Feeds:
Posts
Comments

When Aorta looks like a railway track . . . think about “Extreme” LV dysfunction !

December 18, 2011 by dr s venkatesan

Aorta  is connected to the left ventricle  like a hose pipe.The energy  generated within the LV myocardium is efficiently delivered to  the root of the aorta. Mechano -coupling of LV with  aorta  is important means by which  blood is  is ejected into systemic circulation .

Even though aorta  has  mainly passive  contraction and ( The  wind- kessel effect) ,  the most  powerful contractile force  of aorta comes from   the  transfer of kinetic energy from  left ventricle .

This helps  us to  measure the LV function  simply by  looking at the aortic wall motion.Since aorta is the final common exit for LV  it effectively represents the global LV  function . The  ubiquitous errors during  LV border tracing  and it’s subsequent mathematical  amplification  can be avoided. Here is a  patient with severe LV dysfunction  whose  aortic  motion is depicted . We refer to this as   ” rail roading” sign of Aorta  which  implies  a critically dysfunctional LV . His EF was 23 %  The aortic motion is esepcailly useful in categorizing severe LV dysfunction  from moderate LV dysfunction (The sensitivity we feel is as high as sophisticated tissue motion Doppler protocols .Of course  it may lack specificity !* as hardened  aorta due to aging can confound the aortic motion )

Posted in echocardiography | Tagged , , , , , , , , | Leave a Comment »

Localising Post MI ventricular tachycardia by surface ECG

December 18, 2011 by dr s venkatesan

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

Posted in cardiology -ECG, cardiology -Therapeutics, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , | Leave a Comment »

What is the mechanism of chest pain in mitral valve prolapse syndrome ?

December 17, 2011 by dr s venkatesan

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

Posted in Cardiology - Clinical, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , | 1 Comment »

Abdominal dyspnea : When the stomach encroaches the left ventricle’s living room !

December 16, 2011 by dr s venkatesan

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 !

Posted in Cardiology - Clinical | Tagged , , | Leave a Comment »

Why patients with intermittent WPW are blessed ?

December 13, 2011 by dr s venkatesan

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 !

Posted in cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , | Leave a Comment »

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

December 13, 2011 by dr s venkatesan

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 !

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Coronary artery disese | Tagged , , , , , , , , | Leave a Comment »

This JAMA paper will stun you : Lesser the cardiac risk factors . . . poorer the outcome !

November 27, 2011 by dr s venkatesan

What is a coronary risk factor ?

Right from the days of  Framingham study we have conferred a privileged   place   to  few  cardiac  risk factors.

they are

  • Diabetes mellites
  • Hypertension
  • Hyperlipidemia
  • Smoking
  • Obesity

They are referred to as conventional risk factors .  What is the convention ?  Do they deserve  the  cult  status they enjoy ?

Today we also have a  cluster  of non conventional risk factors like , Lip (a) , low HDL, Homocystenemia , CRP , Apo B etc . Currently ,  in any large cohort of CAD  up to 30 %  do not exhibit even a single conventional risk factor  . This is a huge number .Hence   we tend to give more importance to genetic make up and mental stress etc  .The search is still  on for newer risk factors .

Why some research  findings are difficult to comprehend ?

It is because we are yet to  decode the  intricacies  of  human biology  fully . Our knowledge is so superficial  , as we chase  a pseudo scientific  proofs   for  a  presumed  hypothesis.  The classical example is the concept called good cholesterol (HDL) and reverse cholesterol transport which  is never based on solid scientific foundations.

Take the sorry story of  Torcetrapib

Many consider  low HDL  as an independent CAD risk factor to be a  myth  or else why should we miserably fail  to have any positive effect of  increasing the HDL  levels by pharmacological means . (One argument is physiological  and natural elevation of  HDL  would still be beneficial  . But the issue is still wrapped in a statistical mystery

This  paper from  JAMA   adds further insight into our ignorance about  the  genesis of CAD .

