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Archive for September, 2011

Off label prescription 

  1. Is a great scientific concept
  2. Is a deceit camouflaged  with a pseudo scientific fabric.
  3. Can be encouraged in very selective patient  population and diseases by experienced  cardiologists , as  it may be really useful when no other options are available.
  4. Is diagonally opposite  to evidence based medicine , should be banned in toto !

Answer:

4 is the correct answer .occasionally 3 can be true

Some of the examples of off label indication

  • Statins for Aortic stenosis
  • VSD device for RSOV closure
  • Ivabradine for cardiac failure

By the way how does an off label become on label?

It is not the ” God ” who  gives the label to them

There are few “Demi Gods” sitting aside  in the regulatory corridors of  New york and  Geneva who decide the fate of these drugs and devices . Ultimately the integrity of these organizations that will either protect or injure our patients !

Final message

Medical science grows my mistakes  . . . hence  we should be encouraged to do more of that  . . . so that we can grow !

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ST segment depression is a fairly common observation in anterior precardial leads. It   is  due to

  1.  Pure electrical phenomenon (Referred to as reciprocal changes)*
  2.  Additional  ischemia in LAD territory
  3.  It could imply  the IRA  is  a critically occluded  LCX and STEMI is actually an   infero -posterior STEMI
  4.  Simply  indicate a  multi vessel disease.
  5. Many times  reciprocal changes may simply indicate extensive nature of the  index  inferior MI.

How to differentiate reciprocal ischemia from true  remote ischemia ?*

  • Logically true ischemia patients  should suffer from double dose of angina (Infarct pain plus ischemic). Most of these patients will present in a   scenario of  post infarct persistent  angina . Patients with   pure electrical reciprocal  changes are relatively  quiet and  severe distress is uncommon.
  • In true ischemia  , both patterns are  not temporally related  in time. If its a  pure electrical phenomenon they should be linked in time .
  • Disproportionate ST segment depression  (ST elevation  in inferior lead  is  2 mm  while ST depression in v1,v2, v3 is >  3 mm )
  • Persistence of ST depression even after thrombolysis  or PCI to IRA.
  • Worsening with thrombolysis would suggest ST depression in V1V2 and v3  is indeed an  episode of  true NSTEMI  of LAD , where thrombolysis is contraindicated. (Also  read  – A  related article  dual acute coronary syndrome in this site )
  • Echocardiogram will give us a clue .One can  detect ischemic the wall motion defect in the segment in dispute .(Reciprocals do not show WMA )
  • Coronary angiogram   would provide   definite  answer to the speculations in most  . Still , it may   require a FFR  to confirm ischemia in the contra lateral artery.

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Primary PCI (pPCI) is probably*  the   best modality in the management of STEMI .

( *Probably because ,    we  know “Time” ( fate !) is  still the  most crucial determinate of ultimate outcome of STEMI )

Any experienced interventional  cardiologist will be aware of the surprises  and difficulties  they encounter during primary PCI.

The pPCI  is all about  opening up the IRA rapidly and  wheel  out  the patient  from cath lab at the earliest.

But ,  ironically , an often  under- reported   issue  is the difficulty in  identifying IRA itself  !

One may wonder  , how this can happen ?

Following difficulties  can occur  in identifying IRA during  primary PCI*

(* There are some  hyper-talented  cardiologists who would never consider IRA recognition as an issue  .This article is not meant for them.)

The problems can range anything between the following   queries

  • Where is the IRA?
  • Is that the IRA?
  • No IRA ?
  • Multiple IRAs !

Angiographic encounters during  pPCI  and  IRA  trouble shooting .

