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Archive for December, 2011

Mark E Jospehson  is the man who single-handedly carried  the burden of teaching  generations  of electro-physiologists  from  Harvard  Thorndike electro physiology services , Boston USA. Today , whatever  we know  about the mechanisms of VT , it is because of such great men who  spent thousands of hours  in the  first generation EP labs in early 1970s and 80s  , meticulously analysing   the data emanating  from  over  600   scar mediated VT with complex circuitry .

He along with  Miller published this seminal paper  in circulation 1988 , which gave us  the  algorithm  that localises  Post MI VTs.

Following table summarises their finding.

VT localisation in Infero-posterior MI

The general principles  of localisation of VT  

  • Localising VT following myocardial infarction  is difficult but distinctly  possible with  about 60 % accuracy.
  • Whenever we locate a focus we generally refer to epicardial site of exit not the focus of  origin.
  • Ischemic VTs with complex scars are difficult to locate .
  • The rule  that RBBB VT arise from  LV and LBBB VT from RV is too simplistic  in scar mediated VT.
  • The fact  that IVS is common to both RV and LV confounds the issue .Further, in a given  clinical VT  the origin  , course   and exit points of VT can considerably vary .For example  septal VT can exit  on  either side and  result in  either RBBB or LBBB morphology (Epicardial break thorough )
  • Multiple exit points are also possible.
  • VT induced in EP lab may not be reproducing the same clinical VT. So we have to be careful in what  we ablate and claim success !
  • VT with  structurally normal heart  has   more predictable behavior  , for  example RVOT VT  almost always have LBBB morphology.

Other important rules of thumb are

  • LBBB VT has more localising value .
  • Superior  axis is the most common  axis.
  • Bulk of the ischemic VT are located within the septum either in the apical or basal region .(75%)
  • Infero posterior MI has more complex scars , hence VT morphology is heterogeneous.

The purpose of localising VT is important  only with reference to  ablation.(Of course for academic reasons  as well )   With advent of electro anatomic imaging (Carto ) it is becoming   easier  to locate and track them . Still only a minority of VTs are amenable for RF ablation .

Please note ,  the most common modalities we use  in the management of VT  ,   Amiodarone  and ICDs   simply do not   bother  about   focus of origin  for it’s action !  That makes our job easy !

Reference

http://circ.ahajournals.org/content/77/4/759.full.pdf

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Benjamin Gasul  is a well-known name  in  cardiology community especially  among the old generation . He and  his team from  Cook  county children’s hospital  Illinois,  Chicago,  created a stir among pediatric cardiologists  in late 1950s and 60s . His concept  was rather controversial .He suggested   Tetrology of Fallot can be an  acquired  defect as a sequel to  large   peri-membranous VSD.

He and his team published a series of papers one in 1957 and other in 1963 (JAMA and circulation ) .Later in 1970s  Kieth  and  Tyrrell  from children’s hospital Toronto tried to confirm this. Though they were not fully agreeing with  Gasul  they could not dispute the concept either !

Clinical importance of Gasul VSD

This entity was suspected based on a  curious observation  in children with large VSDs ,  who initially struggle with the defect and   show signs of  failure   . After a critical time frame  (If  they survive )  they  begin to stabilise and some of them do extremely well  in functionality too !

For this to happen , we presume the  quantum of  shunt  must  reduce by any means. Ironically ,  we also know , even patients who are destined to develop dangerous Eisenmenger reaction also live a blissful life for a decade or so  before it strikes  and  take  their life . This is one aspect of the natural history   . . .

While  some ther  children did well without developing  pulmonary hypertension  .This bothered  Gasul .When he analysed those patients (Mind you  there was no echocardiography  those days !)   he found something curious  was happening in the RVOT area. (It was almost like TOF !) This he documented in few patients  who showed progressive infundibular narrowing   acting as a check dam (Artificial banding ? ) and resulted in improvement of  VSD hemo-dynamics  .In extreme situations there was  a significant  right to left shunt as well. It was so tempting  to label it as acquired TOF !

Who are likely  to develop  Gasul  like reaction ? (Reference : Kieth 1978  Heart disease in Infancy and child hood.)

  • Persons with  oblique RVOT angle normal <40 ( 40-60 degrees)
  • Aortic override ride > 30%
  • Patient with anomalous muscle bundle
  • Children with right aortic arch

Why the concept of  Gasul was disputed ?

