“The Sweet Spot”: Why type 2 diabetics fall through the cracks
Case Presentations:
Patient A:
49 year old male with Type 2 diabetes mellitus (T2DM) and CAD with a previous stent to the LAD presents for routine endocrinology visit to discuss his diabetes management.
His A1C is 7.5% and stable compared to last year. He is on metformin and glimepiride.
He asks about new medications he saw on television which may be good for his heart.
He is advised that he is doing great, with his A1C right in the “sweet spot”.
Years ago, his doctor attended a lecture at a national conference where they discussed studies showing that overaggressive management of blood sugar, with an A1C less than 7%, was associated with an increase in adverse cardiac events. Similarly, undertreatment of blood sugar, with an A1C greater than 8% showed an increase in adverse outcome.
With his A1C of 7.5% right in the “sweet spot” he is encouraged to continue his present management.
Patient B:
A 42 year old female with Type 2 diabetes mellitus and obesity with BMI 31kg/m2 presents for a primary care visit to discuss her cholesterol management.
Her LDL-C is 77 mg/dL, HDL-C 37 mg/dL, TG 213 mg/dL.
She is informed that her LDL-C numbers are outstanding and at her age, she does not need to start taking a statin.
However, her TGs are a little high and she was encouraged to work harder on a low carb diet.
Patient C:
A 57 year old male with T2DM and a recent heart attack (STEMI) treated with a stent to the LAD 6 months ago, presents to his cardiologist to review his progress. He has finished cardiac rehab, has been adhering to a Mediterranean diet and been faithfully taking the maximum dose of rosuvastatin at 40 mg daily, which was initiated in the hospital, without any side effects.
Labs from 1 week prior to the visit reveal an LDL-C is 68 mg/dL, TG 216 mg/dL, HDL-C 40 mg/dL.
He is told no additional treatments are needed for his lipids since his LDL-C is below the recommended goal of 70 mg/dL.
Patient D:
A 57 year old female with T2DM, Heart Failure with a Preserved Ejection Fraction (HFpEF) and obesity with BMI 31 kg/m2, presents to her cardiologist following a recent stay in the hospital for 4 days for heart failure, characterized by shortness of breath with fluid in her lungs (pulmonary vascular congestion) and legs (edema).
She was placed on furosemide and instructed to follow up with her cardiologist.
Since then she has lost 8 lbs and feels much better.
On exam, her cardiologist notes that her lungs are clear and the lower extremity edema has resolved.
She is congratulated on the weight loss and her furosemide is reduced to once daily. She is advised to avoid salt and weigh herself daily, while keeping track in a diary.
She asks about newer diabetes drugs she heard about on TV that reduce risk for heart failure hospitalization, such as Farxiga, Jardiance, Invokana and others that reduce cardiovascular risk and help with weight loss such as Ozempic.
Her cardiologist informs her that the drugs are expensive but she can talk to her primary care doctor or endocrinologist about them, since those are not drugs that cardiologists prescribe.
Flying Under the Radar
The cases above represent some of the most frequent lapses and missed opportunities in the cardiometabolic care of the diabetic patient:
Patient A:
Missing the point of landmark clinical trials
It’s about how you get to euglycemia
The failure of previous therapies employed to achieve intense glucose lowering is not a free pass to undertreat. An A1C of 7.5% is not desirable.
Taking the easy way out by persisting with outdated, yet inexpensive (and therefore easier to prescribe) sulfonylurea drugs that have been relegated below several other proven therapies in just about every guideline.
Yes, new branded medications can be expensive and may require labor intensive prior authorizations, but the patient needs to be informed.
Help is on the way with Federal initiative to make branded diabetes drugs cheaper
Farxiga (dapagliflozin) now has a generic
It’s not always about the sugar anymore.
Several clinical trials have now shown that glycemic control has little impact on major cardiovascular events.
Thankfully, we now have many therapies that, independent of glycemic improvement, also improve cardiovascular endpoints
Patient B:
Lack of awareness of guideline recommendations
Reliance on suboptimal metrics - in this case, LDL-C is less accurate and underestimates risk compared with nonHDL-C when TGs are elevated (see Atherogenic Triad:)
Failure to appreciate high lifetime risk and implementing early prevention - another example of undertreating cardiovascular risk in the female (diabetic) patient.
Patient C:
Applying outdated and more conservative guidelines to our highest risk patients - LDL-C needs to be much lower]
Failing to appropriately inform patients of potentially life saving therapies they may be eligible for.
