Beta-blockers In Acute Myocardial Infarction Research Articles

Intravenous beta-blockers in acute myocardial infarction: Perceived versus actual use by cardiologists and emergency physicians

This study sought to determine the relationship between perceived and actual use of intravenous β-blockers by cardiologists and emergency physicians for patients with acute myocardial infarction (AMI). The charts of 35 patients who presented to the emergency department of a community hospital with AMI during a 6-month period were retrospectively reviewed. Members of the departments of cardiology and emergency medicine were mailed a one-page survey pertaining to their use of intravenous β-blockers in AMI. Of the 35 patients only 4 (11%) received an intravenous β-blocker. Three of these 4 patients were either hypertensive or tachycardic and none had a contraindication to β-blockade. A contraindication was present in 15 (48%) of those who did not get intravenous β-blockade. The survey was completed by 11 (100%) of the emergency physicians and 68 (69%) of the cardiologists. Emergency physicians were significantly less likely to report using intravenous β-blockers in AMI patients who were normotensive with normal heart rates ( P = .007) and most (9 of 11) deferred the decision to the cardiologist. Although the majority of cardiologists reported giving an intravenous β-blocker to at least 50% of AMI patients with normal blood pressure and pulse rates, the actual frequency was only 8% (1 of 13). In this institution, cardiologists overestimated the frequency of intravenous β-blocker administration to patients with AMI. Emergency physicians usually deferred the decision on intravenous β-blockers to cardiologists and reported a frequency of use that was much closer to actual practice.

Benefits of non-selective versus cardioselective beta-blockers in acute myocardial infarction in hypertensive patients

To evaluate the effect of current treatment with non-selective or cardioselective beta-blockers on the outcome of a first acute myocardial infarction in hypertensive patients. Peak aspartate aminotransferase was measured as an indirect estimate of infarct size, the occurrence of circulatory arrest from ventricular tachyarrhythmias and in-hospital mortality. A retrospective analysis was performed on data collected in a continuously operating register of all hospitalized acute myocardial infarctions in Malmö, Sweden. A total of 2114 hypertensive patients were admitted to hospital with a first acute myocardial infarction. Of these patients, 323 were treated with a non-selective beta-blocker on admission and 338 with a cardioselective beta-blocker. In patients given a non-selective beta-blocker the mean peak aspartate aminotransferase was 3.02 +/- 0.15 mukat/l, which was significantly lower than the peak (3.78 +/- 0.35 mukat/l) recorded in the patients given a cardioselective beta-blocker. In a multiple regression analysis, treatment with a non-selective beta-blocker was significantly and inversely related to peak aspartate aminotransferase after adjustment for several clinical characteristics. Age, anterior myocardial infarction, peak aspartate aminotransferase, serum potassium and treatment with a cardioselective beta-blocker were significantly and independently associated with the occurrence of circulatory arrest due to ventricular tachyarrhythmias. The relative risk of circulatory arrest in patients taking cardioselective beta-blockers was 1.73 (95% confidence interval 1.16-2.58) and in patients taking non-selective beta-blockers 1.02 (95% confidence interval 0.64-1.66). Advanced age, a history of diabetes mellitus, a history of stroke, anterior myocardial infarction, a high serum potassium level and a high peak aspartate aminotransferase level significantly predicted in-hospital mortality. The relative risk of in-hospital mortality in patients taking non-selective beta-blockers was 0.92 (95% confidence interval 0.64-1.30), and in patients taking cardioselective beta-blockers 0.84 (95% confidence interval 0.59-1.19). The study suggests that current treatment with non-selective beta-blockers may have reduced the enzymatically estimated infarct size and the occurrence of circulatory arrest due to ventricular tachyarrhythmias. Both non-selective and cardioselective beta-blockers may also have reduced the in-hospital mortality in this population of hypertensive patients suffering a first acute myocardial infarction. In a clinical study using with adrenaline infusions in healthy volunteers, we found that beta 2-receptor blockade improved potentially arrhythmogenic variables, such as hypokalemia and hypomagnesemia, but the adrenaline-induced reduction in diastolic blood pressure was reversed. Pretreatment with the new beta-blocker carvedilol preserved the beneficial electrolyte effects without increasing blood pressure during the adrenaline infusion.

Intravenous acebutolol raises serum potassium in acute myocardial infarction.

Hypokalaemia commonly occurs in acute myocardial infarction (AMI) and may be caused by elevated serum levels of adrenaline, allegedly by beta 2-adrenergic mediated influx of potassium (K) into cells. We investigated the effect on serum K of intravenous acebutolol (a relatively beta 1-selective agent) in 50 patients with AMI. Serum K was measured before and 1 hour after drug administration. The same measurements were made in a comparable control group of 30 patients who did not receive the drug. Mean serum K rose from 3.58 to 3.81 mEq/l (P less than 0.005) in the treated group. No significant change occurred in the control group. The rise in serum K could not be correlated with prior beta-blocker therapy, zone of infarction, prior diuretic therapy, or gender of the patient. We conclude that the administration of intravenous acebutolol after AMI raises serum K, despite the fact that this beta receptor blocking agent is relatively beta 1-selective. Since hypokalaemia is associated with an increased risk of ventricular fibrillation, it should no longer be assumed from acute intervention trials with beta-blockers in AMI which had mortality or arrhythmias as end-points, that beneficial effects were necessarily due to limitation of infarct size or to a direct anti-arrhythmic action of the drugs. Future trials should take the effect on serum K levels into consideration.