Beta blockers are vital drugs to limit infarct size and facilitate myocardial salvage. Myocyte death is prevented by reducing MVO2.These concepts originated in early 1980s when thrombolysis was not in vogue .Studies like MIAMI and BHAT were considered landmarks.
Later on , when IV thrombolysis came in a big way the importance of beta blockade in STEMI suffered a little , still it held on to their benefits.
The real problem arose when few enthusiastic cardiologists introduced early multiple blouses of IV beta blockade in the setting of Acute STEMI without realising the potential danger. (In all probability man kind must have lost many thousands of lives with this aggressive beta blocking protocol world over for nearly a decade !)
Fortunately we woke up and in early 2000 , a massive study called COMMIT was initiated to answer convincingly the utility value of routine early IV bet blockade. Rest is history . It clearly showed us the what we were fearing was indeed true. An unacceptably excess cardiogenic shocks were reported in the early IV beta blocker arm .In the same period of time the concept of primary PCI exploded and the BBs were pushed to sidelines
It is a different story altogether . . .
While the funny world of cardiology showed the door for routine early beta blockers in STEMI , it made a stunning U turn in the management of CHF , after being dumped as an absolute contraindication for so many years !
Still COMMIT fails to answer many queries
- Beta blockers in LBBB /RBBB – Probably need to be avoided.
- Beta blockers in bifasicular block – Should be an absolute contradiction
How do you know tachycardia in STEMI is due to high sympathetic activity or cardiac reserve ?
Young men with persistent tachycardia will do well with beta blocker started within 24 hours .
Unless there is s3 or basal rales all tachycardia are to be considered as purely inappropriate and adrenergic
Tachycardia in elderly, women, and diabetic especially the blood pressure hover around 100mmhg is more often a compensatory phenomenon.Meddling the heart rate with BB is vested with a risk.
Finally , if you have a doubt do a rapid echo , if the EF is > 45% one can safely administer BBs
Should we discontinue BBs in those who are already taking it ?
Continuing the beta blocker is thorough the STEMI phase is adviced .(Unless specific contraindication exists )
Beta blocker following primary PCI
The beneficial effect of early Beta blocker even in post thrombolytic era is blunted, it goes without saying primary PCI almost nullifies these effects.
still , beta blockers is to be introduced after a successful primary PCI in all patent for long-term protection.
Do not rush into start beta blocker routinely following STEMI . The risk is not worth taking !
COMMIT study from Lancet 2005
ACC/AHA guidelines on Betablocker and STEMI
The following is taken from the above guidelines When not to administer IV beta blocker seems to be more relevant !
Class 3 recommendation for Beta blocker in STEMI (Evidence A)
1. IV beta blockers should not be administered to STEMI patients who have any of the following: 1) signs of heart failure, 2) evidence of a low output state, 3) increased risk* for cardiogenic shock, or 4) other relative contraindications to beta blockade (PR interval greater than 0.24 seconds, second- or third-degree heart block, active asthma, or reactive airway disease). (Level of Evidence: A)
*Risk factors for cardiogenic shock (the greater the number of risk factors present, the higher the risk of developing cardiogenic shock) are age greater than 70 years, systolic blood pressure less than 120 mm Hg, sinus tachycardia greater than 110 bpm or heart rate less than 60 bpm, and increased time since onset of symptoms of STEMI.
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