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Archive for the ‘Cardiology -unresolved questions’ Category

Is Aspirin’s role become reduntant once the patient is started on oral anticoagulants or Heparin ?

Posted in cardiac drugs, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , on March 13, 2011| Leave a Comment »

Anticoagulants are different from  antiplatelet agents. One acts on coagulation cascade  , while  the other acts on platelet aggregation. That’s what ,we have  been taught  for over a century.The reality is , there is a huge functional  overlap between these two .

Some of the questions   which struggle to get  a clear answer  ( Atleast for me !) 

 What will be the bleeding time in patients  who are on  oral anticoagulants ?

Ans :  Since it  affects only clotting mechanism bleeding time will be normal or near normal .(Is this reasoning correct ?)   But ,we clearly know , Warfarin  increases systemic bleeding risk : Does this risk occur without affecting the  platelet  function ?

If bleeing and clotting are two different phenomenon how warfarin increases bleeding risk ?  If warfarin alone increases bleeding risk  heavily   why  Warfarin – Aspirin  combination  is used  in many  patients with prosthetic valve  ?

In a patient who is  receiving full intensity heparin( say in Acute coronary syndrome )  can we afford to withhold aspirin or clopidogrel ?

Heparin is given  for preventing recurrent  STEMI and antiplatelets are given  for preventing recurrent  NSTEMI !  Is that the answer  ?  How solid is the concept of white clots in  Unstable angina and red clots in STEMI ?  Can a  blood  really clot without help from platelets ?  Can a person really bleed with intact platelet function ?

Final message

We are  far . . . far away  from fully understanding   science of   human  coagulation and bleeding   ! Meanwhile it is a common sight  to prescribe  all in one cocktail  (A LMW Heparin* , an aspirin,  clopidogrel    ) to most of our ACS patients believing   at least one of them will take care !

* Remember the original caution message when LMWH was introduced said ,   LMWH   should not be used along with Aspirin !

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For Primary PCI to be most effective . . . Do it before the Troponin appear in blood !

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , on March 9, 2011| Leave a Comment »

Is there a bio chemical way to measure time window in STEMI ?


It seems so. In this era of hyperacute PCIs  , we are supposed to diagnose STEMI very early .If you wait for troponin  to assit you in diagnosis it  implies  one has missed the golden hour already (At least Three  golden hours to be precise !)

Cardiac enzymes have a unique value in timing a STEMI as  time of   onset of  chest pain is   unrealiable

as the patient (Even the physician !)  may not be able to differentiate pre infarction angina from infarct pain.

In these situation cardiac enzymes provide us a clue.

The time of realse of these molecules are fairly predictable.

  • Myoglobin -2 -3hours
  • Troponin elvation -3 -6 hours
  • CPK –  8 -12hours

Remember  ECG  rarely show a  time lag   in diagnosing STEMI  !

Message

For  maximum benefit . . . try to perform the  primary PCI before the troponin  appear in blood .

Does this  sound a crazy   tip ? What to do . . . truths are very often crazy .

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Is plain balloon angiopasty(POBA) a dead concept ? If so who killed it ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , on March 8, 2011| Leave a Comment »

When  PTCA was introduced  by Gruntzig  in 1977 the whole world was awestruck. All he did was . . . to dilate a coronary stenosis with a balloon. No scaffolding  was ever thought off at that time.  It was a huge achievement .   PCI version 1 was  performed for over  20  years in nearly a million  patients   . Till his death stenting  was  an unknown concept.

When the stents first came in,  it was first used with extreme caution .  From the days of  bail out stenting, it  has evolved  into provisional  stenting, elective stenting ,and  now  what is called  “mandatory stenting”

When  Greuentzig was able to  perfuse the obstructed coronary arteries  successfully  in thousands  of patients  in the 1980s,    with a simple balloon

. . . what is the difficulty for us  to replicate it  in 2011 ?

Unfortunately  advocates of POBA (Plain old balloon angioplasty) are considered  to be  un-scientiifc cardiologists or even carry a risk of labeled as quacks.

