Archive for October, 2012

A truth about half truths!

Arthur  Garson  explores further  .  Click on the Image to get a sample page from Amazon

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Acute coronary syndrome is the number one cardiac emergency .In any coronary care unit there are vital differences  between men and women in terms of ACS presentation and outcome . Though there can be variation in ethnic , geographical   factors .The following is   an observation  from one of the Asia’s oldest  and  largest coronary care unit over a period of 40 years . (Madras medical college Chenna ,India )

There is  very significant gender advantage in the incidence of ACS. The male female ratio is consistently around  4: 1 .This Indicates for every day , men suffer from ACS  by four  fold more .This is a very hard data can not be ignored . Women present to the hospital much later than men .This may be due to increased tolerance of pain, social issues  waiting for their spouse to arrive etc

  • There is a  significant  difference in the pattern of ACS in men and women . Men present with STEMI  and women present with more of NSTEMI . In  NSTEMI  the gender ratio is dramatically equal 1 :1 .
  • Explosive chest pains are less common in women .
  • For some unknown reason  diabetes  afflicts  women with a  greater ferocity  !
  • Similarly  it appears  obesity and dyslipidemia has more significance in women
  • Sudden cardiac death and primary VF is many fold less common in women.
  • Mechanical complications like mitral regurgitation and ventricular septal rupture are several fold higher in women (Weak muscle low muscle mass ?)
  • Thrombolytic success is slightly lower in women than men .
  • The overall outcome in ACS is same as men .Some say women fare  worse  .This is important because while they are protected heavily against development of CAD once they develop it  the outcome seems  exempted  from the gender advantage .The reason for this is not clear

Final message

Women show their  unique way   in ACS  too ! Some   of them are  true  advantages  while  few are disadvantages .The mechanism for these differences  can not be entirely attributable to presence or absence of  estrogen . The hard fact is ,  women always score over men in the tolerance levels and  deal effectively stress situations .  It would appear Women’s body   easily nullify adrenergic triggers .


Reference less cardiology .

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This was question thrown at me ,  in one of the  patient -physician meet .

“I am a 58 year old business man . I am taking tab Atenolol 50mg for over  6  years .I am comfortable with that .My  BP hovers around 130 /80 mmhg .My heart rate is 64/mt . I have recently  moved to a popular city in south India  . Now , my cardiologist thinks Tablet Atenolol  for hypertension is useless  . . . what do you say sir ?

My answer went on like this  . . . causing much  displeasure  to my  colleagues !

Atenolol  is a  wonder drug for management of both hypertension and angina for more than 2 decades .  It is  still useful in majority of patients with HT .

The reason for  current generation of cardiac physicians   shunning  away  from this drug  is  largely  for  non academic reasons . A drug which is  in market for more than  a decade ,  generally becomes a generic one. Generic drugs are  like  orphan drugs !   and patients  who consume generics are inferior ones .This is how market economics want us to think .

Physicians are sincere followers of  science and science is not sacred ,  often times  . . .  it is the creation  of   corporate gimmicks .

Few small  studies ,  one major publication  , few guideline   from  influential    scientific bodies  , cocktail of   seminars  , symposiums   all that  is required to disseminate  a concept !

The second major reason is every physician wants to behave in unique way . He fears loosing  his prestige and  charm  if  he  continues the same drug prescribed by another physician  . Many patients also do not like to continue the same drug for long time  !

And now a few words for the cardiac scientists !

*The concept of central aortic pressure and beta blocker’s lack of control over it are all concocted .Beta blocker is most powerful agent to reduce the shearing stress in the walls of aorta . We know that and we believe in that and we prescribe it for aortic dissection to attenuate the intimal tear . Can it do this  . . . without lowering central aortic pressure ? Think for a moment !

Atenol and Metoprolol : The curious  companions .

Both being   closely related beta blockers ,  what makes  Atenolol  to be frowned  upon   and  still   Metoprolol  is  alive and kicking  !

 My final answer to your question !

Atenolol is still useful in the management  of HT. If your BP is well controlled ,  and you have no side effects,  there is absolutely no need to change  the drug   . . .  if  you are  insisted  , you may consider  changing  your doctor   . . . . . .  rather !

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The  commonest  cause for death in massive pulmonary embolism is 

  1.  RV shock
  2.  Massive Hemoptysis
  3. Primary VF   originating  right ventricle
  4. Refractory Type 1 Respiratory failure

Answer : 1  .(RV shock , RV standstill and RV , RV stunning  is the unequivocal  cause for sudden death in pulmonary embolism . This RV shock occur very early .Once the patient survives the initial  RV scare (say 24-48 hours) usually do well if prompt thrombolysis and anti-coagulation is administered  )

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Conventionally  pulmonary embolism is classified as massive, sub massive  based on

  1. Severity of obstruction
  2. Level of  obstruction in pulmonary anatomy (MPA,Branch PA, Segmental etc )
  3. Thrombus burden
  4. Quantum  of pulmonary vascular bed  compromised

But it is always intriguing ,    the clinical outcome was not linearly  correlating with the above parameters.

