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A young man aged around 40 years, had a STEMI was promptly thrombolysed in a small hospital located about 40 KM away in the suburbs of my city Chennai. They did an awesome job of saving the patient life and salvaging the myocardium.

Now begins the story . . . one of the non-medical person who is the owner of the hospital has an unfortunate working  business relationship with a frighteningly big nearby hospital  which had signed a memorandum of irresponsible understanding . It demanded any  patient who arrives in the small hospital with MI should be transferred at earliest opportunity to them.

So, an ambulance was arranged  and the patient (with a fairly well reperfused heart ) was shifted  in an emergency fashion . It reached desired destination after nicely chugging along the choked chaotic Chennai evening traffic for 45 minutes.

The guy was taken directly to cath lab through the side doors to perform a second salvage  procedure on a successfully opened IRA. Young cardiology consultants  in designer cath suite welcomed the smiling ACS patient to their posh new lab .Did few rapid radial shots, mumbled among themselves for few minutes,  decided to stent  a minimal LAD lesion for a patient who was in  zero distress with well-preserved LV function.

*The relatives of the patients were curious when they were asked sign a fresh set of consent which elaborately  mentioned about possible life risk during the procedure.

The patient’s wife  was clearly  amused and she pointed out to the superior cardiologists about  the earlier briefing by the Inferior freelance cardiologist who treated him in the previous hospital. She recalled , “I was told in confident terms  that  Initial thrombolysis  has been spectacularly  successful and bulk of the treatment is over and risk of complication has dramatically reduced”.

Then why is this distressing risk taking story again ,  she asked ?

The doctors hurriedly explained ,”this procedure is different. We are sorry to say we have no other option but to add  further risk to you” ! but , its all for your good !

Why should I ?  If the initial lysis is very successful  why do you want to meddle with it again ?

No Madam , you are ill-informed , you can’t talk like that .This is what modern  science  is all about. Leave the professional decision to us. We need to check immediately  whether the lysis is really successful .We can’t rely on the ECG.Further, true success lies in stenting the lesion as we fear the ill-fated site may close again.We are  taught to practice protocols based on standard scientific guidelines. This hospital has highest rating in-terms of quality care. That’s why we got updated ISO 2000  NABH accreditation

The women who is a soft ware engineer was smartly and  scientifically silenced in 5 minutes flat !

Post-amble :

What happened  to the patient then ? (When you fear something it happens is in’t the  Murphy’s law ?)

The apparently asymptotic and comfortable patient had uneventful PCI. A  long drug eluting  stent  was  implanted in recanalized  lesion in LAD with around 30 % narrowing that ended with an innocuous looking diagonal pinch. The procedure was uneventful , however next day he developed some fresh ECG changes and chest pain . The worried team took him for another angio found  stent was patent But , ultimately after a stressful 3 days of stay , some thing went wrong he ended up with new LV dysfunction.He got discharged fine with a caution  that , his stent needs to intensively monitored for the next 1 year since technically he had recurrent ACS !

Lessons we don’t learn from such cases.

When two procedures are done to accomplish the same aim (Reperfusion) , but with  differing success rates, expertise, time ,and unpredictable hazards , the benefits from them may not add together. There is clear knowledge deficit here. Scientific data can never provide fair answers to  these questions  as all real life cofounders can never be recreated in study population.

While we expect 1+1 to become  two in pharmaco-Invasvie strategy  ,one should realise it may end up with  either zero or even  – 2 .

1 -1 = 0

-1 + (-1)=  -2 ?

Learning cardiology from lay persons 

The patient’s shrewd wife threw this question ,

After two modes of re-perfusion done sequentially in my  husband’s  heart ,  at a total cost of Rs4.5Lakhs Why he  is  still left with significant LV dysfunction (Which was  around 40% EF.)

The query raised by the lady appeared much more crucial and logical than the ones discussed in many top-notch live interventional workshops we attend every few months!

