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Posts Tagged ‘inferior stemi’

Surprises are hall-marks of medical science . The cardiologists do  get  it ,   in enough doses   from  echo  labs  on a regular basis !   . One such thing is  the total ECG-ECHO myocardial  territorial  mismatch following  a STEMI .  Human myocardial segments are divided by cardiologists  by 17 segments by echocardiogram . Long before  echo came into vogue ,  electro-cardiologists  divided the  heart electrically into three zones to  localise MI . (Anterior , inferior and  the  poorly defined entity  lateral walls* ) .Inferior and posterior  segments are  almost used interchangeably. So , when we have 17  echo  segments to be fit into these three electrical category !   were  bound to have  some overlap . The issues of fitting in septal segments is really complex as septum  is a three dimensionally engulfs all three electrical surface of the heart .

* By the way , anatomists  never agreed about existence of walls in heart.They simply said  , heart has smooth  surfaces that blends with one another.  We cardiologist have  built imaginary walls and struggling to come out it !

We will   try to answer the question that’s been asked here .  “Inferior MI”  by ECG   . . . “Anterior MI”  by  echocardiography . How common is that ?

Possible causes for this wrong call

Technical errors  in  acquiring echo  imaging plane  or  it’s interpretation is the commonest . Many  times  ,  obliquely obtained long axis view  wrongly and strongly  suggests  a septal  MI  instead of   inferior posterior MI. This is  because  in  apical 4  chamber view  bulk of   septum  (Basal and mid third )  lies   in the  infero-posterior region .

wall motion defect

Perhaps ,  misunderstanding this  septal  geography is  the  commonest cause for  erroneously  calling inferior MI as anterior  in echocardiography . (A simple clue is the presence of MR . (It  fixes the infarct in infero-posterior zone with 90% accuracy )

Rotation  and  posture of heart

Alignment of the septum to the rest of the chambers  can influence  , how three inferior leads is going to look  at the septum (There can be  considerable errors  -Electrical myopia ? as these leads are located distantly )  . The plane of the septum is such that  in horizontal hearts  septal electrical activity  will be directed infero posteriorly inscribing a q waves in inferior leads rather than anterior leads . One can expect such ECG /Echo discrepancy in the following subset as well

  • Post CABG patients (Any pericardiotomy will make the septal motion  erratic )
  • Obese persons
  • COPD

There are three  more  situations  ,  which   mystified me   with  definite  ECG/ECHO  mismatch

  1. LVH and STEMI  is always an engima . Counter clockwise rotation when accopany  LVH  that masks anterior MI  electrically . It  however inscribes a   q wave in inferior leads.
  2.  In dominant LCX lesions  ( with at-least  one  major OM    )  and  left main bifurcation  STEMIs  ,  combination of  anterior and inferior  wall motion defects are  quiet common . When a such  a  MI evolves ( with or without  revascularization )   regeneration of R wave can be  time shifted . Septal R wave may appear  much earlier and inferior R may follow or vice versa . .Further,  anterior MI  may  evolve as  Non q MI  making it  ECG blind ,   still  echo may pick up the WMA . So there can be important  ECG-ECHO mismatch in myocardial segmental geography .
  3. Further , WMA  need not  always be an  infarct  .Any new episode of ischemia  can result in WMA . Hence a patient  with inferior Q waves  in ECG may experience anterior wall motion defect meagerly  due to fresh episode of   ischemia (This we should not attribute  to  old anterior  MI. It is also possible intra-myocardial conduction delays can elicit remote wall motion defects.

Final message

By general rule  , ECG  correlates  well  with  ECHO  for localising myocardial segments   . At times ,  it  can  really be tricky , and we  get into above situation  in echo labs.

While ,  it is common to observe  ECGs  to mimic  inferior MI  at the first look  and  subsequently echo  revealing  anterior  infarct ,  the reverse is also very much possible .

The  mechanisms are varied and technical  issues are for more frequent than true clinical discrepancy .The issue has important management implications.

Of course ,  coronary angiogram will pin point the   anatomy , still  it also has  strong limitations in localizing myocardial segments (to which it supplies ) especially with multi-vessel  CAD and  collateral dependent circulation .

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Can you diagnose inferior MI with poor R waves ?

No , you need  a “Q ” that’s  for sure !   Do not diagnose inferior MI without a  q wave  . ( The luxury of diagnosing MI without q waves  is available  only for LAD region )

Any axis deviation ( even 30 degrees) from  base line  can alter the inferior lead qrs morphology to a great extent. R wave amplitude is  primarily determined by the  initial septal depolarisation .  So if the  inferior septum is intact  it will never allow to inscribe a q wave  . Further ,  limb leads are bi polar leads and they are   sum-mated  potential  reflected along the entire  bottom half of the  torso . Hence it is not  reliable to attribute  significance  to presence or absence of  r wave (Unlike  chest leads).

The lung and diaphragm  exert  not only electrical insulation but   also mechanical  alteration of septal profile with phases  of respiration.

Counter point

Not really  . . .  you do not need a  Q   waves  to diagnose inferior MI  ,  electrically  diminutive R  is same as  “Q”

There is  an alternate way of  reasoning  too  . R wave is muscle , We diagnose LVH with tall  R waves so muscle loss should be equivalent to R wave loss .We have innumerable examples where  low voltage R waves are  recorded in inferior leads after a well documented inferior MI.

