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I think it is an Invalid question. Whether you like it or not , medical science and philosophy are always bonded together and its relationship is eternal. It doesn’t make sense to separate them. I think we have misunderstood the meaning of philosophy. While science is presumed truths, philosophy is trying to believe in unknown truths. Philosophical truths are built-into every decision a medical professional takes.

If the expected natural history of any disease is science, unexpected deviations are philosophy. (RT PCR testing for diagnosing  Corona is science, why 90% of them are not infective and don’t transform disease is philosophy) When something is not seen or quantifiable like human immunity, it is a perfect example of concealed science or manifest philosophy.

Taking about what we think we know is science, Talking about what we really don’t know is philosophy. The term Idiopathic syndrome finds a  proud of the place in every specialty in medicine, Isn’t? 

 What will be your answer when your patient wants an assurance that a stent, you had just implanted will not get occluded in the next 6 months or so.“I don’t know, I cant assure you about that”  will be your most likely answer. (Though, we do it in style, hiding behind  the scientific hyperbole decorated with numbers,  also referred to as statistics) Please realize, this is the expression of medical philosophy in the finest form.

Final message 

My Impression is, philosophical truths should be liberally used in a regular fashion right from the first-year medical school to advanced specialty teaching. This seems essential as science in the current times suffers from too much sanctity. This has spilled over to the doctor population as well, and make them appear invincible. 

If only we realize science often trails behind the philosophical truths at least by a few decades, our patients will not be injured inappropriately and prematurely. Mixing science with philosophy in the right composition ( a perfect academic cocktail ) will bring out the best from the noble profession.   

Postamble

Can anyone guess, why scientists are given a doctorate in Philosophy degree  (PhD ) ?

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.

Surprised to see many of my colleagues, physicians and fellows are beaming with new pride even in this troubled corona times. Paradoxically, could see some fresh clinical sense in their approach to problems as well.

Each one of them has a story to tell

  • Sir, I could suddenly diagnose heart failure for the first time with my eyes and ears without NT- Pro BNP or E/E’ . I agree with you sir, textbooks seem to be right. There was indeed basal rales and JVP was elevated. I was astonished I could diagnose CHF clinically!
  • I feel proud, that I have acquired the rare expertise of giving fitness to an emergency appendectomy just by ECG.Its unbelievable, I had the courage of not asking for a pre-op echocardiogram.
  • Oh yes, it was a real flash of bedside brilliance. I could rule out Infective endocarditis, in a patient with prolonged fever, without caring to call for a bed side screening echo for vegetation. I am really proud of my acumen! I realised, Duke criteria is far more deep than our urge to have a glimpse on vegetation.
  • I can’t believe myself, yesterday, I was able to Ignore a 90% LAD lesion, first time in my life, by clinical means without FFR and QFR stuff.
  • This one is again from the Echo lab. I sent home a patient with Aortic stenosis without bothering with all those low flow and high gradient conundrum. I was sure it was severe AS. The dense calcium and LVH were good enough to tell the complete story.

Finally, one of my senior colleagues, who lives half his awake time in cath lab, confessed to me. “Yes,Venkat, it’s all happening right in front of my eyes. Miracles based on absolute truths . I have since learnt the ultimate lesson in cardiology. How to treat, many of my CAD patients, without knowing coronary anatomy, that too without any major adversaries”

Postample

After listening to these sobering stories , I got into a mid-afternoon nap, where in, my good old professor came in my dream. He blessed me with his famous smile and hug for practicing and propagating clinical cardiology, as he taught to me.

But sir, I blinked, sorry sir, I don’t deserve your compliments. It is going to vanish with this dream.Its all about, terrible corona times, which has forced us to deliver this low-quality care based on the antique clinical methods

My mentor’s happiness was short lived, as he realised these guys will soon be consumed again, by the glamor machines that runs medical science.He left silently , still pleading us to try our best.

This post was originally written in 2013.

A middle-aged man with STEMI  came to our CCU.  It is just another case of STEMI and asked my fellow to lyse.

Anterior STEM ecg

But it was not the case . He, told me, Sir, the patient had a syncope following chest pain and he has injured his face and Jaw. He was actively bleeding. When I saw this face, it was indeed  frightening.Strptokinase induced bleeding

What shall we do ? When a patient  with STEMI presents with bleeding facial Injury

  1. Rush for Immediate PCI (Which was  of course not possible in our place as it happened out of office hours! )
  2. Take that ultimate risk and thrombolysis
  3. Give only heparin ( Many times it is as good as  lysis )

We took a (bold ? ) decision to thrombolyse with streptokinase.(After  a CT scan which ruled out any Intracranial bleed like hematoma etc) Clopidogrel was also given.

absolute contrindication for thrombolysis facial trauma

Patient continued to bleed in the initial 3 hours and was oozing in the next 12 hours. Blood transfusion was contemplated, but it was not required. Dental surgeon opinion was sought, his teeth were pulled and a compressive bandage was applied.It arrested the bleeding.The ECG settled down.LV function was almost normal with minimal wall motion defect. He is posted for a coronary angiogram later.

