Feeds:
Posts
Comments

Archive for the ‘Uncategorized’ Category

Cardiology  is  among the top medical  specialty  in the current era. It deserves this  special status as it is probably  the  a specialty  which  is based on maximum  scientific evidence and  involves ,   the  most advanced diagnostic and treatment  modalities.

As on today ,  a cardiologist  can deliver a stent  anywhere along the coronary tree and even  implant  a valve percutaneously . A surgeon can put multiple grafts in a beating heart  with a patient totally awake !

A  person can live with an  artificial heart for months and a cadaver  heart can give  fresh lease of   life to a terminal heart failure patient .

Why such a glorious filed of cardiology  should often   evoke a pessimistic reaction  in the minds of  public and media ?

This is because  for a   simple reason , in the name of technology , we tend to  indulge in scientific excesses.

This article in Circulation is not a  surprise then . . . Click on the link, Thanks to AHA this  comes free of cost !

For pdf article click on  the image

Note : Non adherence , inappropriate therapy,  Class 2b  indications ,  are  simply semantics in stage  play !

Actually these terminologies are synonymous with

  • Guideline violations,
  • Unscientific ,
  • Empirical.
  • Unethical or  even quackery

Read Full Post »

We generally  believe  drugs  and devices are prescribed  by  physicians with strong scientific basis .Unfortunately  it is  not  true  in many instances.  A drug which is approved for one disease is assumed to be useful in a similar disease  (But not tested in  clinical trials ) and it becomes  an unapproved  indication .This is often termed as off label use (A decent terminology for unscientific usage !) .But ,there are pros and cons to this type of physician behavior .

Pros

The best example  is  the role of sildanafil in pulmonary arterial  hypertension(PAH)  . A drug which was introduced for erectile dysfunction , was found to very useful in regressing pulmonary arteriolar pressure  (Mistaking pulmonary arteriole for penile vasculature  !?) .  A new therapeutic concept was born  for a  hither to difficult problem of PAH. This  successful  discovery  was  attributed   to off label  usage  of a drug .

Cons

But this is a rare  success story of off label therapy.  In real world , we  tend  to  overuse this in many situations and harm is anticipated.

Drug eluting  stents was used extensively in off  label situation ( Acute MI in a thrombotic milieu, very small vessels , in close proximity  to bare metal etc all these are non label or off label  use of coronary stents   which  resulted in many deaths )

Who gave the freedom and liberty for the physicians to use a drug or device off label ?

No body gave  it , we assumed ,  we have it .

When somebody uses a drug for an unapproved indication is it not unscientific  and guideline violation ?

It is a violation , but we can afford to do it because every body does so !

Is there any scientific  body to sanction and desanction off label  usage ?

Unfortunately  not !

So what  is the solution ?

Self regulation  . . . Can it  be  a  fool-proof method  ?

or  Is it foolish  to expect it so  in this   era of commerce  ?

Related video in youtube hosted by me.

http://www.youtube.com/watch?v=d2WfLrTiUks

Related article

Guideline violation in cardiology practice

Read Full Post »

The same channels , that  create the  deadly prolonged  QT interval  by  delaying the  repolarisation  in the heart  is  responsible in the for the deafness  as it interfere with inner ear

Mechanotransduction of sound into neural signals .

For proper auditory function  , the cochlear hair cells   needs  a continuous flow of endolymph which  maintain a voltage gradient for  nerve  signal  transmission  .The lymph secretion is  is regulated by potassium channels  KCNQ1 and KCNE1 . Mutations of this gene impairs  the K + content of the endolymph. It results in  a compromised  endocochlear potential (Difference between peri lymph and endolymph potenial )  .This result in irreversible deafness .

Link to   a good   illustration from Medical physiology

Read Full Post »

Cannon Sound

A loud first heart sound (S 1)   which is  heard intermittently in patients with complete heart block (CHB)  is  often referred to as  cannon sound .

What is the mechanism of loud S1 in CHB ?

We know , the intensity of S 1 is  mainly determined by the  relative position of mitral leaflet (To be precise, the  anterior mitral leaflet(AML) )   at the onset of systole.  We also know the  PR interval  has an intricate relationship to  mitral leaflet  position .

