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Posts Tagged ‘acc.aha’

Can we advice CABG for single vessel disease  ?

Yes, CABG  may be indicated  in

  • Critical , proximal , complex  LAD disease   with or without  ostium involvement.
  • Many of the bifurcation lesions with large and significant  side branch
  • Small caliber LAD with diffuse disease .

When these occur  in diabetic  subjects , the  indication for CABG is more certain .

* Present generation cardiologists  would feel  every  lesion  is  stentable and should not be referred to the surgeon .But it should be emphasized here,   technical feasibility alone  ,  does not  imply  PCI is superior and ideal in all coronary interventions.

Can we do a CABG  in  single vessel disease  with  normal  LAD ?

CABG is  very rarely  indicated   for isolated RCA or LCX disease. It should be consciously avoided in this patient population.

This is because the at risk myocardium  supplied by these vessels are far less than that of LAD. PCI  is  preferred    in these vessels .(Ofcourse , after considering medical management  ) .

CABG is  ,  too traumatic a  surgery , to  offer  in this  low  risk  coronary  lesions.

Exceptions

CABG  can still be done in following situations  for non LAD single vessel disease.

  • Left dominant circulation  with  complex lesions in LCX /OMs.
  • It is common to see diffuse , long segment  and severe disease of RCA with normal LAD /LCX system .PCI is not feasible in this subset.
  • Failed PCI
  • Recurrent instent restenosis.
  • Bail out CABG after a acute complication during PCI

One should remember ,  inability to do a PCI  does not  mean ,  the patient  should   land in surgeon’s table .We should recall , from our memory medical management is an effective and established form of treatment in single vessel disease ( Mainly for non LAD , and some cases of LAD also !)


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Angina is classified in many ways .The most useful , clinical classification is stable and unstable angina . While  ,the former generally is considered   innocuous  the  later conveys a sinister  signal to the patient as well as  the physician. 

Why stable angina is  stable ?

In stable angina

  • The patient knows how the pain is going to behave by his past experience.
  • Very predictable .The patient knows at what distance it’s going to come
  • He also knows when  it will disappear.(For some , with rest for others with nitrates)
  • He also knows where the chest pain will radiate.
  • If some thing is unusual it is unlikely to be  stable angina , also any  first episode of angina is considered unstable as one wouldn’t  know how the angina is going to behave !

How is that stable angina has such a learned behaviour ?

The main reason for  the beningn nature of  stable angina is the coronary artery has “stable plaques”

Stable plaques produce stable angina  ,Unstable plaques cause unstable angina

Stable plaque s restrict blood flow only at times of  increased demand( ie supply side ischemia.) There is no thrombus in these plaques.As soon as the exertion ends the angina is relieved.So in chronic stable angina, the patient is stable, the angina is stable , the palque is stable , the coronary blood flow is stable.

Unstable palques have erosion and thrombus , and it interferes with blood flow even at rest .So in  unstable angina, not only the angina is unstable , the plaque is unstable  ,coronary blood flow is unstable. So it is obvious unstable angina , may not be relieved by bed rest.It needs intensive treatment.

Is there a overlap between stable and unstable angina?

Yes. In fact it is more common than we realise.

Read this post https://drsvenkatesan.wordpress.com/wp-admin/post.php?action=edit&post=2177

Related topics

How is a stable palque converts into a unstable plaque ?

How do you identify these vulnerable plaques ?

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                                                    Drugs are poisons , whenever it is administered without valid purpose. it can enter human body  in many ways (Oral, intravenous, percutaneous etc ) And now we have another route namely intracoronary !

                                                   In quest for prevention of restenosis, many of the anti cancer drugs are now delivered directly inside the coronary arteries .These drugs are secreted  like a sustained release  tablet from the drug coated stents.These drugs are expected to prevent restenosis within the stented segment.But, after years of  intense debate and research  , we realised that ,  drugs  eluted from the stent  could damage the distal coronary vascular bed and coronary microcirculation.( And thus came the epidemic of acute stent thrombosis ! )

                                                The tender and sensitive coronary microvasculature  is constantly exposed to  these  powerful anticancer and immmunosuppresive  drugs .It is a great surprise , no body thought of  this dangerous drug -coronary artery interaction ! It required the genius of Renu virmani and others to point out this.

