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If human coronary artery is comparable to live wire , attempting  bifurcation (BFL) stenting is akin to tame a live snake .True BFL  (with Medina 1, 1, 1)  being the most complex of all .The fact is ,we have atleast a dozen strategies for BFL with varying loads of metal abutting the ostia ,side branch and carina.This  would essentially Imply we are still struggling with these lesions .

While current science tends to vouch PCI* for most  BFLs . . . wisdom  might whisper CABG !

Who should do complex PCI ?

Obviously,  not every interventional cardiologist can. Confidence is one thing , but , falling short of minimum standard of care is rampant in India. Newer Imaging tools, techniques are promising , unfortunately  still the gap between, knowledge , science and  reality continue to widen.

* Its true ,some expert Interventionists do a good job !

What is the simplest approach for Bifurcation lesions ?

Final message 

We have come a  long way in BFL. Still , some of the lesions can sting  like a snake ! I am sure, everyone of us would have lost sleep after a complex BFL PCI !( Praying the humble  heparin and DAPT to do the rescue act ! )

bifurcation lesions medina stenting srategies 002

How to escape this double headed threat ?

A meticulous assessment of  patient  &  lesion , mindfulness in choosing the hardware & Imaging , diligent usage of anticoagulants & DAPT and  . . . finally  willingness to listen to your own conscience ,  will ensure a gratifying result that includes abandoning the procedure !

Reference 

For everything in Bifurcation Intervention

The ultimate source : Visit the in this link  European Bifurcation  Club

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

Prosthetic valve implantation has revolutionized the management of  valvular heart disease . The original concept valve  was a ball in a cage valve  , still considered as a  fascinating discovery.  It was conceived by the young Dr Starr and made by Engineer Edwards  .This was followed   by long hours of arguments,  debates and  experiments that ran into many months . The  silent corridors of  Oregon hospital Portland USA remain the only witness  to their hard work and motivation.  At last,  it happened , the first human valve was implanted in the year 1960. Since then . . . for nearly  50 years these valves  have done a seminal  job for the mankind.

With the advent of  disc valve and bi-leaflet valve in the  later decades of 20th century , we had to say a reluctant good-bye to this valve.

There is a  lingering question among many of the current generation cardiologists and surgeons why this valve became extinct ?

Starr and Edwards with their child !

We in India , are witnessing these old warrior inside the heart functioning for more than 30 years.From my institute of Madras medical college  which probably has inserted more Starr Edwards valve than any other  during the 1970s and 80s by Prof . Sadasivan , Solomon victor , and Vasudevan and others .

It is still a mystery why this valve lost its popularity and ultimately died a premature death.The modern hemodynamic  men  working from a theoretical labs thought  this valve was  hemodynamically  inferior. These Inferior valves worked  like a  power horse  inside the hearts  the poor Indian laborers  for over 30 years.

A Starr Edwards valve rocking inside the heart in mitral position

The cage which gives  a radial support* mimic  sub valvular apparatus, which none of the other valves can provide.

* Mitral  apparatus has 5 major  components. Annulus, leaflets, chordae, pap muscle, LV free wall.None of the artificial valves has all these components.  Though , we would love to have all of them technically it is simply not possible.  The metal cage of Starr Edwards  valve partially satisfies this  , as  it acts as a virtual sub valvular apparatus.Even though the cage has no contact with LV free wall, the mechano hydrolic  transduction of  LV forces to the annulus  is possible .

Further , the good hemodyanmics of this valve indicate , the cage ensures co axial blood  flow  across the mitral inflow throughout diastole. .Unlike the bi-leaflet valve ,  where the direction of  blood flow is determined by the quantum of leaflet excursion  in every beat . In bileaflet valves  each leaflet has independent determinants of valve  motion . In Starr Edwards valve the ball is the leaflet . In contrast to bi-leaflet valve , the contact area  of the  ball and the blood in Starr Edwards  is a smooth affair  and  ball makes sure  the LV forces are equally transmitted to it’s surface .

The superiority of bi-leaflet valves and disc valves  (Over ball and cage ) were  never proven convincingly in a randomized fashion . The other factor which pulled down this valve’s popularity was the supposedly high profile nature of this valve. LVOT tend to get narrowed in few undersized hearts.  This  can not be an  excuse , as no consistent  efforts were made to miniaturize this valve which is  distinctly possible.

