Feeds:
Posts
Comments

We all know to err is human , but most of us probably won’t agree medical mistakes , (bulk of which happen in the name of practicing state of the art of science ! ) could be the dominant theme in modern medical care !

BMJ exposes this  well known secret with the help of most authentic data from an apex scientific body CDC , Atlanta .

Reference

http://www.bmj.com/content/353/bmj.i2139#

Oh , it’s a well recannalised IRA  and its flowing TIMI 3  as well.  Now, what shall we do sir” ?, An apparently worried senior resident queried after a second look at the images from a 8 hour old STMEI .Why you sound unhappy  man ?  As if recanalisation is an untoward event” ! I teased my resident !
and went on to ask . . .

What we mean by recannalised  IRA ? (Recan-IRA)

  • It is akin to natural or pharmacological angioplasty (or combination of the two )
  • It can be complete or incomplete from the IRA perspective.
  • It can either result in partial or fully salvaged myocardium.
  • It should be understood even a 30% recanlisation can result in TIMI 3 flow and result in near complete salvage
  • Even a 90% recannalisation may not accrue the same benefit if it has happened late. So its all in timing
  • Spontaneous recannalisation can some times even be  superior  to thrombus aspiration . However , some degree of residual thrombus would be present in most
  • Residual plaque burden is also an important factor that will decide the extent of angiographic recannalisation.
  • Some times the recannalisation  will make the vessel near normal with only luminal  irregularity
  • IVUS/OCT may provide accurate assessment of Recan-IRA , it’s is not logistically acceptable in STEMI setting.
  • After listening to my briefing on recannalised IRA , the fellow looked more confused than before. He bothered to ask again , what am I supposed to do once a well recannlised IRA is detected ?  Should I intervene or not ?

The term recanlised IRA generally convey a hemodynamic  meaning for a successful  early (natural plus or minus pharmacological ) reperfusion .If every parameter is fine , and the lesion is not significantly obstructing better to pause any further procedure ,  as consequences of deploying  stent in a well recannalised segment is not yet clear with a stro ng trend towards harm .The decision is to be taken on individual basis with reference to  symptoms, stability ,  residual ischemia and quantum of incomplete salvage and lesion morphology .

If you believe ,a spontaneously recannalised  IRA has provided a TIMI 3 flow , it is equivalent to well done job of natural thrombus aspiration by  a hidden hand and catheter . Consciously respect that .Most cardiologists would have  realised atleaset once ,  that any aggression on a God handled IRA can be counterproductive !

Is there a non academic angle to this issue ?

Undoubtedly yes , strangely  inspite of a positive phenomenon for the patient , recannalised IRA leads to a difficult debate  in cath lab .Suddenly , the  entire collective scientific wisdom of the cardiologist is put into a stress test. There is direct fight between reality , expectations .True patient benefits , obligations to hospitals , the parasitic  relations with device industry , do have a big say !

Final message

Practicing cardiology is simple , but when scientific and non scientific realities of life are in direct confrontation with patient welfare it becomes a huge struggle and only a determined few can win over this infinite fight against conscience !

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 concept of TAVR(Trancutaneous aortic valve replacement ) is trying hard  to prevail over surgical aortic valve replacement .Two companies Medtronic and Edwards life have their products (Core and Sapiens)  tested and used with varying success.Meanwhile, Boston scientific has come out with a new one , Lotus valve made with stainless steel and bovine pericardium.

 

lotus valve tavr

Lotus valve  seems to have a distinct  advantage* (over the Core and Sapiens ) in terms of easy delivery and adjustment (or retrieval ) of valve till  final position and efficient adoptive steel technology in preventing para-valvular leak.

* Outcome awaited.

Human  trials has started with lotus valve in USA 2014.The REPRISE III trial would compare  one to one Lotus vs core valve . Results will be out by 2017.Unlike many interventions the utility value and long-term outcome of  TAVR  seem to be genuine and patients  waiting for aortic valve surgery can look forward to this as a genuine non surgical alternative.

Responding to this , Medtronic and Edwards are  improving upon core valve with Evolute R /Engager and SAPIEN3 , expected  to give a tough time for LOTUS.

Reference

1.RESPOND registry , REPRISE 1, 2 and 3 trials

2.A review article on TAVR 

Less than a century ago an easy chair  was enough to manage this most important medical emergency of mankind. Of course, at that time mortality of STEMI was estimated to be around 30%.We have since pushed the in-hospital death rate down to less than 10 %  and its around 5-8% currently.(*The lifeless chairs were able to save 70 lives is a different story!)

Heparin , thrombolytic agents, critical coronary care has helped us to achieve this , of course It must be admitted primary PCI also played a small role (at best 1 % ) in our fight against this number one killer.

Now, why not combine  both lysis and PCI ?

