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Archive for the ‘acute coroanry syndrome’ Category

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 % thromotic 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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