The data is from  NRMI registry.

The statistics  reveal  a stunning fact .In  the overall CAD cohort ,  patients  with no major risk factors  experience  highest mortality and the ones with maximum   risk factors have least mortality ! What a shocker of a study ?

http://jama.ama-assn.org/content/306/19/2120

This  paper  would bring  jitters to the population ,  but in the real sense it sends an important message .

A significant population develop CAD without any  known risk factors.(14.5% in NRMI registry )

If a person develops  a CAD without any major risk factor  ,  it seems  . . . it is not at all a  good news   !  rather we need to introspect , why  without any risk factor he or she has suffered CAD ,

One inference is  their vascular system is more vulnerable ! Some hidden factors are operating . How to manage such  patients  without any target to intervene ?   A diabetic dyslipidemic smoker has a   definite  therapeutic target  .

What about these   lesser  humans  who   develop   CAD without any known risk factors  ? They  tend to suffer more !

Is  CAD  due to DM/SHT  is better than  others  ? This study seems to say so ” Known devils are better than unknown ones ”

Final message

Unlearning is an   “essential and fundamental”  component of   scientific learning .  In this progressive scientific world , this applies  most to   medical profession  than any other field !

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Coronary artery disese | Tagged , , , | Leave a Comment »

How does un-accoustomed exertion trigger an acute coronary syndrome ?

November 26, 2011 by dr s venkatesan

Exertion and  acute coronary syndrome (ACS) has a tricky relationship. On the one  hand, it  would  appear they are not related at all  as only a miniscule of patients   give history of recent severe exertion prior to ACS   , while  few others  tell us  a clear- tale of   unaccustomed  exertion ,  just prior to the onset of chest pain.

Here is case history  of a  man  who was rushed to our  ER from  Madras central station ( Our hospital is located just opposite to it !  )

A  48 year bank officer  was  about to board  a train to Patna   . It was a rainy  November  evening ,  his car got struck in traffic .He along with  his family members were rushing to catch the rain  .He had  to run fast with his heavy luggage  .Even as they boarded  the train successfully and occupied their  seats  ,   within minutes  he  developed intense chest pain and sweating . The distressed family de-boarded the train and was rushed to our hospital  . Yes  you guessed it right   . . . he  was showing an extensive ST elevation  in anterior leads on arrival.

So what  has  happened ?  What is the coronary hemo-dynamics during heavy unusual physical exertion ?

The above patient did  not have any obvious risk factor . He vaguely recalled ,   one if his family doctors telling him ,  he had borderline high BP and was never prescribed a  drug . His wife told us  he has been a emotionally  liable individual .

It is well  known  , sudden exertion in an  emotional  milieu   would  result  in  intense  adrenergic drive  . (Here the emotion was anxiety/ fear of missing the train )  Adrenergic drive was  amplified with the  isometric exercise (heavy suitcases ) ,   shoots the intra  coronary blood pressure (normal 45-60mmhg)  into  dangerous spikes . (By the way , what happened to  coronary auto regulation  ?) . We also  realise simple raise  of  intra coronary pressure alone is not sufficient  .These patient  will  harbor at least some degree of  atherosclerosis  which face a  shearing stress and give way /tear  or fissure resulting in  a sudden substrate for intra coronary  thrombosis.  Some of them may manifest  only  as coronary vasospasm  .When sustained  it can also result in a full-blown acute coronary syndrome.

The concept of trigger vs risk factor

One should remember  both physical and mental exertion   act  mainly as a  trigger (They are not  major risk factors  like DM/HT/Smoking /Dyslipedemia) . All that is required ,  for  this   vulnerable population  to fire  is a trigger.  Physical exertion ( especially  isometric)  when  associated with  emotionally charged  brain  sends a  perfect  invitation  for an impending  ACS !

