Feeds:
Posts
Comments

On this special day , wishing all the readers and followers of this blog  an energetic, creative , insightful and  of-course a happy new year 2016 !

Just wanted to share the 2015 annual report of this site with the readers.

wordpress annual report dr venkatesan

Mohandas Karam Chand Gandhi ,  father of my country , India , made these observations in year 1925  about the  fundamental constituents of  violence in society . These words of monumental wisdom came when he was  addressing young Indians in a country- side rally .

mahatma gandhi quotes medical science humanity

Note, his finger points to , what  exactly is relevant to our profession ! He emphasized this  nearly  100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s  current form !

Should we include moral, behavioral and ethical classes  right from the first year of medical  school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !

Here is a  video recipe  !

Please click here to  see more videos from my you tube site

It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

  • 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
  • The medical  world started looking for options to manage CAD.
  • 1970s : CABG was  a major innovation for limiting angina .
  • 1980s: Plain balloon angioplasty a revolution in the management of CAD.
  • 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
  • Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
  • Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
  • 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
  • 2002: BMS are too notorius for restenosis and may be dangerous to use
  • 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
  • 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
  • 2007 : The drug is not  the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
  • All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
  • 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
  • 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we  look back in time and “constantly scrutinize”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

NSTEMI  constitutes a  very heterogeneous population .The cardiac   risk   can vary  between very low to very high .  In contrast ,  STEMI patients  carry  a high risk for  electro mechanical complication including   sudden death .They all need immediate treatment  either with  thrombolysis or PCI to open up the blood vessel  and salvage the myocardium.

The above concept , may  be true in   many situations  ,  but what we fail to recognize   is  that ,   STEMI   also  is  a heterogeneous clinico pathological  with varying risks and outcome !

Let us see briefly ,  why this  is very important  in the management of STEMI

Management of STEMI  has undergone great  change  over the past 50 years and  it is the standing example of evidence based coronary care in the modern era ! The mortality  ,  in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15%  in 1960 /70s . Early use of heparin , aspirin   further improved the outcome .The inhospital mortality  was greatly  reduced to a level of  7-8% in the thrombolytic  era. And ,  then  came the interventional approach, namely primary PCI ,  which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence   for the   superiority  of PCI  , it is only a fraction of  STEMI patients get  primary PCI   even in some  of the  well equipped centers ( Could be as low as  15 %)

Why ? this paradox

Primary PCI   has   struggled  to establish itself  as a global  therapeutic concept  for STEMI ,   even after   20 years of it’s introduction (PAMI trial)  .  If we  attribute ,  lack of   infrastructure  , expertise are  responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world ,   reluctant to do primary PCI  for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI  patients !

All STEMI’s are not  same , so all does not require same treatment !

Common sense and logic would   tell us any medical condition should be risk stratified before applying the management protocol. This will enable  us to avoid applying “high risk  – high benefit”  treatments in low risk patients . It is a great surprise,  the cardiology community has extensively researched to risk stratify NSTEMI/UA   ,  it has  rarely  considered risk stratification of STEMI before  starting the treatment.

In this context , it should  be emphasized  most of the clinical trails on   primary PCI  do not address  the clinical  relevance and the  differential outcomes   in various  subsets of  STEMI .

Consider the following two cases.

Two young men with STEMI  , both present within  3  hours   after  onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL   ,  Low blood pressure , with severe  chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal  or no  discomfort .

In the above example,   a  small inferior  MI by a distal RCA occlusion  ,  and a proximal LAD lesion jeopardising entire anterior wall , both  are  categorized as STEMI !

Do you want to advocate same treatment  for both ?  or Will you  risk stratify the STEMI and treat individually ?  (As we do in NSTEMI !)

Current guidelines , would  suggest PCI for both situations. But , logistic ,  and real world experience would clearly favor thrombolysis for the second patient .

Does that mean,  the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a  random basis  by  not so well experienced cath lab team.

