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Posts Tagged ‘acs’

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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T waves attract less  attention in STEMI ,except for the  fact   tall T waves  implies   hyper acute phase of  STEMI.

What is the duration of hyper acute phase ?

  1. Few seconds
  2. Few minutes
  3. An hour
  4. Few hours
  5. Any of the above

Answer

No one exactly knows  .It can  be highly variable .  So , 5  could be  the correct answer .  

 * Most importantly  hyper acute phase  need not occur in all patients with STEMI as suggested in experimental models.

Some  observations in T wave behavior in STEMI

Mechanism of hyper acute  T waves

It is the pottsium channel dynamics.Transient intracellular hyperkalemia  is thought to be responsible.

T wave as marker of  reperfusion

Inverted T wave in precordial leads are a good marker of IRA patency  especially in LAD

Slowly evolving STEMI

This is relatively  new concept . STEMI with a prolonged hyper acute phase  ,  ie ,  T waves ” dilly dallying”  for hours or even few days have been recognised. (This was  refered  to pre-infarction angina in the past )

This sort of T wave behavior makes it difficult to diagnose STEMI.Enzymes will help , still  thrombolytic guidelines  demand us to wait till ST elevation to occur. This is  unfortunate .But as physicians we are  justified to thrombolyse tall T waves with a clinical ACS .The other simple solution is to shift the patient to cath lab to find what exactly is happening in the LAD ! 

Now , what is new about  T waves in STEMI ?

It is  the localizing value  in LAD infarct

A tall persistent  hyper acute T wave  helps us to localise a LAD lesion .This paper from Netherlands ,  clearly  confirms this observation. The study was done from a primary PCI cohort,   a perfect setting to assess the  T wave behavior  in the early minutes /hours of  STEMI .

Other mysteries about T waves in STEMI

Does hyperacute T waves  occur in infero-posterior STEMI ?

I would believe it is very rare .Our CCU has not seen any tall T waves in inferior lead. Further analysis of the  data from the  above study could answer this question .

How often a  hyperacute T waves transform into NSTEMI ?

This again is not clear.Most of the hyper acute T will evolve as STEMI .But  , nothing prevents it to evolve as NSTEMI a well . After all , a hyper acute T   MI can  spontaneously lyse in a lucky few , ( Who has that critical  mass of natural  circulating TPA )  .If  these natural lytic forces are only partially successful , it may evolve into de nova NSTEMI.

Bi-phasic T waves in ACS.

A benign looking T waves with terminal negativity in precordial leads  can some times be a deadly marker of critical LAD disease.This has been notorious to cause deaths in young men which often correlates with the widow maker lesion in LAD.

What is a slowly evolving STEMI ?

Prolonged tall T wave phase  possibly   indicate , the myocardium is relatively resistant to hypoxic damage .

The most bizarre aspect in our understanding about ACS pathophysiology  is the concept of  time window , based on which , all our  ACS therapeutics revolve !

Does all myocardial   cells  have a same ischemic shelf  life ?  Can some patients  be  blessed with  resistant myocardial cells   when confronted with hypoxia or ischemia ?

                                 It is well-known  , in some hearts ,  the  muscles go for necrosis within  30 minutes of  ischemia,  while some hearts can not be infarcted even after 24 hours of occlusion .So , slowly evolving STEMI is a feature of  myocardial ischemic resistance .This is not  a new phenomenon as we have extensively studied about the concept   ischemic preconditioning .

We wonder there is something more to it . . .  the quantum of preconditioning  can be inherited .Further  , we are grossly ignorant about  the molecular secrets of  non ischemic metabolic  preconditioning  .

Final message

                         T waves attract less  attention in STEMI . Cardiologists are often tuned to look only the ST segment , after all ,  ACS  itself is classified based on  the behavior of this segment.(STEMI/NSTEMI) . We need to recognise ,there is a significant subset of ACS   affecting exclusively T waves.  Shall we call T elevation  MI ? ( TEMI )

Do not ignore T waves in STEMI. It has more hidden electrophysiological  treasures that  is waiting to be explored .

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Acute coronary syndrome  is primarily a disease of blood vessel , which perfuses  the heart.  It can even be a disorder of blood, often called vulnerable blood which predispose  for intra- coronary thrombus .

Mind you  , heart is an innocent bystander ! to the onslaught of  coronary atherosclerosis !

Hence , we  often use two terminologies .

CAD : Pure vascular (Coronary )  disease without  any structural and functional impairment of heart  ( No Angina, No myocardial damage ) Most of the asymptomatic plaques  , non flow limiting  lesions, incidentally detected by the modern coronary imaging gadgets  fall in this category.

