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Archive for the ‘Cardiology – Clinical’ Category

Should we switch “Off” label use of cardiac devices and drugs ?

Posted in bio ethics, cardiac drugs, Cardiology - Clinical, tagged , , , , , , , , , , , , on September 21, 2011| Leave a Comment »

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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Do you fear to deploy DES during primary PCI ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , on September 6, 2011| Leave a Comment »

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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How diabetes modifies hypertensive LVH ?

Posted in cardiac physiology, Cardiology - Clinical, Cardiology -unresolved questions, tagged , , , , , , , on September 3, 2011| Leave a Comment »

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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When does streptokinase beat primary PCI most dramatically !

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, tagged , , , , on August 31, 2011| 2 Comments »

STEMIis numero uno of any medical emergency . The risk of death is maximum in the first  hour.

Here is a patient who presented within 30 minutes  of  chest pain.Enzyme sample was  just sent and a bed side echo  revealed a severe wall motion defect in LAD region.

What would have been  the response from a  current generation cardiologist ?

  • Alert the cath lab . Send the patient direct to cath lab .
  • This did n’t happen as we are in a underdeveloped country and the patient  is poor .
  • Should we worry about that  l ?  Not at all  . . .  He received a shot of   much ridiculed streptokinase injection which  costs 2000 Rs ( 50 dollars) in India  .

And see the result yourself !

Can you imagine this man had a major STEMI just an hour back ?

 Any intervention that is done immediately has a major impact on outcome. When the patient comes to you  early within 3o minutes and  STEMI,  or  actually a TEMI  , T wave elevation MI or Hyper acute MI .

When the patient comes to you early cardiologist should raise  to the occasion and set a new  challenge  .

What is that  challenge ?

The aim should  not to be in  salvaging  the myocardium  , rather   prevent  the  event of   ACS   and   abort the MI process itself !

How is this possible ?  Can you abort a STEMI or TEMI by primary PCI ?

Since one has  to act fast , primary PCI is a likely  loser  9/10 times in aborting a STEMI  .

The best option  is  to do an intervention which can have almost zero door to needle time* .  The good old thrombolysis  administered  at the door itself pips the pPCI  convincingly with a huge cost saving as well .

This is what  this patient received. and  see the result . His angiogram  later  showed a fully recannalised LAD .No stent  was advised .He was put on high dose  statins ,beta blocker  and antiplatelet agents.

*You  can not balloon the patient on the arrival in  door steps  !  .

Final message

Do not ridicule any modality of  therapy for being simple and cheap .  They may be most effective as well .

 

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Drug eluting stents fail in crucial board EXAMINATION in STEMI !

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, Uncategorized, tagged , , , , , , on August 31, 2011| Leave a Comment »

Interventional cardiologist are excessively  talented  guys .They always  lead ahead in innovations  .The only issue is , their  enthusiasm  (   many times  overtake  the pace of science .  In the name of off label indications  they indulge   in drug and device extravaganza   in uncharted territory .

Even as we boast of practicing evidence  based cardiology   scientific  adventures  happen  without  proper  evidence  . . .   rather  we  have wait for evidence to come later .” A clear case of  cart pulling the horse “

The wide-spread of use of  second generation DES in STEMI has not been found to superior to BMS in the  EXAMINATION trial just released in ESC 2011 Paris. It failed miserably ,  when every one took  the superiority  for  granted.( Some may claim  non inferiority is  not a failure , but for a DES which was perceived a revolution,  it is definitely a failure in the  STEMI subset )

Further,  what  EXAMINATION  trial did not  address  is  acute and sub acute  stent thrombosis .Even as the DES is credited  with a dubious  record for  sub acute stent thrombosis ,   there is every reason to  suspect , in  the milieu of STEMI the thrombotic risk of DES  would increase many fold.

The  seemingly  low   incidence  of stent thrombosis with DES  in STEMI ,   in  EXAMINATION  trail  is a statistical mirage .This  trial was  neither  planned  nor powered to address the issue of stent thrombosis.

In the  ultimate  analysis of EXAMINATION ,   One could conclude   Cobalt chromium BMS,  has  cemented  its place ,  more firmly for use in primary PCI.

