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Cardiologists at confused cross roads !

Perils of  limited Intellect & Infinite greed  

When not so appropriately trained cardiologists  do Inappropriate things “use becomes misuse” . . . then, it won’t take much time for science to become total abuse. That’s what happened with the murky world of coronary stents .No surprise, it’s time to firefight the healers instead of the disease !

Now ,Comes the ORBITA study . Yes , it looks like a God sent path breaking trial that spits some harsh truths not only in cardiology, but also in behavioral ethics .Let us not work over time and hunt for any non-existing loop holes in ORBITA. Even if it has few, it can be condoned for sure as we have essentially lived out of flawed science  for too long  Injuring many Innocent hearts !

ORBITA pci vs medical mangement drsvenkatesan courage bari2d ethics in stenting auc criteria inappropriate coronary stenting placebo effect of stenting acc aha esc guidelines chronic st

Yes , its enforced premature funeral  times for a wonderful technology !

GIF Image courtesy http://www.tenor.com

Meanwhile, let us pray for a selective resurrection of  stenting in chronic coronary syndromes  and stop behaving like lesser professionals !

Postamble

Extremely  sorry . . . to  all those discerning academic folks , who are looking for a true scientific review of ORBITA , please look elsewhere !

hole in heart asd vsd hole in raod potholes

https://timesofindia.indiatimes.com/india/potholes-claimed-6-lives-a-day-in-india-in-2016/articleshow/61283355.cms

Continue Reading »

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 !

Postamble

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 !

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

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

 

A 50-year-old man was referred for dizziness, bradycardia and dysphagia .He was very clear in describing his symptoms and  landed up in Gastro- enterology  OPD , from there was referred to my clinic for cardiac work up . His ECG showed a sinus bradycardia HR of 48 /mt.

Screenshot_2017-07-05-19-09-12

Echocardiogram revealed a structurally normal heart as we expected , but was surprised to spot suspicious shadow in para-sternal long axis view , beneath left atrium.

A well demarcated large mass compressing left atrium.  Trans Thoracic Echocardiography  may not be looking at the heart alone ,(Its technically Thoracic Ultrasound though we may refer it as Echocardiogram   )

  • Aortic aneurysm ?
  • Mediastinal teratoma?
  • Bronchial adenoma ?
  • Esophageal mass ?

The Answer is none of the above

As I was wondering what it was, the staff nurse in charge threw a heavy folder with well worked up gastro Investigations.

That moment , diagnosis became obvious , without a need for further scrutiny to my medical acumen.

Note: The barium swallow of the Esophagus reveals the Intimate relationship between the food tube and the heart as it descends vertically downwards posteriorly  . Realise , how the proximity of these two structures could  confuse a physician when symptoms spill over on either way. (I would have expected a lateral view to show the compressive effect of Esophagus on the left atrium the radiologists felt its not important !)

Yes , it is Achalasia of the cardia , dilating the lower end of esophagus with fluid /mass effect  , compressing the posterior surface of Left atrium.He underwent a myomectomy surgery.

Why bradycardia  ?

There is well described esophago-vagal reflex reproducible by stressful swallow or balloon inflation in the lower end of esophagus at D7 level.(Ki Hoon Kang,Korean J Intern Med. 2005 Mar; 20(1): 68–71.)

Achalasia cardia is known to be associated with symptomatic bradycardia, dizziness, and rarely swallow syncope,though this patient didn’t have a classical syncope.The bradycardia is probably due to high vagotonia, (Hugging effect on posterior surface of heart known for rich innervation of vagus.) . Complete reversal  of bradycardia after esophago -gastric surgery is expected.

Implication for cardiologists

There has been instances of patients with esophageal syncope and reflex bradycardia getting permanent pacemaker therapy. I think , clinical or sub clinical esophageal disorders should be included in the work bradycardia before labelling them as intrinsic sinus node dysfunction .(Ref 1,4)

Final message 

The field of Cardiology  is often referred to as a super specialty atleast in India . I disagree with it strongly. Cardiologists are neither super(eme) nor special .We need to be reminded  its afterall a sub-specialty of Internal medicine and each specialist should undergo retro-training in medicine periodically .This patient is a typical example of a gastric problem entering the domain of cardiac Imaging.Strong foundations in symptom analysis and some degree of medical  curiosity will enable an occasional cardiologist to make a correct diagnosis belonging to a remote foreign specialty.

Reference 

1. Palmer ED. The abnormal upper gastrointestinal vagovagal reflexes that affect the heart. Am J Gastroenterol. 1976;66:513–522. [PubMed]

2.Armstrong PW, McMillan DG, Simon JB. Swallow syncope. Can Med Assoc J. 1985;132:1281–1284. [PMC free article] [PubMed]

3.Turan I, Ersoz GBor S..Swallow-induced syncope in a patient with achalasia
4.Dysphagia. 2005 Summer;20(3):238-40  4.Basker MR, Cooper DK. Oesophageal syncope. Ann R Coll Surg Engl. 2000;82:249–253.