Posts Tagged ‘nstemi’

This question always creeps in any coronary care unit.

Often times , there is a significant  histo-pathological overlap between severe degrees of  Ischemia* and  myocyte necrosis . (What is called micro infarcts, lacunar infarcts,  make us over diagnose MI). It is not yet clear , whether leaky myocyte cell membrane can release free cytoplasmic enzymes without actual cell necrosis.
Clinical Implication
Fortunately , there is not much .These bio markers are primarily used as prognostication tools .Many of these patients  need to  undergo early revascularisation. However , It is unwise ,to get alarmed by  just  Troponin positivity  in an other wise comfortable ACS patient.
* Some call severe degrees of Ischemia as Injury ! It is an old thought based entirely on ECG  .There is no specific cellular equivalent of electrical injury current !

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This is a true story  . . . happened  many years  ago under my direct  vision.

A  48 year old women came with significant breathlessness and catchy  sub -sternal chest pain .

“I  was exerting too much in recent days  doctor” , she said .

Her ECG  showed  a tachycardia and dramatic ST depression in most leads .

The ER in charge promptly texted the cardiologist .

The moment he saw the ECG ,he  had no hesitation , to order for an emergency angioplasty  (  How can he plan a angioplasty  , without even  knowing the coroanry anatomy . some one murmured  . May be   . . what he probably  meant was emergency angiogram   the other explained )    Further , he was telling his    fellows  . . . that  this is going top be  tough case and a possible  left main PCI .

An emergency  angiogram was done .  On table  it was a huge  surprise for every one ,  it was a  a classical  text book   look alike normal coronary arteries !

The moment normal CAG was  visualized  the consultant  concealed his momentary  surprise    and went on to say  it is classical case of syndrome  X   with severe micro- vascular disease causing ECG changes !

As  the patient did not give any opportunity to poke her coronaries   she was wheeled out of  wheeled out of cath lab.

Meanwhile ,  first year  fellow came rushing with the blood reports and biochemistry .

Is everything  alright ?   Yeh sir ,  except her Hb %  . . .  it is  5.6  Grams !

The bewildered  consultant *  realized   the  high  coronary drama , that is  been enacted  over the  past 2 hours !  and  learnt  (and taught) a most important  lesson to their fellows !

Hi guys , this is neither  a NSTEMI nor  a microvascular syndrome X  . . . this is simply anemia related  extreme  ECG changes !  We have erred in our reasoning and  our pre cath clinical scrutiny has  gone awry ! 

He went on to say  ,  don’t worry  many times medicine is learnt in  hard ways  . After all nothing adverse has  happened here .

The women was subsequently investigated and handed over to  gynecologist for a probable hysterectomy .

Final message

Please be reminded  , anemia  can produce  variety  of  ECG changes.  In extreme anemia  global ST depression is  common especially if  tachycardia is associated .

The lesson here  is ,  whenever  gross  ST depression is witnessed  with vague chest pain  check the hemoglobin first . This is an unusual story of a women  ,  with simple  anemia  (due to   chronic mennorhagia )   landed in cath table in an acute fashion .  Luckily  she  did not have any  incidental coronary  lesions  that prevented her becoming a  greater cath lab  victim !

* The bewildered consultant is none other than the author  of this blog.

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This  is the ECG  of  a  45 year old man with  H/O hypertension  and  chest pain .The general practitioner who first saw him alerted this  patient about a possible  heart  attack  asked to meet a cardiologist immediately. The cardiologist who  saw  this ECG   tended to confirm  the diagnosis  and advised admission in  a coronary  care unit .

The patient   defied  both  and  somehow landed in my echo lab  .  Looking at the ECG   I also  expected  it to be a  STEMI  evolving into a  Non Q  MI .

I was surprised  to find  only LVH with absolutely no wall motion defect  . There was no evidence of ASH,  HOCM or apical cardiomyoapthy as one of my fellows initially  suspected . His  EF was 70 %.   Cardiac enzymes were sent by then. When  I spent few minutes  with him ,  listening the history , it was very clear  what  he had was  non cardiac pain . In the anxiety ,  no one  got it right  about the character of pain ,which  was localised , lasted  for few seconds and  least suggesed angina.

