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Why mitral valve replacement carries poorer outcome than aortic valve replacement ?

July 6, 2009 by dr s venkatesan

The valve replacement surgery is one of the great innovations in cardiac surgery. The common disorders that require mitral and aortic valve replacement are

  • Degenerative , calcific  aortic stenosis and regurgitation.
  • Rheumatic mitral, aortic valve disease.
  • Ischemic heart disease -Ischemic MR
  • Some cardiomyopathies

The mortality in valve replacement surgeries vary  between AVR, MVR, and DVR.

AVR – 2-5%

MVR 4-12%

DVR  6-15%

Source CTS.net

Determinants of outcome

General factors applicable for both valves

Elective vs Emergency

LV function

Associated CAD /CABG

Co morbid conditions

The following observations  can be  made  in valve replacement surgery

  • Mitral valve function is closely linked to LV function while Aortic valve  is not .
  • AVR  patients always do well than MVR in  the  immediate post operative period
  • Aortic stenosis patients do well than aortic regurgitation .
  • Mitral stenosis patient do well than mitral regurgitation
  • In   DVR  the excess mortality is due to  the addition of MV , not by  AVR .

Aortic valve replacement has better post operative outcome when compared to mitral valve replacement ,Why ?

Aortic valve has only two components namely a  annulus  and leaflets. The prosthetic  aortic valve  replaces both these natural components . Mitral valve has 6 components , prosthetic mitral valve has only two components . Hence  , any prosthetic mitral valve is far inferior to natural mitral valve . The  pap muscle, chordae, and LV muscle fail to assist the artificial  mitral valve.  So , between AVR and MVR   AVR is far perfect  prosthetic surgery and  the hemodynamics   mimic as closely to the natural valve.

Why aortic stenosis patients do better than aortic regurgitation ?

Aortic stenosis  results in severe  LV outflow obstruction .The LV struggles to pump across the obstruction.So , once it is relieved by a prosthetic valve , there is great relief for LV .We know the the aortic valve orifice becomes <1cm2 in critical AS . (Like a pin hole !) .Prosthetic aortic valve at least doubles or triples this orifice and the LV enjoys this sudden relief  and  becomes active or even hyperactive in immediate post operative phase , later  it    settles to a near normal LV function. It has been observed even very severe LV dysfunction associated with aortic stenosis recovers well .

What happens  in AVR done for  dominant or isolated  aortic regurgitation ?

Here the situation  is dramatically opposite.The purpose of  prosthetic aortic valve is  reduce the  aortic valve orifice .

In AR ,  the  left ventricle  is  used to eject  the blood  with ease  across LVOT   without  much  resistance  ,  only to find part of the blood returning  back into the chamber . In  the next beat it does the same and  the cycle   continues for ever .This in due course , dilates the LV  and increases  wall stress and afterload.  LV dysfunction follows .This  takes long time to set in.That’s why chronic asymptomatic AR patients  do so well and they do not require surgery until after the onset of LV dysfunction .(End systolic LV >55mm)

After the aortic valve replacement , the LV suddenly finds  the newly introduced prosthetic valve  a hindrance !. As all artificial  valves  have  less than the natural orifice. LV   takes some time to adapt to the new environment . The EF initially may slightly fall and recovers later.

If pre- operative LV dysfunction was significant the immediate post operative period can be critical.As even a slight fall in EF can result in prolonged hypotension.Many of these   pateint may  require  prolonged inotropic  support.

What are the differences between MVR done for mitral stenosis and MVR done for mitral regurgitation ?

Here again ,  the same principles apply.The Mitral stenosis patients do well following MVR than MR patients.This is because of two reasons .  MR patients  have dilated LV  and may also have associated impaired LV function .A chronic MR is  some   what  a stress reliever  for the LV  ,  as  with every contraction it can decompress a little   bit  . It is an important hemodynamic  fact  ie  ,  presence of   even a  trivial  MR helps the LV to tackle the  it,s  afterload  easily by increasing the dp/dt and also the EF.

So when we introduce a a fully competent prosthetic mitral valve all of a sudden the LV again struggles for some time.

Final message

MVR  patients has less favorable  clinical outcome than AVR .

Coming  soon

How  different is the anticoagulation  protocol difference between AVR  and  MVR ?

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The “not so” benign chiary network

July 5, 2009 by dr s venkatesan

It is the  embryological remnant within right atrium  often observed as , mobile strands within RA extending fromIVC orifice to IAS. Some  times  it is difficult  to differentiate from eustachian valve  of IVC.The network is formed by collagenous material  and mimic valvular tissue

chiary network echo

Incidence

2% of general population . ( Means 10 crore persons  in our world ! )

What is considered  a benign echocardiographic observation for long  ,  may not be innocuous  . It  can predispose to certain clinical events , although rare.