But please remember . . . POBA   is alive and doing well  too ,  in spite of the serious threat  it faces from the current generation interventionists  . It  will continue to have an  important role in  many  situations.

1.In patients with multivessel  disease while the  proximal lesion  deserve a stent  , POBA is preferred in distal lesions  to reduce the overall metal load .

2.POBA has a major role to play in Primary PCI .We need to realise  dying myocardium does not demand  for stents. It simply requires  quick and prompt restoration of  blood flow. POBA can achieve this with flying colors in most situations.

3. Further , stenting  may be  difficult in complex lesions   during primary PCI .Experience tells us , it  is  dangerous to prolong the primary PCI  procedure time. Here POBA is the only choice ,  may be assisted by thrombus aspiration. Stenting may be delayed or even avoided in many STEMI patients. . We know there is huge STEMI population with  pure thrombus with no atherosclerosis.

4.Patients  with  co morbid conditions , who are  likely to have a non cardiac surgery in the near future  and those who  can not take antiplatelet  drugs  POBA will score over BMS/DES.

5.Finally a POBA costs nothing . .All it requires is a stiff  balloon . In this recession prone world  and ever increasing incidence of  CAD  , POBA  could be the  answer.

6. Acute recoil in POBA (Sudden deaths in POBA is  a rare event !) are more of a perceived fear rather than a reality. It can be argued stents  are  primarily used  to make  cardiologists job easy and  comfortable.

7.Cost effectiveness of plain balloon verses stenting was never  properly tested .

Final message

When sudden deaths  due to subacute   thrombois in DES population   is accepted with all those attendant  pride . . . why not we accept a risk of  less sinister event  namely the  late onset restenosis with POBA.

This is a funny world . The DES fiasco is driving us towards stent less world and a bio degradable stent is already being projected as new savior.

Meanwhile no  one can kill POBA thats for sure !  It  will  ultimately   be reinvented  with another exotic study  soon !

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Glagovian Phenomenon : Why it is one of the vital concepts in cardiology ?

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Coronary artery disese, tagged , , , , , , , , , on March 6, 2011| Leave a Comment »

Atherosclerosis  probably ranks first among all  human diseases that cause maximum suffering  to  mankind.Since it is a disorder of blood vessel  it has an easy  access to every  vital organ  in our body to inflict the damages . Histo pathologically , atherosclerosis is an all in one disorder where inflammatory , degenerative and lipid injury  collectively  contribute to the disease progression. Diabetes and hypertension play a vital amplification role.

Atherosclerosis begins very early in life as fatty streaks in every individual and takes different avatars ( or remain indolent)   depending upon the risk factors and life style.

How to estimate plaque burden ?

It has  always been a difficult task to estimate the  atherosclerotic  plaque burden inside the  coronary  arteries.The fundamental flaw for many years is ,  we always thought  if there is a plaque it must  encroach  into the lumen.

Coronary angiogram  , has become the  default investigation  in clinical cardiology . Since it   can  visualize  only the coronary lumen ,  this  flaw  got further  curious  with skewed  interpretation as well.

When things were as it is . . .  Glagov suggested , what  could  possibly be   the  most important  concept in the interpretation of coronary  angiogram .

The concept  suggested  the  atherosclerotic  process  could  actually spread  within the  vessel wall  in a predictable manner .

What determines a plaque to either grow into the lumen or grow away from the lumen?

If we could decode the mechanism of direction of plaque growth we will probably conquer the atherosclerosis  at least by mechanical means . The implications are too many.

A stented coronary artery may be re-engineered to grow the atherosclerosis  towards  the adventia .This could grossly reduce  the incidence of restenosis.

Further , in post Glagov days we realised  mechanical factors like plaque stiffness, eccentricity , plaque mass effect, drifting , lipid core density, medial lysis , elasticity of elastic lamina all could determine the   plaque  movement.

Why compensatory lumen enlargement does not occur in some lesions ?