Even if some practitioners feel there is controversy with the REDUCE-IT Trial (see Something Smells Fishy - The Controversy with Fish Oil), patients ought to be informed of icosapent ethyl (Vascepa) when they fit the indications for it. That’s part of shared decision making.
Patient D:
Passing the buck - assuming some other specialist will take care of it.
We are in an interesting time in medicine, where multiple classes of diabetes medications now have separate indications for improving cardiovascular disease risk - independent of glycemic control.
“I don’t treat diabetes”
It’s not acceptable for a cardiologist to fail to treat the underlying cardiovascular risk in a high risk heart failure patient recently hospitalized, simply out of misplaced fear about a “diabetes” drug.
To put it bluntly, the diabetic patient is left behind due to a lack of cohesiveness across medical disciplines. The PCP, already burdened with everything else, is left holding the bag when the specialists (cardiologists, endocrinologists and nephrologists) assume that the other is going to act. So, nobody acts, and the diabetic patient is exposed to unnecessary “residual risk” when there are potentially effective treatments available. Far too often the patient is left in the dark and never finds out about these therapies.
Instead of fostering mutual trust and building a multidisciplinary community that agrees to take advantage of every opportunity to attack this risk, at every encounter, the opposite often occurs. The cardiologist doesn’t want to step on the endocrinologist’s toes and vice versa. The PCP may yield to the specialist, assuming they had a reason not to act, rather than seeing it as a missed opportunity.
This is why some are trying to create a “cardiometabolic” subspecialty in its own right. Someone needs to put it all together.
Read more in Deep Dive.
CardioAdvocate Checklist:
Cholesterol Management:
Check ApoB
May be used as the preferred biomarker for all patients with high TG, diabetes, obesity, metabolic syndrome or “very low LDL-C” for screening, diagnosis, risk management (Ia ESC/EAS)
European Guidelines:
T2DM at very high risk
LDL-C ≥ 50% reduction, and
LDL-C < 55 mg/dL
T2DM at high risk
LDL-C ≥ 50% reduction, and
LDL-C < 70 mg/dL
If goal LDL-C not achieved with statin, combination with ezetimibe should be used (ECS/EAS Iia)
Combination therapy with lower dose statin, ezetimibe and/or PCSK9i in a patient centered discussion regarding safety, efficacy and cost may be considered (Expert Opinion - many experts prefer a combination approach but recognize the high cost of newer non statin therapies such as PCSK9i mAb, simRNA, ACL inhibitors)
2018 ACC/AHA Guidelines:
DM deemed to be at higher risk: Age 50-75 or multiple risk factors
High intensity statin to reduce LDL-C ≥ 50%
All DM age 40-75 regardless of 10 year risk
Moderate-intensity statin (2018 ACC/AHA Cholesterol Guidelines)
DM 20-39 with risk enhancers - start statin
Type 2 DM ≥ 10 years
Type 1 DM ≥ 20 years
Albuminuria ≥ 30 mcg albumin/mg creatinine
eGFR < 60
Retinopathy
Neuropathy
ABI < 0.9
Triglycerides
Triglycerides are rarely normal in those with dysglycemia
TG > 150 - 499 mg/dL
In the presence of “max tolerated statin”, those with established CVD or T2DM, Vascepa (icosapent ethyl) may be indicated to reduce CV risk (25% reduction in MACE in the REDUCE-IT Trial)
See Atherogenic Triad for more information
Cardiovascular Risk Reduction:
We have arrived at a new era in the management of Type 2 diabetes - don’t get left behind
2 new classes of treatments for T2DM have produced CV benefits (SGLT2i and GLP-1 agonists).
GLP-1 agonists have shown a reduction in CV risk
Ozempic (semaglutide) presently is the only agent in this class with indications to reduce CV risk
Heart Failure: SGLT2i
Consider options for SGLT2i, which reduce CV risk independent of their impact on glycemic control
Reduces Heart Failure hospitalization
Reduces Heart Failure death
The following SGLT2i have indications for Heart Failure
Chronic Kidney Disease: SGLT2i
Check your kidney function
Typically measured with BUN and Cre
Look for the calculated eGFR
Simple blood test panel called a BMP (Basic Metabolic Panel)
The following SGLT2i have indications for preventing declining kidney function in those with CKD
Deep Dive
Patient A:
The #1 killer in diabetic patients is heart disease, particularly coronary artery disease and heart failure.
So, what has been the primary objective in treating diabetes? Controlling blood sugar, right?
