Archive for September, 2012

For ruling out  acute coronary syndrome in   in  men less than 40 years , here is  30 second protocol !

All you require is an ECG and  some degree of common sense ! ( A flattish  T wave is acceptable )

Please note cardiac  enzymes are not required  to R/O ACS in this group !

Vancouver chest pain rule is  a glorified  clinical sense !



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Under physiological condition ,  pre-load , after load , and cardiac  contractility should be a sequentially matching parameters . After load mismatch is an important concept , where myocardial contractility is temporarily  depressed due to  lack of adequate pre-load for a given level of after load .

This is also  referred to as descending limb LV function paradox .

The three  common clinical situation  AL mismatch  occurs

  1. Critical Aortic stenosis              (High aortic after load )
  2. Acute Hypertension                   (High after Load -Normal and  low pre-load)
  3. Severe diastolic dysfunction  (Pre-load is high -After load is normal )

If it happens acutely the myocardium becomes dyfunctional  due to  mechanical non ischemic stunning .Once the after load comes down the contractility improves .

What  is the chronic adoptive response to after load mismatch ?

LVH is the major  chronic adoptive response to AL mismatch.

LVH reduces the wall stress which will reduce the after load  indirectly .

So LVH neutralises the   high  after load .Laplace law at work . (Wall stress is equal to  2 times the radius divided by thickness of the wall )

Here  is the Link to the great lecture by John Ross Jr  in LA Jolla , California in one of the annual scientific session of AHA   more than 25 years ago . http://www.ncbi.nlm.nih.gov/pubmed/966366 .The concept is alive and kicking even today .I am sorry to  note   this  important physiological concept   never received the attention it deserves .  I would vouch , it  can be as   important as Frank starling  principle .

Reference :



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AV nodal tissue is a not compact structure as we would be believe  . But it is a fact ,  AV  node  do attempt  to compact after birth.

It is never complete.

Note the islands of his bundle entrapped .   Image source : M. Paz Sua´rez-Mier J Am Coll Cardiol 1998;32:1885–90 From the Section of Histopathology, Institute of Toxicology and †Department of Pathology, La Paz Hospital, Madrid, Spain.

All specialised cells should coalesce  to form the compact zone .This fails to happen in many . Failure of AV nodal compaction  results  in islands of slow conducting cells in around AV node . Some of them can mutate  , and   acquire fast conducting properties as well . (Accessory pathway )

This failure of AV nodal compaction is termed as  persistent fetal dispersion of AV node .

In the his bundle  same phenomenon is called as his bundle  de-fragmentation .These abnormalities are noted in pathological  specimens  of  Pokkuri sudden death in Asians .

Unexplained sudden deaths and instant bradycardias and complete heart blocks are related to these dispersion of  AV nodal cells downstream . This also explains some of patients with infra hisian escape show junctional characteristics.

Many cardiac pathologists have observed this . Still  there is a  missing  link  .


M. Paz Sua´rez-Mier,Carlos Gamallo  J Am Coll Cardiol 1998;32:1885–90) Atrioventricular Node Fetal Dispersion and His Bundle Fragmentation  of the Cardiac Conduction System in Sudden Cardiac Death

Kirschner RH, Eckner FAO, Baron RC. The cardiac pathology of sudden,unexplained nocturnal death in Southeast Asian refugees. JAMA 1986;256:2700–5.

Hudson REB. The conducting system: anatomy, histology and pathology in acquired heart disease. In: Silver MD, editor. Cardiovascular Pathology. New York: Churchill Livingstone, 1991:1367– 427.

James TN. Normal variations and pathologic changes in structure of the cardiac conduction system and their functional significance. J Am Coll Cardiol 1985;5:71B– 8B.

James TN, Marshall TK. De Subitaneis Mortibus XVIII. Persistent fetal dispersion of the atrioventricular node and His bundle within the central  fibrous body. Circulation 1976;53:1026 –34.

Persistent Fetal Dispersion of the Atrioventricular Node  Association With the Wolff-Parkinson-White Syndrome Claude Brechenmacher, MD; Jean-Paul Fauchier, MD; Thomas N. James, MD Arch Intern Med. 1980;140(3):377-382.

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Why Junctional rhythm has huge variation in P wave morphology ?

