Archive for March, 2011

When LV fails the  lung gets congested and flooded with blood . Similarly when coronary sinus  ,  the major draining outlet of coronary  circulation resists  the incoming blood  flow . . .  myocardium  will  get congested !

This is  the concept  of  retrograde perfusion  in treating refractory CAD with angina . It is a double-edged concept. If the coronary  sinus  pressure is  excessive it may interrupt even  the normal  flow .It should be optimal so that it prolongs coronary micro-circulation time without compromising ante-grade flow. .

Picture courtesy : http://www.dartmouth.edu

Clinical example

We know cardiac failure patients rarely complain of  angina .

Why ? . . The myocardial congestion due to coronary sinus pressure is the most likely explanation.This goes well with the back flow concept in treating refractory angina.

While surgeons tried to link artery to vein  , Interventional cardiologists were smart enough to occlude the coronary sinus partially , that will result in stasis of blood in coronary micro-circulation and hence facilitates oxygen extraction .

Final message

God is a master craftsman. Do not think  there is only  one access to coronary micro circulation.Apart form LCA and RCA there is  a vast network of coronary  veins  traversing  the delicate surfaces and grooves of the heart .

Remember ,they also reach the same micro vascular  bed but in a different direction !

If we  can exploit  them  for myocardial arterial  perfusion we have a real breakthrough   in our hands. . After all , why should we take a vein  from a far way from legs (saphenous veins )  for by-pass surgery  when venous channels are  simply there beside  every branch of a  coronary  artery !

Let us be quixotic , we shall attempt to   congest the myocardium with blood for refractory angina by whatever means ! Mean while let us also remember  what happened to  TMR (Trans myocardial laser  revascularisation ) the biggest technology failure in cardiology in recent times !


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This term is quiet often used in the  main stream cardiology journals  ,  in work places , conferences  , hospitals and even among lay persons . No body bothers to define this terminology.   What exactly this term means ?

It  may  not mean anything  . . . to most  of us  even  as the percentage of inappropriate angioplasty is steadily  increasing over the years .

Picture courtesey : Jupeter Images

What does the term  Inappropriate angioplasty  mean ?

(Choose the correct answer  . . . one or more  may be  true )

A.It simply  means doing  unnecessary angioplasties and has no major implication  to  any one.

B.A form of medical ignorance  or  an unethical act and should be strongly condemned.

C. An acceptable cardiology practice ,  need not be discouraged , as  it improves the quality of life of physicians !

D. A  sure act  of  “error by  commission”   that amounts to   medical negligence .

E.It is a decent term for a major  guideline violation

E. It can be  termed  as medical malpractice as it amounts to harming the patient with or without intention.

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Heart has three layers

  • Epicardium
  • Myocardium
  • Endocardium
  • Epicardium is same as visceral pericardium . If pericardial inflammation dissusely occurs ,  it is bound to injure  the epicardium and subepicardium .

    Does  the  troponins  located deep inside the  myocardium  ?

No .It  can  even be present just few microns below the visceral pericardium  . Hence  severe forms of pericarditis can elevate the troponin levels without any issues .

Is troponin  release related to ST elevation ?

 Ideally  most forms of  pericarditis can be termed as epicarditis. The mechanism of ST elvation in pericarditis is actually a sign of  epicardial injury.In fact ,  there is no easy way to  differentiate  a  slice of epicardial infarct from an   inflammatory pericarditis accurately .

Is there any form of pericarditis which invlove only parietal pericardium ?

We do not know as yet ,  about  existance of such  an entity. It is distinctly possible. However , if present it is unlikely to result in significant  ST elevation in ECG.

In pericarditis ,  troponin release is due to inflammation  or necrosis  ?

Both are possible .Even transient wall motion defects are reported in isolated pericarditis.

What is myopericarditis ?

It is  a general term used  to indicate the above situation . In practical terms Pericarditis + Troponin positivity can be termed as myopericardits. It is well known pericardits can extend to endo- myocardium but it is rare other way  around( ie endocarditis extending to pericardium )

What is pancarditis ?

It is the carditis  involving all three layers of heart ,Cassically occura in rheumatic fever. Fulminant carditis is known to raise the troponin to significant levels.

Does troponin elevation  in pericarditis  occur in all  ?

We are yet to collect adequate data about this .  Diffuse , extensive pericarditis ,gross ST elevation ,  and associated pericardial effusion  correlate with troponin.

Crazy questions in pericardiology

What is the pericardial blood supply ? Is there  an entity called ischemic pericarditis ?

Final message

Do not ever underestimate the  importance of  pericardium  whenever you encounter unexplained ST elevation in ECG.


