Archive for June, 2010

Many believe  modern science is pure and uncontaminated.

I wish it to be true ,  But reality mirror tells a different story !

The following  “spheres of knowledge”  collectively  form the  cardiology literature .

How much ?  each sphere , contribute is any body’s guess !

The same  rule might  apply  in all  medical  specialties.

Readers are argued to add more spheres of  knowledge.

The seventh sphere may be Eg :  “Commerce based cardiology “

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The funny thing in medicine is  ,   simpler the  question ,   greater the  difficulty to answer ! f  Clopidogrel  is   an  irreversible blocker of platelet aggregation . It  probably ,  is one  of the top  cardiovascular  drugs  used currently .It came into human domain as an aspirin killer and failed miserably , and currently piggy packing on the ageless aspirin for it ‘s action. The concept of dual antiplatelet agent is a classical example . The fact  that , Clopidogrel can rarely be used as a successful  mono anti platelet agent while aspirin can do this job with flying colors will unmask the secrets of  antiplatelet drug industry .

Do you know ,  this drug which  is considered  as a   great  antiplatelet drug , does  not even, pass the  basic test of   prolonging  the bleeding time  in a consistent fashion  ?

Still , we are not clear why it  does  or does not increase the bleeding time in vitro or vivo in linear  fashion.We have  confirmed this  in simple bedside experiments. (More dogmatic conclusions   can be drawn  in bed side , than those  double-blind studies) . In many patients 300 mg of clopidogrel failed to prolong the bleeding time even by  few seconds ! Surgeons who operate on clopdogelised patients differ  widely in their  experience  when they do emergency surgeries on them .

The issue is very vital  ,  Questions raised  are  critical  !

  • If clopidgorel  has a  notoriously unpredictable impact on prolonging  bleeding  time , Then ,  is it not  dangerous ? ,  for those millions of patients with DES(Drug eluting stents )  who live at at the  mercy of clopidogrel’s   erratic behavior.
  • Cardiology community  never got shocked  ,  even as  in this era of evidence based cardiology , a drug  which is being used for over 10 years without even a basic monitoring strategy for it’s efficacy.
  • Such is the scenario ,  it is not at all a surprise ,   to find a huge population  of DES patients   who  dial 911 or 108  with   sub-acute sent thrombosis  due to  clopidogrel failure and resistance.

Read this article published in one of the prestigious cardio thoracic  journal and comprehend  yourself   about clopidogrel’s controversy .

Final message

End of life , is  looming large on Clopidogrel , but it has done it’ s intended mission : Increasing the basic cost of cardiovascular   care in general population  .

A costly and a   dubious equivalent to  Aspirin   wrote a  phenomenal    success story in the narrow lanes of  medical wall street !

No doubt , it   will face the same fate as Ticlopidine ,   Prasugrel has just landed to repeat the same old story !

The easiest   job  to do  in   this wold is to fooling around   the public

and  it is an  irony medical professionals  and their patients  are  often

the   victims

Read also the herd mentality in  medical science

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Digoxin is a wonder cardiology drug used for more than a century.We know the pioneering efforts  of  William withering  in detecting the potential  of the unknown  herb  Foxglove.

Mechanism of action

The beneficial effects of Digoxin is attributable  to

  • Positive inotropic  action
  • Vagal action

Digoxin blocks the sodium potassium ATPase in the  myocyte cell membrane .

This cause accumulation of NA + ions within the cells. The excess  Na , then   facilitates  the Na -Ca exchange port .

This pumps in more calcium   into the myocyte.

Increased  calcium means more forceful contraction and that is positive inotropism* .

* This is a  highly simplified version of   Digoxin’s action . It should  be remembered  simple availability of excess calcium can not guarantee  contractility,   as it requires adequate number  of receptors.

Digoxin  is used in which type of cardiac failure  ?

Digoxin is used for both for LV and  biventricular  failure .

Digoxins is still  often  in isolated RV failure  of any cause (Cor pumonale, PPH, Eisenmenger etc)

Digoxin and RV dysfunction

Digoxin  has a tendency  to  hit the atrial muscles  at random causing  multiple short circuiting (Micro reentry )   forming  a perfect nidus  for complex atrial arrhythmias  including MAT .The coexisting    hypoxia  (which is all the more common here )  aggravates the problem .

Inotropism of RV : Does it really exist ?

It is often quoted , RV is a passive pump. It does not mean inotrpism is an exclusive property of LV.