When does  CAD becomes CAHD ?

CAHD : Coronary artery heart disease .Here not only the coronary artery is diseased , but it has it’s mission fulfilled   ie target organ either damaged structurally (STEMI, NSTEMI ) or functionally (EST positive , Chronic stable angina CSA )

Does the heart does any wrong to suffer from Acute coronary  syndrome  ?

No, it is simply not .The fault lies in one or more  of the following   .Generally at-least two these factors are enough to impede blood flow )  . They  combine to produce an ACS.

  • Blood defect
  • Vessel wall defect
  • Slowing of flow (Stasis)

This is called as Virchow’s triad   suggested over 100 years ago . Still valid in the era of per cutaneous  aortic valve implantation.

* The concept of de-linking  disorders of  coronary  vascular disease  from myocardial disease  is vital  in understanding the implications of current modalities of treatment. 

Even though we PCIs target the culprit ie blood vessel , it need to  realised , we  always fall short of real target . . .namely the heart . In coronary interventions  the catheters and wires roam around superficially over the heart  and they never even touch the heart .This is the reason PCIs are struggling to prove it’s  worthiness over medical therapy in many CAHD patients , which can reach deep  into the vessel, heart  and even every individual cells of heart.

Many (or . . . is it most ?)  Interventional  cardiologists have a bad  reputation for ” failing to look  look beyond the lesion” .  It is estimated  a vast  number  of cathlabs  and CABG theaters worldwide  are engaged in futile  attempt to restore coronary artery patency after a target organ damage is done .This is akin to building flyovers  to dead and closed highways .

Salvaging a coronary  artery and reliving a coronary obstruction is an entirely unrelated and futile  exercise to  a patient who has a problem  primarily in  musculature .

The much debated concept of  documenting  myocardial viability  , before revascularisation  died a premature death as the concept  by itself , was not viable commercially . (Viability studies   , tend to tie down the hands of device industry further , some  interventional   cardiologists began to see this concept  as an  interference to their freedom to adventure  )

Of-course , now  we have  other parameters  phenomenon  like  FFR estimation by Doppler , epicardial  -myocardial dissociation, slow  flow , no re-flow are  gaining importance.

Final message

ACS is primarily a disease of blood vessel but it’s impact is huge on heart. We need to look beyond the lesion .Restoring  a blood vessel  patency  to an ailing organ (Heart ) is not synonymous with total  cardiac intervention  and protection . There is lot more to cardiac physiology other than it’s blood flow. Heart muscle is a too complex organ to be controlled by few balloons and wires  which beat around the bush.

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Bio-chemical diagnosis of cardiac injury or infarction is  well  documented modality for many decades. Now , acute coronary  syndrome is diagnosed  by a battery of tests  that  detects the  proteins leaking from the  injured  myocardium.

Nephrologists have long been aiming for  such a  marker for ischemic  renal injury  (Not withstanding the fact , they are already blessed with two age-old molecules  creatinine and BUN !)

Neutrophil gelatinase associated Lipocalin (NGAL)

  • This is 25 Dalton molecule  richly secreted within renal  cortical cells in response to ischemic injury .
  • It is released without  modification in the  urine  .High urinary levels  of NGAL  reflect  acute renal  injury.
  • Early experience shows it  is a  promising  investigation and could  become a regular biochemical test in the near future.
  • Urine level of  NGAL >250 ng/ml , 2 hours   after cardiac surgery  predicts impending renal failure  in the next 24-48 hours .The advantage is , it NGAL raises well before serum creatinine.

NGAL After cardiac surgery

http://cjasn.asnjournals.org/cgi/content/full/3/3/665

Lipocalin following PCI

Bachorzewska-Gajewska H et al. Neutrophil-gelatinase-associated lipocalin and renal function after percutaneous coronary interventions. Am J Nephrol 2006; 26: 287-292.

www.ngal.com

References for  NGAL

http://www.ngal.com/literature/popular_reviews_of_the_nature_of_ngal_with_a_focus_on_acute_renal_injury

Final message

  • Cardiologists  and cardiac surgeons  have started  performing  complex    PCIs and  CABGs in  patients with   delicately  and precariously balanced renal function.
  • While ,  cardiologists   challenge  the kidneys with high  osmolar contrast agents ,  the surgeons stress it with extra corporeal circulation.  Many of these patients also  have co- morbid conditions .
  • Often , the cardiac outcome is directly linked to pre /post procedural  renal function .Nephrologists usually  arrive  late  into the filed (Creatinine SOS calls !).By this time the full-blown ATN sets in many.

Now , we have a tool to identify impending ARF , it gives us  little more time and  flexibility in managing the issue .

