panel here. I would love your guys’ thoughts on how you guys are managing and how you guys are collaborating with some of your folks at your institutions. I know it’s not easy, right, especially if you’re taking care of a patient with diabetes and heart failure, whose swim lane is it in? So I’d love to see how you’ve dealt with this at each of your institutions and how the teams are coming together. Dr. Busch, maybe we’ll start with you.

 Personally, when I’m managing a patient with diabetes, I’m doing the lipids, the blood pressure, and the diabetes drugs. But if I see the cardiologist initiate, I will feel badly if I didn’t initiate the SGLT-2 [sodium-glucose cotransporter-2] in my patient with diabetes. They come prepackaged to the cardiologist with that. There are a variety of types of cardiologists in our community. Some put it in the note, some don’t do anything, and some actually initiate it. The ones who initiate it, I personally call them or text them and say congratulations, you’re an honorary endocrinologist, that’s great that you’re doing that. The ones that put it in the note, when the patient goes back the second go-round, then they’ll probably initiate it if the primary care doc didn’t do it. But there are some who do not do that because it’s a diabetes drug and they don’t want to politically step on the primary care’s toes. We do lipids, I do PCSK9, I am not stepping on the cardiologist’s toes. I do icosapent ethyl if the triglycerides are high. We can each benefit the patient. If you’re seeing the patient and they’re not on it, do something. That’s our job.

But it varies in every community. I’m sure maybe in the Boston community, everyone is more aggressive because you’re in the midst of Harvard.

 Dr. Isaacs, we’ll go to you. How is it in Cleveland?

 We’ve taken a few different strategies. One thing we have is actually a comprehensive diabetes clinic, where patients see cardiology and endocrinology on the same day, which is fantastic because then we can have a conversation and collaboratively decide what agents to start and everything. Another model we’ve had, too, because we use a lot of pharmacists to see patients in between their usual provider visits, is that I’ve been working with one of our heart failure pharmacists to initiate SGLT-2 inhibitors in these patients. What has been nice about that is because, yes, it is easy to start an agent, but some of these patients, they’re on complicated insulin regimens already. It’s nice to have that direct collaboration where I can say, oh, we should probably decrease the insulin by this amount based on their current glucose levels, and she can say, oh, we need to back off these agents, like this diuretic. It’s a really nice to have that collaboration.

 I’ll echo that. I think there’s tremendous variation by practice and by cardiologist. There has been a convergence of quality improvement efforts in the hospital setting to optimize diabetes care as well as in non-diabetic patients with heart failure or CKD, to optimize SGLT-2 inhibitors in those folks. In the ambulatory practices, there has been some quality initiatives that have been variably successful. We had one of my colleagues, an endocrinologist, embedded in our cardiology clinic more for troubleshooting rather than direct comanagement for each of our patients. That worked out quite well in scenarios in which we had maybe subtle questions that may have posed barriers to otherwise starting a therapy.

In general, I would say that the use patterns and the comfort related to the SGLT-2 inhibitors have been picking up, and I think especially in heart failure and CKD [chronic kidney disease] where there is really fixed dosing and almost rare need for adjustment of any other therapy and very little actual monitoring as well. I think it’s actually much simpler than many of the other therapies that we use in heart failure care, for instance.

In contrast, the use of GLP-1 [glucagon-like peptide-1] receptor agonists by cardiologists remains dismally low, even in at-risk patients. That is something that I think continues to need to be disrupted, and hopefully, if oral therapies prove to be successful in modifying cardiovascular outcomes, that may also change.

 Do you think that’s a function of, you know, Dr. Busch mentioned now you have a primary prevention indication for one of the GLPs. Is it more a function of you have not seen the data in patients without diabetes, probably a bigger driver of it? You certainly said that you are seeing an uptick in the SGLT-2 class as it starts to get an indication outside of diabetes status, because obviously injectables are not new to you guys. You have dealt with the Heparins and the Lovenoxes and all that and the PCSK9 inhibitors. It’s not the injection, at least to my knowledge, but you can tell me if I’m incorrect there. Do you think it’s more as that body of evidence starts to grow outside of patients with diabetes, you would start to see some traction there?

 To me, I still do think that the injection issue is a big barrier. We saw this with the PCSK9 inhibitors. Of course, there was a major cost barrier as well. But the use in the community, despite the overwhelming evidence, is markedly low for PCSK9 inhibitors in eligible patients. And I think barriers related to resources, time, and personnel for injection teaching, despite availability of online resources and otherwise more easier pens to use, I think that most cardiologists would feel uncomfortable in titrating and initiating these therapies. The metabolic and glycemic effects perhaps are a bit better and more substantial with the GLP-1 receptor agonists, and so that need for adjustment of concomitant therapies is probably also more relevant to that class of therapy. Again, that may pose another barrier.

A panel of experts discuss their experience with multidisciplinary collaboration of care between primary care physicians, cardiologists, endocrinologists, and pharmacists in patients with diabetes and cardiovascular disease.  