As usual , I started mulling over the issue. There is something wrong with the way , we  understand  the pharmaco invasive approach-PIA .You go with it only if  initial pharmacological  approach has failed.

Of Course ,there is one more modality possible ie Pharmaco -Angio strategy where in, you look at the coronary anatomy and take a call ! This sounds good , the only issue is taking a right call ! My experience suggests wrong calls are the rule and  exceptions are rare. Then a whole new issue erupts about all those non IRA lesions

Final message

So,  til we have gain complete self-control over our evolved ignorance and evolving knowledge , it is better to follow this proposed  funny new ACS algorithm called “Pharmaco -non invasive” approach (PNIA)  in asymptomatic ACS patients  who have had apparently successful lysis.

*Please note, Incidentally  PNIA actually  refers to simple good old traditional stand alone thrombolysis.

Counter point

No one can deny Interventional cardiology carries a risk of untoward effects.Don’t blow this out of proportion. Do you know, how many lives have been saved by routine Pharmaco -Invasive approach ?

I am not sure , my experience may be limited.Let me ask the readers. Is routine PIA is warranted in all asymptomatic , successfully lysed STEMIs ?

100% occlusion of a coronary artery result in STEMI.This includes both thrombus and mechanical component .We are very much blinded till we touch , feel and see the lesion with a wire or IVUS to quantify the mechanical component’s  contribution in the genesis of  STEMI.It is generally believed (True as well ) thrombus is the chief culprit .It can even be 100 % thrombotic STEMI with  just a residual endothelial  erosion and hence
zero mechanical component .However , the point of contention that non flow limiting lesion is more likely to cause a thrombotic STEMI than a flow liming
lesion  seems to be biased and misunderstood scientific fact .

What happens once 100 % occlusion take place ?

Sudden occlusion , is expected to evoke a strong fire fighting response within the coronary artery.The immediate reaction is the activation of  tissue plasminogen system. In this aftermath  few succumb . ( Re-perfusion arrhythmia  generated as VF ) .The TPA system activates and tries to lyse the clot.The volume , morphology, attachment, content of thrombus ,  and the elasticity of fibrin mesh , location of  platelet core would determine the life and dissolvablity of thrombus. Even a trickle flow can keep the distal vessel patent .(Please note a timely TIMI 2 flow can be a greater achievement than a delayed TIMI 3  flow !)

thrombus propgation
What happens to the natural history of thrombus in STEMI ?
Thrombus formed over the culprit lesion can follow any of the following course

  •  Can remain static
  •  Get lysed by natural or pharmacological means
  •  Progress distally (By fragmentation or by moving en-mass )
  •  Grow proximal and and involve more serious proximal side branch obstruction
  • Organise and become a CTO

Factors determining thrombus migration

The interaction between the hemodynamic  forces that push a thrombus distally and hemo-rheological factors that promote fresh proximal thrombus formation are poorly understood. The altered intra-coronary milieu with a fissured plaque covered by  platelet vs RBC / fibrin core,  totally of obstruction,  reperfusing forces , re-exposure of raw areas and  the distal vessel integrity all matters.

While, logic would tell us,  thrombus more often migrates  distally  assisted by the direction of blood flow, an  opposite concept also seeks attention , ie since the blood flow is sluggish  in the proximal (to obstruction site )more thrombus forms in segments proximal to obstruction.

(In fact, its presumed  in any acute massive proximal LAD STEMI , it takes hardly few minutes for the thrombus to  queue up proximaly and  clog the bifurcation and spill over to LCX or even reach left main and result in instant mechanical death.)

What is the significance of length and longitudinal resistance of the thrombotic segment in STEMI ?

If thrombus is the culprit let us get rid of it , this concept looks nice on paper , but still  we don’t  know why thrombus aspiration in STEMI is not consistently useful. We also know little about  the length of the thrombotic  segment .When a guide wire is passed over a STEMI ATO it may cross smoothly like  “cutting a slice of  butter” in some , while in few we struggle and  end up with severe no-reflow inspite of great efforts .Why ?