Here is an article which has   meticulously studied this issue

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For  a police officer who visits a crime site  every one looks like   a culprit. For a cardiologist  sitting in coronary  care unit  all chest pain  will have to look like  an infarct  !  Then only he is a cardiologist !

A rare , but costly mistake occasionally  happens . When a  patient with severe chest pain in the  retro sternal region with ST elevation in ECG , enters the ER  there is little  reason to suspect any condition other than STEMI !

This is how medical  errors takes place

Medicine is an art , we can not take it as granted .Acute MI can present with normal ECG and a dramatic ST elevation need not be MI

Here  was  a patient who presented with this ECG and one our fellows correctly diagnosed the condition .

Most  physicians would have thromolysed this patient or  might have wheeled into cath lab.  We have such events reported from primary  PCI registry .

Key differentiating points

  • Diffuse ST elevation not confining to a arterial territory
  • Absence of reciprocal changes
  • ST  segment with concavity upwards.
  • Echocardiogram and enzymes will be useful

iFAQs  in pericarditis

What is the mechanism of ST elevation  pericarditis ?

It is actually a zone of epicardial or Sub epicardial injury.

What will be the ECG finding if STEMI is associated with fibrinous pericarditis ?

Double dose of ST elevation .Mimics  a re infarction.

What are the dangers of thrombolysing a patient with diffuse pericarditis ?

It can bleed into pericardial  space

What happens

What will be the ECG finding in localised pericarditis ?

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LXR are a unique group of nuclear receptor proteins located in liver as well many body tissues where lipid metabolism is active. They are first identified in liver with apparently no ligands ,  they are  hence referred to as  X (Also called orphan receptors ) .Later  these receptors can be termed as a target receptors for cholesterol metabolites like oxysterols .


How this nuclear receptors modify  the subsequent events could ultimately determine the toxic effects of cholesterol in human body.

An update in NEJM appeared in 2007

The the science of lipidology  is  confronted by  with  suspicious  ,  false targets .We are  biochemically still pitch blind  beyond a point . . . after cholesterol enters  the cell .

We have been targeting cholesterol synthesis by blocking HMGCOA.

Statins though claimed to be the God sent molecule , genuine researchers would agree statins  have a   huge  limitation  and it  is a  hyped up drug in controlling atherosclerosis. In fact ,  it is  believed  (In private ) nearly 50% of people who take statin  atherosclerosis goes  unabated.

Can we modify how  LDL  cholesterol is going to be utilised inside the cell ?

LXR family of proteins along with  RXR are expected to  break  the  barrier.In knock out mice models  LXR agonists are  able to control  and prevent LDL propagation within vascular cells .

The research is ongoing. Let us believe  the right target  has been identified . Nothing is guaranteed as of now . . . but out journey should continue .



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ASD device closure as a modality is constantly improving  . . . but  the consensus is  , it is  yet to catch up with  of  good old surgical  outcome . The key to success is not only in the device but hugely dependent on the technique and pre-procedure evaluation  .In fact , the pre procedure TEE imaging technique  is as important as the procedure itself.

There are lots of discussion about this particular issue. TEE is mandatory we know  but now we realise it is  still better to have a  Real time 3dimensional  (RT3D ) TEE . Rim  size  and ASD  morphology estimation is  the primary aim.

There are  at least 6 named rims for ASD. For a circular  orifice  it  may not be logical to have a fixed number of  6  rims . Ideally the entire circumference must have a rim .( This happens in  central defects )In many,  the complex anatomy of IAS does not allow this. So we are compelled to fix the number of rims to six.

  1. Aortic (Superoanterior),
  2. Mitral (AV valve/ Inferoaterior)
  3. SVC  (Superoposterior),
  4. IVC  (Inferoposterior),
  5. Posterior ( Atrial free wall ).
  6. Coronary sinus rim

One can realise how important these rims are , as  they are the   foundation tissues on which the device is going to be seated for the rest of the patients life.

When do you call a rim is adequate sized ?

5mm is  considered suffice. But it varies depending upon the device and expertise.

Can we deploy an ASD device  in patients   with deficient rims?

Logically the answer is expected  is   “No” but  , many have liberalized the criteria now , after realizing   one may  not have 5mm rim in all six sites in a given patient. If you follow this criteria strictly   you can’t do more than few devices a year !

What is the resolution power of TEE can it miss a 3mm rim  ?

TEE has a good resolution it should pickup any thing equal to 2mm or more.

Which is most important rim and which is the least important rim ?

What are the potential complications that can arise if ASD device is deployed with a critically low rim ?

Having discussed  that every rim is equally vital  ,  we  need to answer this sort of questions  often .  I am waiting to get the  practical tips for the above issue from  my experienced colleagues .  I shall post it soon .