Final message

 There may not be anything called “Absolute contraindication” everything appears relative

I presented this in the weekly clinical meet,  with a tag line of  How to save a patient, apparently by violating a standard guideline. Not surprisingly, It evoked laughter amusement from learned physicians. I wasn’t. Guidelines are meant to guide us agreed.They can not command us. They are not legally binding documents as well! Many lives can be saved if only we have the courage to overrule when it’s required.

Afterthought

Had this patient has bled to death during lysis what would have happened to the treating doctor? (or )If the patient has died due to MI, because of deferred thrombolysis, what would be the line of argument?

2020 update.

This case scenario is a non-issue as of today. With so much experience, we straight away do PCI . Just manage the oral bleeding if any.

 

What is the incidence of Isolated systolic pulmonary arterial hypertension (ISPAH) and its Implication? We attempted to answer this question and found some interesting answers. It was published in the Indian heart journal  December 2007 Abstract issue. More than a decade gone. I think this issue is still largely misunderstood. Fellows may pursue this. One more parameter that can be explored is pulmonary artery pulse pressure and effect on progressive pulmonary vascular disease and PVR. Mean while  PAH definition and classification has changed many times, ISPAH definitely requires a place in the new scheme of things.

The abstract

ISOLATED SYSTOLIC PULMONARY ARTERIAL HYPERTENSION
S.Venkatesan ,G.Gnanavelu,V.Jaganathan , Madras Medical College. Chennai

Pulmonary circulation is a classical example of a low-pressure low impedance circulation. It is generally presumed high output states generally do not increase the systolic blood pressure in the pulmonary circulation. In systemic circulation, there can be divergence of systolic and diastolic blood pressure depending upon the cardiac output and peripheral vascular resistance. This has resulted in separate clinical entity -Isolated systolic hypertension.(ISH). It has been our observation many of the patients with PAH during echocardiographic and cath study were found to have an elevation of systolic pulmonary artery pressure(PAP) with normal diastolic PAP . In this context, this study was undertaken to specifically identify whether there is an entity of Isolated systolic PAH
( ISPAH ) and it’s the incidence in various clinical situations.
We analyzed the echocardiographic data of patients who were referred to our echo lab retrospectively. A total of 4000 echocardiograms over a period of 6 months were reviewed. Majority of these patients were referred for routine screening echo from our OPD. Data from patients who were assessed to have PAH were thoroughly scrutinised. They constituted shunt lesions, RHD,PPH, COPD, pregnancy, and patients with unexplained dyspnea for evaluation Those Patients who had both TR and PR jet were only considered for analysis .The Systolic PAP was estimated with TR jet and diastolic PAP with End diastolic PR Jet. ISPAH was diagnosed when the calculated systolic PAP was more than 30mmhg. And the diastolic PAP was less than 16mmhg  Antenatal women formed 2 % of the study population. A total 72 patients fulfilled the criteria of ISPAH Among the shunt lesions it was most common in large VSD( 4/10), followed by ASD(14/35) and PDA( 1/3) . In patients with RHD it was observed in 12%(15/110) , COPD 10%(15/150), in pregnancy and general population it was 5%(23/450). None of the patient with PPH had ISPAH.The mean Systolic PAP was 38mmhg(R 32- 74) The mean diastolic PAP was 14mmhg(R 8-15).The highest systolic PAP was 74mmhg recorded in patient with large VSD.
It is often presumed hyperkinetic states elevate systolic PAP and reactive elevates diastolic PAP .But it is clear from our study the rule is not that simple. Surprisingly many of the RHD patients had only the systolic PAP raised.It is important to recognize systolic PAP was very high in some of the shunt lesions. Taking this alone as an index of severe PAH is fraught with the risk of declining corrective surgeries in these patients.
Perhaps the most important observation from the study is the incidence of PAH in apparently healthy individuals, which is very significant as it could be the marker of continuously increasing chronic lung disorders due to the worsening environment of the 21st century.

 

A PowerPoint presentation of the paper is available with the author and may be requested.

Fortunately, indications for DC cardioversion in pregnancy is rare. A literature search suggests only about 50 cases are reported. I haven’t shocked electively in pregnancy but occasionally have come closer to it. In this current corona lockdown period, we had a call for a potential shock in pregnant mother with fast AF, which was again avoided by the optional  rate control measures.

Let us see, how often DC cardioversion might be necessary during pregnancy and few tips for its safety.