The concept of PIA (Pharmaco Invasive approach) came into vogue  primarily for two reasons.

1.If thrombolysis and  pPCI are powerful strategies by individual merits why not combine both and achieve double the benefit ?

2. Since pPCI is going to be a logistical nightmare in most points of care and we can’t afford to lose time . So, let us lyse first and consider PCI later !

Unfortunately medical science is not math .One plus one in medicine is rarely two !

Though , it looks attractive , Pharmaco invasive approach  has its own troubles.Fortunately , most of them are man-made, few are beyond our knowledge though.

Following general rules  may help us

  • STEMI  should ideally managed by early thrombolysis (or PCI) in all deserving patients.
  • Don’t wait for PCI if you think , there will be delay or reduced expertise and poor track record of the center in this modality.
  • Pharmaco invasive  therapy is not a default in all STEMI .Do good quality , monitored  lysis , (Not necessarily new generation thrombolytic .(I prefer one hour sustained thrombolytic regimen , not the hit or miss bolus) .As a learned cardiologist we need to assess individual patients according to the type and risk of MI.Its not wise to blindly follow the guidelines ,because these guidelines , though based on evidence never answers a query in a single patient perspective !

The key “branch points”  in decision making  after lysis

  • Invasive strategy  should begin within one hour if the patient has failed  thrombolysis and has developed any mechanical issues.( Mind you, LVF requires good medical stabilization .Rushing  such patients to cath lab without application of mind can be disastrous )
  • If the Initial  lysis is excellent and the patient is asymptomatic  one need not proceed with invasive limb at all.(A significant chunk of apparently failed lysis by ECG are asymptomatic and comfortable , these are patients require delicate assessment regarding further intervention. )
  • If the MI is large and the clinical  stability is “not confirmed” one may  proceed urgently within 24 h.
  • In any case there is no role for invasive approach after 24 hours* Unless fresh ischemia  suspected to come from IRA or  non IRA.
  • Having  said that, there are many centers that do a diagnostic  angiogram alone just prior to discharge  (48-72h) for risk stratification and then take a genuine call for a possible PCI or  CABG. In my opinion it appears a sensible strategy , though a non invasive stress  test pre/post discharge can even avoid that  coronary angiogram !

One issue with Rescue PIA

Though by current definition  PIA is to be done  3-24 hours , don’t wait for the 4th hour if you have recognized a failed thrombolysis earlier than three hours.( Ofcourse , as the gap between P and I gets too narrowed it may  carry some adverse  effects witnessed in routine facilitated PCI -Refer FINESSE study ) Similarly,there need not be a blanket ban on PCI beyond 24 hours if residual ischemia is active.

Final message

PIA is a dynamic  coronary  re -perfusion strategy . Nothing is fixed in science. . The optimal gap between Pharmaco and invasive strategy  can be anywhere between  1 hour to “Infinitely deferred” depending upon individual risk perception and wisdom of the treating cardiologist.

 

 

 

I

 

It was delicate few minutes  in one of  my recent  visits to a corporate hospital , when I noticed an emergency physician  hesitated to follow my advice to  prescribe IV Digoxin for a patient with  Atrial fibrillation and fast ventricular rate.His fear was, his consultant, a modern day cardiologist wouldn’t like it as Amiodarone has become a default drug for atrial fibrillation in that Institution. I could sense. . .he felt so out of place to take on my suggestion.

I reminded the young physician , the uniqueness  of  Digoxin and its  un-diminished value for this particular indication ,still he was reluctant and didn’t oblige.

I realised , it was my mistake to expect  a place for the humble fox glove in corporate crash-carts of centrally climate controlled  cardiology suits !

“Medicine need to be practiced   not only with best science(Truth) but also in a holistic and  cost efficient manner . There is no place for glamor, glitter  and commerce in your prescriptions !  In near future , teaching Medicine to students would  essentially  become  “more of moral” than “science” .

Reference

Link -Which is the best combination for rate control in Atrial fibrillation

medical ethics stastistics www.drsvenkatesan.com

One casual question in my class led to this search for an anatomical mystery. When we were discussing  why left atrial oxygen saturation never reaches 100 % ? ,  it was attributed to desaturated  bronchial venous blood  draining  into pulmonary vein.

How does this bronchial vein enter pulmonary venous circulation ? How many bronchial veins are there ? What  anatomical plane it runs   ?

Surprisingly, even in this hi-tech era of academic excess, literature is sparse for this basic anatomical question. It is reported (In Greys anatomy ? ) Bronchial veins are two in number and both drain to Azygos and Hemiazygos veins (systemic) rather than pulmonary veins.

So is our assumption wrong ?