P waves in junctional rhythm can be

  1. Upright
  2. Iso-electric
  3. Inverted
  4. or  even absent

It depends upon the origin of junctional focus

  1. Site of  entry into RA
  2. Ability to capture inter -nodal pathways  and inter -atrial pathways ,
  3.  VA conduction velocity

Further ,the appearance and timing of P waves will be determined by the underlying structural heart disease also.

Final message

Medical  students  have  grown  up with the belief that  AV junction is a single  focused point .It is  true  in terms  of electrical circuitry  of  normal AV conduction .However  during pathological electrical disorders ( Which arise often because of structural disorder) it should be realised   the AV junction is a huge plane   .   Arrhythmia can occur anywhere from this plane .The entire plane  can become electrically active which may also  acquire the  ability to conduct bi-directionally .

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Hypothyroidism is  a classical example of  generalised edema formation .  The mechanism of which is extensively studied  .Still we are  not clear  about  it .

Content of edema fluid

  • Mucopolysacharides -Hyalinorunic acid
  • Albumin


  • Albumin leak into interstitial and extra cellular space  due to capillary dysfunction.
  • Reduced lymph clearance – probably due to poor lymphatic tone  .

Why hypothyroid  edema  does not pit on pressure ?

For pitting to occur tissue should be compressed and retain the elasticity .This means  the fluid can escape into the cell when mechanically compressed and comes back when the  elasticity of skin  brings  it back to its original status. For this to occur the skin and subcutaneous matrix should be normal in texture.

In cardiac failure and renal  failure   edema is   primarily due to  altered hydrostatic forces and skin  is intrinsically normal .So  some amount of pitting  is retained . In hypothyroidsim and lymphedema  where there is  an intrinsic  pathology  of the  skin   pitting  is rare.

Why constriction and  cardiac tamponade are rare with hypothyroid pericardial effusion ?

Like the generalised slow response of hypothyroid individuals  the effusion is  also very slow forming and is rarely large so tamponade is rare .

The hypothyroid infiltrates which  collects within  the pericardial space it rarely infilitrates  the fibrinous pericardium (The thick outer shell ) .Unless fibrinous pericardium is inflamed or infiltrated constriction is exceedingly rare .Simple epicardial infiltration may cause some restrictive  physiology but not constriction .


Lancet. 1975 Mar 8;1(7906):564-6.Effusions into body cavities in hypothyroidism.  http://www.ncbi.nlm.nih.gov/pubmed/47029

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Intra cardiac foreign bodies are frequent occurrences  in clinical cardiology practice. The common ones  are intra chamber clots , vegetations  and rarely tumors. Some of these masses are very mobile are  precariously attached to the cardiac strutures  . It becomes a cardiac emergency as a major embolic event  is imminent .

While surgery  remains the  mainstay approach in such situations ,   now it seems possible to trap these mobile  masses with help of catheter and retrieval devices   safely.

The only  issue is , while retrieving  these masses   it  should not be let into the circulation and result in  embolisation  . For this we can develop a   porous net (Fishing net like ) that can be  blown in the distal  chamber or Aorta .

Devices can be structured in way  that a single catheter can be used with different  ports  to capture and  filter  and retrieve  the mass . (  vacuum  enabled suction catheters can be additional option  ) .The whole procedure can  be  accomplished with fluroscoy and fluroscopic guidance . Intra cardiac echocardiography might also contribute .

This innovation will    be  a great  value addition  to the  interventional  cardiology   armamentarium   ,would be   be appreciated by clinical  cardiologists . We in our tertiary  teaching hospital   have  felt  the need for a such a device quiet often  .Currently many patients land up  in  surgical tables  for the sole purpose of removing these clots and vegetations  .Similarly left atrial clots becomes  a contraindication for percutaneous   mitral  commissurotomy(PTMC)   . Such capture devices can be very useful.

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Learning and sharing of  knowledge is one of essential qualities of  that make the man kind unique.

But not everyone is ready to do that . A cardiologist from Paraguay shows the way .  . .

Probably a model web site for all academicians .It exemplifies ,  how a medical web site is  to be created and presented .This one is for learning echocardiography .

Though the author calls  , it as  basics it has fairly advanced contents , so it should be useful at levels .