What is the Impact of distal collateral flow in flushing fresh thrombus ?

The efficacy of collateral flow in salvaging myocardium is underestimated. Distal vessel flow if perfused partially by acute collaterals the thrombus load is not only less it’s soft and fail to get organised early that would help cross the lesion easily.

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.

The mechanism of MR in ischemic /Functional is complex. Technically, pure ischemic MR should have a structurally normal leaflet and the subvalvular mechanism dominates But,the combination of the two is also prevalent. In fact, a degenerative component is added to this in many elderly patients.

Mechanism of Ischemic mitral regurgitation

Any of the following may contribute either alone or in in different combinations.

  • Global LV dilatation with or without annular dilatation
  • Spherical left ventricle
  • Altered inter papillary muscle distance (Degree and direction of  posterior vs apical displacement of pap muscle)
  • Chordal shortening /Lengthening/Abnormal tethering
  • Leaflet tenting distance and volume
  • Basal LV dysfunction and Local LV (Sub-mitral) remodeling

We have come a long way ,  since the days of  Carpentier and Duran who did pioneering work .It involved partial or complete mitral annular stabilization with surgical ring technology that  helped us to change the shape of the annulus. Advanced imaging, with 3 D printing will enable us to procure perfectly matched designer valve rings and (may be leaflets also) in the near future. Percutaneous mitral valve Interventions, with clips , valve, are going to dominate the mitral valve therapeutics.

Still, we are largely ignorant about Individual contribution from various components in the genesis of  ischemic /functional MR. This becomes important because the preservation of native valve is better on any day than replacing.  One thing is very clear, even though left ventricle forms part of mitral valve apparatus, the degree of LV dysfunction has no linear correlation with the severity of MR . Its a well-known fact, even severe LV dysfunction (Say < 25 % )may enjoy the company of a perfectly competent mitral valve. It’s interesting to note uniform global LV dysfunction cause more of central MR , while dispropotinate basalLV dysfunction especially the posteroinferior pap muscle cause eccentric jet. One more curiosity is mitral regurgitation improving with worsening disease as contractile force weakens.(Functional MR depends on LV function you know !)

We have witnessed at least two patients who had a significant MR following an inferior posterior MI which was managed medically, showed dramatic regression in the degree of MR  when he had anterior MI later*.The pleasant irony was apparently due balanced dysfunction of anterolateral pap muscle that happened in countering the original postero-medial pap muscle dysfunction.(*Allowing second MI to happen is of course a treatment failure !)

Image source -Christos G. Mihos  Journal of Thoracic disease Vol 8, No 1 (January 2016)

Mitral valve is essentially avascular structure, Still, ischemia affects this valve not by valve necrosis but by other sub valvular mechanisms .Note the MR here is due to poor motion of PML due to ischemic LV dysfunction.

 

Ischemic MR in early hours following STEMI (also NSTEMI) is still a nightmare. We realized in a harsh way, it’s rarely corrected fully even with a successful IRA plasty. (Especially LCX and posteromedial pap muscle that is in extreme distress) In fact , many of the mechanical complications that lead to flash pulmonary edema would need emergency CABG rather than primary PCI. (What to do for Ischemic MR ? An excellent review article( Elsayed Elmistekawy Curr Opin Cardiol 2013, 28:661–665) 

Mitral valve, though looks like an obedient, innocuous structure that  silently does its job , only in special times, it makes us realize, its the most critical part in the entire heart.(Guarding the lung against flooding when the left ventricle experiences turbulent ischemic times during ACS.) Note -Acute MR often kills , not the ACS as such.ischemic mitral regurgitation functional carpentier drsvenkatesan venkatesan madras medcial college 002It looks to me ,the mechanism of MR in various pathologies is comparable to the behavior of a cow grazing in an arc tethered to a poll. Normally its expected to follow a set pattern. If it behaves wayward, one may need to tighten the rope(Chordae), or loosen it, strengthen or move the poll(Pap muscle) . . . still more options like whipping (clipping ) the cow(Leaflet) may be tried. Of course ,ultimately one may need to replace the cow (MVR). EP guys do  have an electrical solution to tame this cow , called CRT to regress Ischemic MR .