The shorter it is ,  wider the leaflet separation  and a longer PR interval makes a mitral leaflet assume a almost closed position   by the time the ventricle contracts.this happens because  a long drawn PR interval fills the ventricle more completely and LVEDV  reaches the maximal levels and LV blood column lifts up the mitral leaflets , and hence the LV  contraction  which follows does not close it with a  bang. In a short PR interval the opposite happens and hence a loud S1 .

In CHB we have variety of PR intervals ranging between  very short to long   ( falling just before the qrs complex) It is not difficult to understand this , as P waves are totally dissociated with the QRS complex  in CHB.In fact p waves have a liberty to fall any where in the ECG tracing , some call this as marching through the qrs complex !.

Hence typically the S1 is variable in intensity , varying between loud to soft.  When  P wave falls just behind a QRS complex , it generates a very  loud S 1  that is called cannon sound .This happens intermittently.

Cannon wave

This is entirely different phenomenon except that it shares the word cannon . Cannon a wave is  a visual finding on the jugular venous pulse.(JVP) .It is a systolic event . It is also seen in CHB as like a cannon sound

This is a giant a wave  in  JVP  when the right atrium contracts against a closed tricuspid valve. In physiological situations atrium contracts with an open AV valves , so that ventricle gets  filled . So atrial contraction  does not does not cause any reflux of blood back into vena cava.

But, when the atrium  contracts and  finds , the AV valve closed  there is no other option   for the incoming blood  to reflux  back into  the neck veins. This is seen as giant a waves called as cannon ” a “waves

With reference to ECG  location ,  this cannon”  a” wave occurs   whenever p wave falls within the ventricular systole ie  the QT interval .The cannon waves also occur intermittently like the  cannon sounds.

What is the  peculiar relationship between cannon a wave and   sound ?

In fact , it is  a non- relationship.  Though  , both the sound and wave   can occur in a given  patient with CHB ,   they can not occur simultaneously .This is because ,  for cannon sounds   to occur  the  P  wave has to fall before  QRS  and for cannon waves to occur the  p   waves must fall after QRS  ie with QT interval .

Clinical significance  of  cannon wave

Complete heart block is the most common situation for cannon waves to occur.

Ironically ,the VVI pacemaker which is used  to treat CHB does not prevent the cannon waves , and atrial contractions continue to occur at random , causing various degrees of intermittent venous reflux into the veins .This may produce, worrisome venous palpitation in some (Usually settles down after few weeks !)

Some attribute , the so called pacemaker syndrome ie giddiness, dizziness to this abnormal venous waves triggering the carotid baroreceptors (Venous -artery spillover )

Will DDD pacemakers  eliminate venous cannon waves ?

We hoped so , it does in fact . But,  it really happens only if the A sense V pace mode . A pace V pace mode with programmed PR interval is not a realiable way to produce AV synchrony. It is  common ,  many of the DDD pacemakers fall back to VVI mode either intentionally or by mode switching  for various reasons.

//

Read Full Post »

There are many  cardiology journals we read , trust , and celebrate  . . .

Many of us are not aware of   few other excellent journals

This is one is different

It is  from  Scandinavia &  deserves a special status.

Read Full Post »

It is said every clinical diagnosis needs to be substantiated with  documented objective  evidence .

Probably,  the commonest cardiac emergency , that can be  diagnosed purely by history is UA.

Yes , unstable angina is a symptom not a  disease entity !

By definition UA is

  • Any  new onset angina  of severe grade
  • Progressive crescendo angina
  • Angina with radiation to new site
  • Angina not controlled by nitroglycerine
  • Any angina after a PCI /CABG

If you read the definition again, you will realise ECG or enzymes never come into the  diagnostic picture .UA can be diagnosed even before one has a look at  the ECG ! So, it is too obvious one can diagnose UA irrespective of whatever is recorded in the ECG. Normal ECG is one such possibility.

When a patient is having severe  compromise  in the  blood supply to his / her heart  , how  on earth ,  it  is possible to have a normal ECG ?

It only tells us,  ECG is not a fool proof method to exclude ongoing ischemia . When we know , ECG can miss even a STEMI  it is not a big deal it misses a UA.

Apart from  the electrical blind spots of conventional 12 lead ECG, following are the other  explanations offered for a normal ECG in UA.We know UA occurs with ST depression(Classical ) , T inversion,  rarely ST eelvation

So UA can occur with

  • Pseudonormalised t waves
  • Pseudo normalised ST depression
  • Cancellation effect of two  opposing  subendocadrial ST segment vectors ( As in multiple active plaques PDA   and LAD lesion )
  • Even Ischemic cascade

Final message

Even though  UA  CAN  occur with normal ECG  , we are uncomfortable to   diagnose  UA without   documenting ECG changes . We should realise this fact , as missing a diagnosis of UA , just beause the ECG is normal  could have very costly consequence !

