Archive for June, 2009

No one can deny ,  there is a huge revascularisation  dilemma  between CABG and PCI  in patients with CAD. This is especially  prevalent in multivessel disease in chronic coronary syndromes.

In acute STEMI , CABG is never considered as a primary revascularisation  procedure.There should be strong reason for this !  Few studies , suggested a role for CABG in acute MI if it is done within3- 6 hours .But it became very clear , by and large CABG for acute STEMI is contraindicated . This especially applicable when q waves are formed.


Performing a complex surgery  on a   blood vessel subtending a  dead  , irritable ,myocardium is dangerous. Even a graft for non IRA vessel has no great benefit in the acute setting. The mortality of CABG in the first 48hours of MI  can be up to 15%.  Primary PCI  opens up the IRA without the hazards of major surgery

Issues  for  CABG in STEMI

Failed thrombolysis :  Rescue PCI  could be useful provided it is also performed within the same time window . In most situations  there is nothing called  “rescue CABG ” 

Some would believe Left main and critical TVD is an  indication for an emergency  CABG. Yes , CABG may be indicated  in this setting , but even here it may be delayed for a week if there is no ongoing ischemia , angina or hemodynamic instability.

Still  , there is a  definite role for CABG in STEMI in the following situations.

  • Mechanical complication- VSR/MR/Free wall rupture
  • Cardiogenic shock
  • Failed  and complicated primary PCI.( Note : Simple failure to open a IRA is not an indication for CABG , there need to be a life threatening situation ! )

 Coming soon

Routine  CABG  is  generally  dangerous and contraindicated   for STEMI ,  while it  is  a great ,  life saving surgery  in  most of  the  refractory  NSTEMI : How ?

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Amiodarone has brought a major change in the medical management of ventricular arrhythmias over  the last  few decades. It is  a powerful antiarrhytmic drug , with all class 1 -4 action  (of vaugan williams classification.) It  has   sodium , pottasium, calcium and beta blocking properties.  Hence there is no surprise, amiodarone is  aptly called a broadspectrum anti arrhythmic as it  acts  on many of the cardiac receptors .

Of course , the major action is thought to be pottasium channel blocking effect(Class 3) that prolongs the action potential duration and refractory period resulting in termination of many re entrant arrhythmias.  While , amiodarone by structure resembles thyroid hormone, takes a long time to reach the steady state plasma levels  .Oral amiodarone takes  up to a week time to exert it’s action.

If amiodarone is a slow acting drug , is it not  surprising  , Why  IV amiodarone is given in the emergency managment of  VT ?

Typically , there is difference between the mechanism of  action between  oral and IV amiodarone

The class 3 property of amiodarone ,  is a late observation following oral adminstration. QT prolongation rarely  occurs  following bolus iv amiodarone . So , VT  terminating effect is thought to be some thing , other than class 3 action. Many believe the combined beta and calcium channel blocking effect could be responsible for rapid reversion of ventricular arrhythmias. The sodium channel blocking action with fast kineticks may also contribute.

Final message.

While amiodarone is a  prototype class 3 anti arrhythmic drug,  it’s  VT terminating property  may  be ,   attibutible to other class action. mean while  , the Class 3 action is responsible for long term prevention of VT/VF .

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Exercise  stress test ( Also called treadmill test ) is an important investigation  not only in patients  with suspected  CAD  but also in  established CAD . In the former  group ,  it helps us to exclude CAD in patients with chest  pain and in the later group ,  it helps us to assess  functional capacity , risk stratification and to detect any  additional ( New or residual ) ischemia.

Stress test being a physiological test , has a huge  advantage of assessing the adequacy of myocardial blood flow without even  knowing the coronary anatomy , while Coronary angiogram (CAG)   has a zero physiological value* in spite of   excellent assessment of the coronary anatomy !

It is an irony , in the assessment of angina we are expected to assess the physiological adequacy of myocardial blood flow ,  we have kept coronary angiogram as a gold standard  over and above the much  neglected  physiological stress test.

