The second in my series of trips down memory lane over the last 30 years is on the treatment of congestive heart failure (CHF).
The second in my series of trips down memory lane over the last 30 years is on the treatment of congestive heart failure (CHF). This comes to mind because of a patient I saw today in the office. Now 62 years old, Mr. N. had not been to the office for about eight years, because he has been getting his care at the local military hospital. I see his wife and had been kept aware of his progress. About 15 years ago, he was on the heart transplant list at the University of Washington after developing end-stage CHF from a viral heart infection as a young man. At that time, a diagnosis of CHF of moderate to severe degree had a five-year survival rate of about 50%, and this patient’s prognosis was far worse than that. He was struggling to just move around the house, and had New York Heart Association Class 4 Heart Failure.
About that time the use of beta blockers and angiotensin converting enzyme (ACE) inhibitors was shown to reduce hospitalization rates, and improve quality of life for CHF patients. Since then, improved mortality rates have been well documented. CHF patients have a reduction of the ability of the heart to pump blood. Beta blockers reduce the force with which the heart pumps, and for many years were considered contraindicated in patients with CHF. To those of us who studied in the 1980s, the use of beta blockers that reduced the strength with which the heart contracted to pump blood in patients whose heart muscle was injured and weak seemed insane. This logical but incorrect thinking led to very slow adoption of this treatment by practicing physicians.
Now we know that the combination of beta blockers to reduce the counterproductive and harmful adrenergic overstimulation of the failing heart, and ACE inhibitors (or their newer sister drugs the angiotensin II receptor blockers, or ARBs) to lower the resistance the heart pumps against (essentially making the pipes bigger) makes effective medical treatment of CHF possible. We can now expect that effective treatment with these medications will prolong life, improve quality of life, and make the words “heart failure” far less ominous. We see objective improvement in these patients by watching their failing hearts improve by measuring the ejection fraction of the left ventricle (ie, the percent of blood in the pumping chamber of the heart that is emptied with each heartbeat.) We can see this improve from levels incompatible with a quality life, to near normal over a year or so on effective treatment in some patients. This was unheard of prior to this type of treatment.
Other major changes in the treatment of CHF have been implantable defibrillators to reduce the risk of sudden risk from ventricular arrhythmias, anticoagulation therapy to reduce strokes complicating CHF, and the development of tests to monitor the failing heart’s level of stress, called the brain natriuretic peptide. Mr. N. has benefited from all of these developments, but the turning point was medical treatment with beta-blockers.
My patient today came in with his grandson, one of three he cares for each day while their parents go to work. This was not what I expected all those years ago when he was a long ways from the top of a long list of patients awaiting a call for a transplant at UW. He has been dropped from that list for years now. I expect him to attend some high school graduations for these grandchildren. Mr. N. helped me overcome my trepidation over what was at the time a treatment change that seemed counterintuitive. Thanks Mr. N.
To read part one of this series of 30 year perspectives, see “Peptic Ulcer Disease — From Curse to Cure.”
Ed Pullen, MD, is a board-certified family physician practicing in Puyallup, WA. He blogs at DrPullen.com — A Medical Bog for the Informed Patient. This article originally appeared online at DrPullen.com.
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