Gasul  concept primarily relied on the fact that  there  would be  some resistance at RVOT  for all those dramatic improvement in failure  as  the children grows .  This he consistently documented in many children who had significant regression of cardiomegaly .

There can be other mechanisms for  the signs of stabilisation in large VSDs.

Relative  reduction  of VSD size as child grows  could be an  important factor .  The falling pulmonary vascular  resistance  allows to  accommodate   the shunted  blood  without  any major issue as RV  after- load regress .

Is concept of  Gasul  alive   in the year 2012 ?

Since  it represent the natural history  of the defect  , most VSDs are closed surgically ,  one may not get an occasion to see a Gasul VSD today . More intriguing is the fact  we will ever get an oppurtunity to  confirm the concept .

Special  situations in  VSD / PS . Can RVOT obstruction  exist with raised pulmonary  arterial pressure ?

This  is a challenge to the traditional teaching . Logically pulmonary obstruction   and  high  pulmonary pressure  does not go hand in hand.Do not get fooled by logic .(We know aorta can record  even  200mmhg  in critical aortic stenosis ).

The respect and command  we give to clinical medicine   even  today is because ,  it can defy logic in  any random patient .

If a  patient with Eisenmenger  develop  Gasul reaction what will happen ? PAH will persist  as do the RVOT obstruction .They are the  blessed  ones and  belong to the category of   Eisenmenger surviving into 4th  5th decades . (Batisda of  Brazil extrapolated this and suggested huge benefits with  PA banding in adult Eisenmenger !)

Summary and verdict

TOF is a cono-truncal anomaly due to defective genes. The Mal-aligned  conal  septum is responsible for RVOT obstruction . Hence  this defect can not be termed as  acquired  , by  any  sort of imagination .

Still , a subset of patient with large VSD  can mal-align their conal  septum for hemo-dynamic  reasons .This  is  especially likely to occur  if the flow is heavy the infundibulum  slides horizontally to generate the obstructive  gradient .  Hence  Gasul was  indeed right when he pointed  to us some of the   grown children with VSD  mimic  TOF .

However,  the controversy remains  whether  the equation  “Adult VSD + IPS” = Adult  TOF  is  true or  false !

Incidentally , the classic book on congenital heart disease by J.K Perlof has a chapter on VSD with PS  and not  on TOF  !  Does it light  a spark ?  Is it worth pondering this question ? Probably not ,  instead we may use our resources to  correct these anomaly  .

Reference

Gasul’s  original article published in 1957 (Only abstract )

http://smj.sma.org.sg/1104/1104smj7.pdf

http://circ.ahajournals.org/content/28/4/560.full.pdf

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Mechanism of chest pain in mitral valve prolapse  include

  1. Mitral valve  has pain fibers , the myxomatous degeneration  of the valve tissue generates pain .* (Not much evidence )
  2. Mitral valve stress, strain ,  stretch and bending.
  3. Mechanical stretch  of papillary muscle or LV free wall (dimple ?  ) as the mitral valve prolapse into LA.
  4. It is a central pain perception disorder .Panicky and anxiety reactions included
  5. It is not chest pain  at all it is simply a feeling of palpitation .
  6. Associated ischemic  heart disease

The commonest mechanisms  are   response  4 and 5 .

The evidence  lies in the fact ,  many of  these people  begin to complain of chest pain only after being aware this problem. MVPS is  often a  fancy entity created by cardiologists  which  unfortunately has  labeled  many of the normal  general population as cardiac patients. Barlow who described this entity  decades ago  would have never imagined  it  would be  so popular and subjected to mis-use . We have proposed a solution for this . The diagnosis of MVPS shall not be mentioned unless it is obvious  and fulfill a strict criteria . The commonest error we make is  an elongated , redundant , hyper mobile mitral leaflet   at   as  MVPS.

It is expected  ,  true MVPS must have all of the following  three criteria

  • Thickened leaflets
  • Clear prolapse of  at least one leaflet in long axis view beyond the plane  of  mitral annulus
  • At least some degree of mitral  regurgitation must be present

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A middle-aged obese man was referred  to me  for  an emergency  echocardiography

The patient was unable to lie  either supine or left lateral  . He could lie down only  right lateral posture  that too for a minute .An ultra fast echo gram was completed . It  was  entirely  normal . His ECG was also normal.

When I  asked for x ray there was a surprise

Note the shrunken thoracic space  on both sides .The  fundus of stomach is  almost fighting for place with left ventricle in the thoracic cavity .