With  due  courtesy  to   Dr  Derliz Mereles I am linking his web site  in my blog .


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Here is  the two versions  of  a  discussion  by a  cardiologist  to his  patient , on the day of his discharge  from a  state of the art trans national  heart health  service in southern  India.

An alluring cardiologist .

  • I have implanted  the  world’s  best drug eluting stent to your block .
  • The block has  vanished without a trace  .
  • You will be free from pain  here after .
  • You can enjoy a new lease of life .
  • You can go for holidays , you can cherish  ,   you can do whatever you want  .
  • Forget about complications  it is negligible .
  • But please take all the drugs regularly .

A Bitter cardiologist

  • This stent is a temporary solution to your problem .
  • Do not think you are cured of your illness .
  • Atherosclerosis can never been cured completely.
  • You have to be careful .
  • Avoid very strenuous activity .
  • It can re occlude at any time even if you skip  the tablets for  few days .
  • After all, it takes only  6 minutes to form a blood clot  .
  • You may  require CABG in  future  as most stents  get blocked  by  5 -10 years .
  • Further , the drug you are taking may develop resistance and you may  recur the same old problem .

Final message

So , the  art of  medicine  is to hide some of  the  unpleasant outcomes from the patient and project only positive aspects to our patients *

* This is often a controversial  issue . Scientifically advanced health care system  do not agree with this . But  I would believe , that is one of the major reasons   they are suffering from huge health care crisis !

I do not agree with  the concept  of empowering  patients with  bitter truths   . This  need not be  vigorously  practiced.   Disclosure of all potential complication  to our patients  , by itself a trigger  such  events  by meager anxiety .

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Which is the “Numero uno”  cause  for  acute stent thrombosis  in real world  Cath labs ?

  1. Hypersensitivity  reaction  to metals
  2. Poor deployment of stent
  3. Inadequate  Anti-platelet  regimen
  4. Drug eluting stent

Answer :  2 .(Indisputably  correct )

It is estimated  at-least 4 out of 10 stents  we implant  is  sub-optimally  deployed .Only a fraction of them go for complication .Coronary endothelium silently  tolerates our  aggression .

How to  prevent this ?

  • Meticulous pre procedure analysis of lesion
  • Preparing the lesion if toughness is anticipated
  • Personal  mind application in stent size  selection
  • A slow , steady  non aggressive PCI
  • Liberal  pre and post dilatations
  • Judious use of IVUS and OCT ( Mind  you a  prolonged  IVUS procedure  can occasionally convert a good deployment into bad one !)
  • A  good quality anti-platelet regimen.

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What are the   structures that  can get punctured and result in cardiac tamponade during PTMC ?

  1. Aorta
  2. LA  roof ( Many parts of LA are extra pericardial . Still ,  if you are good enough !  you can enter the pericardium )
  3. LA free wall
  4. IAS  /pericardial space Interface (Stitch effect )
  5. LV free wall
  6. Pulmonary vein
  7. RA free wall

Traditionally  cardiologist’s major  fear is  confined to  accidental  aortic puncture . With growing  experience  &   inexperience   we  now know   PTMC  is vested with other  risks  for cardiac puncture other than Aorta .

  • LA roof  puncture can occur if the septal puncture is high  and  the movement of sheath over IAS plane is not smooth . ( Animated  to and fro movement across IAS is largely unnecessary !)
  • LA free wall when the guidewire is manipulated.
  • The  right atrial side of IAS  often  over shoots the LA side of IAS . This brings a unique situation where  Brocken-burrogh needle may  enter the LA through pericardial space .One may not be aware of this until you pull back the needle when pericardial
  • LV free wall  rupture is  rare with Inoue technique .Over the wire  balloon technique with a guide wire tip can cause LV injury
  • Accidental  pulmonary vein inflation with the balloon is  always  possible. One has to verify the balloon position in lateral view.
  • RA free wall should not happen  today . Still  a distorted RA anatomy due to associated  tricuspid regurgitation or stenosis . This can bring a surprise element to our understanding of IAS septal alignment .



Joseph G, Chandy ST, Krishnaswami S, et al. Mechanisms of cardiac perforation leading to tamponade in balloon mitral valvuloplasty.
Cathet Cardiovasc Diagn 1997;42:138–46.

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