One would think that if you optimally control blood sugar then you should see benefits in its worst outcome - cardiovascular disease, right? Wrong.
Intense Glucose Lowering:
The UKPDS Trial: (The UK Prospective Diabetes Study (UKPDS): clinical and therapeutic implications for type 2 diabetes) failed to show reduction in cardiovascular events in those treated to reduce an A1C from 8.0% to 7.0% (although, a subset of patients treated with metformin had lower event rates.)
Too many practitioners remain under the outdated impression that they dare not treat type 2 diabetic too aggressively, as this leads to an increase in mortality.
This notion is born out of older randomized controlled trials, such as the ACCORD Trial: (Effects of Intensive Glucose Lowering in Type 2 Diabetes | NEJM), showing that the “intensive” therapy arm in diabetes did worse than the “standard” treatment arm, and the ADVANCE Trial: (Intensive Blood Glucose Control and Vascular Outcomes in Patients with Type 2 Diabetes | NEJM) which showed no significant difference in major cardiovascular events but did show a difference in microvascular outcomes (nephropathy) when randomized to an “intensive” therapy of sulfonylurea plus other medications as needed to achieve an A1C of 6.5% or less.
A breakdown of these two trials is well summarized in this editorial: Intensive Glycemic Control in the ACCORD and ADVANCE Trials | NEJM.
In brief, the ACCORD trial randomized ~10,000 type 2 diabetics with A1C of 8.1% at baseline to an “intensive” treatment arm aimed at achieving an A1C < 6.0%. The “standard” therapy arm aimed to achieve A1C 7.0-7.9%. At 1 year, the intense arm achieved an A1C of 6.4%, the standard arm 7.5% (sweet spot!). However, at 3.5 years the intensive arm was stopped due to an increase in total mortality. The differences in MACE (cardiovascular events) were not statistically different, however total mortality was statistically significant. In the intense arm there was more frequent hypoglycemia requiring intervention and significant weight gain (average 3.5 kg), with 28% experiencing > 10 kg (22 lbs)!
The ADVANCE trial required all patients in the intensive arm to receive a sulfonylurea, whereas the ACCORD trial held no restrictions, thus more use of a combination of thiazolidinediones (TZDs - insulin sensitizers) - in particular rosiglitazone (Avandia), sulfonylureas and insulin utilization.
The ADVANCE trial also combined macrovascular and microvascular endpoints, which was a peculiar decision when trying to establish if glycemia plays a role in major cardiovascular events.
Cardiovascular Risk:
Initially it was felt that hypoglycemia was the culprit for the increase in events, but it was already known that:
Insulin causes weight gain
Rosiglitazone, in a meta-analysis, was associated with an increase in myocardial infarction and other cardiovascular events: Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes | NEJM
Nonetheless, many practitioners conflated the hazardous mechanisms of the drugs used in the trials with the notion that “treating” a type 2 diabetic to a lower A1C% (<7.0%) might somehow place that individual at increased risk of an adverse event. This is short sighted thinking.
Hypoglycemia most definitely is not a good thing and the body will react violently to this very primitive need to maintain adequate blood glucose levels. Therapies that frequently provoke hypoglycemia are associated with a plethora of bad outcomes to include heart attack etc, but the adverse events in the “intensive” treatment arm were not entirely explained by hypoglycemic events. Other mechanisms with adverse off-target effects from insulin, drugs that promote the release of, or sensitivity to, insulin in higher risk patients were likely at play.
It’s one thing to conclude that the therapies employed in these clinical trials did not demonstrate favorable benefits, but it's quite another to conclude that all attempts at achieving euglycemia (normal blood sugar regulation) should be abandoned. Or that therapies that promote euglycemia might also have favorable off-target or “pleiotropic” cardiovascular benefits that have little to do with blood sugar regulation.
About 10 years ago at the American College of Cardiology Annual meeting a lecture titled “The Sweet Spot” which attempted to make sense of these trials and thread the needle between overtreatment and undertreatment of blood sugar in diabetics.
It turns out, it depends on how you get there.
This meta-analysis published in 2015 (Glucose-lowering drugs or strategies and cardiovascular outcomes in patients with or at risk for type 2 diabetes: a meta-analysis of randomised controlled trials) suggests that agents that seemed to promote weight gain, such as PPAR agonists (highest) and DPP-4 inhibitors (intermediate) to achieve lower blood sugars were associated with worsening heart failure. Whereas, agents that promote weight loss were not associated with heart failure.