General principles

We know pregnancy can be pro arrhythmogenic. Most arrhythmias are non-sustained VPDs and APDs.They can be ignored if there is no structural heart disease, or at least postponed till delivery.

Drugs remain the mainstay.

The most common sustained arrhythmia in the young reproductive age group is SVT (AVNRT/AVRT) that can be managed with drugs like  Adenosine and beta-blockers. (Flecainide/Sotalol are found to be safe in pregnancy) . Though IV Verapamil is very effective, it has with some concern for fetus, so better avoided. Please, note many of the SVTs can be reverted with simple vagal maneuvres and oral beta-blocker /Verapamil. IV Digoxin has been widely used in RHD population for AF during pregnancy.

Mind you, even Injections Adenosine, Esmolol do have bradycardic potential and need to be given in monitored setting (No surprise, they are called medical cardioversion with the attendant risk) 

The universal antiarrhythmic drug Amiodarone still might come in handy in any refractory arrhythmia (Including AF) though it comes under the list of contraindication.(Safety of amiodarone in pregnancy) 

One important suggestion to make. Magnesium is a wonder antiarrhythmic drug, a membrane stabilizing agent through its indirect Ca + and K + blocking properties can be a powerful antiarrhythmic agent, especially in VT. This has a unique safety profile in pregnancy.We use it in eclampsia liberally  with the same action to suppress brain convulsions. (Cerebral tachycardia). Please consider IV magnesium  prior to considering  shock in VTs with dysfunctional ventricles as in peripartum cardiomyopathies et(Dose  to 2 g in 10mL of D5W over 1 to 2 minutes)

Consider DC shock only if there is hemodynamic instability.

Hemodynamic instability demands DC version. One practical issue is , what defines hemodynamic instability? In pregnancy, the systolic BP is already in lower normal due to systemic vasodilatory state. An HR>150 makes it further fall to around 90mmhg. This tempts us to label it as unstable. In this situation, we have to rely on patients’ symptoms to define hemodynamic instability. Never try to shock a comfortable pregnant women in whatever tachycardia she is in . (Including some VTs especially from outflow, fascicular, etc  ) Try to use drugs and get an expert opinion. to rule out subsets like cardiomyopathy, documented CAD, LV dysfunction.

When to shift to a cardiac facility?

This question crop up often. It is mainly logistic. May be in peripartum cardiomyopathy /Suspected ACS  with VT require special care.

 DC Shock checklist  & Precautions 

  • Biphasic shocks with energy levels 100 joules ( up to 200). Ideal to give single shock, ok to err on high energy  
  • Pads should be well away from the abdomen. 
  • Synchronized with QRS complex (Machine does this) 
  • In an unusual event of VF and cardiac arrest Defibrillation with 300/320 J (Here unsynchronised) 
  • Check the crash cart ready with essential drugs.
  • Keep cardiologist either on-call (Even a junior resident in labor room give immense confidence) 
  • Rule out  LV dysfunction or significant valve disease by echo (CAD can’t be ruled out though) If echo machine is not available ask the radiology or cardiology fellow to use the abdominal USG probe to document good LV contractility and gross EF% estimate.
  • If intramural thrombus is not convincingly excluded and there is AF and valvular heart disease, better to heparinse  and shock to avoid embolic events.
  • Temporary pacemaker support (Some of the cardioverters has transcutaneous pacing to tide over transient bradycardia that might occur post-shock) 
  • CPR readiness ( Extreme precaution !)
  • Fetal heart monitoring and Emergency cesarian readiness. 
  • Finally, most important consent with patient and family.

Is electrical Insulation of baby necessary or is it possible? 

 It’s not required. Fetus inherently tolerates stress better. Even if,  few joules reach the fetal heart inadvertently it may not mean much. What is, to be worried is maternal hypotension or bradycardia post-DC shock.

Impact on the fetus: Evidence?

The impact on fetal blood flow is not significant. This report from Taiwan  reassures there is no adverse effect by measuring umbilical artery flow (Yu-Chi Wang European Journal of Obstetrics & Gynecology and Reproductive Biology 126 (2006) 268–274)

While we consider DC shock during pregnancy is safe for the fetus, still, shock pads close to the abdomen, amniotic fluid being a good conductor of electricity at least one mother showed a sustained contraction of the uterus and fetal distress. This was possibly attributable to DC shock  Eleanor J. Barnes BJOG 2003 https://doi.org/10.1046/j.1471-0528.2002.02113.

Final message 

Most cardiac arrhythmias in pregnancy are carefully managed by non-electrical means. Of course, emergencies can’t afford to wait. Though two lives are at stake, it’s the mother’s heart that prevails over in drug selection and risk estimation. After all, it is her loving heart, that keeps the fetus alive.

