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Posts Tagged ‘hyperlipidemia’

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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Whatever  is your answer .   It will be   far off from the truth .

What causes  Atheroscerosis ?

The perception  that , circulating lipids directly damage  the coronary endothelium is an  ill proven concept.  Isolated hyperlipidemia  rarely leads to full blown Atherosclerois .

If  LDL moelcules  can penetrate the endothelium  , why the circulating LDL  at a normal concentration of 130mg/dl  fail to do so in vast number of humans   as they criss cross the human circulatory system  at-least a  trillion times  every year ?  So , there  must be something else  operating *It requires a high blood pressure, diabetes , smoking or some form of endothelial injury  (That includes chronic Inflammation )  for the  lipids to  enter the sub endothelial planes and start depositing.

The relationship between serum lipids and plaque burden lacks clarity.

* The argument that 130mg LDL is injurious to endothelium  while  100mg  is not  ,  can  easily be disputed !

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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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10.14prescriptionRXStatins are projected to be  the saviours of human race against the  killer atherosclerosis .Now we have reached a stage  soon ,  where every healthy individual may be administered this drug. There are consistent evidence for statins to reduce , retard , prevent progression of existing atheroscelorosis  and possibly prevent future atherosclerosis.

This  wonder drug acts by blocking the HMG COA enzyme a vital  enzyme that regulates the lipid metabolism within the cells. It is made to appear  as if ,  the  God has  created this enzyme  with the only purpose for human suffering , by blocking this   we  expect  all errors in lipid  metabolism is corrected.

This enzyme is  part of the house keeping  system  that is meant to service the human cellular lipid layers 24hrs a day. If it  is impaired intentionally one can imagine the consequences. That’s what modern science is all about. Luckily God is kind enough the side effects of  blocking this enzyme is seen only in minority. The myopathies that are classically described with statins are due to possible mitochondrial dysfunction .

As the debate still  continues to find the   optimal bottom levels  of LDL  , we have more worries ,  real world experiences have brought us a new issue  namely  the  reduction of HDL with statins. While literature search on statins and HDL  tell  us there is marginal increase in HDL up to 10% the fact is there is marginal fall or significant  fall in many of the patients .

How can this happen ? A  huge difference between real world and trial world ?

statins hdl ldl

* Brands shown  not intentional

Readers are welcome to add their input on this question .

Reference

Visit HDL forum

http://www.hdlforum.org/

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Let us not forget the basics !

  • HT management has been made  easier with the availability of  many  good drugs , at the same time it has become a complex  issue with as many classification and guidelines.
  • The management of HT has evolved over the decades. Now we have realised  HT  is not a simple number game . Reducing the blood pressure to target levels is not  sufficient and is not the primary aim !.
  • In fact we now know controlling the numbers alone is never going to work  , combined risk factor reduction is of paramount importance.
  • HT per se is less lethal but when it combines with hyperlipidemia and diabetes or smoking  it becomes  aggressive.The blood lipids  especially the LDL molecule  enjoy the high pressure environment  ,   penetrate and invade the vascular endothelium.
  • ASCOT  LLA  study has taught us,   for blood pressure reduction to  be effective and reduce CAD  events one has to reduce thier  lipid levels also.So , for every patient with HT there is not only a target BP but also a target LDL level .

picture1

 

Final message

The tip for better vascular  health is  , all  hypertensive patients should keep their lipids to optimal levels and all hyperlipidemia patients should keep their BP as low as possible .

“Keep your LDL  as low as  your diastolic blood pressure  and  let us  keep it around 70 -80

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