 

Reference

1.Yiu S.F.,Enriquez-Sarano M.,Tribouilloy C.,Seward J.B.,Tajik A.J.Determinants of the degree of functional mitral regurgitation in patients with systolic left ventricular dysfunction: a quantitative clinical study. Circulation 2000;102:14001406

2.Mitral valve repair over five decades  Ann Cardiothorac Surg. 2015 Jul; 4(4): 322–334 

GettyImages-865142952-5b5eef884cedfd0050112fa6

Charles river esplanade ,Boston* : A healthy middle-aged man who was jogging quietly, while his heart was under intense scrutiny by the bionic eyes of Apple i-watch’s smart patch electrode. Suddenly, it detected some bizarre ST segment fragmentation (Seems it can predict in advance , Ischemic signals 10 minutes prior to onset of ACS ) The built-in cosmos direct GPS instantly alerted & summoned a titanium powered Space X drone that pulled the patient from the riverside to the nearest human wellness port .

EHANG 184

It dropped him through a remotely accessed split glass roof right inside the hybrid heart lab, to find , men and women chatting with flattish Artificial intelligence panels who readily allowed the robotic arms to hug the patient which engaged the coronary artery pushing radiation free magnetic gas found nothing inside and what would become a perfectly normal human coronary artery .

An amused resident robot gently plucked the patient from the cath table with sheepish laughter and called for another drone to drop the patient exactly in the same place from where he was picked up.The healthy hearted patient thanked the doctors profusely and continued his routine evening jog across the Charles of course with a 16-minute delay!

Next day . . .

Event auditing firm medi-logic mind congratulated the entire cardiac team and its digital health hub for the quality of the network and completing this daring coronary rescue mission in 16 minutes. While the drone to hospital roof time was 3 minutes, the coronary artery visualisation time was perfect.The auditing team had a special mention about the astonishing capability of Apple time watch algorithm that made sure that the patient’s evening routine was unaffected in spite of this life-threatening non cardiac pseudo-emergency. The crowning glory was, the entire expenses amounting to 250000 dollors (after a special money back discount coupon for the first false alarm) were taken care by the patient’s virtual insurance blockchain payment gateway.

*You have just read the news that wasn’t – January 2030 AD

Now, back to reality,

Stumbled on this news clip from pages of Times of India, (20-6-2019) months after I wrote the above piece. I wondered the chase between fact and fiction is becoming  really a close race.

In the evaluation of syncope, history is most important to arrive at a diagnosis. Ofcourse, the first step is to confirm whether its truly a syncope or something else.(Metabolic/TIA or seizure.)We are easily carried away by the urge to order a Holter monitoring routinely. In reality, the yield is too low (<15%) .Even the utility value of Head up tilt (HUT) is being downgraded.

Paradoxically, resting ECG might give important clue in many. One need to specifically look into a set pattern of ECG. It generally falls in one the following in any patient with syncope.

This post specifically may not be exclusive but stresses the importance of resting ECG in the evaluation of syncope. by our urge (Stress testing is not included)

  1. Bradycardia( Sinus Node dysfunction/AV block) Note Brady cardias can per se cause syncope if pause >3-5sec Or it may lead to Brady (Pause) dependent escape VT.

    A pause can be a sinus arrest, Pause or SA block .If pause ends with a junctional escape it becomes a arrest.