I have seen Obstetrician anxiety (which spills over to attending cardiologist too!) can be extreme in such situations. I must admit, Obstetricians, are truly sincere warriors fighting at odd hours to protect the two delicate lives. After all, taking  responsibility brings the anxiety. Cardiologists must understand this and help them out in their difficult times.(without any super specialty ego !)

Reference

  1. Crijns HJ. Electrical cardioversion in healthy pregnant women: safe yes, but needed?. Neth Heart J. 2011;19(3):105‐106. doi:10.1007/s12471-011-0079-3

 

2.Finlay AY, Edmunds V. D.C. cardioversion in pregnancy. Br J Clin Pract. 1979;3:88–94

3.Oktay C, Kesapli M, Altekin E Wide-QRS complex tachycardia during pregnancy: treatment with cardioversion and review. Am J Emerg Med. 2002 Sep;20(5):492-3.

Which drugs are safe?

From BMJ 

Click to access pregnancy_heart_disease_v28_web.pdf

 

Further frontiers 

The DC shock from ICD experience

There have been a good number of women who got ICD for various indications (Commonly HOCM, long QT, ) who subsequently became pregnant, successfully managed during pregnancy.

(One rare study Andrea Natale et ll Circulation. 1997;96:2808–2812 documents at least 10 shock episodes documented in large series of 44 patients without any consequences)

 

 

 

A throbbing query …for so long

Got into this amazing lecture, that Infuses knowledge and wisdom about values in life, in just 14 minutes .Probably, It has more treaures than what we may get, in our entire life time as we search for truths.

I wonder, such thoughts can come only from God’s special messengers.Devdutt Pattanaik seems to be one. 

 

LA volume is one of the critical parameters that define (as well as determines the symptoms) both diastolic and systolic LV dysfunction.Still, we are tentative in the true estimates about the normal range of LA volume. (Upper limit 40ml/m²) .We are surprised to note, the difference between MRI derived and Echo measured LA volume showed a disturbing variation nearing 80 %.

How to measure  LA volume?

While the timing of LA volume measurement has not much controversy (end-systole), and the shape errors are largely eliminated by 3D echo, still why this variation?

It is a telltale error, of either including (or excluding ) the pulmonary vein ostium and complete blindness to LAA during LA border tracing. We know, LAA is physiologically, pathologically, and electrically is a critical accessory of LA. Still, we have so for excluded it from routine LA volume calculations. Is that a right-thinking in the overall evaluation of LA volume?

Normal LAA volume

Though the LAA volume is directly related to its size, shape much great confounder, since it precludes in arriving any mathematical calculation of volume from the area. Direct casts ofLAA and 3D echo to a certain extent will help measure LAA volume. MRI may also do the same.The normal LAA volume is calculated to be up to 20 ± 9 ml. Whatever be the  LAA  volume, one estimate suggests it will reach 25 % of total LA volume. This is very important to know. In fact, In significant LV dysfunction, LAA  is expected to stretch, efface, and dilate and contribute more to LA volume. Both static and dynamic LAA volume status also gives us an idea about potential thrombus formation risk.

(Ref : Measurement of Left Atrial Appendage Size by Transesophageal Echocardiography  Kazuko Yoshimoto et al. J Med Ultrason (2001). 2012 Jan.)

Are we justified to Ignore the LAA volume during routine LA function assesment ?

I don’t know. It may be wise to routinely add LAA volume to LA chamber volume to truly assess  1.Overall LA function, 2.Estimate the risk of thrombus formation and  3.Risk of developing AF. Meanwhile, its found LAA appendage volume might even approach that of  LA volume when it’s pathologically enlarged. (Left Atrial Appendage Volume as a New Predictor of Atrial Fibrillation Recurrence After Catheter AblationPedro Pinto Teixeira et al. J Interv Card Electrophysiol. 2017 August) 

LAA volume is Important for one more reason 

We are getting new data about dynamic LAA volume status during LAA closure.In fact , this particular study (JACC: Cardiovascular Interventions Volume 8, Issue 15, December 2015)  documented how LAA appendage balloons out during volume loading of LA.This study suggests we have to be careful about the hidden potential of LAA to expand and if ignored the device is likely to get dislodged with volume overloading. These observations make it clear we can’t isolate LAA volume when calculating LA volume. 

Final message

There is a strong case for measuring  LAA size & volume separately and preferably be added in the net LA volume Index. We can’t simply Ignore this vital and inherent part of LA , just because its called as an appendage. Of course, even a novice will rank LAA first,  as the pathological hot spot within the entire LA.

Reference

Everything about LAA

Giuseppe PattiVittorio PengoRossella Marcucci,The left atrial appendage: from embryology to prevention of thromboembolism  European Heart Journal, Volume 38, Issue 12, 21 March 2017, Pages 877–887, https://doi.org/10.1093/eurheartj/ehw159