Instead the outcome seemed more dependent on the following .

  1. Degree of RV dilatation
  2. Systemic hypo-tension
  3. RV shock

Image courtesy .www.smartdraw.com

So ,  whatever be the quantum of pulmonary embolism , it is the behavior of RV that is going to determine the outcome.  The current  wisdom   demands , all hemo-dyanmically unstable pulmonary embolsim may be considered as massive or high risk pulmonary embolism and  aggressive treatment  is  to be undertaken.

Counter point

There is  one major diagnostic issue  if we depend more on hemo-dynamic instability . What is that ?

There is no valid method to identify Acuteness / chronicity of   RA, RV dilatation . Consider this  example , a patient with chronic thrombo -embolic PAH presents with  acute deterioration  due to a transient arrhythmia  or  non cardiac  cause of hypotension . He is at  risk of being labeled as  acute pulmonary embolism  since he may  show   some thrombus  in his pulmonary circulation in  CT scan .  However ,  no great harm is done as long as he receives only heparin.



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Mitral valve prolapse  probably is the most common cause for  abnormal added  sounds in cardiac auscultation . MVPS occurs  when  mitral valve tissue  and its accessories  overgrow disproportionately    with reference to  the mitral valve orifice (Also referred to elongated or redundant leaflet) .The net mass  of mitral valve apparatus has an inverse relationship with  LV  cavity volume . Because of  excess motion  ,  leaflet may bulge into left atrium to different degrees and different angulations. This entity  as rule is  benign  in most people . Still ,  rampant diagnosis in the community  (With the  pathological proliferation of   scan centers  )  has raised considerable anxiety .


Hence , the criteria  to  diagnose MVPS are made stricter .Unless the leaflets are thickened and some degree of MR  occurs the  usage of the term MVPS  is  not justified .


Unusual  sounds in MVPS

In many patients ,  AML become so nimble ,  it flexes, bends and   stretches  in both systole and diastole. These leaflets   can generate clicks  not only during  prolapse . Simple folding and unfolding of  long redundant  is known  to produce clicks.

generally folding occurs in diastole and unfolding in systole ( of course in extreme redundancy  both can occur in both phases )

This diastolic  clicks in MVPS has been reported rarely  in literature . It is   more common than we realise .The timing  of these clicks  are  not constant .Audibility is low .It can easily  be confused with opening snap of mitral stenosis .

The spatial  relationship between the sound generation and the anatomical prolapse  does not match . It is always  possible  when  PML prolapses  AML may generate a click and vise versa . Diastolic clicks or opening snaps  are known to occur in some of the severe forms of MVPS.  The first heart sound is not only loud  , the  differential  motion AML and PML  may distort  two componets of  M1  .It needs to be emphasized the loudness  of  S1  can be  preserved even in the presence of significant MR .(Even as the PML prolapses  causing MR ,  an  elongated  AML continues to generate a booming S 1)

Final message

Can MVPS produce diastolic added sounds ?   Yes . . . it can .

Mid systolic click  , and  late systolic murmur  is the classical  manifestation of MVPS . In reality , one can get a variety of noises from prolapsing mitral valve apparatus in both phases of cardiac cycle.


These are all inferred from bed side observation . Luckily  I have found a  reference from a New york state journal of medicine .Other wise my observations would have been ridiculed .  Gone are the days   when we spend  hours together  in  clinical auscultation  of mitral valve motion  .

Today we are  in the era  , working in hi- tech cath labs ,  aiming  to  capture those same  redundant  mitral leaflets  with catheters  and clip its wings to reduce the mitral regurgitation  .

Asking for a phon0-cardiographic  documentation of diastolic mitral click in MVPS    would be a laughing stock among current generation cardiologists  !  Still I would argue for such a study !

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Is this child with Eisenmenger operable or not ?

The answer to this question is  debated for many decades . The old school of thought was  grown with meticulous cath study (Pioneered by Paul wood and his team ) .Calculating PVR is academically fascinating . With  so  many  variables,  assumptions and too much dynamism in a circulatory system , It has never been proven as a  gold standard .

The presence of following  factors points to  possible advantage for  shunt closure .