Sudden deaths from  Starr Edwards valve  .

  • Almost unheard in our population.
  • The major reason  for the long durability of this valve is due to the  lack of  any metallic moving points .
  • Absence of hinge  in this  valve  confers  a huge mechanical  advantage with  no stress points.
  • A globe / or a ball  has  the universal hemodynamic advantage. This shape makes it difficult for thrombotic focus to stick and grow.

Final message

Science is considered as sacred as our religion Patients believe in us. We believe in science. A  good  durable valve  was  dumped from this world  for no good reason. If commerce is the  the main issue ( as many still believe it to be ! )  history will never  forgive those people who were  behind the murder of this innocent device.

Cardiologists and Cardio thoracic surgeons are equally culpable  for the pre- mature exit of this valve from human domain.  Why didn’t they protest ?  We  can get some solace  ,  if  only we can impress upon  the current valve manufacturers  to  give a fresh lease of life to this valve .

http://www.heartlungcirc.org/article/S1443-9506%2810%2900076-4/abstract

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.

Primary PCI (pPCI) is a  glorious revascularization strategy for STEMI practiced for over 2 decades  but still has not proved its perceived mettle convincingly as a large population based strategy. In the mean time, the utility value  of  thrombolysis  was systematically  (Intentionally too! )  downgraded in the minds of both academic and public mind.
Truth can’t be buried for long. Series of revelations are coming up restoring the superiority of early thrombolysis over pPCI even in PCI capable centers.
In 2013, the high Impact STREAM trial argued  for pharmacoinvasive approach within 3 hrs as it was at equipoise with a pPCI. Now, EARLY -MYO  from China vouch  for pharmaco- Invasive approach  till 6 hours. (Just published in Circulation September 2017 )
 
 I think we need to wait for some more time , for another prevailing  falsehood that need to be busted ,(Looking  out for some straight thinking new generation cardiologist to do it !)
What is that ?
Many of us have misunderstood(rather made to !)  that pharmaco Invasive has a defined therapeutic endpoint ie taming  & stenting the IRA . This is absolute ignorance  happening even in state of the art centres ,ironically this beleaguered concept is  backed by peer-reviewed papers from premier journals. The fact of the matter is , If thrombolysis is stunningly successful (Which at the least happens in 50 % ) one can stop with that , it’s also a therapeutic endpoint at least for time being .
Is coronary angiogram a baseline test like ECG ?
That’s what current cardiologists with cutting edge knowledge  seem to believe !  Do you agree ! I am sure I’m not !
 Patients with STEMI who had successful thrombolysis who had an  apparently uncomplicated course (Assessed by strict clinical ECG, ECHO criteria) need not go for coronary angiogram in the immediate future.In fact some good guidelines strongly argue for it and call it as Ischemia driven PCI ! but very few seem to respect that concept.)This will not only contain the cost and ensure the vast majority of Inappropriate (  scientific quackery) coronary plumping activity in human race.
Searching for an elusive data ! Can some one help ?
I have been searching for data , from all those major pharmaco invasive studies (Which is not being reported /shared or analysed )
How many  patients in the “success cohort” after thrombolysis  who subsequently land up with urgent PCI related complications when trying to stent an already reperfused IRA or while tackling  coexisting Innocent or non-innocent non IRA lesions ?
* Complications and adverse events  may be acceptable in patients who had failed thrombolysis or who are  unstable  but even minor adverse events are forbidden in patient with a truly successful and asymptomatic patient.
Final message
So called scientific facts have very short half life !  for the simple reason they are let loose in human domain prematurely !
Reference 

The age old  statistics , 30 % of deaths following STEMI happen even before patients reach the hospital may still be true. But ,there is an untold story that happen regularly in the rehabilitation phase .Its ironical many  apparently stabilised STEMI patients still lose their life just before they get discharged or within 30 days .More often than not this happens in the toilet when they strain for defecation. At least a dozen deaths I have witnessed in the last few years. Of course we have resuscitated many near deaths as well.

What exactly happens to these ill-fated patients inside the toilet  ?

Straining is often an isometric exercise and prolonged strain ends up in   valsalva maneuver , a prolonged valsalva strain realistically shuts both vena cava due to raised intrathoracic  pressure .Vena caval shutdown is equivalent to asystole and imagine the chaos in the  delicately recannalised LAD when the coronary perfusion pressure nose dives (Even the  stented segment in IRA is vulnerable as distal flow restoration may take time   !)