  • When there is diffuse multivessel disease.
  • Thrombus vs  eccentric plaque  both  showing  intra luminal filling defect .
  • Thrombus spill over to adjacent branch or A mid LAD lesion with  stagnating thrombus extending to LCX ostium  mimicking two IRA
  • A bifurcation lesion with both LAD and LCX  ostial occlusion.
  • Multiple active looking  plaques with thrombus
  • STEMI in patients with preexisting CAD . Is it a CTO ?  ATO ? (Acute total occlusion ) A  CTO  ,which is  fed by collaterals from contralateral artery  ,  if this feeding vessel is  occluded even  partially ,  STEMI will occur in CTO territory . Here  , for rapid salvage you need to open the vessel that feeds the CTO territory.
  • Post CABG and post PCI form a special subset . Some times it is very difficult or even impossible   to label a graft as an IRA

Finally and most importantly  , when  there is no visible lesion in any of the coronary arteries   and look  near normal  !   Is that  no IRA  ?  or Wrong diagnosis of STEMI ?  Every one blinks  in cath lab . The consultant  howls the fellow to verify the ECG . Finally it may  well turn out to be an early  repolarisation  syndrome . These are wages we  often pay for the modernity !

How to approach  the situation when one is confused with  identifying the IRA ?

The good old ECG will come to  our  rescue sometimes. Realise in a multivessel CAD  , ECG is also vested with errors.

Echocardiography  rarely  gives a convincing answer to localise IRA. (Segmental overlap , preserved sub epicardial  contraction , residual ischemia all tend to confound )

Most confusions occur between LAD and  diagonal /LCX as there can be a huge overlap in the ECG territory  anterolateral segments

In a infero posterior STEMI, if  you have both  RCA  / LCX lesion and you wonder which  is the IRA  it is easy to solve by looking for RV involvement. (LCX lesions however dominant they are  . 99/100 times can not infarct the RV significantly  !)

If the lesion  is in PDA  the  issue is made simple.

Doing a primary PCI  blindly without knowing the IRA

This is  modern-day cardiology  at its scientific  low ! . Cardiologists  indulge in such  things much more commonly than one would imagine.

Probably  they would reason ,  it is safe to stent every vessel that is potentiality  an  IRA  , rather than  missing it. Though the concept of  multivessel stenting in STEMI   may help   patients with complicated MI ,  like pump failure ,  it generally increases   risk of primary PCI outcome in otherwise stable STEMI. Primary PCI procedure must be as short as possible. The other option is to do plain balloon angioplasty in less deserving vessels.

Important considerations  in the setting of complex multivessel CAD  during pPCI .

  1. Fall back on medical therapy
  2. Staged PCI
  3. Deferred or Immediate CABG
  4. Hybrid procedures like PCI  with CABG

Final message

IRA identification can  indeed be a difficult task  during primary PCI.  Sound knowledge and experience about coronary anatomy and its draining territories especially  in  the setting  of  multivessel  CAD  is essential to avoid errors.

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Do you fear to deploy DES during primary PCI ?

  1. No. Not at all !
  2. May be  “Yes”
  3. Yes, definitely
  4. It depends upon which drug it Elutes !

Answers  that might  decode  the  cardiologist  mind. ( Excuse me  if it errs !)

If the answer is 1 ,  You are the most optimistic cardiologist  and scientifically  updated ,   data driven  cardiologist , and with little concern for the patient welfare.

If the answer is 2 , Your are a cautious cardiologist may be . . . may be . . .  an   ideal one . The chances of you , using a  DES is  still low in  STEMI.

If the answer is 3 , You are a pessimist and  with   anti technology thoughts but still you  have more concern  for  your patients!

If your answer is 4 ,  You are undecided  and probably  ignorant as well . Most likely   you would not use it  for some reason  .You need to read more  on the topic .

By the way , my answer is  response three.

Read further ,  the EXAMINATION trial just released in ESC 2011 Paris .

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This RIFLE  shoots without  bullets . Yes ! it  helps the cardiologist to  trouble shoot  the kidneys which often  suffer from  cath lab cross fires .

As  the cardiologists indulge in sophisticated cardiac procedures ,  in more and  more  sick and co- moribund  patients , it is becoming increasingly  important  for them ,  to   give due  respects  to  other organs as well !

Renal function is an important determinant   in the  over all outcome  in any cardiac patient.

  1. How to assess  the baseline renal function ?
  2. How to measure  the impact  of the  cardiac procedure ?
  3. How to  follow  up and monitor the  progress of  renal function   in coronary  care unit.
  4. How to  reduce the enhanced renal  risk ?
  5. When do you call for  the Nephrology consult ?

