Low Dose β-blockers Effective After Heart Attack

Discharge β-blocker dose was indexed to the target dose used in randomized clinical trials, grouped as percentages of target dose. Follow-up vital status was assessed, with the primary endpoint of time-to-death right-censored at two years.

The results showed that of 6,682 patients with follow-up, 91.5% were discharged on β-blockers. Lower mortality was observed with all doses, but the data showed that of the people who received the full dose, 14.7% died within two years; of those receiving the half dose, 12.9% died; for the quarter dose, 9.5% died; and for the one-eighth dose, 11.5% died. The results indicate that patients who received one-fourth of the original clinical trial β-blocker dose had a 20%–25% decrease in mortality compared to the full dose group. The study was published on September 21, 2015, in the Journal of the American College of Cardiology (JACC).

“Heart attack patients were being treated with much lower doses of beta-blockers than were used in clinical trials. I thought that was terrible quality of care,” said lead author Professor of Cardiology Jeffrey Goldberger, MD, of Northwestern University. “We set out on a mission to show if you treat patients with the doses that were used in the clinical trials, they will do better. We expected to see patients treated with the lower doses to have worse survival. We were shocked to discover they survived just as well, and possibly even better.”

“There is probably not one right dose for every single patient. It doesn't make sense that the same dose will work for an 80-year-old frail man who had a small heart attack as a burly 40-year-old man with a huge heart attack. We now need to figure out how to dose it in individual patients,” added Prof. Goldberg. “This huge gap in knowledge has been completely unexplored. Since this is medicine we use in every single heart attack patient, we ought to figure out how to use it properly.”

β-blockers are used for the management of cardiac arrhythmias, protecting the heart from a second MI after a first heart attack (secondary prevention), and hypertension. They block the action of the endogenous catecholamines epinephrine and norepinephrine, in particular on adrenergic beta receptors located on cells of the heart muscles, airways, arteries, and other tissues that are part of the sympathetic nervous system. They also interfere with the binding to the receptor of other stress hormones, mediating the fight-or-flight response.

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