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Modern medical quotes : Medical research

June 18, 2012 by dr s venkatesan

                                           Essential qualification for becoming a great medical  researcher  is  the    “Fine art of  mis-interpretating  data “                                                     Venkatesan sangareddi MD .Chennai .India

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Exciting new data from Third International Stroke Trial (IST-3)

June 16, 2012 by dr s venkatesan

Thrombolysis in acute stroke

  1. rtPA is indeed useful in acute Ischemic stroke
  2. Elderly need not be excluded (Even > 80y)
  3. Time window : It definitely works up to 4.5 hours and vary likely  to be effective up t0 6 hours.

We are gradually widening the time window  , which was  3 hours a decade ago .It may soon catch up with STEMI window of 12 hours ! ( Mitochondrially myocytes  are not vastly different from cerebro-cytes ! )

So ,  the current role of   of thrombolyis for stroke  is best answered by the editorial  accomplishing  this article !

“The role of stroke and emergency physicians is now not to identify patients who will be given rt-PA, but to identify the few who will not.”

Reference :   A Lancet Break through

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2812%2960738-7/fulltext

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736%2812%2960768-5/fulltext

Coming soon

  • By the way ,  rTPA is prohibitively costly for common world citizens . Please tell us about streptokinase in stroke ? Does the poor cousin match the rich ?
  • Do we have primary cerebral angioplasty ?

 

Please read the comment form Dr  Anthony Andrew Bell it is a must read !

Posted in cerebral circulation stroke, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , | 2 Comments »

Modern medical quotes: Why evidence based medicine is sufferring ?

June 14, 2012 by dr s venkatesan

Posted in bio ethics, cardiology journals, Cardiology quotes, cardiology-ethics | Tagged , , , , , , | Leave a Comment »

Tips in clinical cardiology : Differential diagnosis for constrictive pericarditis .

June 14, 2012 by dr s venkatesan

A  patient who presents with predominantly right  heart failure  is  an interesting clinical challenge . Constrictive pericarditis (CP)  remains  a popular diagnosis in this setting. However  in the bed side clinical  examination (and in cardiology Board exams )  the following  differential diagnoses are  to be  considered .( And ruled out one by one)

  1. Restrictive cardiomyopathy* especially Right  sided .In India endo myocardial fibrosis tops the list
  2. Primary Tricuspid valve disease( Tricuspid stenosis / Carcinoid etc)
  3. Chronic cor-pulmonale in terminal RV failure
  4. Silent Mitral stenosis with right heart failure
  5. Ebstein anomaly
  6. Severe forms of valvular pulmonary stenosis with RV dysfunction
  7. SVC obstruction
  8. Cirrhosis of liver
  9. Porto pulmonary hypertension

( The list is not complete , readers may contribute )

Bed side clues

  • Remember  a deep “y” descent  is  the bed side counter part of   Square root sign  recorded by  invasive RV pressure study
  • Similarly , pericardial knock is the auditory   equivalent (You hear the square root !  . . .yes  )as the ventricle thuds the rigid thickened pericardial shell in very early diastole !)
  • Pulsus paradoxus and kussmal sign can occur in both CP and RCM.
  • If a good LV apex , is  palpated it  goes against CP .
  • Please be reminded , even restrictive cardiomyopathy  will ultimately dilate their chamber pre-terminal and clinical features may be confounded with that of DCM.
  • Silent heart would suggest CP.
  • AV valve regurgitation would favor RCM
  • Features of  Pulmonary hypertension will help confirm Mitral valve disease , Cor pulmonale,
  • Deep  “y”descents  are against  any form of  Tricuspid stenosis.
  • Opening snap of mitral valve is to be distinguished from pericardial knock.( Opening snap high pitched  and occur later than   pericardial knock in diastole   , best heard in expiration )
  • Cirrhosis liver with hypo- proteinimic   fluid retention is  a traditionally close mimicker  .It  may be ruled out by the careful history taking as exertional dyspnea is an exception , if  at all , it is a very late event  in cirrhosis.
  • The issue gets further weird   as chronic constriction can lead on to chronic congestive liver and cardiac cirrhosis .
  • Severe  forms of constriction can invade the myocardium and result in features of myocardial dysfunction .It is more common than we recognise.

How to confirm ?

Following should be performed in that order

  • ECG
  • X -Ray
  • Echocardiogram
  • CT scan
  • MRI

*Cath study is no longer done (Only for academic purpose )

Final message

Even in this era of sophisticated  medical  imaging  , clinical examination  remains the key . One should  realise the importance  of  meticulous  clinical history  ,  sequential examination and interpretation .It  will   “rule out  or rule in”  majority of  cardiac disorders .

