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Archive for the ‘acute coroanry syndrome’ Category

*ISCHEMIA trial breaks not in NEJM or Lancet but in Washington Post and Wall street Journal

After three decades into cardiology profession, one thing is very clear. We work so hard to create pseudo-knowledge and struggle with it for so long and feel awkward and guilty to come out of the mess. But we have to  . . .  in the overall interest of mankind, isn’t?

We aptly call the whole process as continuing medical education, but in the melee, often we ditch some of the precious gems as obsolete. (This tempts me to suggest discontinuing false education is also an option for medical knowledge seekers !)

Confucius has something to say about this issue , which appears more relevant to the medical profession in current times.

Postamble 

We don’t know what’s in store for 2020

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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.

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Evening cardiac clinic is generally a relaxing place until an occasional patient  with vague chest discomfort present with this sort of an ECG .

He was a 68 y old hypertensive and was on Tablet Amlodipine .After a cursory look at his ECG , eyes wandered to look for some specifics. Suddenly ,my  ECG reading skill was stretched . Is it really LVH ? or Ischemia ? I asked for any old ECG which he couldn’t provide. I had to blink  more than a moment , before asking him to describe his chest pain in detail one more time . I got almost convinced it was not ACS  since he was having only localized pain over left side of chest. Still , I didn’t have the courage to send him home. An Echo was done.

Curious to know what the Echo showed ?

 

Yes , you also probably guessed right . It is LVH and there is no wall motion defect either.

How to differentiate between Ischemia and LVH ?

This is a common question asked in the board exams.There are number of ECG clues to differentiate the two .Mostly it will help  fellows  to pass exams. Academics rarely comes to your rescue when patients land with  chest pain  especially at odd hours.

Find the answer in this link

https://drsvenkatesan.com/2009/12/12/how-to-differentiate-lv-strain-pattern-from-primary-lv-ischemia/

 

Now comes the real twister , Does presence of LVH  exclude Ischemia in any way ?

Why can’t be ACS in a patient with LVH ?

When I posed these questions , some one suggested global longitudinal strain  with speckle  tracking to rule out ischemic wall motion defect, my resident suggested  high sensitivity Troponin and Ischemia modified albumin.

Whatever is the technological assistance , one thing  is certain,  we need to finally fall back  on patient’s symptoms . Unstable angina is neither an ECG diagnosis nor biochemical  or Echo diagnosis . (Its all about patient description about his angina , that clinches the  diagnosis !)

It remains a fact normal spot Troponin can never rule out  ACS on time ,( Even patients with unstable angina who  harbor  tight  LAD lesion can be both ECG /Enzyme negative )

When we are not sure ,the traditional coronary care dictum  shall operate .It demands admit, observe, with serial ECGs and enzymes. This protocol cant’t be followed strictly for a variety of reasons . We may have to rely entirely on our clinical Intuition accrued over the years.

A modern-day cardiologist might have a different dictum .The simplest solution in such situations is a diagnostic radial snap shot coronary angiogram .It is an easy way out  . . . , and avoids the trouble of spending wasteful minutes of personal conversation with the patient .The ethics of outsourcing history taking , patient record review or even clinical examination has pushed the definition of professional competence in coronary care into murky grey zone.

One more reason we should hesitate to rush these patient to cath lab is the detection of  incidental insignificant CAD (Which will loom larger than life when they are wheeled in from  ER)  that will  lead on to  further inappropriate chain of events.

How relevant is clinical acumen in modern era ?

Clinical acumen in medicine can never be taught in class rooms or read in text books. It is the innate ability to  combine  knowledge, experience ,skill  and  lastly (and most importantly) courage to ignore conflicting and pervasive data from new generation Investigations. Instead of helping us ,they often directly affect our increasingly vulnerable native medical cognition.

Even if some one is blessed with a good clinical acumen it seems to have little value many times as power of Investigations and fear of missing a event will prevail over it ! I have been victim of this phenomenon many times and not able to follow what my mind preach me !

What happened to this patient ?

I had to admit him against my  wish (Of course I was safe!)  He too got admitted reluctantly and was observed till morning , spent Rs 5000 for pack of investigations and stay , was discharged without any issues with a diagnosis of simple Hypertension and LVH.

The non academic bug  didn’t stop there  . . . again  contrary to my conscience  I had to suggest  optional coronary angiogram to rule out true CAD as a precautionary statutory advisory !

 

Counterpoint 

How do you know this is really not CAD  ? I won’t believe unless and until I see the CAG and its normal.

Ok, Let me post his angiogram if he decides to  undergo it.

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

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

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

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

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hemodynamics of ffr lad valsalva 2

 

 

 

 

 

 

 

 

 

 

 

 

 

Other modes of sudden toilet deaths

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

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

How to anticipate and prevent these  deaths ?