Despite newer therapies and updated guidelines demoting sulfonylureas (like glimepiride) way down on the list of medications to choose from to treat diabetes, they continue to be frequently prescribed as the next agent following metformin (second-line) or sometimes first-line in the real world.
Sulfonylureas (like glimepiride):
Sulfonylureas are insulin secretagogues, which promote the release of endogenous insulin from pancreatic beta islet cells. They have the propensity to promote hypoglycemia, weight gain and fluid retention - all of which are cardiovascular risk factors (Sulfonylureas and the Risks of Cardiovascular Events and Death: A Methodological Meta-Regression Analysis of the Observational Studies | Diabetes Care.)
Thiazoladindiones (TZDs - like rosiglitazone):
TZD’s are peroxisome proliferator-activated receptors (PPARs) that work by increasing insulin sensitivity by acting on muscle, adipose and liver to better utilize glucose and reduce glucose production.
In November 2007, the FDA issued a black box warning for rosiglitazone (Avandia) due to an increased risk of heart attack. It was removed from the market in early 2010.
Not all TZD’s are the same, however. Pioglitazone remains a helpful medication for many patients with diabetes.
The story of rosiglitazone (Avandia) underscores many important lessons in science and medicine:
The better we adhere to evidence based medicine through randomized controlled trials (RCT) and meta-analysis, the better off we are.
While not every clinical question can or ever will be answered by an RCT, when it can, we should.
Not everything that sounds right, is right.
Often, only large trials can detect harmful off-target effects of certain drugs.
Cardiovascular Benefit - what we’ve all been waiting for.
Fortunately, we now live in a world where we have several treatments that can be employed against diabetes and reduce cardiovascular events! Finally, right?!
In 2015, the EMPA-REG Outcomes Trial was published showing that empagliflozin (Jardiance), an SGLT2 inhibitor, when used on top of standard care, reduced the “primary composite cardiovascular outcome and of death from any cause.”
Since that publication, these and other therapies have exploded:
Canagliflozin and Cardiovascular and Renal Events in Type 2 Diabetes | NEJM
Dapagliflozin and Cardiovascular Outcomes in Type 2 Diabetes | NEJM
But even still - see how long this takes? EMPA-REG was published in 2015…
There are pluses and minuses regarding this delay: It takes a while for the entirety of the peer-review process to take place, for journal publication, for FDA label indication updates, for replication with other drugs in this class and for general acceptance in the cardiometabolic community and then the broader general medical community.
Another axiom of medicine is - “you don’t want to be the first to try something new, but you don’t want to be the last either.”
In between the time from when positive outcomes from a large scale randomized controlled trial are accepted as the new standard of care - and the time until it is widely implemented in real world medicine, many lives would have been saved or improved. This represents an example of where we can do better.
SGLT2 Inhibitors (sodium-glucose transport proteins 2)
SGLT2 inhibitors lower blood sugar by inhibiting glucose reabsorption through the sodium-glucose transport protein in the kidneys. Glucose is therefore excreted in the urine. This causes a mild diuretic effect, which can help with fluid retention, blood pressure and promote some weight loss.
However, since the urine is a little sweeter, it can increase the risk of urogenital infections like a rash or urinary tract infection. Bacteria and yeast like sugar too. Good urogenital hygiene can prevent this.
Drugs in this class:
Farxiga (dapagliflozin)
Jardiance (empagliflozin)
Invokana (canagliflozin)
Steglatro (ertugliflozin)
BRENZAVVY (bexagliflozin)
These drugs are currently branded (expensive and may require prior authorization), though dapagliflozin (Farxiga) has now been released as a generic.
Given the history with intense glucose lowering and rosiglitazone, the FDA mandated cardiovascular safety trials. Any new diabetes drugs were required to at least prove they didn’t promote cardiovascular risk.
Most of the SGLT2i now have multiple indications other than improving blood sugar control in type 2 diabetes.
Separate indications include:
Type 2 Diabetes
Type 2 Diabetes with established cardiovascular disease (CVD) to reduce CV death
Heart Failure (HF) - reduce the risk of HF death and HF hospitalization
Chronic Kidney Disease (CKD) - reduce risk of sustained decline in eGFR (kidney function), End Stage Kidney Disease, CV death and hospitalization in adults with CKD
The Discovery of a New Treatment for Heart Failure
Somewhat surprisingly, SGLT2i were found to improve cardiovascular risk, mostly with regards to heart failure and heart failure hospitalizations.