We do not know the exact reasons . We may call it a fate . . . shall we ?

Curious blessing  : Atherosclerosis  for  some unknown  reason  blesses a  few with coronary artery  dilatation rather than narrowing .

This is called coronary  ectasia . Medial necrosis , weakness of internal elastic lamina or  destruction paves way for plaque shift towards the adventia . It is estimated , if the medial necrosis occurs in at least  50 %  of  circumference of vessel wall   it will  result in ectasia .And  paradoxically if  the media  shows resistance   the plaque grows into the vessel wall.

Endoleak  and Glagovian phenomenon.

Endo leak is the Achilles heel of   endovascular intervention . In fact , many would  consider  it as  a dignified terminology  for graft failure . Endo Leak   occurs when  the artery outgrows the stent  graft and bllood starts  collecting  in the graft vessel -wall interface . When the  scaffold is  placed  within the lumen ,  one may wonder how it is going to prevent  the  artery  dilatation . (Which is basic defect in any aneurysm}In fact , the aneurysm does continue to grow  along with   centrifugal  atherosclerotic  forces ,  possibly by  Glagovian phenomenon .

This makes it obvious  endo- leak is a distinct threat in every vascular  intervention.


Final  message

Most cardiologists  think their ultimate  job  in this world is to  deploy  a stent deep inside a LAD  or RCA.  While a few others indulge in more exotic  adventure of  crushing a plaque ,  trap the debris and  catch it with a  with  a basket .

There  are bigger and bigger   blind areas  in the vessel wall ,  infiltrated with  deadly atherosclerosis which is conveniently ignored  .If only we realize   this fact  , we  can move forward in our war against coronary atherosclerosis.

Of course the good old   medical  interventions  . . .  exactly try  to address  these issues . Let us  think  straight , and  not succumb to glamor  in cardiology !

http://heart.bmj.com/content/84/5/461.extract

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One more cause for dynamic LVOT obstruction : Abnormal Aortic angle ?

Posted in Cardiology -unresolved questions, tagged , , on February 23, 2011| Leave a Comment »

Inter-ventricular septum is generally in parallel alignment with Anterior aspect of root of aorta.

Have a look at this echo form a 65year old man

Note the classical bend of basal IVS encroaching the LVOT. Aortic valve opens normally.

 

The basal septum Projecting into LVOT

Pseudo LVOT gradient. It was about 25mmhg which is not significant.

 

 

  • Sigmoid shaped IVS can  cause a unique  LVOT  profile .
  • Present in elderly . The exact mechanism and  mechanical and hemodynamic   implications are not known .
  • It can rarely cause  dynamic LVOT obstruction.
  • When these patients develop Infero posterior MI there could be further collapse of IVS into LVOT .

Relationship between Aortic angle , Hypertension, HCM

Many of the HCM patients may show similar features .When ASH is confined only to basal IVS. HCM should not be diagnosed instead it is  often a defect of aorta /IVS alignment .

Abnormal  aortic angle  with that of IVS  may  make the IVS appear sigmoid.

If  patients  with abnormally angled aorta develop hypertension ASH and sigmoid septum is  more pronounced .

IVS dragging by mass effect  on aortic root is possible and Aortic regurgitation may ensue

Reference

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Why doing a coronary angiogram is much easier than interpreting it !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged , , , , , , , , , on February 6, 2011| Leave a Comment »

Coronary angiogram is probably the commonest invasive cardiac investigation done  world wide. It should run into millions every year. The procedure once thought dangerous  is now performed in few minutes in day care centers . While doing a  coronary angiogram  has become a minuscule task to most cardiologists, interpreting  it correctly remains a huge task !

Many  of the young cardiologists  get fascinated in   doing a coronary  angiogram and hardly spend enough time and mind in interpreting it.