  2. Look PR interval specifically(A bifasicular block shouldn’t be missed .It can be more dangerous than say a congenital CHB)PR interal represents condcution from SA node to Purkinje fibres in ventricel. The importance is directly linked to the location of the block than propably the degree of prolongation. Please note HV interval > 70 ms in any patient with prolonged PR is cause for concern,
  3. Preexcitation/Delta waves (Though Narrow QRS AVRT rarely causes syncope its very much possible during  Antidromic tachycardia. (AntiVRT), Antidromic AVRT or Accessory pathway with short RP <250ms need to be documented. Concealed paths are safe , but delta appearing during stress testing is extremely unsafe
  4. Post-excitation /Epsilon waves. (often noted in lead V 1, A marker of RVOT dysplasia as in ARVD. Also referred to as Fontaine wave who discovered it by bipolar cheat leads over V1 )

    Note the epsilon occurring after the qrs Indicating RVOT dysplasia

  5. Q waves (Markers of old MI -Scar Induced VT)
  6. High voltage QRS LVH /HCM /Aortic stenosis
  7. RV strain/S1Q3T3 pulmonary embolism.(Syncope is a common presentation with PE especially with minimal exertion or change in posture)
  8. Early coupled VPDS (R on T location a trigger for VT) Wedesky effect. The terminal portion of T which correspond to supernormal period.

    The significance of VPDs directly related to its prematurity than its focus of origin.The one that falls on the vulnerable period .Late phase 2 and phase 3 are more vulnerable as triggered activity

  9. Brugada (Type 1 with T inversion riskier, Camel hump less dangerous Joseph Brugada,

    Brugada syndrome -Note three types . Type 1 is typically risk prone. Please note it is the late ST declining component and the T iversion that confers the risk not ST elevation per se.The type 2 with a camel hump is confered with least risk

  10. Malignant ERS pattern (Most ERS or safe / Maligant forms infero lateral forms risky only at times of ACS not spontaneous risk
  11. J wave syndromes –Overlapping with Brugada /ERS Charles Antzelevitch,J Arrhythm. 2016 Oct; 32(5): 315–339

    ERS syndrome are so common. In the absence of sycnope, it should be ignored straight away. Recently it received too much hype among cardiologists increasing the anxietywhich is not warranted.

  12. Long QT Interval (Hypokalemia commonest, Congenital next Peter J. Schwartz,Long-QT Syndrome Circulation: Arrhythmia and Electrophysiology. 2012;5:868–877
  13. Fractioned QRS (Most often seen in DCM ischemic /non-ischemic confer VT risk usually with LV dysfunction, these are candidates for CRT-P/D as well)
  14. T wave alternans Fluctuating T waves indicate repolarisation alternans .It elevates risk of VT Narayan SM J Am Coll Cardiol. 2006 Jan 17;47(2):269-81
  15. Exercise Induced VT/ CPVT is to be considered seriously in all unexplained exertional syncope. Behere SP, Catecholaminergic polymorphic ventricular tachycardia: An exciting new era. Ann Pediatr Cardiol. 2016;9(2):137–146.

What next after ECG ?

After ruling out neuro cardiogenic syncope by history, one has to perform a good quality echocardiography that can clinch structural heart disease .In cardiomyopathies like ARVD or RCM MRI studies will be of immense value especially the LGE/DEMRI that picks up the scars and fibrosis as in sarcoid or tuberculomas etc. Event recorders are popular, may have a slightly better yield than Holter.EP studies are required in few as diagnostic or more commonly as a part of therapeutics.(Please note, EP lab Induced polymorphic VT has Zero diagnostic value as any normal human heart can be induced to VF by repetitive stimulation)

Management

The main purpose is to exclude serious primary electrical and or structural heart disease. However, fortunately, the most common cause of syncope is neurogenic or reflex mediated. It requires reassurance and fluid repletion Fludrocortisone,/Midoridine (Alpha receptor agonists are promising) Pacemaker/ICD is indicated in few with brady/Tachy -Brady .ICDs/RF ablation are Indicated in Ischemic VTs channelopathies with inherited VT/VF like Brugada. One important question still not clearly answered is when to refer a patient with syncope to Electrophysiologist. ? For me , it appears only a fraction may need it.

