Only 1% of Heart Failure Patients Receive Optimal Medical Therapy at Appropriate Doses
Yesterday’s post showed that optimal medical therapy (OMT) reduces heart failure hospitalizations by 70% in patients with type 2 diabetes and CKD. Despite this dramatic benefit on a deadly and expensive condition, only 1% of heart failure patients are on adequate doses of OMT medication. That huge disconnect makes no sense unless you consider this. We do too little too late! Most heart failure occurs as the result of hypertension, diabetes, and heart attack. Patients with these conditions have increased angiotensin II, HMG CoA reductase, and aldosterone activity already, especially if they are obese. These factors increase oxidant production and activate the signaling pathways that increase scar formation, kill heart muscle cells and produce cardiac enlargement. Patients who have had a heart attack have increased sympathetic tone. The beta blocker interferes with that.
If you wait until disease is advanced, other problems like chronic kidney disease limit the ability to titrate heart failure medications to adequate doses. If you reduce blood pressure to 130/80 with medications that block the effect of angiotensin II and aldosterone, you are interfering with progression to chronic kidney disease and heart failure. If a patient has a heart attack, sympathetic tone, angiotensin II, and aldosterone are increased. Blocking these factors precisely interferes with progression to heart failure and chronic kidney disease. When the ejection fraction falls below 50%, make sure your patient is on medication that blocks the effects of angiotensin II and aldosterone. The journey to heart failure has begun. If they have had a heart attack, add carvedilol. You can do all that for $12 a month. If heart failure progresses, add a SGLT2 inhibitor like empagliflozin which works in patients with or without type 2 diabetes by activating AMPK. Preventing heart failure and heart failure hospitalizations is less about controlling risk factors and more about precisely interfering with the molecular biology that causes heart failure in the first place. Your primary care cardiometabolic team can make a huge difference.