The hi tech imaging  modalities should be used only to confirm , risk stratify and  plan management . If you skip the clinical  part , one  may still arrive at a correct  diagnosis  but there is  high chances of erring in  management.

(Cardiac pearls lie in the bed side not in cath labs !   Here is  one such pearl  . Not every constriction  require surgery !

Please note about 20 % of constrictive pericarditis are  transient !)

Posted in Cardiology - Clinical, cardiology -Therapeutics, myocardial disease, pericardial disease | Tagged , , , , , | 3 Comments »

Break through in Brugada syndrome ! . . . always carry this vital data in FINGER tips !

June 10, 2012 by dr s venkatesan

Brugada syndrome continues to fascinate  us for two reasons.

One , it deals with mysterious sudden  deaths of young  men and women

Two , it is one of the  fine  examples  of how  advances in molecular biology , links  physical defects in ionic channels to  sudden electrical  death (Most of them  are due to inherited defects  sodium channels  of myocyte cell membrane )

While high risk subsets of Brugada are easily managed , it is  the asymptomatic  ones  that bother us.

The following are some of the  difficult  questions ,   a  cardiologist faces when dealing with   patients , who exhibit  only Brugada pattern in ECG .

  1. Should I go for an EP study Doctor  ?
  2. Will  I  require an ICD  Doc ?
  3. Do I carry a significant risk of  dying  suddenly  ?
  4. Do  I need a genetic test for sodium channel mutation ?

Fortunately,  we can answer  all these questions with much  courage than before.

(Thanks  to the European Finger registry published in 2010  !)

“No” is the  clear  answer for all of them !

Summary from the FINGER registry. 

(France  , Italy, Netherlands, GERmany)

The registry included 1029 consecutive individuals

(1) Aborted SCD (6%);

(2) Syncope otherwise unexplained (30%);

(3) Asymptomatic patients (64%).

In the  follow-up of 31.9 (14 to 54.4) months . A total of  7 death occurred .

The cardiac event rates per  year was 

  • 7.7% in patients with Aborted SCD,

  • 1.9% in patients with syncope

  • 0.5% in Asymptomatic patients.

Predictors of cardiac  event

  1. Previous syncope
  2. Spontaneous type 1 ECG

Non predictors ( Surprisingly there were more non predictors ! )

  1. Gender has no predictive role
  2. Familial history of SCD,
  3. Inducibility of ventricular  tachy-arrhythmias during  EP study,
  4. Presence of an SCN5A mutation

 

Follow up

PRELUDE study  almost reaffirms  Finger data

(PRogrammed ELectrical stimUlation preDictive valuE)

Just publicized in JACC 2012 from the pioneer of   Brugada Silvia  Priori of   university of Pavia  Italy

Reference

http://circ.ahajournals.org/content/121/5/635.full.pdf+html

http://content.onlinejacc.org/cgi/content/abstract/59/1/37

Posted in cardaic physiology, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias | Tagged , , , , , , , , , , , | 2 Comments »

Tips and Tricks in cath lab : Cortical sense and Guidewire crossing !

June 9, 2012 by dr s venkatesan

Years ago ,  I  remember asking my professor during  a balloon mitral valvotomy workshop .

How  is that ,  you  are able to  puncture the  IAS  effortlessly and efficiently sir ?

Every thing is in the feel  Venkat ,  he used to say !

What  feel ?  I  used to wonder !

Now , I  realise the guide wires  and catheters are just an  extension of our hand and fingers.

When we   tackle  CTO lesions we should   be  able to feel  and differentiate the  capsule and dimple .

More sensitive hands (Brains)  can tell whether the guide wire  is poking the vessel wall or the lesion .

Of-course ,  now  we have sophisticated OCT, IVUS, and camera  tipped ( Is it really there ?)   guide wires to guide us.

Still ,  a cardiologist  who  is able to feel the  lesion intimately  . . .  would be  a clear  winner !

How to feel a lesion ? (Plaque palpation ,  Hitting the calcium  , Feeling  the  thrombus  !   Cuddling the  foramen ovale  etc )

Key word : Guide wire tactile sensitivity .We are familiar with   guide wire torque .Now , a new technology  that can transmit the feel of the target lesion  ,  to the hands  of  the operator  would be very much desirable .

Two point discrimination  and temporal cortex  plays a critical role here. Irrespective of  the hard ware  used   , how  the  brain  perceives  touch is going to determine whether you are going to cross  a difficult  lesion .