While they proved to be a nice addition to several therapies already available for HFrEF (Heart Failure with Reduced Ejection Fraction - due to a weak pump Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction | NEJM, Cardiovascular and Renal Outcomes with Empagliflozin in Heart Failure | NEJM), of particular value, was the benefit to the enigmatic subgroup of heart failure patients called “HFpEF” - the so-called “diastolic heart failure” due to a stiff left ventricle, with difficulty relaxing between beats. Previous treatments for HFpEF centered around treating the underlying causes, but no specific therapies for HFpEF - until now:
Dapagliflozin in Heart Failure with Mildly Reduced or Preserved Ejection Fraction | NEJM Empagliflozin in Heart Failure with a Preserved Ejection Fraction | NEJM
Chronic Kidney Disease
Since then we have now seen separate indications for chronic kidney disease as well:
Canagliflozin and Renal Outcomes in Type 2 Diabetes and Nephropathy | NEJM
Dapagliflozin in Patients with Chronic Kidney Disease | NEJM
Empagliflozin in Patients with Chronic Kidney Disease | NEJM
GLP-1 Agonists (Glucagon-like Peptide-1)
Drugs in this class:
Semaglutide subcutaneous injection (Ozempic), oral tablet (Rybelsus)
Dulaglutide (Trulicity)
Tirzepatide (Mounjaro)
Ozempic and Trulicity are both indicated by the FDA to reduce risk of major adverse cardiac events (MACE) in those with T2DM and established CV disease.
Semaglutide demonstrated ~ 25% reduction in cardiovascular death, nonfatal myocardial infarction and nonfatal stroke (collectively called MACE): Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes | NEJM)
Dulaglutide also demonstrated CV risk reduction, with a 12% reduction in MACE in diabetics on top of standard therapy, regardless of preexisting cardiovascular disease and in a broad range of glycemic control - thus presumably a lower risk patient population.
Patient B:
This case illustrates a few missed opportunities:
Standards of Care in Diabetes - 2023 Guidelines recommends “high-intensity statin therapy in individuals with diabetes aged 40–75 years at higher risk, including those with one or more atherosclerotic cardiovascular disease risk factors, to reduce the LDL cholesterol by >50% of baseline and to target an LDL cholesterol goal of <70 mg/dL.”
Looking closer at the lipid panel (TC and nonHDL-C intentionally not provided), one sees that the TG are elevated (> 150 mg/dL) and the HDL-C is low (< 50 mg/dL). This should alert the clinician that the LDL-C is being underestimated. Looking at nonHDL-C, which is all too frequently not listed in the lipid panel but can be calculated by using math (ugh!) by subtracting HDL-C from TC. Using ApoB is even better. This is perhaps one of the biggest reasons for “residual risk” and “flying under the radar” in the diabetic patient.
Young female diabetic patients are often undertreated for their risk. While a CAC CT score to assess for early plaque development by way of coronary calcification has been shown to “de-risk” many patients, including diabetics, a score of “0” really only tells us her “short term risk.” Lifetime risk remains high. The common phrase “Even lower is even better, for even longer” applies to this patient.
Patient C:
There are several points to be made here:
This patient is lucky to be alive. 50% of such heart attack victims die at home.
The European Society of Cardiology (ESC) and the American Endocrine Societies (AACE) would characterize this patient as “very high risk” and “extreme risk,” respectively, with goal LDL-C < 55 mg/dL and nonHDL-C < 80 mg/dL.
The Standards of Care in Diabetes - 2023 recommend high intensity statins be used in diabetics with established ASCVD to achieve > 50% LDL-C reduction and a goal LDL-C < 55 mg/dL. Ezetimibe or PCSK9 inhibitor should be added if goals are not achieved.
If it’s the 2nd vascular event for this patient, the ESC would shoot for LDL-C < 40 mg/dL. After suffering a near death experience with a STEMI, many would not want to wait around for the next one before taking such measures.
One thing is for sure, < 70 mg/dL as a goal LDL-C in a post STEMI patient, is simply not getting the job done.
Here is where it is helpful to point out the elevated TGs.
In this patient, getting a complete lipid panel (rather than just the ApoB that the savvy clinician may prefer), reveals the elevated TG's that now become (like it or not) a prerequisite for additional potentially life saving therapies.
In the REDUCE-IT Trial, those with established cardiovascular disease or diabetes with residually elevated TG’s of 135-499 mg/dL despite maximum tolerated statin therapy achieved a 25% further reduction in cardiovascular events (MACE) when treated with icosapent ethyl (highly purified eicosapentaenoic acid, or EPA, under the trade name Vascepa) 2 grams twice daily on top of statins.