Read Full Post »

STEMI is the commonest cardiac emergency . Many believe , we  are close to  conquering  it .  It is hardly the truth .

  • The  mortality is  up to  30 % out of hospital and another 6-8  % within CCU  and another 2 %   at  30 days due to recurrent ACS   .This  is followed by an   annual attrition rate OF 25  due to progressive LV failure  .
  • The commonest mode of death is electrical,  ie primary VF.
  • Mechanical deaths are also equally important. Free wall rupture carries 100% mortality . Ischemic MR, Ventricular  septal rupture (VSR ) may also result in deaths.

Here is a case history and ECG of a  patient with STEMI .

After thrombolysis , the paradox happened . ST elevation  increased by 4mm and soon the patient became restless with worsening pain and became silent instantaneously ,  with monitor showing EMD and asystole .A diagnosis of free wall rupture was made.

What we used refer  in our CCU (Madras medical college Chennai .One of the oldest CCU in  South Asia )

as   “Action pontentialisation”  of surface ECG . This ECG finding has  great  clinical significance .

Here is a zoomed up view of a qrs complex of  the patient , which is very

closely resembles an action potential

Picture courtesey  http://ocw.tufts.edu/Content/50/lecturenotes/634488/634591

Pathological basis of  “Action potenial”  Like ECG

  • When the ST elevation is huge and wide it mimics  an action potential .
  • Myocyte action potentials are normally recorded epicardially in physiology lab where a  micro electrode with glass pipettes directly enter the myocyte.
  • A giant ST elevation and a sustained dome indicate , the quantum of  electrical injury is  very large and the  ECG electrodes is picking up the myocyte electrical events like that of a intra cellular electrode.
  • It is to be recognised  ,  ST elevation in chest leads is substantially taller than limb leads   because the exploring electrode  is located just above the myocardium . But,    when a  huge  ST elevation  is recorded  over a limb lead (as in this patient )  one can imagine ,   how intense the electrical  charge  of  the myocardium  should  have been  !

This heavy downpour of electrical energy that  emanate from the myocardium   means two things

  • The area of infarct is very substantial
  • The tissue in question is  very unstable .

Clinical correlates of  action potential ECG

  1. Damage is transmural , the   infarcted area is soft, friable and often hemorrhagic .
  2. The pericardium is also  likely to get involved in the injury process .
  3. The myocardium is  rupture prone or already torn .
  4. Even minor hemodynamic stress can be fatal in these patients
  5. An episode of vomiting, a fall in blood pressure,   an episode of  LVF or a short run of VT is suffice  to result in a fatality.

The death happens by a sudden rupture ,  EMD and asystole .

Can a life be saved  by the much fancied Emergency PCI  ?

Not really. The PCI  can not reverse the myocardial damage ,  so it’s role is little . But , any way it should be done and  .  .  . it  will  be done  in most institutions to give the benefit of doubt (Of course , with  a definite the risk of doubting  !)

What is the risk  of  PCI in these situation ?

The infarct related artery * if opened up can convert a bland infarct into a  “angry red”  hemorrhagic  infarct .This   is as good as  giving  the patient ,  a  farewell  party for his journey to heaven !

Note : Primary PCI  definitely  saves life in STMI . The  * is applicable only in persistent ST elevation , late after an acute MI.

How could  have the above death prevented ?

As one of the comments to this article  suggested, we need to have methods to identify impending rupture early and accurately .This should  followed by a prophylactic  surgical intervention (Reinforcing the friable myocardium – with a patch or mesh  )  .This is again not  a easy decision to make .

Final message

When the ECG  assumes  a shape of an  action potential ,  it is often a sign of  imminent  death  . Even though it may sound a pessimistic  view  it is often the truth  . Of course , an  emrgency PCI or  CABG  are  the only options available , we have  to be remember the above truth  ,   as we   play  those sophisticated  games  within their coronary arteries.

Read Full Post »

As the name suggests   dilated cardiomyopathy  would imply  cardiac chambers will dilate , at least some time in the course of the disease .It can be minimal, mild or massive. A new entity called  non dilated cardiomyopathy is also gaining wider acceptance . (That will be dealt seperately )

Logic would suggest , the first chamber to dilate in DCM  should be the left ventricle because it is  facing the direct load of systemic blood. But we also know , whenever  LV is stressed , left atrium comes to it’s assistance .

