Archive for April, 2014

I share my thoughts after going through this  85 page  land mark document !

acc aha 2013 guidelines cholesterol ncep

In whatever way I look at it  ,It  keeps  both physicians and their patient population guessing  in a  confused sate regarding their cholesterol levels  the treatment modalities !

It seems to revolve around a single point agenda,  how to fit a single drug called statin in the scheme of things !

What  if  ,  a new  drug comes and statin is  proved  not an angel  in our fight against the evil  of  atheroscerosis !


acc aha lipid guidelines atp 3 ncep  nhlbi dyslipidemia

Summary as  I interpreted

“All healthy and unhealthy human beings should ask only one  question

whether they can some how  benefit from taking statins  ? “

If your answer is yes ,  administer the statin  not in  low dose but in moderately high dose ! (It  appears  there is little role for low intensity statins )

There  is generally no  need to to monitor the lipid levels as long as patient is comfortable.

Disclaimer :  *Sorry , the Intention is not to  hurt the hard work of a elite panel who toiled for years to bring this much awaited guidelines on lipids and atherosclerosis! but to express my view , biased though !)

A mini research

To confirm my assumption I did a curious word search in this 85  page document .

For words statin , diet and exercise

  1. Statin appeared  814 times
  2. Diet appeared 8 times
  3. and exercise just once in the entire document !

statin search acc document statin acc aha 2013 guidelines statin acc aha 2013 guidelines 2

The importance of  diet and  body activity  which  are  the  primary   determinant of serum lipid levels is mentioned  in a cursory fashion in this  global guideline meant to control the total  cholesterol load  and atherosclerosis of our population .

Meanwhile . a drug which  acts in a  physiological  cell servicing  metabolic path way in a complex fashion  is glorified 814  times !Do  you still  think this post is is biased ?



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medical morality

Tree of life : When professional morality suffers a mortality . . . human health becomes a causality !

Greatest threat to the future of  human health is  . . .

  • Not from  exotic  infectious agents , bird flu  or  mosquito  fevers
  • Not from  epidemic of cardio vascular disease
  • Not from  thousands of  published  diseases in ICD code
  • Not from  aging population and failing  vital  organs
  • Not from  lack of availability of life saving  drugs and devices
  • Not from  lack of  hospital beds.
  • Not from  good sanitation
  • Not from  hunger and poverty
  • Not from  lack of para medical workers
  • Not from  lack of health awareness and education

But from  . . .

  • The way  health care is administered in this planet .
  • The way  noble professionals are created .
  • The way  trivial health  issues prevail over  major  health crises  that  wallop the health budgets.
  • The way by which  medical morality is systematically destroyed
  • The way   “concept of  health” is  sold  as a  buyable  commodity by insurance companies.
  • The way  medical journals churns out  junk articles in the name of research.
  • The way corporates indulge in  delirious pursuit  to  increase  bed occupancy rate of their  patient  ware houses (Also called Hospitals)
  • The  way greedy drug companies aim to increase the per capita drug consumption of  ill informed  homo-sapiens  by discovering  pseudo  drugs for pseudo  illness
  • The way   health insurance policies are misused
  • The way  rich spend billions for reconstructive  cosmetic  surgery while the poor die for want of basic medicines !


Link to a wonderful  article  on moral education for our kids in medical school !

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What happens to diastolic blood pressure in severe Aortic stenosis ?

Traditional answer: The diastolic BP remain unchanged. Only systolic BP falls as it is related to LV  stroke volume .(What we refer to as systolic decapitation of BP  )

Reasoning :Diastolic BP is related to peripheral vascular resistance , hence aortic stenosis has  little impact on diastolic BP .

 Further analysis

If we assume only the systolic blood pressure  is bound to decrease in  AS , at one  critical point of time*  systolic BP  should  approach  the diastolic pressure and pulse pressure should approach zero .This can not happen , hence at that point  diastolic pressure will also fall.

*What is that  point ?

No one really knows !

Correct answer

In severe aortic stenosis  both systolic and diastolic pressure falls , but the fall in systolic BP is more striking .

* Though it is customary for clinicians  to discuss them in isolation both systolic and diastolic  blood pressure are closely coupled parameters..In the absence of peripheral run off one of the  strong determinant of diastolic BP  is . . .  systolic BP !

