Heart failure is a major contributor to cardiovascular morbidity and mortality in patients with diabetes.
Type 2 diabetes mellitus (T2D) is a global pandemic affecting 30 million adults in the United States.
Among the greatest risks associated with a diagnosis of T2D is the increased risk of developing heart failure (HF), which is doubled in men and quintupled in women.
Heart failure is emerging as the most common and more big cardiovascular complications of type two diabetes.
When heart failure develops in patients with type two diabetes the prognosis is ominous.
The development of heart failure in patients with type two diabetes, is largely attributable to concomitant hypertension and coronary artery disease.
Not only is HF one of the most common cardiovascular complications of T2D, it is also the most disabling and deadly.
In some patients with diabetes, myocardial dysfunction is present even in the absence of coronary artery disease, valvular disease, and the sequelae of associated cardiovascular risk factors has led to the use of the term diabetic cardiomyopathy.
Patients with a metabolic syndrome have increased risk of heart failure, with 2/3 developing heart failure with reduced ejection fraction.
There is a doubling of the risk of incident heart failure in patients with diabetes compared with subjects without diabetes and stable heart disease.
Cardiovascular complications: include coronary artery disease, stroke, atherosclerosis, hypertension, and heart failure (HF) are related to diabetes,with approximately 33% of patients hospitalized with HF being those with diabetes.
The development of HF with diabetes is particularly prevalent in older patients.
Diabetic cardiomyopathy is defined as cardio pmyopathy in the presence of diabetes without other concomitant causative processes, such as coronary artery disease, to explain the development of cardiomyopathy.
Mechanisms of diabetic cardiomyopathy include: effects of hyperglycemia, advanced glycation end products, autonomic dysfunction, microangiopathy, subclinical mycardial necrosis, mitochondrial dysfunction, lipotoxicity, potential genetic abnormalities, sodium hydrogen exchangers and adipokines..
Over a 10-year follow-up period a Mayo Clinic study found 21% of participants with diabetes developed HF, independent of other causes.
In a subgroup of the cohort with normal left ventricular filling pressure, diabetes was still associated with increased risk for the development of HF.
Prevalence of diabetes and prediabetes is high among patients with heart failure.
More than 1/3 patient hospitalized for heart failure without a diagnosis of diabetes have impaired fasting glucose or impaired glucose tolerance.
Prevalence of diabetes in patients with heart failure ranges from approximately 25 to 40%.
The increased risk of heart failure with type 2 diabetes is related to obesity and insulin resistance leading to increase oxidative stress, inflammation, fibrosis, apoptosis, glucose toxicity, and lipotoxicity, which could produce structural heart abnormalities, subclinical myocardial injury, and ultimately heart failure with either reduced or preserved ejection fraction.
There is increased risk of heart failure with thiazolidinediones.
There is an increased risk of heart failure hospitalization with certain dipeptidyl peptidase-4 inhibitors.
The promotion of myocardial glucose uptake by insulin may be unfavorable for the failing heart, especially with aggressive glycemic goals: there is increased mortality in aggressively treated patients with diabetes associated heart failure.
Sodium-glucose co-transporter 2 inhibitors (SGLT2 inhibitors) reduce the risk of incident heart failure for T2D patients.
More recently, 4 large SGLT2 inhibitor cardiovascular outcome trials, EMPA-REG OUTCOME, CANVAS, DECLARE-TIMI 58 and VERTIS CV, of empagliflozin, canagliflozin, dapagliflozin, and ertugliflozin, respectively, demonstrated a significant reduction in HF hospitalization among T2D patients with and without established CVD.
Reductions in HF hospitalization were significant and consistent across each of the trials.
In the DIRECT-TIMI 58, the largest trial with the highest proportion of patients without CVD (10,186 of 17,160), investigators reported a significant reduction in HF hospitalization.
These results suggest that dapagliflozin, and possibly the SGLT2 inhibitors class as a whole, might serve as a disease modifier for patients with pre-clinical CVD/HF.
Dapagliflozin (Farxiga) received FDA approval to reduce the risk of hospitalization for HF in primary prevention patients with T2D.
Clinical Practice Guidelines on Diabetes, Pre-Diabetes and Cardiovascular Diseases recommend starting with an SGLT2 inhibitor or GLP-1RA before metformin in newly diagnosed T2D patients who are treatment naïve and either have established CVD or are at high CVD risk.
The 2020 ADA Standards of Medical Care in Diabetes include SGLT2 inhibitors and GLP-1 RAs as second-line therapy after metformin for patients with established CVD or at high CVD risk.
For patients with high ASCVD risk, established chronic kidney disease, or HF, guidelines suggest an SGLT2 inhibitor may be used as part of the glucose-lowering regimen independent of a1c and in consideration of patient-specific factors.
Recommendations suggest an SGLT2 inhibitor for patients with T2D who are at high risk of developing HF, diabetic kidney disease, clinically evident ASCVD, or any combination of these conditions.
The current guidelines provide strong recommendations for the use of SGLT2 inhibitors for the reduction of incident HF among T2D.