But still , the cardiology community by and large , fails to consider  this an important issue.This is proven by the fact, usage of DES is  still increasing  and used mainly as an off label indication.

Read this land mark article from circulation

picture1

http://circ.ahajournals.org/cgi/content/full/115/8/1051?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&author1=renu+virmani&andorexacttitle=and&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=1/1/2007&tdate=12/31/2007&resourcetype=HWCIT

 

Questions that need to be answered

  • What is the long term effects of drugging a coronary artery ?
  • Is no reflow or slow flow  more common after DES , because of the adverse drug reaction in the distal vascular bed ?
  • If a patient  with  DES  undergoes a CABG later what  would be  the impact of the  drug on the graft ? Will the functional vasodilatation   affected ?

Final message

                                  A drug , to get a legal clearance it has to undergo  hundreds of rigorous tests . Finally it is cleared for that  specific indication for which it is tested  .Just because a drug is cleared for one purpose ( Paclitaxel for malignancy ) it does not mean it is safe to use for any other  purpose for which it is deemed to be useful . Exactly the  opposite is happening   in the  the field of interventional cardiology . No body wondered to think what would be the effect of these drugs on the normal coronary endothelial cells and vasculature.Is it not a crime ,  without analysing this particular issue  , dozens of drug eluting stents have been released in the market . And now,  sounds of crying  foul is heard world wide !

Let us thank  , the so called negative forces in cardiology  for making this an  issue . In science ,  the watch dogs should bark  at  times of danger not wag the tail !

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Drug eluting stents : A slap on the face of Evidence based cardiology . . .

Click the BMJ link or read below

 

venkat-bmj

It is often said science is sacred and unfortunately we forget ,  science is not a heavenly creation and it is the creation of scientist of varying grades of integrity fueled by the vested interest of medical industry . It has been a almost a daily affair , some of the devices and drugs are recalled or found to be unsafe on patients.

Now the big cat has come out .The Drug eluting stent has fallen from Hero to Zero in a short span of 5 years. It was projected to have zero percent restenosis in 2002 . And now we realize it is Zero percent truth.

What has started as anecdotal reports of late stent thrombosis has indeed become an epidemic in all DES patients. The five studies that has been published in the NEJM this month (March 2007) has convincingly proved how unsafe these stents are in most of the coronary population .

Millions of patients in whom this stent was implanted will carry an impending stent thrombosis and possibly an SCD . Who is to take care of them ?

The DES story is a clear cut case of getting premature approval for a dangerous form of treatment inside human coronary arteries.

It is amazing how the scientist’s eyes are shut by the illusion of knowledge and lure of wealth. How foolish they were to think drug which was administered via the stent will selectively prevent vascularisation and leave the normal endothelium intact . Now they realized , one should not suppress the endothelial growth around the stent and got the fundamental point wrong. Which was the key reason for the astonishing episodes of late stent thrombosis. When we play with biology of nature we have to be little more careful .God has created man and his heart for over a million years . One can not alter it by a 6 month follow up study of DES .

When ICDs were exposed last year , of similar disastrous outcome they were recalled and explanted . How are we going to unstent the millions of coronary arteries ?

Somewhere along the line the medical professionals have lost the battle against the Wall street and NASDAQ . Or how else we can explain repetition of similar events.

The wages for the modern technology , the patients have to pay a heavy price.

Let us all hope common man with common sense will reign supreme over the sixth sense of the uncommon man . . .

“Ignorance is better than illusion of knowledge”

Dr Venkatesan Sangareddi MD , Assistant Professor of cardiology , Madras medical college Chennai, India

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Stents are mechanical  devices like  a  spring ,  used to  keep an artery open after a PTCA or PCI.

des-why4

                                Bare metal stents(BMS) were found to have restenois rate of about 25%.  So it was perceived a stent should have it’s own protective coat , so that it won’t get restenosed.For this the researchers thought  anti cancer drugs are ideal as they block cell proliferation and thus neovascualrisation and restenosis.Alas, they were found dismally wrong ,  after all , neointiaml proliferation is only a part of the problem of restenosis  and simple blocking of cell growth is insufficient . The issue doesn’t stop with that, the anti cancer drugs incorporated within the stent simply can not differentiate normal from abnormal cells and

DES effectively blocks the normal endothelisation over the stents and make this highly vulnerable for acute stent thrombosis .