Complex concepts

1. What happens in combined aortic stenosis and regurgitation ?

In  combined AS and AR   we get  pulsus bisferiens. implying  AR will  elevate the systolic blood pressure in spite of obstruction.

2.What happens in associated systemic Hypertension  and aortic stenosis . (Which is very common combo in elderly )

Since HT will increase the  aortic pressure , the LV-Aorta gradient tend to fall.

However ,this  does not happen always as if the original cause for HT was  dependent  more on the stroke volume rather than peripheral mechanisms .

3. Aortic stenosis with aortic  atherosclerosis .

A stiff aorta augments the percussion wave amplifying the symbolic BP and blunting the  classical anacrotic pulse of AS.

4.What happens to BP  during exercise in  severe AS ?

Exercise demands raise in systolic BP and temporary reduction in diastolic BP due to peripheral  vaso dilatation in exercising muscles.

If a fixed  crtical AS does not allow the systolic BP to raise  as required , diastolic continue to fall pulse pressure should still become wide .

Excercise testing is a tricky business in AS. Some have attempted it to assess the functional capacity.(Read below)



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A 76 year old man with history of recent stroke presented with acute chest pain  and his ECG  showed ,

ischemic rbbb

It was diagnosed as Anterior STEMI .Since he had co-exciting renal dysfunction also he was not considered for thrombolysis (Primary PCI not feasible !)

IV  Heparin bolus followed by infusion was started. Patient  had a comfortable night stay. The ECG taken on the morning  looked like this.


ischemic rbbb 001

Do you call this aborted STEMI or a simply an Ischemic RBBB ?

Transient RBBB due to Ischemia in  LAD territory(with septal compromise ) is very much possible during ACS. But , it is a rarely discussed entity unlike ischemic LBBB .

We know qRBBB  complicating anterior STEMI is much commoner than LBBB , still transient ischemic RBBB in non STEMI setting seems to be uncommon .Is it possible propensity for  Ischemic RBBB is different from necrotic RBBB ?


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LV ejection fraction (EF) is the most commonly used  LV systolic functional index.Since , it is an  easily acquired parameter,  it’s popularity has zoomed among both learned and novice cardiology professionals .(Not withstanding the serious shortcomings!)

In one of the evening rounds  in my CCU , a young cardiology fellow told me about a  patient  with acute  anterior MI with ST elevation V1 to V5.

The patient  was lying supine with trunk up . HR was 110 . BP was  100 /70 There were few basal crackles .The patient was undergoing  lysis with streptokinase.

It was  suggested  to me by the  fellow  that  the patient is  going in for “Impending  cardiogenic shock since his EF is just 30%”

That prompted me to ask this question

How good is the EF  a measure  of size of MI during STEMI ?

EF during  STEMI  is highly variable parameter.The following are important con-founders in LV EF measurement during STEMI.


  • Acute ischemia induced LV dysfunction .(Ischemic stunning from  the watershed zone  significantly over estimate LV dysfunction)
  • Mitral regurgitation  if present will underestimate it
  • Effect of tachycardia and bradycardia can be significant
  • The posture of the patient and  measurement errors (A good Simpson score is rarely  possible in a sick patient )
  • Associated  hemo -dynamic drugs like NTG/Dopamine etc which alter  pre and after load   and changes the frank starling forces.

* Please recall  , LV EF is never included as a criteria to diagnose cardiogenic  shock, confirming the  flimsy  nature of this parameter during acute phase of STEMI !

Final message

The purpose of echocardiography during STEMI is to rapidly identify any mechanical complication , not to waste time in calculating EF.

EF is not a good indicator  to  quantify the extent of STEMI  or it’s prognosis. LVEF cannot be used  to risk stratify STEMI in the first  48 hours .One can expect  the true LV function  to prevail only  at discharge.

Ideally ,LV  function should be reevaluated by 2 weeks to get a fair idea of true myocardial function .By this time all  confounders will resolve.

Clinical implication

Since many of us are suffering from an academic obsession and blindly follow the scientific guidelines, a hurriedly diagnosed  “severe”  LV dysfunction post STEMI may land our  patients to  inappropriate intervention !


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