Most of  us  succumb to the popular occulo  coronary reflex and describe a coronary  artery  lesions as though it is a  number game . It is very rarely we use the quantitative angiography tools available  in the machine. We need to meticulously  analyse   the length , morphology , distal flow, thrombus  , collaterals  etc . (FFR a new avatar tries to do some justice )

Calling   atherosclerois   by numbers alone,   such as  50 %  LAD  and 70 %  diagonal    20 % left main  is a huge  insult    to the deadly  & diffuse  disease process of atherosclerosis .We are paying the penalty for it .This is  the fundamental  flaw in our  reporting , that  makes every coronary intervention redundant.We must first  remember  we are looking at the lumen not the wall of coronary  artery.

Coronary  interventions is not about removing obstructions but  regression of  atherosclerosis  load within the coronary artery , prevent progression of it and ultimately reduced cardiac events and improve  survival. It  is obvious, it can not be achieved by wires and catheters alone . At best they can be adjuncts.One can  easily understand  why medical therapy  scores over wires  as it can take care of the overall disease process.

But still  ,  most* of  the  learned cardiology community  considers medical therapy   to be an adjunct to coronary intervention  , which  is  a  gross ignorance at it’s best !

* This is my perception. If  I am proven wrong ,  I am happy our patients  will be benefited !


Final message

Do not reduce  the importance of coronary angiogram   to a  farce  number game !

Do not get excited  by visualizing your patient’s  coronary artery. It may make you richer by few thousands. Realise , what you are seeing in a CAG is a fraction of coronary  circulation.

It is estimated coronary  circulation we visualize  daily in cath lab as epicardial coronary arteries  is less than  2  % of entire cross section of coronary  circulation.

This means we are 98 % blind ! ( or  2 % wise  !) .Spend  adequate  time and  mind to interpret it correctly  , so that logical and useful  ( non ) interventions can  be done .This only can make you a  true cardiac professional and your patients will respect you.


//

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What is “Partially successful” or “Partially failed” thrombolysis ?

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology-ethics, tagged , on January 26, 2011| 1 Comment »

Nothing in this world is black and white. In fact,  most events are in between . The irony is , our brain  always wants to view  things in two distinct entities !

  • Success or failure
  • Beautiful or ugly
  • Good or bad
  • Win or lose,
  • Rich and poor etc . . . etc

So it is no  surprise !  cardiologists  also travel in the same boat !

They classified  the events after thrombolysis   into two dogmatic categories . Successful  thrombolysis or failed thrombolysis   . . .  as if no other event  can occur in between .

Traditionally 50% regression of ST segment is called successful .   What  about 30%  and 40 % ST regression ?

Further , there is an important caveat  in the timing,  as we  traditionally assess ,  90 minutes of thrombolysis .

Consider the following  situation  :

  1. Thrombolysis  is failed at 90 minutes, but  succeeds  at 120/180  minutes ?
  2. Is 50 % ST regression at 180 minutes is as bad  or as good as 25 % regression at 90 minutes ?
  3. How to label a patient who  is extremely comfortable in spite of ECG criteria of failed thrombolysis ?(Surprisingly this situation is fairly common !)

So, without finding answers to some critical questions , we have defined the success  of thrombolysis with  half baked data .

This is exactly , is the reason we  are unable to do a  valid  study on failed thrombolysis, rescue PCI etc .  We know the results of rescue PCI  ,  always  been  contradictory to the general logic !

It is estimated a substantial number of  STEMI patients following   thrombolysis   fall into a category of partially successful thrombolysis implying partial restoration of blood flow and salvage. The correct definition for  successful thrombolysis and reperfusion should be at the myocardial mass level , and  not at the level of coronary artery.The ECG  is the best available indicator.

Implication for having a  poor definition  of  failed thrombolysis

It is not a rare sight to wheel  in , a patient to a cath lab  with label of failed thrombolysis dangling in his neck  who is clinically  stable  (Has a less than required 50%  ST regression , but a definite, favorable trend with a 30 % ST regression  at 90 minutes  )

How many cardiologists will be willing to abort a CAG/PCI  , as a repeat ECG just  before puncturing  in the  cath lab reveals    successful  thrombolysis ? (little  delayed though !)

