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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.

One of my well-educated patients asked me, how ready is our state health services. How many ventilators do we have, he asked? I told him, we have enough but short of it only technically. I had great difficulty in explaining to him that ventilators are not the antidote for coronavirus.

I continued, even if we have an unlimited number of ventilator and other gadgets, the major determinant of the outcome is going to be the overall viral load, severity of lung Injury and other system involvement. Finally, it is the patient’s ultimate fighting power along with the forbidden word in medicine, ie fate.

However, judiously timed, non invasive assisted breathing (CPAP etc) might have a major role , since it could avoid pushing mild cases in to ventilators.

This pyramid tries to explain there are many other ways, by which, we can successfully tackle this pandemic other than critical care.

Corona management strategies prevention

(Please, take it in a proper perspective. It is not intended to undermine the importance of critical care.)

Emerging trend In India

Things look positive .The virulence of covid here seems to be less pronounced.(1000 cases with 25 deaths). As of now , it appears, the take off slope from phase 2 to 3 struggles to sustain.It could still be an assumption, but would love to see it as a fact.

Indian Government is on the right tract and we should all be glad about the steps taken, inspite of the collateral social suffering of the lock down.

Looking forward to celebrate the summer folks !

Even in the best of non-Corona times 90 -95% of STEMI population in our country (the rich and famous included) are discriminated by denying life-saving primary PCI. Instead, they are subjected to an inferior and near-forbidden therapeutic modality called coronary thrombolysis or its slightly less inferior cousin pharmaco-invasive strategy. Now, thanks to corona, for some time it’s going to be near 100% discrimination. 

Fortunately, “Corona” or “No -Corona” this discrimination has never harmed in true sense in the real world.

 My feeling is, there is going to be little overall impact on ACS /CCS  outcomes with current “Acute cath lab distancing” protocols. If at all,  it might accrue some invisible benefits. Of course, few random lives could be saved in heroic cath lab maneuver in complex STEMI and NSTEMIs (which are not possible due to prevailing situations)

Final message 

Things will settle down. Cardiologists need to introspect with the large pool of outcome data,  emanating from the underused cath labs. It is a natural cross control study available free of cost and effort.

I wish, I can say loudly, many of the IRAs and the myocardium in distress will definitely welcome this sudden turn of events. Let us continue to keep a watch on our ‘distance with the cath lab’ even after Corona settles down.  

Presentation

A 38-year-old women,with  episodic chest discomfort, mild dyspnea, and occasional non-productive cough. She was investigated in a non-emergent fashion.  After an abnormal X-ray chest, A CT scan was requested.  (*X-ray chest is Intentionally not posted here to add some curiosity factor)

This is probably one of the most curious Images in cardiology I have stumbled upon. At the first look, it seemed a baseball has replaced a heart. Is it not?

Most curious Image in cardiology

Posted with Creative Commons Attribution License CC-BY 3.0. Afzal et al. Dept of Internal Medicine, Florida Hospital, Orlando, USA.Cureus 10(11): e3566.

When you see such a large round shadow occupying an area exclusive meant for the heart what will you think? The following thoughts came in.

  • A Hydatid cyst of heart ?
  • An Aneurysm from a chamber of the heart?
  • Pericardial mass
  • A granulomatous cardiac mass
  • Aortic aneurysm?
  • A mediastinal mass (Teratoma, Lymphoma)
  • A foreign body?

Answer: It turned out to be none of the above. The best part is this woman was diagnosed, undergone surgery and cured of the condition.

Find out from the link and read yourself about this curious case report from  online journal Cureus, . Hats off to this journal, doing a great job of dissemination of knowledge without much restriction as other peer-reviewed ones do.

 

Acknowledgment 

Original source of Image  : Afzal A, Mobin S, Sharbatji M, et al. (November 09, 2018) Rare Case of Giant Asymptomatic Left Coronary Artery Aneurysm of 10 cm Associated with Coronary Cameral Fistula. Cureus 10(11): e3566.

Reference

A review of giant coronary artery aneurysm

1.Crawley PD, Mahlow WJ, Huntsinger DR, Afiniwala S, Wortham DC: Giant coronary artery aneurysms: review and update. Tex Heart Inst J. 2014, 41:603-608. 10.14503/THIJ-13-3896

As human life enters an extraordinary new phase ,”Digital distancing” is also critical for Corona(fear)control.Let us make all mobiles into “non-smart mode” for the next 30 days at least . Use TV time judiciously. Just listen to radio for official Govt.Communication.No panic buying. Help the needy. Let the economy shrink considerably and get rid of all the wasted expenditure.

Meanwhile, let us use this lockdown period to find a  “fresh purpose” for a meaningful life. “God will definitely bless us”

The anger of Corona is sure to settle down very soon and will start living with us in complete harmony, like billions of other organisms do.

How far we are from a vaccine? 