(Note : Streptokinase  or TPA does not  vary it’s action ,  whether given by  an ambulance drive or a staff nurse or even a  cardiologist !  .In contrast ,  the infrastructure and expertise have the  greatest impact on the success and failure  of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc)  need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

The field of cardiology has seen great men over the centuries. Few women have permanently stamped their presence  in that history .Jane Somerville can be termed mother of pediatric cardiology along with Maude Abbott She has a fascinating life history , having  worked  in Royal Brompton  , Imperial  and Guys London.She was mentored  by  pioneers like  Paul wood , Blalock and others .She is primarily interested in the pediatric cardiology especially congenital heart surgeries .The classification  of pulmonary atresia with VSD  goes with her name.

jane somerville

Dr. Jane Somerville : British cardiologist , (b-1933 )

She carries the credit  of  starting  the Pediatric cardiology world congress in 1990 ,is the founder of GUCH (Grown up children with congenital heart disease.) .

Here is a rare  interview  from he  to Dr Robert Califf  for Heart.org. For  those,who like to  have a glimpse of  cardiology in its vintage  times , don’t miss it.Dr Jane addresses the past treasures , explores specific issues of facing pediatric cardiology  and frank expression about the issues of women being a cardiologist  in a man’s world.

 

She has a foundation in her name that helps the children and adults with congenital heart disease.

somerville foundation

Reference

The landmark paper in BHJ 1970

pulmonary atresia

 

Men are from Mars , and  Women are from Venus  ” . . . Do you agree ?

Many probably witness the much talked  differential behavior among the gender  every day. Its argued , men take more risk in life ( often  senseless !) , some go to the extreme to  suggest  Men are Idiots and decorate them with a  provocative title  MIT (Men Idiot Theory ) (Mcpherson 2011).Risk taking is important in life, but at  what cost ? Does women (Who  are caring by nature )  help themselves  and the society by less risk taking behavior ?

I stumbled upon this rare piece of writing from BMJ which  would demand  in depth analysis  into this gender phenomenon based on  evolutionary biology and genetics.

This article concludes, Yes, men  . . . indeed  tend to take some foolish risks in various life situations that result in potential harm.

Gender difference in medical outcome men are from mars women venus male idiotic theory darwin theory

What is the influence of MIT on medical profession and patient outcome ?

Now , Iam compelled to ask  a hypothetical question .Does women medical professionals take  less aggressive stance and low risk taking behavior  and in the process result in less mortality and morbidity to our patients  ?

I would think the answer to that question  would be in affirmative .I wish  BMJ or anyone  should design a study on this issue.

Reference

1.Harris CR, Jenkins M, Glaser D. Gender differences in risk assessment: why do women take fewer risks than men? Judgm Decis Mak2006;1(1): p. 48-63.

2.Eckel CC, Grossman PJ. Men, women and risk aversion: experimental evidence. In: Plott CR, Smith VL, eds. Handbook of experimental economics results. Vol 1. North-Holland, 2008:1061-73.

3.McPherson J. Women are from Venus, men are idiots. Andrews McMeel, 2011

4.Northcutt W. The Darwin Awards: The official Darwin Awards: 180 bizarre true stories of how dumb humans have met their maker. Orion, 2004.

 

 