Left atrium does this    by total self sacrifice ( by all  means!)  increases  it’s  force of contraction, elevating it’s  mean pressure or even increasing it’s rate (AF) .

Like most  other critical questions in cardiology  ,  the factors that determine LV dilatation in DCM ,  is  also poorly understood !

  1. Is it the after load ?
  2. Is it the  muscle mass ? or it’s turgid  or flabbiness ?
  3. Is it the interstitial integrity?
  4. Is it the blood volume ?(LVEDV ,  LV residual volume )

When the issue is complex , it is  usual  to  make the   the unknown  genetic defects  ,  the scapegoat !

As of now the most important determinant of LV dilatation  could be  the behavior of the desmins, the gap junctions and myosins the titins etc

If  the LV of a DCM patient  refuses  or  resists  dilatation what  might happen ? Is it good or bad for the patient ?

Here is a catch .  A  LV  that does not dilate  obviously should be  be good for the patient  is in’t ? Medicine is not that simple.

When   LV  fails to  dilate  it means it has become  too  stiff and rigid    and pass on the  burden to  to LA which  faces the music. And in the process it dilates.This is the reason , we  observe  diastolic dysfunction in vast number of DCM patients.( Currently it is estimated > 75% DCM will have significant diastolic dysfunction )

So , now we can imagine how complex the sequence of hemodynamic stress in DCM that determine the chamber enlargement.( RA, RV  dimension in DCM is a separate issue !)

So now answer this question :  Which chamber dilates first in DCM ?

  1. Left ventricle
  2. Left Atrium
  3. Any of the above
  4. Both of the above dilate simultaneously

The answer must be 3 .

Why  recognising this sequence of  chamber enlargement  in DCM   is important ?

  • It gives us an opportunity to assess the dominant mechanism of LV dysfunction.There are reports , where some  DCMs  have more diastolic dysfunction than systolic dysfunction  .This will have important therapeutic implication.Further , many of the infiltrative   disorders of LV can have features of both DCM & RCM .
  • When a RCM begins to dilate it is usually  a harbinger of terminal heart failure. But,  it need not be always true .  A small restrictive LV  , when  dilates ,   may acquire a  slightly improved diastolic properties , as the  LV becomes more placid . And ,  if it happens the LA size may regress.
  • The role of LV restriction devices like, Acron mesh, Dor procedure, plication  in refractory  DCM is not well defined. All these   modalities actually  adds  a small dose of diastolic dysfunction in these patients who have grossly dilated ventricles. This fact is  very important  , as presence of any preexisting  significant diastolic dysfunction in DCM makes  the role of LV restrictive devices and surgery a big question mark !

Read Full Post »

STEMI is the major cardiac emergency .The acute mortality is about 20% (Both prehospital and in CCU )  STEMI occurs whenever a coronary artery is occluded  suddenly in toto .We traditionally believe that STEMI occurs only in the major  epicardial vessels. (LAD/LCX/RCA .)

The total length of   coronary tree is much  longer than the length of the three vessels put together.The diagonals , the ramus, the OMs ,the septals  run for varied  distances. The caliber of these vessels can be quite large.It is estimated the diameter  of   first diagonal ,   the first OM  or the   ramus can be as big as LAD proper in 30% of CAD population . Law of statistics tells us sudden occlusion can occur any where in the coronary tree in  ACS prone patients.

What is the real incidence of side branch STEMI ?

The  dogmatic answer is   ” We do not know”

Will we ever know ?

How will a  Diagonal / OM /Ramus   or PDA   STEMI  behave ?

It is surprising this question is not addressed by us  for  so long . Some may even question  the existence of  such an entity(Side branch STEMI ). This is most likely ,  reflect our ignorance on the issue . We know  bifurcation lesions at  the   side branch  origin is very common . Further , thrombus can migrate from a main stem to a side  branch  immediately after formation .