If only we have better methods to risk stratify patients following thrombolysis , we can avoid

  • Huge costs incurred
  • Expected and unexpected hazards of doing an emergency  intervention in an adequately salvaged STEMI
  • Hundreds of cardiology man hours can be saved  for better purposes .

Final message

Classifying thrombolyis into  success  or  failure  is a  skewed  way of looking  at this important  issue .

It is an irony ,  cardiologists often  triage LV dysfunction , valve disease , cardiac failure  etc  into 4  grades (  minimal  , mild , moderate or severe  ) . It is  still a mystery ,  why thrombolysis  is never graded  like that ,  and it is always considered as  all or none phenomenon !

There is a substantial number of patients  with partially successful ( or shall we call partially failed !) thrombolyis  .This group must be given adequate attention or inattention  . There  is a urgent need for a through review of how we look at  the post thrombolysis status  . It is better to use the newer imaging modalities like PET/MRI more  liberally to identify  exact sub group  of failed thrombolysis who will benefit form revascularisation .

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5 minutes crash course on Ventricular septal rupture !

Posted in cardiac surgery, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Echo library and gallery, echocardiography, myocardial disease, tagged , , , , , , , , , , , , , , , , , , on January 14, 2011| 2 Comments »

We know,  electrical deaths constitute the bulk of sudden cardiac deaths in MI.  Mechanical deaths due to pump failure, muscle rupture , valve leak , also cause significant deaths   .(Surprisingly many of the mechanical deaths   may also   fulfill  the sudden death criteria !)

Free wall rupture is  invariably a fatal event. Papillary  muscle trunk  rupture  leads to severe LVF and unless intervened sure to result in fatality.

The ones who tear their interventricular septum  are some what blessed ! Here ,  the rupture does not result in instant death as there is  no loss of blood ,   instead , there is an  volume over load of right ventricle  followed by the  left ventricle  after a  few beats. Hypotension is the  rule. Even though this is a major complication there is something about  VSR which makes it unique.

Sudden giving way of IVS has  a decompressing effect on the ailing left ventricle.This many times  bring a  temporary relief to LV and if the patient survives the first few hour he is likely to stabilise  further . In fact , sudden deaths within 24hours after the onset of VSR is an exception.This defect always gives the cardiologists and surgeon some time to plan the management. We need to use this time judiciously.

The natural history is delicate . Five themes are possible

  1. Very unstable – Instant death( Fortunately a  rare theme )
  2. Unstable – Deteriorating further
  3. Unstable to Stable * fit for discharge even without surgery
  4. Stable from the onset and  continue to be stable* .
  5. Stable to Unstable (Probably the most common theme )

* Pleasant themes occasionally witnessed !)

Here is 55 year old women came with extensive anterior MI with lower septal rupture.(She belonged to type 3 of the above scheme)

)

Note the septal rupture is visible even in 2D Echo

 

Color flow showing significant shunting from LV to RV.This shunt depends upon the LV contractile function, LVEDP and ofcourse the RV pressure

 

If there is severe RV dysfunction or bi ventricular dysfunction flow across the defect is inconspicuous.Brisk left to right shunting may be an indirect marker for good LV systolic function and absence of significant pulmonary hypertension.Both imply a better outcome.

The main determinant  of survival is the  underlying LV dysfunction and associated co morbidity(Renal function ) and complications .

Infero -posterior ruptures tend to be complex and  may have multiple irregular tracks  that makes it difficult to repair.

Investigations

Echo cardiogram is the mainstay .Serial echos should be done to assess the mechanical function and the progress of VSR.Hemodynamic monitoring may be done without injuring the patient .

Medical management

  • Often supportive , but  effective . Dobutamine infusion can maintain a life for few days.
  • Paradoxically , LV dysfunction and elevated LVEDP restricts volume overloading of VSD.
  • Associated MR, Arrhythmias  need to be taken care of .