It is estimated it may take at least a year. Might happen earlier too. There are at least 12 companies working on creating a vaccine. Let us hope breakthrough happens at the earliest 

vaccine tracker

 

Viruses are essentially lifeless molecules (A nucleic acid RNA/DNA) .In the case of CoRoNA, it is the inbuilt RNA that acts as a commander in mischief. Ironically, it gets to life only when it attaches to the host cell. How a small bit of nucleic acid with a lipid cap infects a cell and becomes a deadly factory of new viruses and spread through the body remains a deep biological mystery.

Someone asked me , “Can we kill the Corona en masse”? The answer is frighteningly simple, we can’t kill them really, because they don’t have life in the first place. At best, we can deactivate or make it dormant and reduce its spread.

I just got contaminated with coronavirus . . .Is it a death sentence?

Even if you forcibly feed COvid 19 at random to 100 persons 80 % will be near normal or with a mild respiratory infection. You may wonder how can so many people are positive for Covid 19, and comfortable. We are still far away from understanding the complexity of how this virus will behave in a given human body.

This is because we are not clear what is the exact port of entry and how the first cell reacts to it.The way the body deals with it is entirely different if it attacks the respiratory tract through aerosol or it enters gastric tract (Imminent death with acidic PH ? we don’t know )

The mysterious interaction of genetic susceptibility, response to initial entry, epigenetic memory and subsequent immunological activation, will determine whether one is going to get simply infected and completely decimated.

Healthy humans enriched with good protein diet are expected to have good immunity. However, it can never be foolproof. It is obvious, there is something more than a host stress response readiness.(The fighting power and the fitness of your Immune cells T,B ,K,NK cells, infinite number of Interstitial scavenger cells and molecules)

When you are stressed the Immune system is activated or deactivated?

As expected the answer can be both. Then, how does the body will fight it over? Cells start synthesizing defense molecules. Unfortunately and paradoxically, cortisol is a major hormone released at times of emotional stress, that can severely compromise the immunity. Steroids are firefighters but cause collateral damage.

So its easy to conclude, positive emotions have positive immunity and negative emotions like fear, anger, distress can pull our immunity down.

Fear is a thought virus

Technically and biochemically, every human thought is a neurotransmitter. A neurotransmitter is nothing but a chain of amino acids synthesized in response to DNA/RNA codecs. So, straight away there is an obvious link between thoughts we harbor and the fighting power of the body. Why depression and anxiety affect the infection rate ?
The effect of various emotions on the Immune system is a big emerging topic. Fear-mongering about Corona and the manic digital dissemination of the virus of fear could turn out to be a great Immune system dampener.

One of my wonderfully healthy friends wanted to estimate the fighting power of his body’s immune system in case he is affected by Corona. He asked, whether his blood can be mapped and give a reassuring report?

I said no, it is not possible. Just take all the precautions. Reassure yourself that you have all the Immunity to fight. That’s it.

This following article elegantly explores the link between emotions and Immune response.

Final message

Can viruses befriend “fear” that reduces host Immunity and help self propagate? No one can be sure. But, I wish “unrestricted courage” acts as a vaccine to Corona, which can ooze from the brain free of cost.

Postample: What will happen to this pandemic?

It will (and should) settle down taking its toll. Preventive measures are gratifying. We need to learn from China, how they blunted the steep ascending curve of propagation.(Of course it started from there)

Who is responsible for such global pandemics?

I am sure, this is the toughest question, probably with no answer. Is it man-made or God made ? If you strongly believe, God will never punish human beings without a reason, then the answer is simple. Now, the world is under freeze. Its one way of arresting the mad growth of artificial,materialistic, biased economy. Corona could be a whipping force on mankind and let us use it to heal and unite fellow human beings.

Now, some positive news from CoVid 19 positive population

The false positive results are too high with currently done active screening tests.

This study from China says positive predictive value of a positive test is just 19% .It would mean 80% error rate. So, don’t really get unnerved with a positive test.

https://www.ncbi.nlm.nih.gov/m/pubmed/32133832/

Aortic dissection is a unique cardiac emergency that tests our collective understanding of vascular anatomy and pathology .It poses the ultimate challenge to the expertise and wisdom of both cardiologists, and surgeons.

It’s all about freezing the Time 

The philosophy of management swings between near-total Inaction* in some (As in most Type B & few Type A as well ) to “No holds barred” approach in others. (In most Type A and few Type B).

*Read it (also) as medical management that includes powerful Aortic pulse attenuation therapy with beta-blockers ( Unfortunately medical management is considered as Inaction by many current generation cardiologists)

Advanced Aortic Imaging is the key

A rapidly focussed TTE usually confirms the diagnosis.TEE might be used but carries a small risk of directly aggravating dissection when performed in an unstable patient. Conventional CT provides good (but limited) information, spiral MDCT delineates the vascular anatomy in a more clear way. MRI probably scores over and adds flow dynamics.