Every step becomes  vital . Do not ever think , a  cardiologist’s job is over  once few  stents are deployed . Wheeling   out a  sick  and fragile diabetic  with borderline  creatinine    out of the cath lab  may be  considered   as a procedural success  , but the real success happens only after  every organ of the  your patient  comes  out  unscathed  after the procedure .  In this  context  , we should first aim to  become a nephron  savvy and a nephron friendly cardiologist .

I have witnessed  cardiologists  spend hours  together  in cath lab with liberal injections of contrasts  even in  elderly  who have delicate kidneys .Cardiologist should realise  kidneys are soft and gentle  organs  which unlike the heart  , do not  know  how to cry  (Angina) at times of stress  as they lack  well developed pain fibers  (unmedulated  type c fibers to be precise!) .Only thing they  know  is ( like touch me not plant !)   they  strike work  the next   next morning (What we refer to  technically as Acute renal  shut down !)

Now , we see little  interaction  occurring between a  cardiologist and nephrologist  prior to PCI , even though  those two organs ( The   respective experts behold )  are  constantly in touch  with each other , every minute ,  by neural and hormonal mechanisms. The new generation organ  specialists  has to learn  a lot   from these sincere , interactive  , democratic  human   biological system.

Coronary arteries can gulp any amount of dye but  not the renal  arteries .The   future looks still more frightening ,  as we have a variety of devices lined  up  to invade human vascular tree (TAVI, Renal ablation, per cutaneous aortic pumps etc)

So what should we do ?

  • Patients  prone for  CIN should be promptly  recognized .
  • Ask repeatedly  the question .  Am  I   sure  ?  . . .does this patient  require this  procedure at all ?  If  so , have I taken all the precautions ?
  • Use the nephrologist’s services more liberally

Finally ,  read the basics of  nephrology   lessons  once again .  The international consensus group has  classified   the Acute kidney  injury  (AKI)   with a  simple and lovely criteria  for  risk  triaging .     It is a  five faceted ,  inverted  (Tip less ) triangular  cartoon called  RIFLE .

The beauty of  RIFLE   lies in its  simplicity . All  it requires  is  serum  creatinine   (eGFR)  levels  and urine output.  Let  every  cardiologist  master this scheme of AKI . It will immensely  help  our  patients   and make us  a  complete  physician   instead of   being  labelled as a  “master of  an  organ”   or   ” An accessory sub physician”

The CIN prevention recipe.

Source Catheterization and Cardiovascular Interventions 69:135–140 (2007)

References

For review about Contrast nephropathy (CIN)  there are lots of excellent articles.

One company is trying to find a new  solution for  this complication . Let us welcome it ! The device is called rena  guard .

Renal Guard : A new technology to prevent CIN

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Left ventricular hypertrophy (LVH) is the most common structural abnormality of the heart. Hypertension and LVH are close associates . Still ,not every one with HT develop LVH .  So,  there  obviously  is a missing link . Similarly , diabetes  in the company of   hypertension  love to  target the  heart muscle with more vigour .  The  incidence of LVH  can be near  100%  when DM  join hands with HT.

So, what is the secret ?

Sustained elevation of afterload  due to high BP   inflate the myocyte ,  result  in myocyte hypertrophy , which is more of a physiological response.  The diabetes mellitus  adds some spice to the hypertensive LVH.

Diabetes causes glycation of  myocyte cell membrane  proteins . This  opens the  flood gates  and  the  cell permeability barrier vanishes. Hence there is exudate collect in the  cardiac interstitium. This is  equivalent to diabetic microangiopathy seen in retina and  kidneys.

There is  well established link between diabetic LVH and microalbuminuria  , suggesting  a  protein  leak  equivalent  in   heart  (Myocardial proteinuria)  . The only difference  here  , is the  protein leaks into the interstitium   instead of  renal  tubules  .  As we know interstitial leak is a  powerful  stimulant for   fibrotic reaction and  new cell growth. Fibroblasts in combination with extracellular matrix  and macropahges form  a rigid  and timid myocardium . If the patient is also a dyslipidemic(  which is usually the case !)  the leaked LDL , TGL adds to the chaos .

