Introduction
In acute MI, beta blocker therapy can reduce the risk of death when started early. This evidence is seen in STEMI though there are no randomised trials when it comes to non ST elevation myocardial infarcts. Beta blockers were first discovered by Sir James Black for which he was awarded the Nobel Prize in 1988. Since then, there have been great advances in research and development of beta blockers, with newer generation drugs having an effect on the production of nitric oxide.
The effects of beta blockers
Beta blockers have a number of clinical effects. Some of the relevant ones include reduced heart rate, reduced oxygen consumption, anti-ischemic effects, increased myocardial protein synthesis, shift from free fatty acid to glucose metabolism and peripheral anti oxidant effect.
In the ischemic heart, they reduce heart rate, improve coronary circulation by improving diastolic circulatory times and reduce catecholamine release. This has a protective effect on the heart, which is particularly important in STEMI.
Role in STEMI - Evidence
In the prethrombolytic era, the early use of metoporol in the Goteborg trial found that intravenous usage within 12 hours of ischemic pain onset reduced LDH levels and also reduced 90 day mortality by 36%. Other trials showed that early metoprolol use led to a significant decrease in development of definite infarction and reduction in tachyarrythmias with metoprolol, especially when treated within 7 hours of symptom onset. However, there was no statistical difference in mortality.
In the thrombolytic era, the TIMI IIB trial found that immediate beta-blockade produced no improvement in cardia ejection fraction and neither did it reduce mortality.
The COMMIT study was a landmark trial that found that early use of metoprolol in acute MI patients did not significantly reduce in-hospital mortality. However, it reduced the risk of re-infarction and ventricular fibrillation. Interestingly, the risk of cardiogenic shock was markedly increased. This translates into safer use of beta blockers later in acute myocardial infarction, once the patient is clinical more stable.
The American Heart Association now recommends using beta blockers on day 0 -1 if there is evidence of high blood pressure or atrial fibrillation. If there are signs of heart failure or a risk of cardiogenic shock, it is better to avoid this completely. Always re-evaluate the need for treatment if early use is contraindicated.
2 new trials have emerged over the last few years that have put in doubt the early use of beta blockers. The METOCARD-CNIC trial found that pre-PCI beta blockade reduced infarct size in anterior MI only. However, this finding has been placed in question by the Early BAMI study, that found no difference in any kind of MI.
Recommendation
When considering beta blockers in acute STEMI, always evaluate the risk and benefits. If safe, consider use after the first day or at least prior to discharge, provided the patient is stable.
In acute MI, beta blocker therapy can reduce the risk of death when started early. This evidence is seen in STEMI though there are no randomised trials when it comes to non ST elevation myocardial infarcts. Beta blockers were first discovered by Sir James Black for which he was awarded the Nobel Prize in 1988. Since then, there have been great advances in research and development of beta blockers, with newer generation drugs having an effect on the production of nitric oxide.
The effects of beta blockers
Beta blockers have a number of clinical effects. Some of the relevant ones include reduced heart rate, reduced oxygen consumption, anti-ischemic effects, increased myocardial protein synthesis, shift from free fatty acid to glucose metabolism and peripheral anti oxidant effect.
In the ischemic heart, they reduce heart rate, improve coronary circulation by improving diastolic circulatory times and reduce catecholamine release. This has a protective effect on the heart, which is particularly important in STEMI.
Role in STEMI - Evidence
In the prethrombolytic era, the early use of metoporol in the Goteborg trial found that intravenous usage within 12 hours of ischemic pain onset reduced LDH levels and also reduced 90 day mortality by 36%. Other trials showed that early metoprolol use led to a significant decrease in development of definite infarction and reduction in tachyarrythmias with metoprolol, especially when treated within 7 hours of symptom onset. However, there was no statistical difference in mortality.
In the thrombolytic era, the TIMI IIB trial found that immediate beta-blockade produced no improvement in cardia ejection fraction and neither did it reduce mortality.
The COMMIT study was a landmark trial that found that early use of metoprolol in acute MI patients did not significantly reduce in-hospital mortality. However, it reduced the risk of re-infarction and ventricular fibrillation. Interestingly, the risk of cardiogenic shock was markedly increased. This translates into safer use of beta blockers later in acute myocardial infarction, once the patient is clinical more stable.
The American Heart Association now recommends using beta blockers on day 0 -1 if there is evidence of high blood pressure or atrial fibrillation. If there are signs of heart failure or a risk of cardiogenic shock, it is better to avoid this completely. Always re-evaluate the need for treatment if early use is contraindicated.
2 new trials have emerged over the last few years that have put in doubt the early use of beta blockers. The METOCARD-CNIC trial found that pre-PCI beta blockade reduced infarct size in anterior MI only. However, this finding has been placed in question by the Early BAMI study, that found no difference in any kind of MI.
Recommendation
When considering beta blockers in acute STEMI, always evaluate the risk and benefits. If safe, consider use after the first day or at least prior to discharge, provided the patient is stable.
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