(4D Phase-contrast MRI showing slow helical flow in the false lumen and high-velocity flow in the true lumen. Computational flow dynamics will help assess entry point, plane of dissection, calculate false lumen Index, pressure and wall stress in true lumen and Aortic branch compromise etc . Image courtesy. The Lancet Volume 385, Issue 9970, 28 February–6 March 2015, Pages 800-811)

What is Non-A Non-B dissection?

This is a newly recognized subgroup. It’s not a surprise as the imaging modality improved we found the existence of this subset. In Non-A -Non-B Dissection initial tear involves the Arch and threaten to go retrograde A or antegrade B. We also realized there could be an apparently illogical transformation of type B becoming Type A, later on, due to late retrograde dissection.

The incidence of Non A , Non B dissection is about 10% (Ref 1). Here the outcome between surgery and medical is confusingly sitting at equipoise.

The traditional Debaky and Stanford classification didn’t address this subset.Though some other classification Like (DISSECT (Ref 2) /PENN (Ref 3) tried to clarify .

A new classification based on Type ,entry and malperfusion appear perfect.

TEM classification of Aortic dissection

This is a practical classification that uses Stanford as a base model but adds entry point and branch vessel compromise. This is analogous to TNM classification of tumours.(Hans Hinrich Sievers et al)

Where does EVAR stand ?

The management strategy of dissection of Aorta got an important makeover in the last decade (for good mostly ) as interventional cardiologists and radiologists landed in the hitherto to surgical domain with endovascular reconstruction (EVAR) .It is handy mainly in the complicated type B and complicated Non A and Non B . One more viable possibility is the hybrid approach of combining EVAR and surgery in delayed presentation of Type-A.

Single point Principle in Aortic dissection management

Rapid sealing of the entry point and arresting the false lumen progression wherever it is and by whatever means (especially in Type A dissection ) reduces mortality significantly.

Though exit points are important for comprehensive management, one need not waste time to locate and search for exit points. In a specific group of patients, it may not be visible or even absent altogether.

Another critical determinant

Detection and tackling the retrograde dissection and involvement of coronary ostium distortion and damage to Aortic valve , and pericardial invasion is the key to reducing early mortality in Type A dissection

The final outcome in God’s domain

The IRAD and other global registries in Aortic dissection has taught us important lessons. We are continuously learning and the patient outcome is improving.

Still, one unresolved statistical ( metaphysical ) mystery is how to identify? that small subset of patients who are lost because of inappropriately early aggressive Intervention who would have otherwise been pushed into natural survivors of Inaction or less action.

Reference

1.Sievers H-H, Rylski B, Czerny M, Baier ALM, Kreibich M, Siepe M et al. Aortic dissection reconsidered: type, entry site, malperfusion classification adding clarity and enabling outcome prediction. Interact CardioVasc Thorac Surg 2020;30:451–7.

2.Dake MD, Thompson M, van Sambeek M, Vermassen F, Morales JP;DEFINE Investigators. DISSECT: a new mnemonic-based approach to the
categorization of aortic dissection. Eur J Vasc Endovasc Surg 2013;46:175–90

3.Augoustides JG, Szeto WY, Desai ND, Pochettino A, Cheung AT, Savino JS et al. Classification of acute type A dissection: focus on clinical presentation and extent. Eur J Cardiothorac Surg 2011;39:519–22

Metanalysisfor Non A Non B dissection

Professional medical practice demands to put always the patient’s interest first. Unfortunately, current practicing methods threaten doctors to yield to patient’s whims & wishes which are influenced by significant non-academic forces. The principle of Informed consent is gradually losing its true meaning. Who is informing what ? and to whom?  is becoming a hazy conundrum in complex two-way confabulation based on severely battered evidence-based medicine.

pateint empowerment

Some of the conversations not heard in silent corridors of big hospitals

Why did you stent his LAD ? , He had triple vessel disease Is’int CABG Ideal?

“Yes , I agree. What  can I do , the patient  chose to get stented”

Why did you replace his keen joint, it was not that bad isn’t ?

“Yes, I agree but the patient chose it.”

Why did you do the cesarian madam? the pelvis was fine, she was contracting well  Isn’t?

“Yes, I agree, what to do. The patient decided it”

Why did you do the endoscopy, you are sure it was simple dyspepsia right? 

“I agree. What to do? The patient wanted it”

Final message 

We all agree patient empowerment is a critical component of health care delivery and management. I am afraid it can very easily go wrong and take a bizarre direction. Many times I felt it has seriously Interfered with professional decision making.

Still, I am not able to come to terms with this awkward situation. “How can  patients  (or their health care provider) enforce me to do a procedure on them , which I feel is Inappropriate or Injurious to them !

Missing you Dr.Hippocrates