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Archive for the ‘Cardiology lipids /dyslipidemia’ Category

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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  • Diabetes mellitus is a pro-coagulant state,especially so in severe uncontrolled states.(1)
  • This is mediated by increased  levels of   plasminogen  activator Inhibitor.(PAI 1 and 2
  • This tilts  anti-fibrinolytic  forces towards thrombosis.
  • High PAI-1 is an Independent risk factor for MI in young individuals (3)
  • During STEMI the success rate of  fibrinolysis is significantly lower in diabetic population because high levels of PAI 1 .
  • The triad of DM,Obesity, Insulin resistance is a powerful predictor of  poor  response to thrombolysis.

 

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I’m trying to get  a right  answer for this question for quiet some time. The literature on lipids is so vast  , one can never finish reviewing it.There are   nearly two dozen journals that  deal with lipids ,Atherosclerosis, obesity ,and vascular biology .

Yet  , the answer to this simple question is elusive to us .The Irony is complete when we have evidence for   two diagonally  opposite responses 4 and 5 .

My interpretation of the issue

Any lipid molecule if exceeds a critical  level ( Only  if   . . . associated with hypertension, or diabetes or smoking ) can penetrate the vascular endothelium. ( HT-pressure injury , Smoke- Endothelial dysfunction  due to Nitric oxide depletion) DM -Glycation of cell membrane  , finally some  unknown inflammatory component )

Though evidence  for direct endothelial  injury is more for LDL ,  less for TGL (Almost nil  for VLDL , but  TGL has more VLDL in it !)

Strangely ,these molecules , express a mob psychological behavior .In isolation they appear innocuous. But ,in an  unfavorable   setting it shows signs of  revolt. If a group of  LDL molecule start attacking a  dysfunctional segment  of endothelium , the other molecules  like TGL and VLDL fractions would love to join the crowd  and inflict further  damage . (Of course ,the lonely HDL may watch the chaos silently !)

Questions to ponder

If LDL is a sharp knife like molecule  trying to injure the blood vessel , every normal human being is potentially threatened  by this  lipid fraction . Mind you,  this is a physiological molecule  traversing the human vascular system  at concentration  of 130mg/dl  at the  velocity of blood .

So it is  foolish  to blame this  physiological molecule for all our ignorance.

I recall one recent definition for hyperlipidemia

The lipid levels at which a patient develops vascular injury is considered high for him !

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Statins have revolutionised the treatment of coronary artery disease .Intensive lipid lowering is the fundamental prerequisite in the management of both acute and chronic coronary syndromes. One question  is  always difficult to answer , ( rather reluctant to find the answer )   “The effect of statins on the HDL cholesterol”. Logic and the mechanisms of action would suggest HDL is not much affected , but in reality  I believe , in a given patient statins  do  reduce the HDL by at-least 10-20 % .This might have some significance. However ,  the marked  reduction in LDL  may nullify the adverse effects of lowering HDL.   Does this happen in all

What does the scientific evidence say ?

It says the opposite .  It seems  HDL is raised by statins that too significantly . The following paper also  suggests mechanism of  HDL  elevation by statins .It is Independent  to that of LDL reduction , I believe .

This JAMA article  adds more evidence

http://jama.jamanetwork.com/data/Journals/JAMA/5100/jpc70001_499_508.pdf

This paper  from  the  premier  Journal  of   Lipid research  agrees  to the   mechanism of  HDL reduction by statin  is a complex process  but still  it vouches for it .

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3035518/?report=printable

In spite of  all these  evidence . . .   it  remains a  huge suspect . . . from my personal point of  view ( My patients are  my evidence !  )

Coming soon

The above articles also raise an important  concept of dysfunctional HDL.  Simple raise  in HDL is not suffice . . .it should be functional as well !

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