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

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

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

Final message 

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

Postample 

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

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

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

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

Reference

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

Further reading

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

 

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Now , some one wanted to know,  Can we diagnose unstable angina without Chest pain ?

Crazy question isn’t , Angina by definition  should have chest pain .There is nothing called silent angina , only silent Ischemia  .

  • We know Ischemia can occur silently .
  • We also know STEMI can occur silently (About 10 % of MI do occur without any symptoms )
  • If STEMI occurs  silently  why not UA/ NSTEMI combo ? (Collectively called as  NSTE-ACS)

The debate goes like this .If stable angina can present with equivalents ? what prevents  “Unstable angina”  to present with  Anginal  equivalents without chest pain ?

If  a diabetic patient who had a silent MI in the past  . . .  subsequently  experience  severe episodes of resting ischemia  , will he feel the pain , that is supposed to occur  with his  “unstable angina”  or not ?

Hmm , difficult to guess right,   So it seems highly plausible  UA/NSTEMI  do  occur silently ! Literature hasn’t looked into this specifically. Chest pain is built integral  into definition of UA , infact it is a symptom  complex rather than an disease entity by itself, while NSTEMI is ECG and enzyme combo ! Making the term  NSTE-ACS  look  perfect.

Any other technical explanation ?

The concept of Ischemic cascade says angina occurs last, well after biochemistry , wall motion defect and ECG , hence its distinctly possible for UA/NSTEMI present to be painless !

Final message

Anginal pain perception is related to intactness of neurogenic circuits and also probably the severity of Ischemia.If full thickness myocardial necrosis can be painless in few, nothing prevents from an episode of UA/NSTEMI  be truely painless .

Clinical implication of this conundrum

Can we admit a patient as UA/NSTEMI with out chest pain ?

Yes, it would seem so .

No, we can’t .

Indeed we can , if ECG changes are there .

No, we can admit even with normal ECG if its real unstable angina.

This is the crux of the problem in ERs all over the globe. Our knowledge base is simply not good enough. Every one of us has seen Troponin positive silent NSTEMIs ! but . . . to me still something is missing in the link .

Modern day approach 

Pain or no pain,any  fresh ECG changes ( Both T and ST shifts*) should be rushed to cath lab.Whenever you are not sure .Always better to err on the side of over investigation.That’s the mantra ! So ,you do an Angiogram , find an Incidental intermediatroy lesion which may not be responsible for the ECG changes but you are compelled to go after it FFR//iFR , OCT, IVUS and so on !

*There is huge list of non Ischemic ST/T shifts in ECG that can be read elsewhere .

Counterpoint

Can’t agree with this article. Foolish to diagnose UA without chest pain. Never  treat ECG  in isolation unless its a convincing  ST elevation or depression with clinical input and thorough scrutiny of  past record . Realise , how important is  the basics principles of medicine taught  by Oslers and Cushings a  century ago.

 

 

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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.

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Hot debate in STEMI

Acute total obstruction (ATO) of coronary artery is an emergency .Opening it  by pharmacological or catheter is the  standard ( logical ) protocol.However, time plays a crucial role in this coronary re-perfusion game.It can either be a sure shot of success or end up in total spoilsport. One more issue as important as time is from the overflowing scientific data  fired  by different regulators  in conflicting directions  (Also called knowledge) .

What to do with STEMI coming late ?

  • ATO with cardiogenic shock is an  absolute emergency at any time.
  • Symptomatic ATO  other than CS beyond 24 hrs still  considered  emergency for most.(Symptom should be true angina )
  • Hemodynamic instability is misunderstood term . Stabilizing it medically is not forbidden.

Asymptomatic stable ATO  beyond  24-72 hours can be  semi emergency, true emergency or as cool  as a cucumber depending upon the cardiologist’s wisdom , experience or inexperience  and the  Institutional Integrity !

*Please be reminded ,LV dysfunction is not an absolute indication for urgent intervention unless it is due to ischemic dysfunction attributable  to a critical non IRA lesion

When does a ATO become safe CTO ?

1 month , 3 months, 6 months ?

Why we are  not defining a sub-acute ATO ? or CTO in transition   ?

Is living peacefully with sub acute ATO or CTO a coronary crime ?

We don’t require a debate , whether these  questions are worth answering  or not !

Final message

Though cardiac professional  are committed  to open up occluded arteries to save  lives , reality is repeatedly teaching different stories ! The greatest danger of keeping an artery open( In disputed indications ) is the newly conferred risk of sudden closure and the attendant  unpredictable aftermath !

Or should we conclude : Living with CTO is ok , but don’t intentionally create one by denying PCI in late  post STEMI ATOs

Anti-thought

Arguing closed artery is better than an open artery is straw man argument and inability to interpret positive things in science.  However it may still be right  when science suffers  from hostile incursions from non academic forces.

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