DES  at best ( *With all those conditions apply , Dual antiplatelet etc) can be equal to BMS,  while  BMS at any  day ,  would  casually will  win over DES without any conditions at a  huge cost advantage.

The above analysis is diagonally opposite to that of general  perception  that  emanated  from Paris  ESC meet 2011   trial   .

Please remember EXAMINATION trial did not reach its desired primary end point  !

That is  a strong point  against it  .What do you think ?

Reference

http://www.theheart.org/article/1272077.do

A  TV  debate on Examination  trial from EURO PCR

http://www.oxfordjournals.org/our_journals/eurheartj/ehjvideo.html

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What is the function of moderator band of right ventricle ?

Posted in cardiac surgery, Cardiology - Clinical, cardiology-Anatomy, Cardiology-Land mark studies, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , on August 30, 2011| Leave a Comment »

Moderator band is a ubiquitous structure  found inside right ventricular   cavity , often overl0oked by cardiologists. God has created no structure  without any purpose ! Moderator band has important role to play  both in physiology and pathology .

Image credit and courtesey : Whoever has created

The table attempts to summarise  the features  of moderator band. The  structural and functional behavior of moderator band  in , RV cardiomyopathy , RV non compaction and arrhythmogenic  RV dysplasia is not fully studied yet  . Reference :Content is taken from various sources and with a personal input in few places.  The anatomical data is largely taken from the pioneering  work of cardiac  pathologist and morphologist  RH Anderson of  United kingdom.

Here is an article  from my institute Madras medical college  published in Indian journal of Thoracic and Cardiovascualr surgery in 1982.

An autopsy study  on moderator band   by Paul Ravindran and   Solomon victor

http://www.springerlink.com/content/g35616v662976g1r/

http://circ.ahajournals.org/content/67/6/1268.full.pdf+html http://www.ncbi.nlm.nih.gov/pubmed/20235167

//

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What is geographic miss during PCI ? How do you classify it ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, tagged , , , on August 22, 2011|

A stent missing a  lesion after a PCI  is referred to as geographical miss.

It can be metal missing a lesion ( in BMS )or a drug missing a lesion  with DES.

Geographical miss is  obviously  more important with DES ,   as both metal and drug can miss a lesion ! (A double miss !)

Read a related article in this site. Geographical Miss : Difficult coronary Runways . . .

What are the types of  geographical miss ?

A.Longitudinal

B.Axial

Longitudinal miss is more of a technical failure (Interventionist error ) While  axial miss  is  often a  design or concept failure .

Longitudinal  miss results in edge lesions ( either  stent inflow or outflow lesions) .Axial miss result in discreet  in-stent lesions .

Please remember ,  axial GM  is  much more common .

What is definition of  axial geographical miss ?

Inadequate inhibition of intimal hyperplasia within the region of stent .

Mechanisms of  geographic miss in DES era

  1. Stent  vessel diameter mismatch  (Less drug vessel contact)
  2. Low drug dose -Pharmacological error
  3. Stent radial strength more than the desired force per unit area . This excess  stress  effect  might interfere with drug release.
  4. Some degree of vessel injury is needed for drugs to percolate. (A very smooth deployment may not release the drug  properly )*

*A modern day cardiologist  is expected not only to deploy the stent properly , he has to make sure drugs reach the target cells . What an  irony  cardiology can be  .  . . a  too gentle  PCI  can show up a  negative face ! when we want to poison selectively  the atherosclerotic plaques .

What is the incidence of GM ?

In  STLLR trial which looked specifically the issue of GM  the incidence was very high ,  an astonishing 65 %

How to recognise it ?

Longitudinal miss can be identified by conventional angiography.

Axial miss is very difficult to diagnose . IVUS,ICT will  help.

Many times it is an after thought  when patient presents with  an event.

What can we do once we recognise it ?

Unfortunately nothing much can be done to reverse the miss especially the axial ones.

longitudinal miss can be corrected by a over lapping stent .(Still ,  we do not know the implication of double metal doses  dragging an edge of lesion !)

Can  “Geographic miss”   be termed as  a failed PCI ?

Clinically , technically , logically and morally  Yes .

But  practically  “No” ,  as GM  takes much longer time to manifest as a clinical event  ,  by then , no one   would  really attribute  the event as  procedure  related  . And of course ,  we have numerous other  excuses to convince our patients.