Of course, the limitation of stress test is that ,  it has only 75%  specificity(  to rule out CAD ) and about 80% sensitivity (To detect CAD ) .In simple terms  stress test is likely to miss  20% times to miss a CAD  in patients with CAD  and 25% of times falsely diagnose CAD  in patients without CAD.

In the above statistics  ,  coronary angiogram was considered   gold standard . The problem with this data is that , CAG is not the real gold standard ,but it was  nominated  as a gold standard . We now know normal coronary angiogram is not equivalent  to  normal coronary arteries and vice versa.

While both test have limitations , it is logical to believe CAG has an edge over stress test since it visualises the anatomy. But ,  once an obstruction is demonstrated by CAG, stress test scores over in assessing the physiological impact of the lesion.

Is a 70% LAD lesion significant or not ?

Stress test will give vital information to answer this question.If this patient performs 10-12Met exercise without symptoms it means , the obstruction is not impeding the flow even during stress. He may do well with medical therapy.

What does a positive stress *mean for the patient and for the physician ?

(* A false positive EST in LVH, anemia, baseline ST shifts are included in discussion )
  • A positive stress test  with or without angina at low workload <5 METS  indicates very significant obstructive CAD either in left main , or proximal LAD/LCX. They should get immediate CAG.
  • A positive stress test at load  5-10METS  is again significant and patients should get early CAG
  • A positive stress test with angina at good work load >10-12 mets  would indicate insignificant or minimally obstructive  CAD.
  • A positive stress test at  the peak of exercise  at good work load > 10-12METS without angina could indicate a false positive or very minimal CAD.

For the physician , the proper way  of interpretation  should be , the fact that a person performs 10-12  METS  indicate the myoacardial blood flow  would  be  more than adequate in most life situations. Knowing the coronary anatomy serves no purpose here, as no revascularisation will be attempted even if he is going to have a significant CAD ( Which again , is also highly unlikely ) .He should be managed with appropriate lifestyle (Diet, activity, relaxation )  anti anginal drugs,  aspirin , good lipid control and plaque stabilisation with statins .

Can a  patient with critical left main  or proximal LAD  perform >10METS in exercise stress test ?

No , large clinical experience (Also refered to Class C evidence  by ACC/AHA!) indicate no patient with critical  left main or equivalent disease  can perform 10 METS  excercise

While  ,  EST may be less hyped investigation, but it is the  only  noninvasive test , ( that too , simple and  cheap ) that can rule out * a significant left main  or equivalent almost   100%  correctly .

Now that,   the results of COURAGE  and BARI 2D have clearly indicated medical therapy is best form of management  in chronic  CAD , ( except in severe obstructive CAD in vital locations)  a  positive EST  at > 10-12Mets  , has absolutely no indication* to for doing a CAG.

*Some would advocate a policy of  doing a  CAG as a baseline investigation in all patients with positive EST  to know the coronary anatomy and will not proceed onto revascularisation if there is insignificant lesions.

Further ,  real life experience has taught us , routine  CAG in these patients

  1. Increases patient anxiety as he is given a report with a diagram of obstructed heart vessels
  2. Leads to multiple cardiac consultations
  3. Divergence of opinions
  4. Finally end up in  the likely hood of a inappropriate  revascularisation for a  insignificant distal CAD.

Final message

Every patient,  who has positive stress test  , ( Please note , it could  even be  true positive  )  need not undergo CAG .  Most  interventional cardiologists could  feel  otherwise , but one should also  remember ,  There is one  more role  for the interventional cardiologist ie  , to intervene when inappropriate interventions are done to their patients.


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NSTEMI constitutes an important sub group of ACS. In fact it  forms the major  group. Real world data would indicate it   UA/NSTEMI could form up to 75% of all admissions for ACS in any cardiac emergency units. Risk stratification of NSTEMI is important and  is available. It is  one primarily with clinical features , ECG and troponin positivity. Classifying NSTEMI   with reference to underlying patho anatomy is not available.

Classifying  NSTEMI based on the following is  is suggested .

A.Based on the  extent  of infarct.( For example there is no entity called extensive NSTEMI  unlike STEMI)

B.Based on the Location of NSTEMI .