The sudden systemic hypotension leads to  fall in coronary arterial pressure proximal  to the lesion. The normal physiological response to proximal fall would be corresponding distal fall maintaining the flow gradient . If the microvascular bed is damaged( loss of capacity to vasodilate ) this distal fall may not happen promptly .So its acute standstill of flow  across IRA ( or even Non IRA if it has a lesion )  triggering events that rapidly destabilise  unless intervened.

.

hemodynamics of ffr lad valsalva 2

 

 

 

 

 

 

 

 

 

 

 

 

 

Other modes of sudden toilet deaths

*The opposite process , ie sudden spikes of blood pressure (In contrast to hypotension of  Valsalva strain ) can  occur as straining is equivalent to Isometric exercise which increase afterload .This can either cause LV failure, another episode of ACS, myocardial stretching, even tear it and result in mechanical complication.

  1. Acute LVF triggered by spikes of BP /new onset ischemic MR.
  2. Free wall rupture and tamponade.
  3. Emboli getting dislodged from LV during strain

How to anticipate and prevent these  deaths ?

  • All complicated STEMI patients should have special rehabilitation program.
  • A simple rule could be patients with persistent ST elevation with  are prone for further events.They should be flagged. (Stented / TIMI flows matters very little !)
  • Restrict all vigorous activity for minimum of one to two weeks ( I am not a believer of pre-discharge stress test even in uncomplicated MI  )
  • Use laxatives adequately.
  • Western toilets may have an hemodynamic advantage. Indian closets that require squatting which increase the venous return , ultimately it compromises coronary hemodynamics more. We don’t understand as yet ,what will happen if one perfoms a valsalva  and  squatting simultaneously.(Which will prevail over the other ?)
  • Finally toilet shouldn’t  be locked during rehabilitation for safety purposes.
  • All post STEMI pateints should have registered with emergency contact and alert service ready.

Has primary PCI has reduced the sudden deaths  in Post MI period in current era ?

I’m afraid , I can’t say a dogmatic yes . May be ,to a certain extent , However,  it has created a new subset of perfectly  stented still prone for ACS.A physiologically or pharmacologically  recannlised IRA generally heals by themself. A Stented IRA  hands over  the responsiblity of healing the injured IRA to us  .Ofcourse ,we try to do it  with lot of difficulty  .(Different versions of  confused DAPT  regimens !)

Final message 

Please note , “discharge to 30 day mortality” following STEMI   which is  upto 2 %  .It is the most neglected  and  mismanaged phase in coronary care .Toilets are definitely not a benign place for them and all the good work done by you in cath lab and CCU can be nullified in few Innocuous looking seconds !

Postample 

Is Toilet room death amounts to  negligence / mis-management  inside hospital ?

May be there is a reason for this argument. When to ambulate in complicated STEMI is a big question. ? Though we have guidelines some of the patients are reluctant to use assisted service.

I think its a calculated risk , and  there is trade off between the benefits of early ambulation and potential exertion related risk.

One such argument by a cardiologist in a medicolegal situation goes like this. “I thought my patient’s heart  is stable enough to use toilet , it misfired , hence it is just an error of  judgment. I can’t be faulted.  Though this argument appear logical , many times it can’t hold water in court of law !”

Reference

1.Siebes M, Chamuleau SA, Meuwissen M,   Influence of hemodynamic conditions on fractional flow reserve: parametric analysis of underlying model Am J Physiol Heart Circ Physiol. 2002 Oct;283(4):H1462-70

Further reading

Cardiac rehabilitation NICE guidelines  : Myocardial infarction: cardiac rehabilitation and prevention of further cardiovascular disease 2013

 

How often you assess the success of Primary PCI with degree of  ST segment regression or resolution ?

I posed this query to a  freshly hatched , Intelligent and energetic cardiologist in an upscale dedicated heart care center.

He said, “No, we don’t .We always go with TIMI flow in IRA .TIMI 3 flow with less than 30% narrowing of IRA is success, that’s it ! He continued ,very often ,we don’t even Insist to take serial ECGs after the procedure .  . . forget about analysing ST segment  !  His body language seemed to suggest,  he didn’t expect such a question (Silly !)  from me , talking about ECG  in this era of hyper Interventionism where we literally live within the coronary artery !