It is sometimes assumed Aortic rim may not be that important .Here is a   good discussion  for  ASD closure with deficient aortic rim from Saudi Arabia  . http://www.rmsolutions.net/rmfiles/SHA21/028002.pdf

Meanwhile let us learn . . .

How to perform the “all important” pre- procedure TEE ?

The following article which also  includes video clippings will be immensely useful for all those enthusiastic cardiologists.Thanks to JACC  for making this link free .

Three cheers to AMRITA team from India


A stylish article on the topic

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Action to  control cardiovascular risks in diabetes (ACCORD ) : The accord long-term follow-up results are just out  in NEJM  March 2011   http://www.nejm.org/doi/full/10.1056/NEJMoa1001286

The ACCORD study which created a huge buzz in 2008 when it was prematurely terminated  for fear of  bad outcome ,  with aggressive blood sugar lowering (Hb A1 c <6 %)  .The  negative  trend was confirmed in the aggressive* group even after switching to non aggressive group  at further 1.7 years follow-up  till late 2009.

*Intensive /Aggressive is used interchangeably in this article .

Why should aggressive glucose lowering be harmful ?

This  question is  struggling to get  a  logical answer for over 5 decades. To answer this question,  it  need to realised  our  fundamental understanding of  diabetes  itself  is  flawed ,   as  we have equated it with high blood sugar.

                                                    A  persistent state of  high blood sugar   can never be  used  as a  synonym for diabetes melites.  There is much . . . much  more , to it  !    Patients ,  lay persons and pharma industry  may  think  like  that   but  it is unfortunate many  physicians  have the same thinking   pattern .  The fault lies there .

Diabetes is a systemic metabolic disorder  apparently due to lack of insulin( or relative excess of it ! as in insulin resistance ) in which hyperglycemia is one of  grossly visible abnormality.

It is estimated there can be at least 100 invisible or less visible  biochemical abnormality in every diabetic individual.In fact , DM has more profound effect on lipid metabolism  than carbohydrate metabolism. Almost every microproteins   in our body  gets glycated . That  can be either be  reversible or irreversible .We know how difficult it to reverse diabetic nephropathy or retinopathy

If we realise the above reality there is absolutely no surprise why lowering blood sugar alone  does not reverse diabetic complications !

The second major issue is the modalities we  use  to target the  blood sugar 

Right from the days of early sulphonyl ureas  and biguanides ( of  Tolbutmide and Phenphormin etc ) one thing was very clear (or unclear  ! ) vigorous control of blood sugar has always been a doubtful intervention in controlling  diabetic complications .

                                                If  high blood sugar causes  excess mortality,   why  bringing it to  normal levels  does not reduce long-term mortality convincingly  ?

Is the Madness  lie in the methods ?

It seems so.  ACCORD study has strong reasons to suggest the  worse outcome in aggressive management is due to multiple , drugs used in a random fashion.

Then there  is always this  question  . . .How good is HB A1c  to assess the adequacy of DM control.  ? Biochemically this molecule still has lots of issues regarding its reproducibility.

Individuals who control blood sugar  by  natural means and by minimal drugs seem to do well. Early diabetics and  pre diabetics  should be our targets.

One should also remember the drugs we have today to control DM  have yet to prove the long-term safety records (Say for a span of 30-40 years)

Modern medicine  usually does not bother about the future  . . . it simply shrugs of the issue  with a caution statement . . . that the ” Drugs  you take  are well-tested and  thought to be  safe and useful with the current level of research !”

What is aggression in DM management ?

No one has defined it so far. But the any of the following may fit in with the  definition

  • Any DM patients prescribed more than  two drugs and Insulin
  • Premature start of Insulin
  • Lack of diet and exercise management  and  trying to substitute them with  incremental drugs and insulin 
  • Finally ,any patient who is always tensed up about his HBA1C and switches his physician  frequently  end up in  early complication   than the ones who follow simple non pharmacological approach.


How good is the idea  ,   to define aggressive thrapy  with reference to HBA1  levels ?

ACCORD defines aggressive approach  with HBA1C   as less than 6 %  and   Non aggressive as  7-8%  ( or  is it 6-7 %)

Not withstanding the limitations of HBA1C , there can be many patients who will require multiple drugs and insulin to maintain the HBA1C  even  at  7-8 %

How do yo label  them ?  Aggression by  number of  drug used   . . .  but still  considered  Non aggresive control  by HBA1c  criteria .

If ACCORD study fixes the indiscriminate use of drugs as a cause for bad outcome ,  then the very definition of aggressive approach need to be changed !

 Final message

ACCORD says it all . Never be aggressive on diabetic patients. The aggression we show with drugs can be more dangerous than the deadly diabetes itself.

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