medical education critics cardiology evdnce based medicine growth ethics

Every time , patients ask me  what diet he or she  should follow , Iam sort of  amused , as my understanding of diet and cardio vascular disease is at best primitive.I used  go with a standard single phrase  advice “Anything in moderate should be okay  “
What about going for a saturday night party doctor? One of  my shrewd looking  patient who was recently double stented with DES , asked.
Human body is a biological marvel.While medical professional divide it  into various systems  for our convenience. God doesn’t  think that way .He has no systems in mind when the body was designed . There is no wonder , the alimentary system and hematological system has to interact on a daily basis  with the help of circulatory system  to keep the  body alive. Platelets are unique blood cells that exist primarily to plug physiological bleeding if any  or for self-healing at sites of tissue injury.
 platelet lipid ldl tgl triglyceride ineraction 002
With human vascular system increasingly invaded by various metals and wires , platelet are a confused lot since their original biological functions are altered. They simply don’t know whether  fight these foreign body , aggregate over it , flush or simply pass over these .Adding to this  the powerful anti-platelet drugs targeting critical functional pathways .No wonder every other cardiovascular  patient  consumes at least one anti-platelet drug.
It seems diet  can have direct influence of platelet function
With human beings desire to add style to food consumption and eating habits  competing with  top slot of purpose of living , we often forget it is same prevent us from living a good life.
There has been numerous anecdotal and study population and experience  acute coronary events are more common after a heavy meal especially a fatty one .The immediate suspect has been high triglyceride and chilomicrons in blood stream shunted  intestines .
It is logical to expect , these high TGLs some how act a s trigger for pro-coagulant trigger .With the core thrombus  rich platelets it is assumed platelet stickiness is augmented and  maintained  by transient raise in triglyceride formation(Reference 1,4,5)
Glycerol component of  TGL is know for  its sickness and  making the companions wet.
The million dolor question is , at what level of TGL and which forms of TGL make the platelet cry and attract each other ?
Diet, anti platelet drug efficacy  ?
 Now , patients with coronary stents has to live at the mercy of these anti-platelet drugs. The drug resistance(Clopidgrel) is  threatening to be major issue.Like warfarin do we have real issue of dietary binge and acute neutralisation  of anti-platelet drug efficacy that can trigger acute stent thrombosis . This is potentially  important  area of study .
Final message
So does a fatty meal  a new trigger for ACS ? It may sound an alarmist statement .but as of now , its difficult to ignore this.So my advice for that  the that smart young man with soluble stent  was to avoid binge dinners that carries a definite risk of interfering with  stent maintenance .
Reference

What are the mechanisms of cyanosis in  cyanotic heart disease ?

Most of my fellows have difficulty in answering this question. (It is not the lack of knowledge though !)  In my view ,cyanosis can occur , by six  different  modes

  1. Reduced pulmonary blood flow  with some form of anatomical obstruction in RVOT with a communication between ventricles  (TOF physiology  ) , atria or both
  2. Reduced pulmonary flow with obstructive pulmonary vasculature (Eisenmenger physiology )
  3. Wrong way origin ( RV to Aorta/LV to Pulmonary artery ) : Transposition physiology
  4. Simple mixing of arterial  and venous  blood channels within the atria  ,ventricle or great vessel  without RVOT obstruction .This, in fact can causes increased  pulmonary blood flow (Technically left to right shunt ) and still there is cyanosis (These are called as Admixture lesions )
  5. Isolated Right to left  shunt very rare ( Pulmonary AV fistula , SVC to LA )
  6. Complex combination of first 4 (Like bi-directional shunting , TGA combines ,  AV canal defect , with varying degree of pulmonary obstructive disease) Note : TOF and Eisenmenger are physiologically mimic each other , the  only difference is site of resistance to pulmonary flow. RVOT vs Lung vasculature )

For advanced readers only

Now, is it possible for “Net” left to right shunt to  result in cyanosis ?

Yes*.Very much possible. The bulk of this group is referred to as admixture lesions with certain caveats.There should be an obligatory mixing without contribution from RVOT obstruction or raised PVR( *Please note theoretically  admixture can either be right to left  or  left to right shunt )

All pure admixture lesions are in fact net left to right shunts. (TAPVC, Single ventricle , Common atrium , Common AV canal ,Truncus, ) This is the group we have been traditionally calling cyanosis with increased pulmonary flow.

Its may also to be noted with  surprise admixture lesions often  has less intense cyanosis than other forms as long as pulmonary blood flow is normal and the lung does its job perfectly .