The link to STLLR  trial which gave us the startling data about GM .


http://www.ajconline.org/article/S0002-9149%2808%2900350-0/abstract

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Nesiritide : Death of wonder drug and a concept ?

Posted in cardiac drugs, Cardiology - Clinical, cardiology -Therapeutics, tagged , , , on August 20, 2011| Leave a Comment »

Medical science is  nothing ,  but trying hard all possibilities. Most innovations die .Only a fraction will survive .

That does not mean we should not try ! The greatness is in accepting the failure.  The wonder drug which was an analogue of human atrial  naturetic peptide    (BNP)  Nesiritide   , died a peacful death on July 7th 2011 .

Long before , in year 2005 ,  Eric Topal in a hard hitting  Editorial  of  NEJM  wanted to hang this drug .

But it was a case of prolonged  death sentance .

http://www.nejm.org/doi/full/10.1056/NEJMp058139

Should we  pity with the drug companies  and forgive them for delaying it’s  exit ,  enable them  recover the  cost involved  .

Meanwhile , Nesiritide might have died ,  the  concept of  BNP analogues may need to be explored further.

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What is the best intervention for critical in-stent restenosis (ISR) ? Do we have an universal recipe ? !

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Land mark studies, tagged , , , , , on August 17, 2011| Leave a Comment »

How do you tackle  In-stent restenosis  (ISR) ?

  1. Deploy another BMS
  2. Use a third generation  DES
  3. No . . . first  generation DES(Paclitaxel )
  4. Consider Plain balloon angioplasty.(POBA)
  5. Refer for CABG.
  6. Fall back on medical management.(Ingloriously  referred to  as  “No option” patient !)

Answer:  Please  note , there is no single response answer for this question .

Instent restenosis (ISR) is   commonly seen with BMS .This is primarily because  we are busy blaming DES  for stent thrombosis  and we do not want to give a double blow to DES .There is a  significant population  roaming with ISR  involving  DES .  BMS is in vogue for nearly 2 decades, hence it is natural to see more of it.  In due course ,  DES  is expected to catch up with BMS  and would lead in ISR as well .

The issues in PCI for ISR

Though any of the above 6 strategies may be appropriate ,the urge to put another stent within the IRS ,  prevails over all other options in most centers. This is more off an Interventionist talent  show off  !

Please remember , the common  principles  must apply in all patients before an PCI  . Simply stated , this  principle involves  assessing  symptoms, residual  resting  ischemia, myocardium at risk  during stress, viable muscle mass etc .Lesion characteristics  should come last in the work up. ( A cardiologist  should not  report  a coronary angiogram  , if   does not  not know  basic clinical parameters.)

It is  good  to have a  rule  that  “reserves  intervention”  for ISR  only if the  patient  has refractory angina. 

Can you promise  relief from dyspnea

Contemplating  PCI for  patients with dyspnea as the main symptom is really tricky one.Unlike angina ,  dyspnoea  can be attributed to so many factors other than coronary blood flow.(Apart from LV EF , Iscehmic MR,  A transient diastolic dysfunction , lung function , volume status, renal function , physical conditioning etc)

Opening  ISR in the belief it would improve LV function is highly questionable even if viability is documented.

What is the most important step in the decision making prior to PCI for ISR ?

* Most important step  in ISR management is  probably  spending  sufficient time ,  involving  experts ,  ” democratically  debating”  the indication and techniques  in your institutional cath conference.

Once you document the necessity of intervention* The following things  are possible .

  1. If  the patient has diffuse in-stent stenosis , especially  the  proximal ones or that  involves  branch points,  it is wiser to refer  them for CABG.
  2. Discreet and focal ISRs can safely be attempted for repeat PCI.
  3. BMS or DES  ?  This  is  debated. Current preference is to use  a DES. (Many feel ,first generation DES -(Paclitaxel)  scores over Everolimus in this situation )
  4. Is POBA  possible for IRS ? Can a balloon do a job where a stent has failed ? . No  body is trying it .Many Feel guilty to  do it .  POBA for IRS is a failed concept without even trying it !  One  way of reasoning  is IRS occurred  only  because stent was  never indicated in the first place  in that  location  and a POBA would have been the choice in the initial attempt itself .So let us not make the second error !  ( May be , if  Gruientzig is alive today ,  might have  used  POBA  for ISR very effectively ! )

Issues for which  we will never ever know the answer !