Clinical presentation of side branch STEMI

  • Acute presentation is identical  to  that of a major main branch STEMI . The  pain  can be severe , the primary arrhythmic threat is real . Ischemic VF , once initiated does not  modify it’s  character  according to the  quantum of insult .
  • ECG is the major variable.  You ,  don’t expect gross , ST elevation in many leads as one would see in LAD MI /RCA MI.
  • The  age old teaching that  an ECG can be entirely normal in acute MI ,  could actually imply the side branch STEMIs . When a small D2 or D3  gets occluded the ECG may not pick up the ST shifts .
  • The commonest site of atherosclerosis apart from proximal LAD is the bifurcation of PDA in RCA.  STEMI due to PDA occlusion is  the most  difficult thing to recognise. Many of them have very subtle ECG and clinical findings.
  • There has been reports of acute complete heart blocks with isolated AV nodal infarcts. Here sudden cardiac deaths are reported

It is very much possible ,  many of the  side branch  MIs   may be wrongly diagnosed as unstable angina by us , for the simple reason the myocardial necrosis is not large enough to produce ST elevation .They may actually respond to thrombolysis ,  as there is total occlusion in the coronary artery.  Since, they do not manifest ST elevation there is a lost opportunity here  . This ,   probably  is the population in TIMI 3B  trial that showed some ( statistically   insignificant ) benefit for   thrombolysis in NSTEMI.

Is primary PCI justified in side branch STEMI ?

May not be . The chances of side branch STEMI   to result in LV dysfunction and progressive adverse remodeling is considerably less . The hazards of primary PCI for exceeds the risks of  MI  due to a   septal  or diagonal branch lesion .

Final message

  • STEMI due to   branch coronary artery  occlusion is a less recognised entity among ACS.
  • Cardiologists ,  need to  look into this  issue with little more seriousness as it could represent a new  intermediate risk  category   among the much  flaunted  classification  of  acute coronary syndrome. Triaging and risk stratification of  ACS  needs  a revamp.
  • It is possible  many of the UA  patients  ,  may in fact represent total occlusion of side branches.
  • There is a  definite  case  for showing less aggression in these patient  subsets  ,  provided we are sure  about  the location of lesion.

Counter point

* Identifying  a side branch STEMI with confidence  may be very difficult at bed side in an emergency . Implication of wrongly  calling a STEMI  as benign  can be  dangerous . So it will be argued ,  one need not do this exercise of traiging STEMI into main branch or side branch .

Image courtesey

Coronary tree : http://www.southcharlestoncardiology.com/64cta.html

Read Full Post »

Modern medicine promises   healthy new lives  to millions. We all , enjoy  the   fruits of  great scientific discoveries.  But do we  realise , medical science is nothing but experiments done on live  human beings . All  treatment modalities   are under constant scrutiny.  A great drug becomes the most harmful drug over a short time.

A drug or a device which is banned in one country is freely used in other country , marketed by the same parent company . How on earth this can happen ?  A device  ( Eg : A stent )  which is found  inferior  can  still can  be used legally elsewhere ,  hiding the information .

  • Do we divulge all vital information to our patients ?
  • Do we reveal all our conflicts of interest to our faithful patients ?

Informed consent is  the  “greatest  invention” in medicine . That is democracy in medicine . Doctor  patient conversation is   supposed to be  most noble of all communication !

But . . . this is under  genuine threat .  In this ” New medical AVATAR ” truths  remain only as thoughts , they  rarely  come out as words or action !

One such  situation a  physician  often  faces  in his office ,   as he is compelled  to act against his  conscience

If only we  have an ability to  read  his silence it will go something like this  . . .

For the sake of  Science &  Commerce , I have to implant this device  in your heart , and  my gut feeling says  ,  you will do much better without this device as well !   But ,  I am sorry . . .  I can’t avoid it .

Doctors are not be blamed  . . . rather  , we can’t blame  any body

Patients believe in doctors , and doctors believe in science  And the irony is ,  doctors have no other option as they are  coerced to  believe ,  in whatever is published  as science even if it is  half baked , unproved,  unapproved or  even dangerous science .

Let us prey for the genuine science to prevail  at least in human health  and the mankind  reap the maximum  benefits !

Let us  recall  Mahatma Gandhi’s    “Seven Social sins”   That included one  advice for the scientific world  nearly a century ago when it  was at it’s infancy !

Seven Social Sins By Mahatma Gandhi


  • Politics without Principle
  • Wealth Without Work
  • Pleasure Without Conscience
  • Knowledge without Character
  • Commerce without Morality
  • Science without Humanity
  • Worship without Sacrifice

– Young India, 22-10-1925

Read Full Post »

« Newer Posts - Older Posts »