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This article is in response to the prevalent belief  about  primary PCI for STEMI   endorsed by world cardiology forums. (Caution: A highly personalized version)

Time window in STEMI

  • Is the window half-opened  or half closed ?
  • Is it open at all ?
  • Or ,does it open only for primary PCI  ,and tend to close down  bluntly for thrombolysis

Modern medicine   grew faster than our thoughts .We have witnessed the audacity of advising  arm-chair treatment  for MI  till later half of   last century . Now we are talking about  air dropping of patients   over the  cath lab  roofs  for primary PCI.

Still ,we have not conquered the STEMI. While ,  we have learnt to “defy  deathin many patients  with cardiogenic shock , we continue to lose patients(“Invite death “)  in  some innocuous forms  of ACS due to procedural  complications  and inappropriate ( rather ignorant !) case selection.

Note : The ignorance  is not in   individual physician mind ,   it is prevalent in the whole cardiology knowledge pool.

The  crux of the issue for modern medicine is ,  how to reduce risk  in patients who are at  high risk and how not to convert a low risk patient into a high risk patient by the frightening medical gadgets.

In other  words ,  arm chair treatment for STEMI was  not (Still it is not !) a dustbin management . It has a potential to save  70 lives  out of 100. What many would  consider it as  ,  nothing but  the natural history of MI .

Medical management of STEMI is ridiculous !

That’s what a section of  cardiologists try to project by distorting the already flawed evidence base in cardiology. Some think it is equal  to no treatment. Here we fail to realise, even doing none has potential to save 70 lifes out of 100 in STEMI who reach the hospital.

Out of the  remaining , 10 lives   are saved by aspirin heparin (ISIS 2) and the concept of coronary  care . Another  7  lives are saved by thrombolysis (GUSTO,GISSI) . PCI  is shown to save saves one more life (PAMI).The remaining 6-7 % will die in CCU  irrespective of what we do .

Of course , now medical management has vastly improved since those days  .  A  thrombolysed ,  heparinsed ,  aspirinised ,  stanised  with adequately antagonized   adrenergic ,  angiotensin system   and   a proper coronary care ( That takes care electrical  short-circuiting  of heart)   will score  over interventional approach in vast majority of STEMI patients.

Now comes the real challenge . . .

When those 70 patients who are likely to survive  , “even a arm-chair treatment“, and the 20 other patients  who will  do a wonderful recovery with CCU care ,  enter  the cath lab  some times in wee hours of morning  . . .what happens  ?

What are the chances  of   a patient  who would otherwise be saved by an arm-chair treatment be  killed by vagaries of  cath lab  violence  ?(With due apologies ,statistics reveal  for every competent cath-lab   there are at least  10  incompetent  ones  world over !)

In the parlance of criminology , a hard core criminal may escape from  legal or illegal shoot out  but an innocent should  not die in cross fire , similarly ,  a cardiogenic shock patient with recurrent  VF  is  afford to lose his  life , but it is  a major medical crime to  lose a simple branch vessel  STEMI (PDA,OM,RCA )  to die in the cath lab,  whom in all probability  would have survived  the arm chair treatment.

Why this pessimistic view against primary PCI  ?

Yes, because  it  has potential to save  many lives  !

Time and again ,  we have  witnessed  lose of   many lifes  in many  popular hospitals in  India ,  where a   low risk MI  was  immediately  converted  to a high risk MI  after an primary  PCI with number of complications .

I strongly believe I have saved 100s of patients  with  low risk MIs by not  doing  for primary  PCI in the last  two decades.

*The argument that PCI confers better LV function and longterm  beneficial effect is also not very convincing for low risk MIs .This will be addressed separately

The demise of comparative efficacy research.

Primary PCI is superior to thrombolysis  : It is agreed , it may be  fact in academic sense .

Experience has taught us , academics rarely succeeds in the bed side.

“superiority studies can never be equated  with comparable efficacy”

Only the  questions remain . . .

  • Where  is comparative efficacy  studies in STEMI ?(Read NEJM article )
  • Why we have not developed a risk based model  when formulating guidelines for   primary PCI ?
  • Is primary PCI for a PDA /D1/OM infarct worth same as PCI for left main ?
  • Is high volume center guarantee  best outcomes ?

Who is preventing comparative efficacy studies ?

Primary PCI : Still  struggling !

This study from the archives  of internal medicine tells   us , we are still scratching  the tips  of  iceberg (Iceberg  ? or Is it something else ?)  of  primary  PCI

Even a  pessimistic approach can be  more scientific  than a optimistic  !