Further reading (2018 ESC guidelines)

A middle-aged man a Biotech engineer, who is just back from his annual health check, sitting in front of me with a deeply anguished face and said “Doctor my LDL is 130mg, and my diastolic BP is 90 mmHg and fasting sugar is 120 mg .I am very much worried about my future”

Wait , let me go through your file, I said ,

Isn’t a serious Issue doctor?

No, its not ,

But , doctor, I have read about ASCOT, SPRINT and HOPE-3 trials. I guess they tell us to keep the LDL, blood sugar and diastolic BP all these three parameters around 80. Isn’t doctor? He went on to add, that his old fashioned family physician has asked to continue the beta blocker. He said he is also aware of the fact, how JNC has ditched the beta blocker to the graveyard since they don’t do anything to central Aortic pressure. He continued, “Last year my routine coronary calcium score was beyond 300 . Shall I go for a regular coronary angiogram to ensure my SYNTAX score is around zero doctor” ?

I was quite shocked with his academic prelude, and asked him, by any way, he is a physician or a cardiologist?

No doctor, I am purely a non-medical man but follow all health related stuff from wall street medical bulletins. I am a busy man, still, work out regularly. I have important targets, ambitions to fulfill and lot to achieve in life. But, this LDL and BP is really bothering me doctor.

Yes, I got it . . . I understand your anxiety. Don’t get worried about all these biochemistry and hemodynamics. They are just numbers. Some of them will fluctuate to the tunes of your wall street as well.

Really Doctor?

Yes, we are all unlucky, in one sense you know. We are living in a man-made (scientifically) insecure environment. Great men in the past never had to bother with these silly numbers that currently define health. Alexander the great , neither had his Macedonian master health check nor he looked up for his lipid particles, (he was counting his horses Instead) Did Chengiskhan ever knew about his BP ?

Medical ethics master health check up holistic medicine life style nutrtion

If only these men were worried about these fancy number the world history would have been rewritten.

They didn’t even know an organ called the heart that is pumping 5 liters of blood every minute, until Harvey found the circulatory system 1000 years later. Still, they conquered the world. If we take world history millions of men and women have tasted the pinnacle success without really bothering to know their periodic Individual organ function status.

Here is one more story from my country, The Raja Raja Chola the great built this biggest Hindu monument called Brgadheeswara temple in Tanjavur ,Tamil Nadu , India in the year 1010 .

Raja raja cholan

A fictitious query – Who did FFR for Raja Raja Chola (947-1014AD) when he had vague chest pain from suspicious LAD lesion just after his war with Rashtrakuta empire .He went on to Live for 67 years conquering much of India without a single health check and ECG in his life time

It was an unparalleled kingdom of South India where millions of happy men and women who lived a healthy life with absolute faith and trust in their village healers who did the magic with Indigenous leaves, herbs, secret medical formulas based on ancient wisdom.

Longevity with a purpose

The anxiety to live long often keeps our lipids , sugar and blood pressure high . . . and sets a vicious cycle. Today ,this has become a perfect ground for the saviors of health care to trap us in a cartel who are conferred with an almost divine power of defining who is healthy and who is not.

Many times philosophers have felt longevity and the urge to live long, lacks a matching and meaningful purpose. Lack of purpose, as well as extreme obsession with a purpose, are equally dangerous. The purpose of life can never be equated solely on the longevity of our life. Life long fear and anxiety about possible illness and death is not welcome.

Human life span is mystical journey determined by genes as well the environment and its interaction with each other (Epigenetics) It’s destined to face challenges.Substantial of them can be managed without anyone’s help. I will be happy if you don’t ever need the help of cardiologist to get rid of fear and anxiety induced by general health awareness.