What a grave error in coronary cognition ?  . . . thats commited  day in day out of cath lab  all over the globe !

TIMI flows across IRA lesion tell  more about epicardial patency while the humble ECG  reveals the true myocardial reperfusion.

So ,which will you use for assessment for successful reperfusion ? Ideally both , right !

But , as of 2017 ST segment regression is not considered worthy to  define success of pPCI  by the all powerful world scientific cardiology community .This is unfortunate (Or Intentional ?) we have  ignored  this Inspite periodic research papers showing the importance of the same.  (Link to this land mark Brodie BR AJC 2005)

Do you know , none of the  trials that celebrated the superiority of primary PCI in the last two decades used  ST segment criteria. But then ,we realised much later even TIMI 3 flow can have near zero myocardial perfusion. So ,can we now say all these trials are invalid ?

We also never bothered to include no reflow as a liability during pPCI. We have enough data to say even restored No reflow during pPCI has worrying long-term outcome  as reocclusion and tissue level perfusion is dismal .(Can we call it a pPCI failure equivalent ?) This is because the Cocktail  of anti no-reflow drug  we administer often give us a momentary satisfaction with transient myocardial blushes ! (Only to occlude minutes later as the patient is wheeled out of cath lab .We will never ever know how often this happens  !) This is because , microvascular bed integrity is notoriously unpredictable and defies the conventional salvage time window . We have seen patients with ultrafast pPCI ending up with severe LV dysfunction.

to-succeed-in-life-you-need-two-things-ignorance-and-confidence-quote-1

Final message

If you apply the ST regression criteria by 90* minutes after  pPCI (as we do for lysis ) the true success rate of pPCI will emerge .My prediction would be , if you do that routinely  the hype of perceived superiority of pPCI might go down the drain (At Least in all low risk STEMI ! ) Let us do a large-scale trial comparing ST regression with TIMI flows, blushes ,frame counts etc and rediscover the true face of our beleaguered coronary microcirculatory sense !

*In fact ST regression should occur much early with pPCI than lysis (May be 10 minutes after restoring IRA patency ! )

Post-ample and a Quiz !

If coronary thrombus laden IRA  is the chief culprit in STEMI battle field , Why is that Immediate , routine aspiration of thrombus in the ground zero is counter productive ?

That’s what the sophisticated mega trials of coronary thrombus  TASTE, TOTAL revealed.  I’m looking for an answer !

Reference

 

Counter point (and adding more confusion !)

Surprisingly , a Danish(DANAMI)  study showed  ST regression may not be Important in pPCI .This appears curious , especially when it suggests , ST segment regression didn’t occur because of more complete revascularisation by PCI !

Left main bifurcates into two , that’s  the classical anatomical behavior of LCA. (Or it trifurcates) When left main divides , it tends to share its diameter between its two siblings LAD and LCX with considerable  whims and fancies.(Though Finet* et all thought it has a working rule !) * From  Biomedical Engineering, Cardiovascular Hospital and Claude Bernard University France

Now , have a look at this , its a rare example of  how a left main might Ignore the rule of bifurcation just like that !

Left main simply continues as left main* after giving off a casual side branch from mid left main shaft .Yes , Its a innocuous looking LCX which would be non dominant as expected

LCX arises exactly mid way in left main , (Technically LAD begins at this point ) but , can you find any difference in the left main after giving off  LCX branch.

Can we say left main continues as LAD without a bifurcation ?

Or shall we say  left main gives off a premature early side branch ( true LCX)  non bifurcating  branch ?

It is an unusual anatomy and  as expected , this patient had a dominant  RCA .

What could be the clinical implication for such a premature  LCX ?

We can only guess . May be nothing !  Obviously ,these patients are immune to develop true bifurcation lesion. Does it in any way mean they have anatomically blessed coronaries !

 

Reference 

1.Finet G1, Gilard M, Perrenot B Fractal geometry of arterial coronary bifurcations: a quantitative coronary angiography and intravascular ultrasound analysis. , EuroIntervention. 2008 Jan;3(4):490-8.