In future any of the following combination of  stents  will occur in tackling ISR.

  • DES covered  BMS
  • BMS covered DES
  • Two BMSs
  • Two DESs
  • Paclitaxel covered Everolimus
  • Everolimus covered Cypher.
  • Overlapped DES and BMS
  • DES covered beta irradiated IRS
  • Rotablated BMS (Yeh metal crushing !)  followed with  DES jacket !

How does the two metals ,  two drugs in various combinations interact with  the tender coronary  endothelium ?

Endothelium is an endocrine organ. It has  to secrete as  many pro and anti homeostatic molecules (Nitric oxide, endothelin etc).This has to be  kept in mind when we develop newer and exotic devices. Of course ,  we claim our  aim is primarily  to provide  relief  to  our ailing patients , but, as things stand today  , there is a distinct risk of  converting human coronary arteries into corporate playgrounds !

Reference :

http://circ.ahajournals.org/content/100/18/1872.full.pdf+html

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During primary PCI , when you encounter severe multivessel disease what will you do ?

Posted in cardiac surgery, Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese, tagged , , , , , on August 15, 2011| Leave a Comment »

Surprisingly it is common !

A .Abandon the procedure call the surgeon for an emergency CABG

B. Open the most critical lesion.*

C.Attempt to open and stent all possible lesions.

D.Send the patient back to CCU for a conventional  thrombolysis or attempt a intracoronary thrombolysis.

Answer : All  can be a right response depending upon the available expertise ,  time window, associated complication and hemodynamic stability etc .

* Please note ,the most tight lesion may not be the culprit artery. Though there is high chance for that  being the culprit , it  can be very deceiving   especially when  there is multi-vessel  CAD with  chaotic collaterals.

The site of lesion and site of infarct can unimaginably remote.  (A traffic snarl at remote flyover  can have its impact  right on the busy commercial street due to diversions ! ).

What will happen if you open  a non culprit artery first mistaking it for a culprit ?

This could lead to  dangerous turn of events as whatever little perfusion the patient was getting through the ill-fated  IRA will be challenged by the fresh diversion  facilitated by non IRA angioplasty. Extreme caution is required.

Emergency CABG  within 3 hours  of MI even though advocated  by few ,  is still considered a risky  way to reperfuse  the heart.(In India  there  is  nothing called primary CABG!)

An energetic interventional  cardiologist would vouch for opening all lesions . Only thing  , he has  to  make sure is  , the patient also has enough energy to withstand  his  onslaught. Never   non culprit lesion if a patient is stable . 0ur aim is not that.If the patient  is in shock or impending LVF one can justify opening  few more lesions  that improve total muscle function which can be vital.

What about fall back on thrombolysis?

This may be seen a defeatist attitude ,  but  when the aim is  in the  well being of patient ,  there is no defeat or success. If severe  CAD is encountered and both  CABG / PCI  or not an option,  the cardiologist need not feel guilty or  humiliated to refer him back for thrombolysis. (Of course , Intracoronary thrombolysis  is  an option !)

Final message

Primary  PCI  is often made  to  appear ” As  a  kids play”  by many modern  day cardiologists . It is not so.  It requires a team effort. It is  race against time.   Feasibility depends largely on the coronary anatomy. The failure rate of  primary  PCI is often camouflaged .(Currently Success of pPCI is boasted at 95%)   Logically it should include pPCI ineligible anatomy as well . Many still do not understand the real purpose of pPCI.   The aim is to salvage the myocardium  at risk , sure and fast. Never attempt for total revascularisation in an emergency situation however tempting it is !

In young persons with discrete single vessel disease  the procedure is simple and outcome is straight forward. In elderly , diabetic , STEMI on  preexisting CAD,  diffuse  multivessel disease  ,   complex main left,  bifurcation lesions , one requires  lot of brain sense  to provide optimal outcome . Many times that sense includes abandoning the procedure !

Please read a related article in this site  Primary CABG

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