• Ilke Sipahi, E Murat Tuzcu, Katherine E Wolski, Stephen J Nicholls, Paul Schoenhagen, Bo Hu, Craig Balog, Mehdi Shishehbor, William A Magyar, Timothy D Crowe, Samir Kapadia, and Steven E Nissen.
• Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
• Ann. Intern. Med. 2007 Jul 3; 147 (1): 101810-8.

BackgroundIn patients with myocardial infarction, beta-adrenergic blockers reduce recurrent myocardial infarction and total mortality rates. However, whether a direct influence of beta-blockers on coronary atherosclerosis contributes to reduced recurrent myocardial infarction and total mortality rates is not known.ObjectiveTo assess whether beta-blocker therapy is associated with reduced atheroma progression in adults with known coronary artery disease.DesignPost hoc, pooled analysis of individual patient data from 4 intravascular ultrasonography (IVUS) trials.SettingFour IVUS trials conducted in the United States, Europe, and Australia.Patients1515 patients with coronary artery disease.InterventionThe original trials used 3 different statins, a calcium-channel blocker, an angiotensin-converting enzyme inhibitor, or an acyl coenzyme A-cholesterol acyltransferase inhibitor.MeasurementsChanges in atheroma volume, as determined by IVUS after adjustment for possible confounders by using linear mixed-effects models, were compared in patients who did and did not receive concomitant beta-blocker treatment.ResultsPatients who received beta-blockers (n = 1154) were more likely to have histories of myocardial infarction, angina, and hypertension than were patients who did not receive beta-blockers (n = 361). The estimated annual change in atheroma volume was statistically significantly less in patients who received beta-blockers. This was true for univariate and multivariable analyses that controlled for history of myocardial infarction, angina, and hypertension (mean [+/-SE] atheroma volume, -2.4 +/- 0.5 mm3/y in treated patients vs. -0.4 +/- 0.8 mm3/y in untreated patients; P = 0.034). Accordingly, atheroma volume statistically significantly decreased at follow-up IVUS in patients who received beta-blockers (P < 0.001) and did not change in patients who did not receive beta-blockers (P = 0.86). Additional adjustments for low-density lipoprotein cholesterol level, concomitant medications, and clinical trial did not change the results.LimitationsPatients were not randomly assigned to beta-blocker therapy, and interventions other than beta-blocker therapy could have influenced the changes in atheroma volume. Whether progression rate of atherosclerosis as detected by IVUS predicts cardiovascular outcomes is unknown.ConclusionsThe analysis demonstrates that beta-blockers can slow progression of coronary atherosclerosis. The findings provide additional support for the current clinical guidelines advocating long-term use of beta-blockers to treat most forms of coronary artery disease.

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