No wonder he is severely orthopnic  (But fairly comfortable on erect posture )

He has a distended abdomen .He is  now waiting for a GE consult. His other complaint is belching   . Is that some form of gastric obstruction ?

I’m posting this image to re-emphasise the  classical  teachings in medicine .

Human body is  a highly integrated  biological  system .We in the name of modern science  has  disintegrated in to  multi organ entity.

This patient was labeled as acute pulmonary edema and the treatment was about to be started.

Here is a patient  with dyspnea and orthopnea  entirely  due to a non-pulmonary and non- cardiac cause !

                                                        All youngsters  . . .  always be alert  . Clinical medicine  is  notorious  for  throwing   surprises , especially when you least expect it !

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There were times medical  profession’s  only purpose was to take care of the sick . Modern  principle of living  has contaminated  every walk of life .Medical profession  leads  by example in this race .

How can one justify celebrating a disease in a grand manner in public domain  in the name of increased awareness  ?

I am shocked to find an ad in a recent  The  Hindu Ad  (25-11-2011)

Some of the words  used are terrible and highly objectionable . It amounts to an  insult to all diabetic patients.

  • Diabetes award !
  • Diabetic  Carnival !
  • Join us in the fun of diabetes !
  • Glitz and glamor of diabetes!
  • Festival of diabetes !

How can a patient celebrate his illness ?

I think  the news paper  which  publish such ads  should also show some sensitivity .

I agree there are lakhs of diabetic patients who do require  intensive treatment  but the fair held in the air conditioned corridors of  a trade center is  never  going to address  this issue.

( Can I ask these organizers to  help and  serve the real diabetic burden in ill equipped public hospitals  across  our state ? )

It  is simply a commercial extravaganza   creating a fear complex among the healthy , rich men and women and make a living

out of   human anxiety . 

Who sponsors these medical  award nights ?

For those who are unaware  of the games doctors and pharma companies play,  here is a shocker – large amounts  of money is pumped into  such public events.

This is part of  a  larger board  room  strategies ( Can it be a conspiracy  !) to increase the per capital consumption of drugs of our population . And no doubt   doctors are integral part of this scheme with or without intention .

While MCI can penalize  a individual doctor  even for accepting a pen as gift from pharma company ,

they can do nothing but simply watch  as millions are  exchanged  in the name research , health education ,  and awareness .

The height  of  the  irony is  , these events are sponsored by WHO and the world  forums as well  !

Ironically   the  doctrine of  modern medicine  seems to suggest   . . .“Ethics is   primarily for individual physicians and do not  apply   for institution ”  This is the single   most dangerous  concept that is  playing havoc with human health”

It closely mimics the principle  of   war justice  . An  individual shooting another individual  is a definite  crime ,  while  multiple  individuals  killing  multiple   individuals   is not a crime , it is a war !

Disclaimer

The author has no  personal grudge  against any hospital or organization instigation. It ‘s   an expression  against so many commercial activities that occur  in the medical filed on day-to-day basis !

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WPW syndrome is the prototype of cardiac pre- excitation . The accessory  AV pathway short circuits the ventricle .Since  there are two options  available   for the  incoming  atrial  impulse  to reach ventricle ,  often  times  the qrs is contributed by both .Hence a  fusion  occurs  within qrs complex and stretches it wide   ,  it also  generates a delta wave and short PR interval .

The complexities of  conduction   properties and refractionaries of AV node and  accessory  pathways determine the degree of pre- excitation. When an optimally timed  APD  gate crashes  into the  accessary pathway it gets blocked ,  only to recover little late ,  unfortunately  invites AV nodal impulse  from below  . This facilitates a  re- entry circuit from ventricle to atria and result in classical AV reciprocating tachycardia .

Antegrade conduction through AV node is  physiological and  benign as it inherently checks the heart  rate . Antegrade conduction  occurring through the  accessory pathway  (which  constitutes the pathological  component  ), is   potentially  dangerous  as it lacks the  electrical breaks (Technically called decremental conduction )

What  is the  specific  ECG evidence for  antegrade conduction thorough accessory pathway  in ECG ?

Delta  waves

So,  what does it mean if there is absent delta waves  in WPW syndrome ?

It can mean three things

  1. Concealed pathway
  2. Manifest pathway , but intermittently  blocked pathway.
  3. It is not WPW syndrome at all .

We know concealed  pathways are  safe* as it allows only retrograde conduction. ( Safe  regarding   risk  of  sudden cardiac death ,  still unsafe for AVRT !)