*Please note Isolated classical left to right shunts , ASD, VSD, PDA can never cause significant cyanosis unless there is reversal of flow .However ,many Eisenmenger physiology are show net Left to right shunting only ( 1.2-1.5 : 1 or so ) but with a definite right to left component .What we call as typically bi-directional shunt .

Is single ventricle with PS  admixture lesion or TOF physiology ?

Though single ventricle in isolation is an admixture lesion, when it has associated RVOT obstruction it ceases  to be admixture by definition  as mixing is augmented by the obstruction rather than by simple mixing.The complexity could be understood in certain situations  where admixture lesions  like common AV canal  go for raised PVR .Here the various quantum of contribution to cyanosis is mind boggling. (Original admixture, augmented by RVOT resistance, differential mixing at atrial and ventricular level  , hypoxia  at lung level due micro pulmonary AV fistulas in grade 4 heath Edwards etc )

Can TOF behave  like an admixture lesions ?

Technically Yes.If the RVOT obstruction is minimal , (What was called then as pink Fallot ) We haven’t  understood this entity properly for so long.Atleast  I was baffled to read when J.K Perloff mentioned in his book  during my DM fellowship days,  that  TOF can manifest  with predominant left to right shunt with little or absent cyanosis.

The  aortic override in TOF facilitated by large malaligned VSD make it a sort of admixture  situation as  RVOT resistance is too little to offer any resistance, (rather it welcomes more blood from left side ! ) So , should we call it simple VSD physiology , admixture physiology or  just acyanotic forms of TOF ?)

Further reading

An excellent review article on this rare topic of  admixture physiology

  1. Jaganmohan A Tharakan Admixture lesions in congenital cyanotic heart disease Ann Pediatr Cardiol. 2011 Jan-Jun; 4(1): 53–59.

 

Wall motion defect , in patients after CABG is fairly common.These  defects are difficult  to interpret  as the mechanisms can be multiple.Though the commonest wall motion defect appears to  involve the interventricular septum. it can occur anywhere in antero-lateral zone.

The mechanism attributed is  the effect of pericardiotomy , which surgeons as we understand leave it open after grafting  .This can cause lack of localised ventricular interdependence and results in a a brisk septal movement (bounce )It is an indirect effect .

post cabg wall motion defect

Note the, wall motion defects are confined to the exposed areas of the heart during cardiac surgery .In short axis echocardiography it correlates anywhere between 9 to 3 O clock position. Though interventricular septum is not covered by pericardium in the true sense , there is a indirect bounce effect over IVS due to interference with anterior ventricular interdependence .

More commonly a direct wall motion defect in the 12 to 3 O clock position in short axis is seen .This can closely mimic true wall motion defect as pericardial adhesions can tether these segments. Careful observation is warranted.Myocardial thickening is the key differentiating feature.

What is the physiological impact of these wall motion defects ?

It is generally considered benign (It is !) .Though in echo it looks awkward and suggest desynchrony. The real issue is , it can  mislead the echocardiographer to errors in calculation of that universally  sacred parameter called EF %

Importance of  knowing pre existing wall motion defect.

This has to be reviewed with old reports as it can wrongly create a new wall motion defect de-crediting the surgeons.

New pathological wall motion defect.

Of course it can happen due to peri-operative ischemic insult or infarct . However , It need to emphasised transient wall motion defects are common post CABG due to apparent hypoxia.This seems to be more pronounced with on pump surgeries than off pump .(Expected though) In my opinion, 2-4 weeks cooling off period is required before  a meaningful assessment of  wall motion post CABG.

Late pericardial reactions and localised constrictive features has been reported.

Disappearance of wall motion defect : How  common ?

Any disappearance of WMA is welcome . It happens rarely though . Some of the post ACS population (Both STEMI and UA/NSTEMI) can experience this ,  as they could harbor  zones of myocardial segments afflicted by  ischemic stunning rather than true  necrosis , that might  disappear.

 

Follow

Get every new post delivered to your Inbox.

Join 523 other followers