Editor's Note: This article was originally written by Charles Whitcomb, M.D.
Congestive heart failure (CHF) is one of the most common reasons for hospital admission in the United States and most Western European countries.
The most common cause is coronary artery disease and myocardial infarction (heart attack).
Hypertension and what is called hypertensive heart disease is next on the list.
Patients with congestive heart failure have a markedly increased for death.
Patients with CHF usually present to the hospital with signs of fluid overload.
They become short of breath due to the buildup of excess fluid in the lung.
The fluid excess interferes with the transfer of oxygen from air to blood.
Classically this has been attributed to abnormal heart muscle function where the heart muscle is weakened (by heart attack, hypertension, viruses or other causes) and can no longer pump blood efficiently.
In the last two decades it has become apparent that many patients (up to half in many studies) do not have weak heart muscle.
Rather their heart is stiff and requires higher pressure to fill it between heartbeats.
The period between heartbeats when the heart fills is called diastole, and this form of heart muscle disease is called diastolic heart failure.
Much less is known about this form of CHF in spite of the fact that up to half of the heart failure treated in hospital in diastolic CHF.
The most common identifiable cause of diastolic heart failure by far is hypertension.
Systolic heart failure (the kind with weak heart muscle) is treated with diuretics ("water pills") to relieve congestion and improve symptoms.
Long-term benefits have been shown with ACE inhibitors and beta blockers, both classes of drugs originally used to treat high blood pressure.
Logically it was thought that these agents would also be useful for diastolic heart failure as hypertension is its most common precipitant.
Diuretics do relieve symptoms in diastolic heart failure (a more politically correct term in cardiology is "heart failure with preserved ejection fraction"-go figure).
A couple of recent trials have suggested that inhibitors of the angiotensin system (ACE inhibitors and angiotensin receptor blockers) and beta blockers may not work as well in this form of heart failure as had been previously thought.
I-PRESERVE is the acronym for a large trial reported at the American Heart Association meetings in November.
The angiotensin receptor blocker irbesartan provided no additional benefit to patients with CHF with preserved ejection fraction over conventional therapy.
Two weeks later an analysis of all the previously published trials with beta blockers suggested that these drugs also provided no additional benefit in these patients.
These results were surprising and contrary to the conventional wisdom.
They point to our lack of understanding of this very common cause of heart failure.
They are sure to spark more debate and hopefully more research into the appropriate treatment for this common disease associated with great functional limitation and premature demise.