This complication is unique to DES and can result in SCD.Further ,during the last 6 years of DES , we recognised the restenosis rate has increased form the much hyped O % to almost 15% and it’s still growing . These  complications  has made a huge question mark over the future of drug eluting stents !

des-coverage

The concept of DES may not die , but which drug it should elute should be answered ! This  again is  going to be a long battle. So it is currently   adviced,  based  on common sense ( With due respects to  those RCTs  funded by industry )

Whenever you encounter a block within the coronary artery* Ask the following  questions in sequence  ,

  • Whether we can leave it alone  with medical therapy  ,  if the answer is no , proceed  to the next step !
  • Is there a possibility for plain balloon angioplasty in a given vessel (POBA, Yes !  the concept is not dead yet !)
  • If you decide a stent is required , Will  the  bare metal  do the job ?
  • In multivessel CAD  , Did the issue of increased metal load on the  long term outcome was considered ?
  • If lesions appear complex,  should we  not strongly consider CABG as an option ?

However  if we  have the habit of  ask ing the following  question  you are likely to deviate from scientific approach  

Is it possible to put a stent  across  the block ?

Yes , will be the answer most of the time ,and the patient will invariably get one or more stents  and carry a life long  stent related problems.

*The rule does not apply in Acute coronary syndromes

Also read this letter  posted by the author published in  British medical journal

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                                      One of the important principles of  post PCI care is,   we need  to be very careful  till the metal struts are fully endothelialised . This is of vital importance as improper endothelialisation  is a powerful trigger and nidus for a  imminent thrombosis and  acute coronary syndrome.

stent

It is a billion dollor irony , the much hyped DES does exactly what we don’t want ! and still it’s  usage is  increasing world wide .  The drugs (Anti cancer agents)  which coat the DES   are the villains as it  prevents  the  metal struts  from being endothelialised  and  keep the metal surface  raw and vulnerable , while the  much maligned  bare metal stents allow  this natural endothelialisation  process  without any interruption ! So right now it is mandatory  to administer dual antiplatelet agents  life long( life of the stent !)   for the patients with DES.

 Just look , at the following image of  a stent in vitro at  30 days follow up

des

des-2

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                                Hypertension is the most common clinical  cardiovascular entity.Left ventricular hypertrophy (LVH) is  an important consequence of  HT.In fact, it is considered as a end organ effect or damage. Others being brain, kidney, and peripheral vascular disease.Knowing about LVH is important because it has been linked to increased cardiovascular events.

lvh-4

                              Though LVH is considered  as a close companion of  HT  it is  surprising  only a minority (15-30%)  show evidence of LVH .Some  experienced clinicians (Level C evidence)  quote even lower < 10 %  .Traditionally LVH was detected by ECG and now it is replaced by echocardiography.

What determines the LVH ?

It will be suprising to note , answer to this question  is  still not  clear .

  • Is it the duration of elevated blood pressure ?
  •  Is it the absolute level of blood pressure ?
  • If so , is it  the systolic BP  , diastolic BP or the mean BP ?
  • Or is it related to the etiology of HT ?
  • There has been no significant correlation between the above parameters

When we don’t know  the answer to a question in medicine , the answer will  generally will be inside the genes !

So in HT also the major determinant of LVH is in the genes that determine the myosin heavy chain  response .

and also ACE gene polymorphism.ACE genes are involved in the expression of growth factors within the myocardium.

An excellent study  on the issue http://www.nature.com/jhh/journal/v17/n3/full/1001523a.html#tbl1

It implicates , gender, age, race etc in the genesis of LVH

Final message

So , the  myocardium does not respond with LVH   in all patients with HT.It happens only in a minority* .Duration of HT can be an important determinant , but  the major factor is  the alteration of genetic switches  within the myocytes How this switches are going to  behave ,  is largely inherited .Regression of LVH is also not uniform again implying lesser role for hemodynamics. (Some studies revealed ACEI have maximum regression  of LVH , later disputed )

*LVH is more consistently seen  in hypertension due to reno vascular  or parenchymal disorders .It is also an observed fact , a  combination of diabetes and HT is more likely to result in  LVH.

The other major issue  that needs explanation in HT/LVH  is   , how much of LVH is due to  myocyte hypertrophy perse  and how much is contributed by interstitial cell hypertrophy(Non myocytic hypertrophy)

This issue will be discussed soon

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