Currently , NSTEMI simply means there is an infarct some where in the heart ? Should we not localise it ? Is it not surprising , we have not attempted to localise  NSTEMI  so far ?

C.Based on the coronary anatomy : RCA NSTEMI vs LAD vs LCX NSTEMI.

The reason is two fold.

1.NSTEMI is often patchy , subendocardial . Some times  only islands of infarct can occur.But , .How common is segmental NSTEMI ? May not be common, still if wall motion defect occur it must be an segmental MI.Some estimate wall motion defect in NSTEMI is around 25%.

2.Is  there any clinical purpose for localising NSTEMI ?

Some would  think there is no real  purpose. That does not  mean ,  we should not attempt to do it. In fact there is an  important reason ,  we  need to  localise  NSTEMI. Triple vessel disease ,  is the common pathology underlying NSTEMI. They often have  multiple critical lesions as well. Identifying the  the  culprit lesion is not an easy task. If we know the site of infarct ,  however small it may be , it  helps us fix  the coronary artery.

A real dilemma could occur in patients  with NSTEMI , who has a  90 % lesion  in  RCA and  50 % proximal LAD lesion  . We ( tend to !)  take it as granted  ,  RCA  lesion is likely to be responsible for the NSTEMI. But  the real culprit  could be  the  recannalised LAD .  If it is so ,   the 50%  LAD lesion  could   be  more important and if you leave it free there is a strong  likely hood of recurrent UA. If we could some how located  the NSTEMI in the LAD region in this patient  , he could  get a PCI for LAD as well.

Of course , there is  an   universal approach available “Doing PCI for all suspected culprit lesion however mild it may be ”  . Unfortunately , it  increases the metal load for the  patient, which is an independent risk factor for a future ACS.

How to locate NSTEMI ?

So , it is often helpful to locate NSTEMI  . Of course ,  it needs little more efforts. A very meticulous echoc cardiography can aid in locating  the subtle  wall motion defects in NSTEMI . Perfusion studies/PET studies may be indicated in occasional patients.Myocardial contrast echo can be useful.

Coming soon

Difference between Anterior NSTEMI and inferior NSTEMEI

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In  thrombolysis  of  STEMI ,  there is a   less  published ,  but   interesting observation . It is  often noted , variation  in the efficacy of streptokinase according to the time it was administered.It was most effective in the evenings and least effective in the early morning hours. The mechanism  is thought to be  due to  ,  pineal gland driven   endocrine   spikes    ,  that result in  a  less pronounced  progoagulant activity in the evening hours.    There could be a therapeutic significance for this phenomenon.

The following paper was presented as an abstract in the cardiological society of India annual scientific sessions in New Delhi in 1999.


Download full PPT presentation stemi thrombolysis ppt

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When  a doctor is confronted by serious  doubt  ,  what will be the outcome for the patient  ?

Can  doubting  be beneficial for a patient ?  . It seems so ,  according to  EBM which  stresses   about statistical outcome at every turn of events in a  patient who  is critically  ill .

Is  something ,  always  better than  nothing   ?   Our  limbic  system tends to think so .  It  may not be true. But  in  dire situations ,   many  things  (Proven , unproven)  need to  be tried  however doubtful it ‘s  efficacy  may be  .This is  akin to an  emergency in an  airplane. Even here there need to be a logic.

Then ,this question  arises . How do we make  sure ,  we have a  dire situation on hand  ?

This is the key issue ,  in  the  decision making  for the   critically ill patients .  It  needs  experience ,  only experience !  Though the principle of uncertainty  is the fundamental rule in medicine ,   EBM  aims to bring some degree of certainty in medical therapeutics.

ebm evidence pci coronary

Benefits of doubting in coronary care unit.

In  a  sinking patient  with cardiogenic  shock  , try  the maximum treatment . Even if , the patient is  in severe shock  , take him to the  cath lab ,  try  open the coronary artery . Give the benefit of doubt  to him even though the chances of reviving him is less than 10%.

Risk of doubting in Coronary care unit.

A.Elderly STEMI  with SHT,(Arriving late ,  with  an unknown time  window  after an MI ) To thrombolyse or not ?  . There is  no benefit of doubt here.  Do not thrombolyse. Here , apply  the benefit of doubt against thrombolysis .