Isn’t prevention better than cure Doctor? I came for a possible coronary angiogram . . . but you have really confused me doctor!

No , I am not doing that Intentionally. From your angle its prevention of potential hidden disease. I am talking In a larger perspective, Master health checks many times end up as medical witch hunting. I am bothered about technological contamination that is all too pervasive among the health care system, especially manifesting as new non-existing diseases. (Skewed and tinkered normal curve )

We, the modern men . . . with all six senses intact, tend to make our life miserable with all these digitized biological data and deeply mined medical images from Innocuously good organs. Some times, we seem to more worried about artificial intelligence and least bothered to know the advantages of being naturally ignorant.

Life is not live data that is in motion. Have a good purpose in life, be physically active, think right, eat well, life shall be lived with peace. Please realize many pockets of the world had been more peaceful, healthy, and cultured in the past, than the current glorious and glamorous times. Of course, life expectancy has definitely prolonged with breakthroughs medicine but It’s not clear it has any positive impact in terms of overall global well being.

Please wake up , you are in the middle of patient consult story … Doctor!

Oh yes , thanks. As a parting advice, I sermonized, homo-sapiens are generally programmed to live for about 100 years except in a fraction who have either true incurable disease or those who succumb to a bad fate.

I realized , what should have been a simple prescription for an ARB +Thiazide + Statin and a stress testing , turned out to be an unsolicited compulsive lecture on life’s purpose, and philosophy etc I said sorry to my patient.

He silently got up. His body language was clearly not convincing enough to suggest, he has accepted my confabulations. He left the clinic with a humble thanks probably looking for a more saner physician!

.

Somehow the concept of  Evidence based medicine (EBM )never excited me in spite of great strides it has made. Probably the main reason for this is, EBMs origin, quality, and credibility is currently severely compromised. (Though It appears to ooze science 24/7 and make us believe in it too !) Herewith, sharing some of the forbidden thoughts(with lots of pun)  for a (un)successful practice of EBM. This is definitely not meant for young and novice medical professionals. Strictly for the ones who can segregate sense from non (S)

Evidence-based Doubting 

 

Reference

 

Yes, Its “evidence-based fun”. Forget all those anti-platelet trial dramas … showing in the cardiovascular theatres near you . There is only one genuine drug , that’s the good old humble Aspirin . Mind you ,none of other  actors can ever be imagined for primary prevention.

By the way , there is absolutely no controversy for the role of Aspirin in secondary prevention after established CAD.(We know , how Aspirin has taken up a critically  Integral role in saving the life of the stents  as well as  patients,  post PCI)

Oh , what a disgrace for this drug when it comes out of the glamorous cath lab zones. Its use is often frowned upon for preventing simple CAD. (All due to a single factor, fear of bleeding ? No , its exaggerated in most studies)

Overlap between Primary and Secondary prevention 

In primary prevention of CAD , what do we attempt to prevent? How do you differentiate established CAD from  “Established coronary atherosclerosis  but Non-established CAD ?”

The fundamental flaw in this perceived controversy is in our inability to define what is significant CAD in the asymptomatic population.Do we need a clinical event to say, established CAD?

For the attention of  evidence-based script writers , a long query  . . .

“How much evidence we have to conclude , that a  patient with manifest clinical CAD carry more risk for a  recurrence  than an asymptomatic  high-risk pateint  who is likely to develop the first clinical event (with a bang that could be a major ACS ) due to underlying silent Atherosclerosis.?  

Reference 

Click  here to for more  unscientific review on primary prevention of CVD.

 

 

 

 

*When I tried to condense three decades of my learning into the medical profession in three lines, I scribbled this. Sorry folks, if It doesn’t sound scientific for some of you! 

By the way, What is successful medical practice? Success for the Doctor, patient or both?  The answer to this question is never simple.