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A Paradigm Shift in the Treatment of Type 2 Diabetes and Heart Failure
1Department of Cardiology, Keio University School of Medicine.
Insights
Diabetic patients face high heart failure risk despite controlled risk factors. Current guidelines are insufficient, highlighting the need for new approaches targeting kidney-brain-heart interactions.
Area of Science:
- Cardiology
- Nephrology
- Endocrinology
Background:
- Diabetic patients have a higher risk of heart failure (HF) even with controlled myocardial infarction (MI) risk factors.
- Current treatment guidelines primarily focus on MI prevention and are inadequate for preventing HF in diabetes.
Purpose of the Study:
- To investigate the mechanisms underlying HF development in diabetic patients.
- To advocate for updated treatment guidelines based on a comprehensive understanding of HF pathophysiology in diabetes.
Main Methods:
- Observational study analyzing risk factors and HF development in diabetic individuals.
- Review of clinical evidence, including the impact of sodium-glucose-coupled transporter (SGLT)-2 inhibitors.
Main Results:
- Despite optimal management of blood glucose, blood pressure, lipids, and smoking, HF incidence remains elevated in diabetics.
- The pathological kidney-brain-heart coupling contributes to HF by shifting the hemodynamic set point towards cardiac overload.
- Sodium-glucose-coupled transporter (SGLT)-2 inhibitors demonstrate efficacy in slowing chronic kidney disease progression and reducing HF hospitalizations and mortality.
Conclusions:
- Current MI-centric guidelines are insufficient for preventing HF in diabetic patients.
- A holistic view of HF pathophysiology, emphasizing the renocardiac syndrome and kidney-brain-heart axis, is crucial.
- Targeting the kidney-brain-heart axis may offer novel therapeutic strategies for diabetic HF.
Abstract:
Despite good control of all risk factors for myocardial infarction, including blood glucose, blood pressure, lipids, and smoking, the probability of heart failure is significantly higher in diabetic patients than in healthy individuals. This observational study shows that the current treatment guidelines, which focus on the prevention of myocardial infarction, are insufficient in preventing heart failure development. Now, understanding the mechanisms of heart failure in diabetic patients and developing treatment guidelines based on these mechanisms are urgently needed. Instead of narrowly viewing that heart failure is caused by poor cardiac function, we need to take a bird's-eye view that heart failure is caused by a shift in the hemodynamic set point (blood pressure, heart rate, circulating blood volume, and autonomic balance) toward overloading the heart due to the persistent drive of the pathological kidney-brain-heart coupling. Clinical evidence, which shows that sodium-glucose-coupled transporter [Na+/glucose co-transporter (SGLT)-2] inhibitors slowed the progression of chronic kidney disease (CKD) and reduced heart failure hospitalizations and deaths, underscores the importance of the renocardiac syndrome in heart failure development in diabetic patients.
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