May not be.We realise these are only two visible and named bronchial veins .It is learnt they  probably carry only about 13 %  of bronchial  venous blood to systemic venous circuit.

bronchial venous drainage bronchial circulation

Image showing right and left bronchial veins draining to Azygos and hemiazygos veins.

 

It is assumed , remaining  87 % of  bronchial  venous blood drains to pulmonary  venous  circuit in an invisible  fashion (By unnamed twigs ?) desaturating  the LA blood by about one percent from 100 to 99 %. This is our current understanding. I haven’t come across any specific human  research that quantifies the bronchial venous channels and it saturation . It’s gratifying  to find one study specifically looked answer this question  in sheep study .(Charan H.B  et all Reference 1 )

 

where does bronchial vein drain drainage circulation pulmonary vein saturation

True physiological bronchial venous drainage seems to be  different from anatomical bronchial venous circuits .

 

Clinical implication of bronchial venous circulation.

In physiology it may not be important . However bronchial circulation (both arterial and venous)  can take many anatomical tracts when pulmonary micro vascular bed is structurally and functionally altered as in  COPD,   , pulmonary atresia  with aorto-pulmonary collaterals , congenital left to right shunts,post Fontan  circulation pulmonary AV malformations,lung tumors  etc .

Hemoptysis in acute pulmonary  venous hypertension is thought to be due to rupture of these bronchial veins as elevated pulmonary venous pressure reflect into bronchial veins  (As in mitral stenois and other conditions. )  This again would vouch for bronchial veins draining to pulmonary veins.

Final message

As on today , it can be concluded bronchial vein drainage goes both systemic and pulmonary venous circuit.Bulk of them appear to end in  pulmonary veins though clear anatomical evidence is lacking.

Post-ample

Exploring human anatomy appear a  grossly unfinished agenda even today, especially the micro and histo-anatomy. Teachers of basic sciences  should impress upon youngsters entering the medical school to pursue translational  research relevant to specific clinical  problems.

Students  may contact   <drsvenkatesans@yahoo.co.in> for specific areas of clinical cardiac anatomy topics that still requires answers.

Reference

We know, atrial fibrillation is the commonest clinical cardiac arrhythmia , that is extensively studied , subjected to exotic investigations and state of the art treatment strategies.Interestingly , this arrhythmia also drags the economics of cardiology practice of a community in a big way with heavy influence on drug , device and usage.We know, RF ablation of pulmonary vein is one of the modern ways to manage this arrhythmia.

Iam sharing this article from medscape by an EP specialist Dr. Jhon Mandrola , surprisingly exposes our fundemental ignorance about this arrhythmia and the near futility of certain procedures.

http://www.medscape.com/viewarticle/865209?src=WNL_infoc_160625_MSCPEDIT_v2&uac=44538BX&impID=1137861&faf=1

Scientific cardiology has forced us to believe ACS management must be catheter based and all others are inferior  and  those who pursue the later , carry a risk of  being labelled as unethical in near future. However ,experienced cardiologists will know  where the truth lies.

Now,in the interventional cardiology board rooms  there is a big  debate going on regarding the value of early total revascualrisation in STEMI with multivessel CAD.Suddenly , every lesion looks suspect ( Ex,current or future culprit ! ) and all stentable lesion are stented  either in an emergency or semi emergency fashion (The new age post PCI dialogue goes something like this “I have tackled one culprit , other one seems to hide in LAD ,  we will arrest it  next 48 hours or so* ? ( This is the concept of  deferred or staged  non-IRA stenting )

*Ironically it brings   one more dubious therapeutic time window in ACS !

ptca ira non ira multivesssel pci

The recent  studies like  PRAMI, PRIMULTY ,CvLPRIT are trying to find out an answer to this issue  and suggest acute multivessel PCI may be  good strategy. Some of them advocate a FFR guided non IRA intervention , knowing fully well micro-circulatory bed is completely altered by the index acute thrombotic event.( Mind you , for FFR,  we need to induce maximum hyperemia with Adenosine in a highly varying local autonomic milleu within the thrombus clogged capillary network)

Final message ( Intentionally biased !)

Till we learn or unlearn  it is vital to go with conventional wisdom.Don’t pursue a random hunt for coronary culprits in acute phase of  STEMI.Many of them are innocents and likely to suffer in cross fire.Tender coronary arteries need some rest,peace and time to heal thyself  . Just keep away , they will definitely say big  thanks with folded hands !

Reference

1.Gershlick AH, Khan J, Kelly DJ, et al. Randomized Trial of Complete Versus Lesion-Only Revascularization in Patients Undergoing Primary Percutaneous Coronary Intervention for STEMI and Multivessel Disease: The CvLPRIT Trial. J Am Coll Cardiol. 2015;65(10):963-972.

Follow

Get every new post delivered to your Inbox.

Join 588 other followers