Can you electronically amplify tactile feeling like sound amplification ?

It may be possible in near future. But it has  other issues  like   hypersensitiveness

Can a physician with defective cortical sensory  system  face difficulty in catheter based  interventions ? 

I have observed at least  two  cardiologists with diabetes  , acknowledging  major  difficulty  to  feel the palque and  cross  the  lesion   (Due to autonomic  neuropathy ?) With many  cardiologists  rapidly aging  , the quest  for intervention  goes unabated   (Still  unwilling to quit !   )  one may  experience  cortical dementia  as a hurdle for  guide wire manipulation . These issues need  to be tested  in  real  world .

Final message

It  is   fascinating  ,  how the feel  of  coronary plaque  reaches  our brain . It is picked  by the tip of  guide wire , travels about 150cm , handing over the weak signals across the  gloved fingers ,  reaching all the way through cervical spinal cord and spino-thalamic tracts ,  brainstem  and finally to the  cortex.

There are  multitude of factors that determine   the success of   complex  angioplasties . I realised  suddenly , Intact  cortical sense  could  be an  important one,  among  them . Let us train our brain  centres for this specific sensation of cath lab hardware . After all ,  the brain is  maneuvering force in any cardaic intervention !

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Tough calls in cardiology : Refractory hypotension in septic shock and the role of Hydrocortisone in Septic shock ?

June 5, 2012 by dr s venkatesan

Time and again cardiologists are called to opine  in critically ill ICU patients with  hypotension.  The circulatory shock of septic shock  is often refractory  . Many  times it  degenerates  into multi -organ failure . The mortality remains high in- spite modern treatment .Even in those patients who recover , they require prolonged  inotropic support  (for days or even weeks)

Here is a  recent call I attended to .

A 44 year old   febrile   , ventilated patient  (With a pneumonitic patch , PEEP of  6 , near ARDS )  ,  precarious renal function and altered sensorium , maintaining a blood pressure of 100/70mmhg with high dose dopamine and nor- adrenaline  , monitor showing a heart rate of 125 /mt sinus  .This status -quo  has continued for more than 72 hours. To my surprise,  the ICU physician told  me there is  in-fact a  minor improvement in general condition than before  . After blinking  at the patient’s  file for few  minutes  , I did a customary bed side echocardiogram .The only positive finding  I  found was  his  heart was  structurally normal  and EF was  64 %  , still the right heart chambers were struggling  to do it’s job   fighting with the PEEP.

The physician had  a very  specific query  from the cardiologist . How to wean the inotropic support and shift him off  ICU ?

(The poor patient  has no  insurance  , and has to shell  Rs 10000 everyday  which is equal to his monthly income ! )

A very  valid question indeed   !   After all  , cardiologists  claim to  have special  knowledge  and wisdom about disorders of  vascular system .

Heart being normal , the crux of the problem is loss of vascular tone. (Autonomic dysfunction ) .How to improve it ? I  discussed the following suggestions.

  • Early passive muscle exercise (Augmenting  muscle tone and transforming it to  into arteriolar and venous tone )
  • Venous support ,stockings etc.
  • Ensure adequate intra-vascular  fluids
  • Sodium supplements
  • Corticosteroids.
  • Fludro-cortisone , the mineralo-corticoid may have a specific advantage as it could retain sodium in vessel wall that can be exchanged with smooth muscle calcium and improve vascular tone .
  • ECMO is  often a pre terminal intervention .
  • Will power . We know vascular  tone is in fact neurogenic in origin .The tone flows from brain stem .Administering  will power could be a useful intervention . (parental infusion of fighting spirit !)It can be done through pep talks from  close family  members   in   conscious patients .(One controversial advice is to allow  near and dear  into bedside , ICU phobia may delay recovery of vascular tone !)
  • Finally  I suggested , a  vascular consult from the GOD  . Organised prayer .  There is some evidence ,  even  proxy prayers do exert benefits in unconscious patients .

After a 15 minutes stay in the ICU , for doing nothing  I  received a significant consultation fee  , and I left the  place  sheepishly  with a  definite dose of guilt !

Reference for role of Hydrocortisone in septic shock

The CORTICUS study

It has no overall impact but hastens recovery from septic shock . Even though the study appears to denote a negative connotation

it has the role in selected individuals .http://www.nejm.org/doi/full/10.1056/NEJMoa071366

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , | 1 Comment »

A great 3-D Echo course from European society of cardiology . . . free of cost !