The moral of the story is   listen to the patient  however dramatic the ECG may look !

What is special in this ECG ?

It is common for LVH with ST depression to be  mistaken for  ACS/NSTEMI

Here , there were  other  observations that  added  more  complexity .

  • Presence  of  ST/T changes in inferior leads(ST elevation in lead 3)
  • Bi-phasic  T wave in v1 to v3
  • ST elevation  in precardial leads

In LVH  it is usual  to note  ST depresion , how do you explain ST elevation in LVH ?

ST elevation in LVH   may occur in  leads  v1 to v3   . It is very rare  for LVH to inscribe  ST  elevation in   v4 v5 v6  .   Why certain  leads elevate the ST segment while others depress  in LVH  is not clear. It may represent  incomplete LBBB pattern where the ST segment deviates opposite to the  dominant QRS  complex. Septal  hypertrophy often elevate  while free  wall  hypertrophy depress the ST segment . Since V5,V6 leads are free wall oriented , these leads  record  classical  ST depression .

Importance of Bi-Phasic T waves

Please remember  Bi phasic T waves are notorious for it’s  unpredictability. An  innocuous looking bi-phasic T waves  (especially  with dynamic behavior )   is a  harbinger of proximal  LAD or even left main disease.

Finally , what will be ECG  changes if a patient with classical  LVH  who  develops a  real  STEMI ?

  • LV strain  pattern normalises ?
  • Further ST depression  occurs ?
  • No great changes . ECG  Looks near normal ?

Answer : ?

What is the significance  of   Bi-phasic T  waves : A  link to  a related post

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Acute STEMI is the numero uno of  all medical emergencies. Hundreds of life are lost every few hours in our planet.Significant  chunk of them  do not   even reach the hospital alive  . While the emergency crew has many vital responsibilities , the cardiologist job starts only after the patient reaches the hospital .  Hence  the ambulance  crew  need to act much more sharper. Please remember even the  skills   of the driver  will have a direct impact on the myocyte survival.

The symptom to first  medical ( or second  hospital ) contact could be as vital  as a primary PCI procedure itself . A 3 minute traffic jam can kill 3 thousand myocytes ! One could imagine the importance of  decision making process here.

Distance from  the point of contact to PCI lab , the anticipated delay ,   intensity of traffic  matters .

Is it not funny ,  to realise  when   we  have  a reperfusing agent on hand , within the ambulance and the vehicle stuck in  the traffic jam  waiting to reach a  reperfusion  room situated  50  km down the high way !

( One may wonder why can’t we thrombolyse every one  routinely  in the ambulance  and do  the PCI later in  . . . But surprisingly  this    concept  simply does  not work  !)

When we realise , even in  a well developed country like Netherlands ,  time to shift  to cath lab is a big issue (Read the following article )  we will never ever know , how much of myocardium  is consumed  by traffic jams  in  a  country like India  , where   the traffic   scenarios   can be  more chaotic  than a  VF  !

Events  that unfold following a STEMI  are crucial

It begins with chest pain recognition.

Call for first help Spouse/Family doctor /Neighbor

Call for 911/108 . Ambulance arrival time and boarding

Administration of  Aspirin + clopidogrel*

Meanwhile spontaneous thrombolysis will begin in most of them !

A promptly administered Aspirin and clopidogrel   a shot of heparin and a lytic agent within 30 minutes is distinctly possible and may be more  effective  at a fraction of cost.

Highway thrombolysis

Even though current studies still  . . .do not  favor primary PCI over thrombolyiss in the first hour ,  most of the cardiologist  do show some  favoritism  towards pPCI for some unknown reasons.

So by default ,  many of the   ill fated  STEMI patients    enter  an  unrealistic  hemodynamic   race  in the deadly highways and urban lanes our country !

For every minute  that goes by ,  the patient  not only loses  his  muscle but also the  golden opportunity to get salvaged by the thrombolytic agents .

Since ,  a delay  beyond  one hour eliminates the indication of thrombolysis  (if a cath lab is available in the vicinity  ) many times   traffic delays  convert a potential   hyperacute  thrombolysis  into a say . . .    3-6 hour old  PCI .(Should we feel happy about it ?)