Another example  for untoward  effects of  exertion

A middle aged man who had  impaired glucose intolerance and dyslipdemia  was referred for an  EST.He did complete  12 minutes of  Bruce  protocol  comfortably . But  on the same day evening  ,  he felt  uneasy  and came to our ER ,   only to record a full blown STEMI .

These events may be rare but if properly understood   these  patients can teach  us  few   lessons in the genesis of ACS and coronary hemodynamics .

Special  issues  about   exertion in post PCI patients

One of the purpose of doing  PCI  for CAD  is to improve the  functional  capacity  (and possibly to prevent future ACS) . Paradoxically ,  we  continue  to have  some apprehension about subjecting post PCI  patients  into early stress testing . (I remember reading some guidelines that advice us to  avoid stress testing strictly for 6 months post PCI  ! Is it true ?)

If a  cardioloigst  is  not too comfortable  putting their  patients  into a  treadmill  post PCI ,  it only implies they doubt their efficacy ! It   would  also imply  these  patients   should  not be allowed to exert to their full capacity in day to day  life events as well .(Attention  cardiologists   . . . Yeh  . . . we have a  fundematal problem on our hand !)

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

Early surgery for infective endocarditis (EASE Trial) answers a terrifc debate !

November 23, 2011 by dr s venkatesan

Modern  day cardiology can do wonders. It can revive a sinking  patient in cardiogenic shock with IABP , LV  assist ,   multivessel angioplasty and bring back  life . On  the other  hand  , a young man with an infected mitral valve who is put on  intensive  antibiotic  regimen   , progressively deteriorates  throws an emboli into brain ,  raise his urea  creatinine  , cardiac   failure worsens and finally succumbs .

This is a clear case of failure  of medical therapy in infective endocarditis .  It is almost certain  surgery would have saved him .

Why  the delay ?

So the question that is been debated for so long is   “When to intervene with surgery in IE”  ?

While we show extreme  urgency for ACS , the same is not shown  with IE.This is going to change in the future .Thanks to the  EASE trial (Early surgery  in  endocarditis )  This land mark study from Korea  is likely to revolutionise  the way we will look into the  problem  of infective endocarditis. It was presented in the just concluded AHA annual scientific sessions  in Orlando

This was  our  observation  too . The issue was discussed in  the year 2008 .It reminds me ,  every  learned  thought or opinion is in fact a paper  but unfortunately modern science does not accept a  fact without evidence of a  study . Until then  it remains  as a crap !

I am glad  to note   genuine concepts will some day  get ratified . Kudos to the Korean team.It is a great study to do with  many ethical issues.

Click below to read the related article

Link to EASE Trial  http://www.theheart.org/article/1313215.do

Next question  on the cards

Should there be  a time window above which medical therapy should be   deemed (Doomed !) to have  failed  , so that the patient becomes a default candidate for surgery.

Posted in Cardiology - Clinical, cardiology -Therapeutics, Clinical cardiology, Infrequently asked questions in cardiology (iFAQs), myocardial disease | Tagged , , , , , , | 1 Comment »

Exclusive guidelines for late presentation of STEMI

November 22, 2011 by dr s venkatesan

  • Acute myocardial  infarction is the number one cardiac emergency .
  • About a million papers and articles are available in  medical literature about STEMI.
  • Management of STEMI when they present early is addressed by every text book.
  • It is  really surprising to note there is no  simple and  specific guidelines  to manage STEMI when they present late to the ER .
  • Such a scheme is vital for physicians,  as experience suggest almost 40 % of all STEMI arrive late and are ineligible for specific reperfusion strategies.

The following  flow  chart is  exclusively meant for usage in STEMI when they  arrive late >12 hours .

This is a personalised version based on working in one of the oldest CCU in  Asia which handles  about  2000 acute coronary syndromes every year with a mortality rate of 6-7 %  Hope one can bear with it !

Please click on the chart for a high resolution Image

Comments are welcome

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese | Tagged , , , , , , , , , , | 6 Comments »

« Newer Posts - Older Posts »