RV has to generate about 30mmhg to pump the blood into  the lungs.

In cor-pulmonale the RV works against an afterload of around 50-70 mmhg  , making  RV inotropism  much more important  concept.

Rate control in atrial fibrillation Digoxin lowers the heart rate by vago mimetic action ,  primarily in  AV node  and to a  certain  extent in SA node .Ventricular rate reduction  is the prime requirement  in the management  atrial fibrillation and this property  is still the crowing  glory of  Digoxin.

Though beta blockers and  verapamil  can be used as rate controlling agent ,  lack of negative  inotropism makes  digoxin    prevail   over , especially in severely dysfunctional  ventricle .

But , one disadvantage of Digoxin is , since it requires  a vagal traffic to mediate it ‘ s rate controlling effect , it  is less effective ,  when there is  high sympathetic activity as during exercise.

What is the action of digoxin on interventricular  septal contraction ?

Digoxin , simply does not know where it acts when administered in cor pulmonale  ! We believe in cor-pulmonale the maximum action would be the area of maximum dysfunction .This is purely  an assumption. In cor -pulmonale septum shifts it’s loyalty from LV to RV as the later is the distressed chamber.So , logic would be there  is a theoretical  compromise of LV function in  patients with cor -pulmonale. These factors make  the   inter ventricular  interaction and dependence a complex one.

Some believe  the improvement of sub clinical LV dysfunction in cor pulmonale may be more important factor in giving relief  to  the patient’s  symptom.

What are the other RV inotropes ?

Doubtamine has some RV inotropy  .This again may be due to a spill over effect from LV rather than a primary RV inotropism .

As such , there is no great breakthrough  in creating a powerful isolated RV  isolated RV inotropic dug.

Probably  the best way to  give relief to RV is to reduce the pulmonary artery pressure as invariably sever PAH  is the predominate  accompaniment

(Nitric oxide ,  Epo prostenol etc)

Final message

  • Digoxin , indeed has  some useful  role in cor- pulmonale .
  • But ,the benefits are more pronounced in late stages of RV failure.
  • Since the dose required to get an optimal RV inotropy is high the safety margin  is reduced.
  • Since there is a propensity   for complex atrial  arrhythmias  ,  it has to be used very cautiously in management  of   atrial fibrillation due to cor pulmonale .(Than in other forms of AF)

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AV nodal reentrant tachycadia(AVNRT) is the commonest mechanism of SVT. It is divided into slow-fast, fast-slow, slow-slow , representing the two limbs of he circuit.

Slow -Slow circuit is  the rarest  type of AVNRT.  It should be appreciated  ,  the scientific validity of  slow-slow circuit is  applicable  only in relative terms . A virtually  similar antegrade and retrograde limbs with identical conduction velocity and refractory  properties  , can neither  initiate  nor  sustain an AVNRT.

Caveat in the definition of slow -slow AVNRT.

Even though ,  we call it   a  slow-slow  tachycardia , one of the limbs need to be faster than the other.  So , every slow -Slow AVNRT in reality will have  two types

  • Slow- Slow ( Still , faster than antegrade slow) mimic a slow-fast physiology
  • Slow( Faster than retograde slow )  -Slow closely mimic typical  fast slow .

Implication for electrophysiologists  and   points of contention for the ablationist !

  • In Slow -Slow AVNRT ablation we do not know exactly ,  which of the slow pathway is being ablated , unless we specifically  analyse  the post ablative  data.
  • Very often it is not done.Every one in the lab is happy , for breaking the tachycardia circuit. Only after the procedure is over , we may realise the tachycardia is not really killed as it finds an alternate highway to complete  the short circuiting of heart.
  • We need to  suspect this type of AVNRT   prior to the  procedure .Electrophysiologist  shall  spend little   more time and a wide area ablation done , in the vicinity  of coronary sinus ostium can be attempted. .

It is not a smart practice to advocate  wide area ablation as a routine protocol in all AVNRT

as it directly  increase the rate of complication >

Final message

A   hurriedly  done slow pathway ablation  which  may  temporarily terminate the AVNRT ,only to recur later as  the retrograde  slow pathway may again form  a substrate  .The area of slow conduction  acts as a turnaround gateway and capture  the  retrograde fast  pathway which  could be  available in plenty in the anterior aspects of AV node  .   (Note : The unablated  slow pathway  now  form the antegrade  circuit )

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