  1. Mistaken for right atrial mass
  2. May produce  innocent murmur
  3. Catheter entrapment within RA
  4. Infective endocarditis of the network , and tricuspid valve
  5. Abnormal P waves and trigger for  atrial tachycardia
  6. Disrupted chiary network  prolapsing into RV
  7. Associated  foramen ovale  may induce  streaming  .This maintains  an embryonic right atrial flow pattern into adult life and directing the blood from the inferior vena  cava preferentially toward the interatrial septum

Reference

http://content.onlinejacc.org/cgi/content/abstract/26/1/203

http://ats.ctsnetjournals.org/cgi/content/abstract/76/4/1303

http://content.karger.com/ProdukteDB/produkte.asp?doi=10.1159/000096780

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Why we look lead V1 to diagnose RVH but look at V4R , to diagnose RV infarction ?

July 2, 2009 by dr s venkatesan

The right ventricle  is a unique  chamber of the heart . It is the anterior most chamber and  triangular in shape.  Even though  the walls of RV are  not  clearly demarcated ,   it does  have  anterior ,  posterior, and lateral free surfaces   . Anatomically it has a inflow  body, apex and outflow portions . The apex of right ventricle , blends with the lower IVS at an acute angle.

How does RVH occur anatomically ?

The anatomy of RV is such that  it does not allow  it  a concentric  RVH ( like LVH ) . In fact , there is a  disproportionate free wall , anterior  wall   hypertrophy  many  situations  like  PHT/Pulmonary stenosis. The  infero posterior aspect of RV rarely show hypertrophy.

Since RV is the anterior most chamber, located just beneath the left border of sternum   RVH brings the RV  further closer to chest wall .This makes the V1 lead to show  tall R in V1.

What happens in RVMI ?

Unfortunately, when we  refer to RVMI , we generally do not make any efforts to locate or estimate it’s  size.  Since RV has , anterior , lateral and posterior surface  , the site  and  the  extent of the  mI will have a major impact  on the  ECG  features .

Most often  the RVMI occur as a  part of infero posterior MI  .Hence ,  it is uncommon for the anterior surface of RV to get involved.  But ,  it can be involved if  RCA gives of a   large RV branch  that reach the anterior surface of RV.

Anterior RVMI can occur as a part  of LAD MI  , if a large conal branch cross the RV surface.

What prevents the lead V1 from showing the  ST elevation of RVMI ?

  • Most of the RVMI do not involve the anterior surface of the RV so , less chances for ST elevation
  • Further , if a true posterior wall  MI  occur as a part of  RVMI (Which is often the case !)  V1 can never  show ST elevation  as the  posterior MI  tend to have a ST depressing effect in the V1, V2 leads.
  • Extensive IWMI , can have reciprocal ST depression in V1-V2.This again , prevents V1 lead to show the ST elevation

So many times , even though V1 lead is just sitting over the chamber RV it fails  to  pick  the  ST elevation forces of RVMI

Advantage of V4 R ?

V4R records remote RV forces , as these  signals are not contaminated by the inferio posterior ST forces. Hence  a  1mm ST elevation in right sided chest leads have good sensitivity  and specificity to diagnose RVMI .

When can V1 show ST elevation in RVMI ?

If the RV anterior wall is predominantly involved (Ie Anterior RVMI ) ST elevation can occur in V 1 like a anteroseptal MI.

rvmi ecg

Rarely a q RBB can occur in V1 in isolated RVMI.

Final message

V1 lead , though anatomically proximal to RV has less value in diagnosing RVMI since this lead picks up  Infero posterior  negative ST forces  and  the anterior  forces of RVMI get neutralised . So relying on lead V1 to diagnose RVMI is not adviced , except when  the anterior surface of RV is predominatly  involved.

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Primary PCI is great for STEMI but “Primary CABG ” is not why ?

June 28, 2009 by dr s venkatesan

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.

Reasons.

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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How oral amiodarone differs form IV amiodarone ?

June 28, 2009 by dr s venkatesan

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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Should all patients with positive excercise stress test (EST) undergo coronary angiogram ?

June 26, 2009 by dr s venkatesan

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.

//

Posted in Cardiology - Clinical, Uncategorized | Tagged , | 13 Comments »

Why we are not classifying NSTEMI ?

June 22, 2009 by dr s venkatesan

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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Circadian variation in thrombolysis efficacy : Streptokinase works best in the evenings !

June 22, 2009 by dr s venkatesan

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.

CIRCADIAN

Download full PPT presentation stemi thrombolysis ppt

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“Benefit of doubt” and the “risk of doubt” in cardiac care”

June 19, 2009 by dr s venkatesan

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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Therapeutic issues in STEMI :Persistent sinus tachycardia following thrombolysis

June 16, 2009 by dr s venkatesan

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

Or

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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