  1. Pink Eisenengers ( Complete  lack of   clinical  cyanosis   )
  2. Clinically mild cyanosis  but  Oxygen saturation   nearing 92 %  (We  have seen an occasional  patient  with 98 % )
  3. If Echo shows  a dilated left atrium and left ventricle (VSD,PDA) it indicates a significant L-R shunt.
  4. Lack of septal bulge towards  LV (This Indicates  RV has  still  some  useful life in it ! )
  5. Pulmonary  flow velocity > 1.5m/sec indicates fairly good flow across RVOT (Qp/Qs calculation is  almost impossible in bi-drectional shunt )
  6. Pulmonary artery diastolic pressure  <  3o mmhg
  7. Pulmonary artery pulse pressure > 50mmhg

*Oxygen, Tolazoline test in cath lab has  limited value.

**Temporary balloon occlusion and watching  for reversibility is not useful (As fall in PAP and  PVR is a long term affairs )

Final message

Scientific cardiologists may feel awkward  to read this message .

  • With mortality for shunt closure in   Eisenmenger  reaches  nearly 50 %  ,  it is essentially a 50-50 guess game !
  • We  often depend on our collective  clinical acumen (Also called as  Gut  feeling   . . .”I some how feel  this child will do well ! “
  • Most  importantly  surgeon’s  experience and expertise would  finally prevail  over cardiologist !

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Failed thrombolysis is a well debated concept, while failed primary PCI is a conveniently neglected phenomenon .

How to assess successful reperfusion following PCI or thrombolysis?

I do not know how many  of us know this vital fact !

Coronary angiogram is squarely beaten by the humble  ECG in assessing the effectiveness of myocardial  reperfusion . This is not hard to understand as  coronary angiogram *  can  tell us only  about epicardial  patency ,  while ECG  sends vital perfusion  data from within the  myocytes ! Which do you  think is superior ?

And now  interventional cardiologist have realised this fact . they  measure the ST segment  regression instantly once the primary  PCI is  completed . How ?  An ECG is recorded from  right inside the infarct  related artery .

*Of course myocardial blush score , TIMI frame count are poor alternatives !

This paper just published in CCI is  a fascinating revelation .


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Anginal equivalents are distinct  (often vague  ) symptoms that occur in response to myocardial Ischemia , instead of angina. Dyspnea or shortness of breath  is the commonest anginal equivalent . The incidence and exact mechanism  is not clear. Both angina and dyspnea are sensory  events . Both are  perceived  at the level of cortex. Angina occurs when ischemic  muscle  triggers pain signals from the   nerve  twigs engulfing the myocytes membranes  and the vasavasorum.

Dyspnea during myocardial  ischemia  is multi-factorial

  1. Signalling error .( Mismatch between respiratory /Cardiac  receptors  neural traffic)
  2. Cortical perception disorder.
  3. Autonomic neuropathy (Blocks pain signals  but still may carry  myocardial stretch response)
  4. Coronary sinus lactate –  Biochemical /Chemo receptor stimulation
  5. Isolated  Ischemic LV relaxation defects  , and resultant elevation of LVEDP
  6. Ischemic systolic stunning  and secondary  diastolic dysfunction  (elevated PCWP  pulmonary stretch receptors stimulation )
  7. Ischemic MR . Eccentric MR jets and regional and segmental elevation of pulmonary venous pressure has been reported. (Unilateral and segmental pulmonary edema)
  8. It is possible  ,  Ischemic wall motion defect per-se  can induce myocardial stretch and create a feeling of dyspnea.

Out of the above eight factors  which is  most important  ?

The most popular and easy to comprehend   mechanism   is number 5 : Ischemic diastolic dysfunction .

(Fellows will be appreciated if they  know this !   )

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How to manage an  asymptomatic 45 year old man with  90 %  mid  LAD lesion  , with  FFR  .9   who is  stress test  positive at 9 Mets  ?

Six  cardiologists and six responses   . . .  and the elusive seventh sense

  1. FFR is most scientific test to assess  physiology of coronary stenosis  . I will  go with that  and put this patient under  medical management.
  2. I agree with FFR, still the  patient has no symptoms  , but why the hell is EST  + ve ?  I am confused  .
  3. I would definitely stent the lesion irrespective of the symptoms .
  4. I would order a stress thallium . I do not believe in FFR
  5. The data provided  is insufficient. I would like to this patient in my clinic , and if necessary  may  order a fresh CAG.
  6. For a 90 % LAD  lesion FFR should not have been done in the first place .That is the root of the confusion. He should have received a stent long back .

Final message

FFR is  a terrible concept   for two reasons . One ,  it never bothers about flow across  a lesion. It simply  relies upon  pressure drop. we all know  there  is an intricate relationship   between pressure and flow . Simple pressure drop can never be  expected to translate into incremental flow in biological systems .The  second major limitation is  it  ignores the  morphology of the lesion . We know an eccentric soft  lesion with a  good distal   FFR  is  live  coronary explosive .

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