Interestingly, the risk benefit was independent of TG lowering, leading many to believe that high TG’s merely identify a very high risk patient population, benefitting not necessarily from the TG lowering itself, but rather some other mechanism (see Something Smells Fishy - The Controversy with Fish Oil)
The benefit also was seen proportionate to the percent saturation of red blood cells (RBCs) with EPA, meaning, those who absorbed more, fared better.
Patient D:
This case is perhaps the most emblematic of the struggles in treating the cardiometabolic risk of the diabetic patient.
No single discipline wants to “own,” or take responsibility for treating the cardiovascular risk of the diabetic.
Not the endocrinologist (aside from those who specialize in lipids). Why? Several reasons:
They're not accustomed to it. Endocrinologists who treat diabetes tend to focus on glycemic control and have not had to consider the cardiovascular risk - because until recently, glycemic therapies had never shown any positive cardiovascular impact (negative in some cases).
One would think that if the leading cause of death and demise in the diabetic patient is ASCVD, then surely improving dysglycemia, the main derangement in the diabetic, would result in improvement of its most common bad outcome, right? Nope.
Quite the opposite. As touched on in Patient A, the more aggressive treatment arms for diabetes in clinical trials showed cardiovascular harm.
When another promising agent, rosiglitazone (Avandia) was removed from the market due to its association with worsening heart failure - that was it - The Institute of Medicine and the FDA had had it. From then on, any new drugs for diabetes would need to prove that they at least didn’t worsen cardiovascular health.
But nobody expected that the diabetes drug pipeline would bring therapies that actually improved cardiovascular health - and seemingly independent of glycemic control!
Endocrinologists are getting on board - perhaps faster than cardiologists.
The Standards of Care in Diabetes - 2023 calls for the “addition of specific SGLT2 inhibitors or GLP-1 receptor agonists that have demonstrated CVD benefit is recommended in patients with established CVD, chronic kidney disease, and heart failure.”
The American Association of Clinical Endocrinology Consensus Statement: Comprehensive Type 2 Diabetes Management Algorithm – 2023 Update - ScienceDirect has easy to follow algorithms for all cardiometabolic diseases associated with diabetes. The “glycemic control” algorithm recommends SGLT2i and GLP-1 receptor agonists for those with known ASCVD, high ASCVD risk, Heart Failure, Stroke/TIA and CKD. This is “independent of glycemic target and other T2D therapies.”
But far too many are either stuck in their ways, or can’t be bothered with the prior authorizations.
It’s easier and far cheaper to prescribe inferior sulfonylureas and TZD’s, than the more expensive and branded drugs that have been shown to reduce cardiovascular risk.
Not the cardiologists either. If it has to do with diabetes management, it’s icky, complicated and foreign to them.
For cardiologists, that part of Internal Medicine is quickly disposed of upon entering fellowship training - as it was for this author - when the attending interventional cardiologist asked “why are you prescribing metformin? You’re a cardiologist - you don’t treat diabetes anymore.”
That was not necessarily true then - and it certainly isn’t true anymore.
Cardiologists do not want to concern themselves with a heart failure medicine that may require them to alter any of their other diabetes medications, such as lowering or discontinuing their sulfonylurea (glimepiride). Diuretics? Sure, no problem. But not blood sugar medications. Too messy.
They don’t want to be responsible for educating their patients about urogenital hygiene when using SGLT2i (makes the urine sweeter, which may increase chances for bacterial or yeast infection down below), for instance. Nor the issues of delayed gastric emptying with GLP-1 agonists such as nausea, diarrhea or constipation.
They can’t be bothered with prior authorizations so they punt back to endocrinology or their PCP.
But there is hope…most cardiologists will aim to follow cardiology guidelines.
These therapies are all over the guidelines now and have received Class I recommendations for the treatment of patients with type 2 diabetes with established CVD or high cardiovascular risk to prevent heart failure hospitalization…and for the treatment of those with HFrEF; Class 2a for HFmrEF and HFpEF - independent of whether diabetes is present or not (2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines).
Cardiologists are beginning to tow the line, but opportunities continue to be missed.
Additional References:
Here is an interesting take on insulin resistance, described by Dr. Jason Fung during his interview with Dr. Peter Attia on his podcast: Jason Fung, M.D.: Fasting as a potent antidote to obesity, insulin resistance, type 2 diabetes, and the many symptoms of metabolic illness - Peter Attia
