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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