When WHO can be influenzed and make a pseudo emergency pandemic  and pharma companies  make a quick 10 billion bucks  ,  Realise how easy  it is  for the   smaller ,  mainstream cardiology literature  to be  hijacked and contaminated .

Final message

Why we reverently follow the time window for thrombolysis,  while  we rarely apply it for PCI ?   This is  triumph of glamor over truth . The open artery hypothesis remains   in a  hypothetical state with no solid proof  for over 2o years since it was proposed.

Apply your mind in every  patient , do a conscious decision  to either thrombolyse  ,  PCI or none . All the three are  equally powerful approaches in tackling a STEMI , depending upon the time they present .Remember , the third modality of therapy comes free of cost !

Never think ,   just because  some one  has  an access to a sophisticated cath lab 24/7   , has a iberty to overlook the  concept of time window  !

Remember  you can’t  resuscitate   dead myocytes , however advanced your enthusiasm and   interventions are !

Realise , common sense is the most uncommon sense in this hyped up human infested planet.

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Once in a while the ACC/AHA comes with knock out articles. Here is a  must read  topic for every cardiologist.

How to diagnose MI in ECG ? Sounds , insulting ?

After reading this you should change the way 12 lead  ECG is looked at . . .

Experts from the article

  • How to make the best of lead AVR  ?  Just invert it and you get a + 30 degree lead which  was hither  to unavailable .A new window of opportunity to diagnose   antero lateral MI .
  • Shuffling  the 12 leads to a have an anatomically contiguous  ECG
  • Know , how to label STEMI  with a  .5mm ST elevation  (Minimal STEMI ?)

And lot more exciting  tips  !

If you  think ,  all these are new stuff in cardiology you are grossly mistaken .These concepts are more than 10 years old (In Sweden it is 25 years old ! )

When  European heart journal published  the article   “Myocardial Infarction redefined ”  in year 2000 many missed out the importance . For those who missed it (just  10 short  years have gone by )    ,  Let us update ourself  at least  in 2010 !

Thanks to ACC and JACC.

Click on the link

For PDF article click on the Image

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Human body is  now  approached by many of the physicians as  collection of  multiple  organs . This is  the price we pay for modernity in medical science. The era  of great physicians  in general medicine has gone . Now, a  super specialist  of one organ  is  rarely concerned about what is happening to the patient’s  other organ ,  it is  considered    foreign to him  ! While ,  this is the dominant thinking pattern of   modern-day specialist

Let us  travel intime  and  go to the year 1954 . . .

Three  physicians from Michigan ,USA  published  one of greatest observation in clinical sciences , namely the ECG changes in various forms of stroke .

Now , a shrewd physician  , will  suspect a subarachnoid hemorrhage (SAH) by looking at the ECG when the clinical situation demands . But , what we need is every one should develop that skill . We have seen errors happening  even in big institutions (or is it because it is big ?)  when  an elderly person comes with deep T  inversions with or without  altered sensorium being rushed into  CCUs  & cath labs instead of  neurology units.

We  need to teach  our junior  colleagues  . . .  That ,  ECGs of patients with  acute neurological syndromes  (ANS)  can mimic as acute coronary syndromes (ACS) ( especially in elderly ) .

The following ECG changes * are observed during stroke

  • Deep  T wave inversion –   Sub arachnoid hemorrhage
  • Cerebral thrombosis   –      Prolonged QT interval, U WAVES
  • Cerebral hemorrhage –      ST segment  shifts /T inversion

 

The ECG changes tend to occur very early after CNS injury.May last up to 1 week. They are not useful to identify the type of stroke. But , deep T wave inversions strongly suggest SAH rather than ICH or thrombotic stroke.

What is the mechanism of these ECG changes ? 

It is a clear proof that heart and brain are interconnected by neural network. All the noted changes occur during myocardial repolarisation . (ie ST segment )  The current thinking is  (Ofcourse , it is same as our thinking  in 1950s !)  it is mediated by adreneergic surge  initiated by CNS insult  transmitted to  myocardium by the sympathetic system.

Why should SAH produce more  ECG changes than others ?

It is possible the net adrenegic drive from the brainstem and spinal cord will be greater in SAH as it  spreads the entire CNS  through the cerbro spinal fluid. While localised ICH and infarct is  likely to generate less adrenergic impulse. 

Reference

Read the link to circulation 1964 .With courtesey to circualtionaha.com

http://circ.ahajournals.org/cgi/reprint/9/5/719.pdf

This came 50  years  ago , we still quote their work and no one has improved their work . 

Final message

If  only  we make the  clinical bed side teaching as a  regualr habit ,  we  do  justice to   our  great  physicians of the past ,   who enriched  our  life  with their  clinical  skills  and  passion for knowledge  sharing .

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