In the September 2005 issue of Diabetes Care, McDonald et al. (1) showed that β-blocker therapy after myocardial infarction (MI) was not associated with reduced mortality or fewer recurrent events in people with type 2 diabetes in routine practice. This contrasted with studies performed before intervention with drugs such as ACE inhibitors and statins were available. These studies showed a significant decrease in mortality and reinfarction post-MI in diabetic subjects (2, 3). The authors conclude that the benefits of β-blockers are attenuated in the era of multiple interventions.
I believe that there is another reason for the decreased effectiveness of β-blockers in the modern era. When the older studies were preformed, the majority of β-blockers used were nonselective β-blockers that blocked both the β1 and the β2 receptors. Selective β1 blockers, unless used intravenously at the time of the MI, have never been shown to decrease reinfarction or mortality post-MI (4). In contrast, nonselective β-blockers (propranolol and pindolol) with normal ventricular function, as well as carvedilol with decreased ventricular function, have been shown to decrease cardiac events and mortality post-MI.
Therefore, I believe that the shift in effectiveness of β-blockers post-MI is not due to multiple other interventions but to utilization of β1-blockers, which—especially at lower doses—have not been shown to decrease mortality or reinfarction. A reanalysis based on the use of β1 selective and nonselective β-blockers could prove or disprove this theory.
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D.S.H.B. has received honoraria from GlaxoSmithKline, Bristol-Myers Squibb, and Aventis.