Pathological  effects of  diabetic LVH

  • Increased LV mass
  • Early LA enlargement
  • Early diastolic dysfunction
  • Prevent regression of LVH  even after good BP control

Can  diabetes per se cause LVH without Hypertension ?

Yes .this is also possible , but it  is less recognised.Diabetic LVH  can be a part of generalised organomegaly seen.(Right from the days of fetus diabetes has a  tendency to increase solid  viscera  size –  Large babies in  diabetic mothers , diabetic kidneys rarely shrink !)

Other factors that are related to LVH in diabetes include

  • Female Gender
  • Insulin resistance
  • The lipid connection – Hypertriglyceridmia is linked to LVH

Can tight blood sugar control reverse diabetic LVH ?

We hope so . It may not happen in real life .it depends upon the extent of interstitial invasion of abnormally glycated proteins.

Can echocardiography identify diabetic LVH from hemodynamic LVH of SHT ?

The diabetic LVH is fundamentally different in that ,  the classical septal hypertrophy is uncommon, instead the overall LV mass is increased .This is logical,  as septal LVH is more often reflect hemodynamic stress .

Diabetes  infested myocardium   bright echoes arise  from within . This is due to reflection from  interstitial  proteins.

The newer modalities of echocardiography  like integrated back scattering  analysis can characterise  tissues.

Tissue doppler  myocardial spectral analysis  can identify LVH contributed by DM..

Final  message.

What we know about LVH ,  is far less than we do not know !  , especially when  a patient has a combination of DM and HT. The interaction between them  is so intimate ,  we fail to recognise individual contribution to the process. If only we decode this  mystery , we can intervene better in the  pathological progress of  LVH.

http://care.diabetesjournals.org/content/28/9/2255.full

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 Inter atrial septum(IAS)  is a delicate structure , formed by a  “curious IAS  embryological process”  , when  two septums ,  two ostiums  cross each  other .They  fold  and unfold  like  curtains  in different times ,  ultimately result in a  single membrane separating LA and RA  with a  central physiological   hollowness called foramen  ovale .

All along this process ,  blood has to shunt  from  RA to LA  untill the baby comes out ,  when the direction reverses that  result in the flap  of foramen ovale locking  against the septum secundum with raising LA pressure . So , basically the genesis of  IAS is all  about growing,   resorbing  and  sticking of two septums . This starts in utero and continues well after birth. One can imagine  complexity of  the factors that determine the thickness of IAS.

The IAS thickness varies between 2mm to 4  mm . With increasing use of trans esophageal echocardiography and also the need for cardiologists to puncture the IAS , it is becoming important to study the anatomy of IAS in detail.

A new  cause of  thickened IAS  is reported recently .

 This is refered to as Double Inter atrial septum,  fused like a sandwich  with a  potential space  in between  .

The embryological basis is not clear. (A septum primum and secundum fusion ?)

The PFO   is an  oblique orifice in many .It is some times refered to as tubular PFO . A large tubular PFO can mimic a double IAS.

An  aneurysm of IAS  may get  fused to appear like a double septum

or Is it  IAS dissection which  give an appearance like double IAS ?

Personal perspective

  • It is very difficult to embryologically  explain the concept of double IAS .  I would think  , it is  double layer  of single embryological  septum   with a  potential  space  in between .
  • It is possible an intra mural hematoma (Spontaneous or acquired ) may cleave the septal plane and mimic a double IAS   when the   thrombus gets dissolved later.

Other causes of thick IAS

Septal thickness an issue during transeptal puncture . During PTMC and left heart catheterization a thick septum may be a hurdle.

Infiltrative  myopathies especially amyloidosis is known for a very thick non -puncturable IAS  

Reference

1.http://ejechocard.oxfordjournals.org/content/9/5/707.full

2. http://www.ncbi.nlm.nih.gov/pubmed/16950474?dopt=Abstract

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