Intermittent WPW

Intermittent pathways are equally  safe  as intermittent absence of  pre-excitation   indicate  the  presence   of naturally occurring     breaking system within accessory pathway . Are these  accessory pathways blessed with some AV nodal cells ?  May be !  . Histological studies do suggest that .This explains   intermittent missing of delta waves  which is  electro-physiologically a good sign

(We also know   there are exclusive slowly conducting accessory pathways like  Mahim and variants  )

If  one is lucky to observe this phenomenon in ECG  it can be termed as  a poor man’s  EP study  . ( Which requires specialized methods to document the refractory period of accessory pathway  to be   < 250 msec)

Techniques to  screen for or / unmask this concept.

Whenever  we  diagnose  WPW one has to look   ,  whether the patient  harbors  this phenomenon .

  • Holter monitoring has a useful role in this regard .
  • If there is nocturnal   disappearance of pre- excitation it would  suggest a safe  accessory pathway.
  • Similarly , if pre- excitation disappear during exercise  stress  testing it  would indicate a  type of intermittent WPW syndrome.

Final message

An astute cardiologist shall  look for this intermittent nature of delta waves  and  help avoid a costly and  potentially harmful EP study !

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How early one can shift a patient for rescue PCI after failed thrombolysis ?

  1.  Wait for at-least 24  hours.
  2. A minimum  cool off period of 2 hours is required.
  3. It is never an issue . Rush the patient  immediately to cath lab
  4. The question does not arise  . Often times ,  rescue PCI is a dead concept  as  sufficient damage has happened !

Answer

The irony of  medical science  lies in our belief that every medical query  has a specific answer ! In reality it is rarely true.   In this instance , any of  the above can be a correct response.

A patient with  failed thrombolysis can belong to any of the  64 possible combinations*  based on  time of  thrombolysis , extent of  MI,  associated complications, co- morbid conditions , presence of symptoms . (For example there is  a sub groups of patient with  failed thrombolysis still  asymptomatic  and comfortable )

The issues for rescue PCI  do not  arise  in a   sinking STEMI (Cardiogenic shock ) , or  STEMI with persistent angina. There  is  no  management issues in  these patients  .They need to be rushed to cath lab. Unfortunately  in  impending  LVF or manifest LVF (But not in shock )  decision making is tough , as doing a PCI in patients  with basal crackles  and hypoxia is a real challenge .These are the patients who are likely  to hit hard  from the hazards of the procedure .Extreme caution is required.

I have seen  significant cohort  of  asymptomatic hypotensive patients getting converted into   drug resistant, IABP dependent refractory shock after PCI  ,  making every one look  pathetic  !  The  only solace for the interventionist  is  the gratification  of  stenting the  IRA !

This  happens  , in spite  of having  multi national trained  in house critical care anesthetics and  dual core processing IABP  . Realise  what we need is delicate decision making ,  So use extreme diligence in selecting patients with impeding shock .

Your medical management can  provide  more teeth to stabilise your patient than a PCI .If you are doubt discuss with your learned colleagues .  ( If you  do not  ask for evidence for  this statement , probably  it would confirm  you  as  an  experienced   cardiologist  !)

Real issues pushed to the sidelines ?

While the real issue  in the timing of rescue PCI  may be  different , the discussion traditionally  revolves around   hemo-rheological aspects . We know  the lytics and PCI do not combine well for two reasons.

  • Pro-coagulant nature of lytic state .
  • Excess bleeding risk at puncture site.

Now ,  we have evidence to say fibrin specific lytics  TPA, TNKTPA has less of this issue . ( NORDISTEMI)

Patients who receive  fibrin specific lytics  can  safely  be  taken for rescue PCI  in case it is needed without any increased risk .

Bleeding complication  has dramatically reduced as radial procedures are done often even in emergency setting.

Vascular occlusive devices  have added to our comfort.

* The definition of failed  thrombolysis by  itself is not standardized . Is it symptom guided ?  or ECG / enzyme / echo guided  ? A patient with  infarct  related chest pain (dull aching )  after thromolysis can be labeled as post infarct refractory angina and rushed for emergency angiogram .(This is due to our ignorance  about  the  residual pain signals  through  type c pain fibres  for up to 24 hours )

Final message

The indication and  timing of rescue PCI is  primarily  related   to the  overall   patient profile  rather than the bleeding or pro-coagulant issues .

Although   pro-coagulant  lytic state is based on weak scientific  foundation , it  is a blessing in disguise  as it  can  act  as a deterrent  in restricting  inappropriate rescue PCI !

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