Surgeons role

  • Very Vital.
  • Experience counts.(Individual as well as  Institutional )

Timing of surgery

Continues to be a controversy . Surgeons love to operate in a stable patient. But they need to realise , surgery is often needed to stabilise  many  patients. . The issue of tissue friability  is blown out of proportion in the literature .When a  life is  is at danger we can not worry about  friable tissues !

The rule of thumb could be

  • Operate as early as possible in unstable patient.
  • Post pone surgery in stable patient as late as possible ( Late here means . . .elective non emergent surgery )

Surgical options

  • Simple VSR closure without  knowing coronary anatomy
  • Simple VSR closure after knowing coronary anatomy
  • VSR closure with CABG ( total revascularization)
  • VSR closure with partial revascularization

In our experience  each of the above , has a role in a given patient depending upon the logistic , financial , social and even  the available expertise. (A good surgeon in bad Institution !)

Is coronary angiogram mandatory  before attempting to close VSR ?

Logically yes. If it is not available  just do not bother .  But, many times , when issue is saving lives , we can not afford to be too scientific , many lives have been saved by not following  such strict  protocols .A simple emergency  thoracotomy and closure of rupture site (Without even touching the LAD ) can be a distinct  and viable option in  a selected few .

Role of cardiologists

Contrary to the popular belief the role of cardiologists is minimal , except  to prepare  the patient and hand over to the surgeon.

Interventional approach to close  a VSR  is currently  be termed as an  adventurous option ! The VSRs  can assume unpredictable shapes  and the  tears can be multiple  in  different planes. The devices , catheters and  other hard ware are not specifically made to tackle these  issues  .An acquired VSR  should never be compared with congenital VSD.

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TRANSFER-AMI study : Transfer with caution . . . bumpy roads ahead !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology journal club, cardiology journals, Uncategorized, tagged , , , , , , , , , , , , on January 14, 2011| Leave a Comment »

Preamble

The much published TRANSFER -AMI study  has few important queries to ponder about.It was supposed to test the role of routine PCI following  thrombolysis. In other words it compared  rescue only strategy with routine strategy.The caveat is , even among  failed thrombolysis, the   rescue strategy has not convincingly proven superior to medical management  (if the time is lapsed ) as much of the damage is done .

In essence , Acute MI is  more about time management than drug or cath lab management

  1. Why the 67 % of  standard therapy cohort underwent PCI. Technically , you are supposed to transfer for rescue only if there is a  failed thrombolysis ?That is the standard approach , if  most of the cases are any way land up in cath lab , then you are trying to compare two similar groups .
  2. Why the rate of   failed thrombolyis with TNK-TPA in both arms not disclosed ?
  3. How can a 92% of study population be in class 1 Killip still considered to be high risk group ?
  4. Why the recurrent ischemia  was very vaguely  defined and still included and clubbed with primary end point along with deaths. If only recurrent ischemia was removed from primary end point . . .this study will straight away land in a regret bin.
  5. Why there were 6 additional deaths at 30 days  in routine early  PCI group ,  What was he cause of death ? Mind you these deaths have happened in a 92 %  Killip class  one cohort . Is it  not important ? The trend looks vitally   significant .We can not afford take refuge under a false  statistical roof .
  6. How many patients died or  developed MI  because of the early PCI in-spite of having  successful thrombolysis.This again could be vital . Complications during intervention  for a failed thrombolysis may be acceptable. While ,complications , when we try to  improve upon the already  successful thrombolysis is simply not acceptable .

Will the investigators share their experience ?

Finally

Why the title of the paper says it is about “Routine angioplasty” and  the conclusion emphasizes  it is indeed   “high risk subsets ofangioplasty” (While the study itself involves a 92 %  least risk Killip class 1 ) .  Why this double dose of confusion ?  (Is it deliberate  ! Which i think is unlikely )

NEJM please take note of this  . . .

All that glitters  are  not natural glitter . . .some are made to glitter !

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Newer observations about tall T waves in STEMI

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , , , , , , , , , on January 9, 2011| Leave a Comment »

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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