June 3, 2012 by dr s venkatesan

Who said  knowledge comes at a cost . Here is a great resource . Everything about 3D echo

A sample of   3D echo  evaluation of  mitral valve anatomy

http://www.escardio.org/communities/EAE/3d-echo-box/3d-echo-atlas/mitral-valve/Pages/normal-mitral-valve.aspx

Posted in Cardiology teaching websites, Cardiology-Land mark studies, valvular heart disease | Tagged , , , , , , , | Leave a Comment »

Primary PCI : Making “Non-Sense” out of sense !

June 2, 2012 by dr s venkatesan

In the management of STEMI , many  of us  believe  , contraindication  exists only for thrombolysis . In fact  , there is  a big list  of contra’s for primary PCI as well  . Few  books mention about it and  few discuss about it  . It comes under many broad categories .Time , technical, patient  and  concept  related

  • Late presentation > 12 hours (This is the most important  contraindication  . 12 h is the time taken for  death of  myocytes . Myocardium will not  bother by which modality it is going to be rescued ! It simply  won’t give any  grace time  and never feel privileged to be rescued by PCI !)  The supposedly time independent beneficial effects of PCI  was  never proved convincingly !
  • Uncomplicated , fully evolved, spontaneously re-perfused   ( successful  )  STEMI  (At-least  10 % of STEMI population  ) . This is  common in RCA STEMI .
  • Primary PCI  should not be done in  low volume centers with poor expertise  ( less than  2 -3 per month ?)
  • Lack of sufficient hardware .
  • Co-Morbid conditions
  • Very elderly ( Controversial … some may call it as an  absolute  indication ! Such is the status of EBM in 21st century !)
  • Any recent bleeding conditions carry equal risk as that of thrombolysis

The list of relative contradictions  that are  widely reported in literature  for thromolysis may apply in PCI as well .The risk of bleeding is many fold higher when  multiple anti-platelet agent /Heparin are used .The usage of 2b -3a is also rampant in many centers .  A recent hemorrhagic  stroke is  an absolute contraindication  for PCI as well.(If only you do a PCI without anti-platelet  agents).With number of complex anti-thrombotic drugs knocking the d0ors of cath lab , the problem is set to grow further.

Final message

Never underestimate the  potential  peri -procedural bleeding risk during PCI  .It can easily  exceed that of a thrombolytic agent  in susceptible individuals !

Primary PCI is a great innovation and is a gift  of modern science to human race . But , when  selecting the patients  ,  many of us  continue to interpret  this issue  wrongly. We seem to think , in a given patient  , if  thrombolysis is contraindicated  ,  he or she will automatically become eligible for  primary  PCI.  It is a dangerous assumption and  is rarely true  . There are umpteen number of situations were both are contraindicated . I  argue the  intervention community to publish specific guidelines with absolute and relative contraindication  for primary  PCI as well .

After thought

If  a patient is not eligible for both thrombolysis  as well as PCI what to do ?  Is it not a crime to watch a patient with STEMI simply losing his myocytes ?

It may seem so  , when we look at  superficially   but  be reminded even simple heparin therapy has saved many lives in such a situations .

Link to related You tube video

Reference

That  elusive  uncommon  sense

Posted in Cardiology -Interventional -PCI, cardiology- coronary care | Tagged , | 1 Comment »

What are the mechanisms of hypoxia in Acute pulmonary embolism ?

May 31, 2012 by dr s venkatesan

Hypoxia is most important feature of acute pulmonary embolism.

It occurs due to variety of mechanisms

  1. Ventilation perfusion mismatch is the major  mechanism  ( Normal ventilation /Reduced perfusion)
  2. Atelectasis of lung  ( Left to right shunt)
  3. Loss of lung volume due to pulmonary infarct  contribute later
  4. Low mixed venous Oxygen saturation  (Tissue hypoxia -more extraction )
  5. One more important cause is right to left shunting  across PFO  due to sudden elevation of right atrial mean pressure reflected from RVEDP .

Can  acute pulmonary embolism be diagnosed  with out Hypoxia ?

Surprisingly many standard text books mention hypoxia is a soft sign . In fact , Braunwald’s  text book of cardiology  do mention about it .

Significant acute pulmonary embolism can not occur without affecting o2 saturation .

However , it is possible sub acute  pulmonary embolism could occur with normal oxygen saturation.

Final message

Hypoxia is indeed a hard sign  for most events  of major pulmonary embolism . It can even be termed as an essential criteria .A hypoxic , tachypenic patient in  sinus tachycardia with echo evidence of  new onset RA or RV dilatation is almost 100 % specific for acute pulmonary embolism . ( This becomes 200 % if he or she has DVT as well !)

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