Heart is not like a rigid structure built with  bricks . . . . so , its too architectural mindset to describe cardiac chambers to be made up of walls. Rather , Its a four chambered muscle mass moulded together in a complex 3D interface with distinct surfaces rather than walls. It’s also important to realise, since the heart is positioned (rather hanging )delicately in the middle mediastinum resting on the diaphragm , its subjected to one more dynamism due to respiratory motion blurring the definition of surfaces as well. (Vertical vs Horizontal)

4415_21_26-heart-human-posteriorly

Posterior surface is now referred to as infero-posterior

The posterior aspect of heart contains essentially the venous channels and the atrium (LA in particular)pulmonary veins and coronary sinus.  This happens right from 8 week heart open stage when venous end of lower straight heart tube folds up and posteriorly .

cardaic-looping-posterior-wall

It should be recalled only a small portion of lower aspect of posterior wall is alloted to left ventrilce.Instead the Infero diaphragmatic surface is formed by two-thirds  the LV and one-third Right ventricle.

anatomy-of-heart-posterior-wall-mi-lcx-rca-grays-grants-anatomy-netter

Image courtesy : From the great Netter

Nomenclature  issue 

The term posterior wall is now abandoned in most Echocardiography texts its replaced by inferior .The implication is more for Electrophysiologists with reference to accessory pathway localization

What is true posterior wall MI ?

As discussed before ,posterior surface of heart is different from posterior aspect of left and and right ventricle.

What does leads V7 V8 V9 record ?

It actually records electrical signals arising from posterior  aspect  of heart.  Left atrium,  pulmonary vein along with insulatory  effect of lungs dampens the potential . This makes the sensitivity of ST elevation  in posterior MI is low.

Blood supply of posterior surface

It’s highly variable.Both RCA and LCX arteries contribute with its  posterior left ventricular branches (PLV)

It can be inferred , LCX has more territorial rights than RCA in this unique zone of heart as the artery covers more posterior areas.

Read a related article

Back pain from anterior MI : Is it possible ?

 

 

Hippocrates is bestowed with the Immortal  tag “Father of Medicine”, not because he invented  any miraculous gene therapy or a modern virtual imaging of human organs, nor did he found any magic drugs .He didn’t receive a single award  even from his local village, forget about any Nobel prize to him !

hippocrates

Mind you , he lived before Christ ,2ooo years ago , there was nothing in the hands of noble professionals, not even a piece of paper and pencil to note down patient’s symptom .They didn’t even know what organs human body contained no basic medical tests . They just had a pair of hand, working brain with six senses , strong will to work hard and most importantly a caring mind and a constant search for answers to lingering scientific queries .

good medical practice hippocrates medical oath ethics drsvenkatesan dr s venkatesan

Yes, Hippocrates is still holding the post of father of medicine because he was the first human  to propagate  thought that human diseases are not evil forces beyond our control, it may have scientific basis , every disease has a specific cause that arise from derangement of body function.

More important than this , he formulated a way to practice this profession in a dignified manner. He also predicted common sense may prevail over science  in innumerable instances. Going through his quotes , one could wonder , he probably predicted technology might hijack human Intellect as well !

hippocrates quotesQuotation-Hippocrates-disease-Meetville-Quotes-149262Now,we have every thing. Students read medicine  in animated 3D class rooms , physicians  get a deluge of body system data &  images beamed straight into their ipad . One can perform  complex interventions with ease in almost every  organ or  even replace it , if it doesn’t work .

Still , as on 2017  ,there is something huge , that is missing  in the Noble profession when compared to ancient days  (2 millenniums before!) when people thronged Hippocrates  clinic in the remote Koss Island of Greece, where he used to sit  with almost  nothing , but was able to offer definite cure for many .

What is that missing link  ? Without realizing  what it is, we enter the Noble profession and fervently  take the  customary Hipocratic oath . For many (or most ?)  of us it is amusing to read and practice that. Life has moved in  fast lane since then. It is a tragic truth , Hippocratic oath  have become  redundant , obsolete .or outright humiliating for few !

Final message 

Whatever you say, still Iam compelled to feel sorry for that “Good old man” who miscalculated the Integrity modern day Noble professional , (I would say, Mr H failed to  realise doctors are also made from ordinary human beings ! )

It’s ok . . . here is a “Doctor’s life maintenance” manual : Keep reading it periodically !

British General medial council , has done a wonderful job . It has published a practical life maintenance and behavioral guide for  doctors  which I feel is most important text to be read periodically and of course  followed  !

Link to Good medical practice