The bad news—heart failure cases will increase from 5.1 million in 2012 to 8 million by 2030 because of our aging population. Major efforts to improve health and reduce costs have been implemented but have resulted in only small improvements. The number of patients with heart failure is increasing despite these efforts.
Even now, Medicare patients with heart failure generate 34% of Medicare spending. Forty percent of patients in the Medicare population who die have a diagnosis of congestive heart failure as a contributing factor. Forty-two percent of Medicare admissions are related to heart failure along with 55 percent of readmissions. These patients cost almost $42,000 a year and most of the cost is related to hospitalizations.
Having heart failure is like having many forms of cancer in that half of these patients are dead in five years. Twenty-two percent of patients hospitalized for heart failure die within a year. This is so frustrating, because we know what causes heart failure and how to prevent it. Rather than tiny improvements, a huge reduction of 70% of heart failure admissions can be accomplished.
Globally, among all causes of congestive heart failure (CHF), heart artery disease accounted for the highest proportion (26.5%) of CHF in 2017, followed by high blood pressure (26.2%). Diabetes induced heart failure also represents up to 26% of CHF cases. Please note that the epigenetics and molecular biology of these conditions are related. The same molecular mechanisms lead to all of these “risk factors” and heart failure itself.
The good news. We understand much more about heart failure and how to treat it effectively. The master metabolic growth switch mTOR coordinates growth with food intake in the fetus and child. Let’s call it the food switch. This switch is universally switched on in heart failure to cause the heart to grow, but this is not healthy growth. Many muscle pumping cells in the heart die and they are replaced by scar tissue because of food switch activation. This change is universally present in heart failure and it may be due to several different hormones or enzymes that are switched on by weight gain, lack of exercise and tobacco smoke.
The 70% reduction in heart failure admissions over 21 years occurred because the protocol for treating these people with diabetes and chronic kidney disease contained multiple interventions that inactivate the food switch—lisinopril, losartan, and spironolactone for high blood pressure; statins for cholesterol; and metformin for diabetes. Diet and exercise do the same thing. The combination of those interventions with aggressive lowering of pressure, sugar and cholesterol produces these remarkable results.
Just imagine the clinical and financial impact of a 70% reduction in CHF admissions to the hospital. That potential is real if we undertake the system reengineering that the National Academy of Medicine recommends. We can do even better than that. The protocol that generated that reduction did not include medications like empagliflozin for diabetes or spironolactone for high blood pressure. Both medications reduce heart failure hospitalizations by a third. This is another concrete example of the way we can improve health and lower costs now. Will we?