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Higher beta-blocker dose does not increase survival after acute MI
New findings from the OBTAIN registry demonstrate similar survival outcomes after acute MI among patients treated with various doses of beta-blockers.
The registry enrolled 6,682 patients with acute MI. Researchers compared outcomes between those who received no beta-blockers or those who received doses ranging from more than 0% to 12.5%, more than 12.5% to 25%, more than 25% to 50%, and more than 50% of the target dose.
The primary endpoint was time to all-cause mortality during a median follow-up of 2.1 years.
Most patients (91.5%) were treated with a beta-blocker on discharge, with a mean dose of 38.1% of the target dose. Those who received a beta-blocker, regardless of dose, had lower mortality rates compared with those who did not receive a beta-blocker (P < .0002).
Multivariable analysis indicated that risk for mortality at 2 years was similar among patients who received more than 0% to 12.5% of the target beta-blocker dose (adjusted HR = 0.862; 95% CI, 0.677-1.098), more than 12.5% and 25% (HR = 0.799; 95% CI, 0.635-1.005) and more than 25% and 50% (HR = 0.963; 95% CI, 0.765-1.213) compared with those who received more than 50% of the target dose.
Additional multivariable analyses incorporating more covariates and propensity score analysis revealed no significant improvements in outcome with higher beta-blocker doses, the researchers wrote in the Journal of the American College of Cardiology. Low-dose beta-blocker treatment (≤ 25% of target dose) was associated with a significantly lower mortality risk compared with high-dose therapy (≥ 50% of target dose; HR = 0.857; 95% CI, 0.734-1.002), according to initial multivariable analysis. However, adjustment incorporating an extended covariate set eliminated the significance of this association, according to the results.
Patrick T. O'Gara
“Current practice is characterized by the use of low-dose beta-blocker therapy post-MI,” the researchers wrote. “To date, no data support this practice, as all the randomized clinical trials used higher target doses. Because these trials did not include titration studies, the present findings are not in conflict with the randomized trial data. Importantly, further research is needed to establish optimal (personalized) beta-blocker dosing after MI.”
In a related editorial, Viviany R. Taqueti, MD, MPH, and Patrick T. O’Gara, MD, both of Brigham and Women’s Hospital, Harvard Medical School, cautioned that these findings should be interpreted with caution. They noted that the researchers “conclude appropriately that we cannot ascertain a dose-response relationship between beta-blocker dose after MI and mortality from this observational study.”
The study, however, raises important questions about beta-blocker use after MI, according to Taqueti and O’Gara.
“Broadly, the work … highlights the inherent limitations of a 1-trial, 1-drug, 1-dose approach to treating entire populations, especially when individual responsiveness cannot be predicted,” Taqueti and O’Gara wrote. “We look forward to a personalized approach to [CV] care that moves toward patient-specific drug target effects while reducing major morbidity and mortality, but recognize that this will require a better partnership between us and our patients.” – by Adam Taliercio
Disclosure: The NHLBI funded the study. One researcher reports consulting for Celladon, Outcome Research Solutions and Zensun. Taqueti and O’Gara report no relevant financial disclosures.