Posts Tagged ‘stemi guidelines’


Verdict ?

Only complicated or high risk  STEMI,  would require immediate anatomy based management. Please note, this population at worst is never beyond 20 % of all STEMI. Hence more than majority of  patients  can be managed effectively without CAG.

My reasoning tells me,though knowing the  coronary anatomy appear vital  , it is rather the physiological impact of those  anatomical lesions  that will determine the outcome. So,post STEMI, if at all , we need to investigate, it should be about the  adequacy of the over all blood supply to left ventricle.This is done by a pre or post discharge sub maximal stress /nuclear test .If it’s negative with a good exercise tolerance  CAG will never be required as any critical flow limiting lesion ( that would require intervention  )is excluded with near 100% surety.

Postamble :Try asking  any neurologist , how often they demand to know cerebral arterial  anatomy for managing stroke  ? You will get a real surprise answer !

Read Full Post »

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.

Final message

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.

Read Full Post »

                                                    Drugs are poisons , whenever it is administered without valid purpose. it can enter human body  in many ways (Oral, intravenous, percutaneous etc ) And now we have another route namely intracoronary !

                                                   In quest for prevention of restenosis, many of the anti cancer drugs are now delivered directly inside the coronary arteries .These drugs are secreted  like a sustained release  tablet from the drug coated stents.These drugs are expected to prevent restenosis within the stented segment.But, after years of  intense debate and research  , we realised that ,  drugs  eluted from the stent  could damage the distal coronary vascular bed and coronary microcirculation.( And thus came the epidemic of acute stent thrombosis ! )

                                                The tender and sensitive coronary microvasculature  is constantly exposed to  these  powerful anticancer and immmunosuppresive  drugs .It is a great surprise , no body thought of  this dangerous drug -coronary artery interaction ! It required the genius of Renu virmani and others to point out this.

But still , the cardiology community by and large , fails to consider  this an important issue.This is proven by the fact, usage of DES is  still increasing  and used mainly as an off label indication.

Read this land mark article from circulation




Questions that need to be answered

  • What is the long term effects of drugging a coronary artery ?
  • Is no reflow or slow flow  more common after DES , because of the adverse drug reaction in the distal vascular bed ?
  • If a patient  with  DES  undergoes a CABG later what  would be  the impact of the  drug on the graft ? Will the functional vasodilatation   affected ?

Final message

                                  A drug , to get a legal clearance it has to undergo  hundreds of rigorous tests . Finally it is cleared for that  specific indication for which it is tested  .Just because a drug is cleared for one purpose ( Paclitaxel for malignancy ) it does not mean it is safe to use for any other  purpose for which it is deemed to be useful . Exactly the  opposite is happening   in the  the field of interventional cardiology . No body wondered to think what would be the effect of these drugs on the normal coronary endothelial cells and vasculature.Is it not a crime ,  without analysing this particular issue  , dozens of drug eluting stents have been released in the market . And now,  sounds of crying  foul is heard world wide !

Let us thank  , the so called negative forces in cardiology  for making this an  issue . In science ,  the watch dogs should bark  at  times of danger not wag the tail !

Read Full Post »