B. Chest pain with  LBBB (Thought to be new onset LBBB ) don’t ever rush to thrombolyse.  Wait for the enzyme result . Don’t try to thrombolyse your doubt , instead  thrombolyse the  confirmed thrombus !

C. Patient with persistent ST elevation following thrombolysis ,in an  otherwise asymptomatic and stable patient. Don’t  pass on  ” your doubt ” of salvaging   at least  some myocardium  by rescue PCI .Rescue  should be done before death. You can not resuscitate  dead myocytes.

Final message

The concept of   giving  the  benefits of doubt  to the patient   is a widely prevalent practice  in medicine .This concept is alive  and popular , not because it has proved effective, but because of the primitive   human perception and cognition  , namely “Something is better than nothing ” !

Common sense and logic would suggest , whenever  there is  a benefit  for doubting there would be a  equal (  or  even  more ) unmeasured  hazards and risks . This  becomes  especially  true ,  when   a   physician makes  a therapeutic move  based on doubting than on conviction .

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Sinus tachycardia in the early hours of STEMI is  a very common arrhythmia. This seemingly simple problem can be really worrisome to many cardiologists and give sleepless nights(While the patient may sleep comfortably !)

The importance of sinus tachycardia in STEMI  primarily lies in answering the following question

A.  Is it compensatory sinus tachycardia ? ,  Where in  , the left ventricle is struggling to maintain the cardiac output and works more  per minute to maintain the vital cardiac index


B. Is it a non compensatory -Inappropriate Sinus tachycardia ?  It is a simple  response to heightened adrenergic tone  and   increased neural traffic from the injured ventricular myocardium . (or  high  baseline anxiety levels  )

It should be recalled , tachycardia in any form is  detrimental  following STEMI as it increases the MVo2 ie myocardial oxygen consumption. This is the reason ,  beta blockers are administered in this situation. Compensatory tachycardia  denotes , myocardium is working at it’s reserve capacity  , to prevent an  LVF that is impending . Hence ,  one should recognise , the compensatory tachycardia can not be  tampered  with ,  as we like ! .

How do you clinically differentiate a largely benign inappropriate tachycardia from potentially  harmful compensatory tachycardia ?

It is not an easy task. Heart rate  is typically around 120/mt   in  compensation to impending LVF.  While inappropriate tachycardia has no limits , it can exceed up to 140 or so . Further , tachycardia due to LV dysfunction has reduced variability.( Typically hovers around 120( +/- 5) .In stress or anxiety  heart rate  fluctuates  more .

Accompanying S3 suggest compensatory tachycardia . Even a few basal  crackles would make a diagnosis of  LVF .

The definite way to differentiate  could be   ( Also the dangerous way !  ) looking for  therapeutic worsening to beta blockers .

How to control the sinus tachycardia in STEMI ?

Beta blockers are  the  mainstay. Any of the beta blockers ,  metoprolol, atenolol, carvidilol can be used.Oral metoprolol up to 50 mg can be used. Beta blocker usage is primarily useful in non compensatory tacycardia. It should be  realised , the wide spread routine use of intravenous beta blockade has largely been discontinued as it has adverse outcome.The greatness of carvidilol,  in cardiac failure mainly applies to stable chronic cardiac failures. So ,  it is important to  recognise,  carvidilol can not be used liberally ,  in sinus tachycardia associated with impending or manifest LVF in STEMI.

*The potential source for tachycardia like dopamine,  dobutamine etc should be excluded.

Other options are

Digoxin ( Not withstanding the critics ,  it is still useful in acute MI with persistent sinus tachycardia ,The advantage is ,  it can be used without a need to differentiate whether it is compensatory or non compensatory!)

Ivabradine , a  wonder drug supposed to reduce selcetively  reduce the sinus rate without negative inotropic action could be tried.(Data lacking for this use )

Final message

Sinus tachycardia ,  may be seen as a simple arrhythmia .  but, the circumstances  in which it occurs , it’s mechanism and  the limited therapeutic options , narrow safety margin of beta blockers  , makes it a interesting clinical issue.

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