Here , we need to know TIMI 2 flow achieved easily by thrombolytic  agents is  quiet effective in preventing myocyte death.

Fast  track   shift to PCI

Helicopter drop over cath lab -( Distant dream ?  or better to be in dreams )  It has been noticed even a helicopter was squarely beaten by the  thrombolysis  in terms of  early  and  timely  reperfusion.

Fast -Slow track PCI ?  (Like fast slow AVNRT !)

Unexpected delays on  road  , in  many countries  financial issues  /Insurance sanction etc  contribute to the time delay significantly . What starts as a fast track  protocol  peters out  into  slow race (Late primary PCI ) and may even  end  in a grinding halt.(No primary PCI )

Worse still  . . . some of these patients  are made   unsuitable  for  thrombolysis  as well !

Final message

Management of STEMI  is gradually becoming a team effort.  The emergency crew , the command , the destination hospital all need to be  alert  and proactive. When the  initial  anticipated delay  is getting prolonged , get the ground staff  in  cath lab  ready for  an  emergency landing .

A word of  advice  for  the ambulance crew .Involve them  more   in the decision making  as  they   are in a better position to calculate the  possible delay.  If delays  are anticipated  propose a thrombolytic order and get clearance from the command and administer the lytic agent as early as possible.

It is highly likely , restoration of   TIMI   2  flow  right in the middle of   national highways  is much  . . .   better than a   TIMI 3 flow  that  is going to come  later   . . .in  a distant  cath lab .

Finally use the common sense  liberally  before you  act   . . . unfortunately it has become  the most elusive  sense for man kind  !

References :

Here is a study that gives a fresh insight into this  enigmatic issue of pre-hospital thrombolysis vs primary PCI


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NSTEMI is a  common clinical problems in CCU.

When we say  NSTEMI it can mean any of the following

  • NSTEMI with ST depression
  • NSTEMI with T  wave Inversion
  • NSTEMI with Biphasic T wave
  • NSTEMI with normal ECG
  • The irony   called STEMI evolving as  NSTEMI**

By default most of  us think ,  if it is NSTEMI  . . . there  must be ST depression. This thinking is  not logical but traditional. Still,   ST depression may be the  common presentation. NSTEMI with ST depression  has much worse outcome than other forms.

The following ECG is from a 45 year old man with a vague mid sternal  chest pain for 48 hours.

The unusual type of NSTEMI with Bi-phasic T waves

His echo showed wall motion defect in LCX territory .A diagnosis of NSTEMI was made.The predominant finding was biphasic T waves .

**One may wonder  why can’t we call this ECG as a  Classical STEMI ?

There is a 2mm  ST elevation ,  with a infarct as well  ? But , the point  here  is there is no business for T waves to get bi-phasic or inverted in the early hours  of  a  classical STEMI .

This  exactly has happened here. Hence we can not call  the above event as  STEMI . Instead it  is ,  STEMI   evolving into NSTEMI . So  a combination of  features of STEMI/NSTEMI occur together. The best description for above  entity is  STEMI in transition to Non Q MI

Read the related article in my site  Is the terminology of Non Q MI still relevant or obsolete ?

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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


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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Cleveland clinic is a leading centre for cardiac care .Major technological breakthrough occurs from this institute than any other place. Thousands of articles come out every year. Some articles , get global attention and make  a huge impact. These are usually related to a new hi- tech modality like CRT devices or percutaneous aortic valve deployment etc ,etc.

                                                Some articles , which are very important  may not get the due  attention . Journal editorial boards often  have a scorecard called impact factor .That is ,   how  a  journal  is  impacting the practice habits of  medical professionals . Ideally we need to have to grade individual   articles with impact factor .Many articles may not have any significant  impact  however good the impact factor of the journal.

Here is an article,  which excellently depicts the principles of management of ACS.  It was published in 2003 JACC,  by Steven Nissen  from Cleveland,  Ohio .It deserves more attention . Every cardiologist , involved in ACS management should read this, especially the interventionist.

Link to article placed her with courtesey of JACC

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