How do you diagnose old inferior MI by ECG ?

  1. Near normal ECG with degeneration of q waves and regeneration* of  R waves
  2. Residual T wave inversion
  3. Simple low voltage inferior leads
  4. Slurred or notched qrs  complex in 2 3 AVF
  5. Rarely with atrial abnormalities and AV nodal prolongations

The concept of regenerated R is well established . And it brings to the age-old debate of R with live muscle Q is dead muscle

Regeneration is salvaged muscle (Natural salvage , awakening from hibernation etc)

How good is Echocardiogram in diagnosing old Inferior MIs ?

Surprisingly , echocardiography do not help much either .Technically inferior transmural MI  is expected to  leave  a residual wall motion defect.  But many times it do not. Many non q inferior MI (Is there such an entity ?)  do look perfectly normal by echo .

The primary reason  for this is ,  infero-posterior surface is anatomically remote and it makes  wall motion analysis difficult .Newer tissue motion analysis (Velocity vector imaging)  could aid us better.

Some times a trivial or mild  mitral regurgitation is the only sign of   old inferior MI  as  the pap  muscle  lags behind in it’s  functional recovery  while  free posterior wall is  fully salvaged and contracting well .

Final message

It needs  that extra bit of   of  knowledge to  expose  our ignorance.

Even in this  maddening   scientific  era  we have valid  reasons to  go back to fundamentals  of  R wave and Q  wave genesis in MI ,  where clarity  is lacking .

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Myocardial infarction (STEMI)  occurs in two distinct arterial  territories .The anterior LAD circulation and postero- inferior RCA/LCX circulation.The incidence is equally shared.

There has been some  learned and unlearned perceptions about Inferior MI.

Inferior MI is less dangerous than anterior MI.  True or false ?

Answer: Essentially true in most situations.

Reasons.

Inferior wall of the heart (strictly speaking there is no walls for heart , only surfaces , which blends with adjacent areas)  inferior wall  is formed by diaphragmatic surface and posterior surface.Inferior MI can occur by either RCA or LCX obstruction.The outcome of inferior MI is determined by mainly by  the extent  of   LV myocardial   damage it inflicts.To  quantitate this  we need to know , how much of LV is supplied by RCA , or LCX or combination of both ? This depend on the coronary dominance .It is estimated , the bulk of the LV is supplied ( up to 75%  ) by LCA. This becomes further high in left dominant circulations . In fact , it is believed LV can never get involved in non dominant RCA occlusions. This has brought in a new terminology  called “Small inferior MI”.Inferior STEMI due to PDA  occlusion or in a co -dominant circulation is not yet studied

Apart from the above  anatomical considerations the following clinical observations  have  been made regarding inferior MI.

  • When thrombolysis was introduced , many studies  suggested the the ST elevation in inferior  leads toched the isolectric levels  in most situations even without thrombolysis.Technically, this implies spontaneous , successful thrombolysis are more common in RCA. Among the thrombolysed ,persistent ST elvation is a rare phenomenon.
  • The well known difference in the conduction defect between anterior and inferior MI  is an important contibutor for better outcome in the later.(AV blocks in inferior MI , are often transient, non progressive, supra hisian location rarely require permanent pacemakers)
  • During acute phase cardiogenic shock occurs in a minority (That too , only if RV shock is included )
  • Even in the follow up the ejection fraction in inferior MI is  almost always above  40%. In many EF is not affected at all.
  • Progressive adverse remodelling of LV is rare

When can Inferior MI be dangerous ?

Anatomical factors

Inspite of the  above  factors  inferior MI can not be taken lightly . Especially when it  extend into posterior, lateral , (Rarely anterior) segments.

While  posterior extension  is often  tolerated , lateral extension is very poorly tolerated .This is probably explained as  the extension involves the vital free wall of LV and the laplace forces could precipitate LVF. Free wall rupture is also common in this situation.

Posterior extension , predominantly involves the surface of RV which is less important hemodynamically. Of course incidence of MR  due to it’s effect on posterior mitral leaflet can be trouble some.

inferior MI ECG

High risk clinical catagories.

Out of hospital STEMI  are at  equal  risk irrespective of the territories involved  .This is because,  primary VF does not differentiate , whether  ischemia comes from RCA or LAD .

  1. In elderly , dibetics and co existing medical condtions  the the established  benign   character  of  inferior MI disappear, as  any  muscle loss  in LV has equally adverse outcome.
  2. Even though  inferior MIs are immune  to cardiogenic shock  , a equally worrisome  prolonged hypotension due to high vagal tone, bradycardia, plus or minus RVMI can create trouble. Fortunately , they respond better to  treatment. Except a few with extensive transmural RVMI outcome is good.
  3. Presence of  mechanical complications of  ventricular septal rupture , ischemic MR can bring  the mortality on par with large anterior MI.

How different is the clinical outcome of infero-posterior  MI with reference  to the  site of  coronary arterial  obstruction   ?

The sequence of  outcome  From  best to worse  : Non dominant RCA* → Dominant RCA but distal to RV branch → LCX dominant with large OMs

* It is believed   an  acute proximal  obstruction of a  non dominant RCA may not be mechanically significant, but can be electrically significant as it retains the risk of primary VF and SA nodal ischemia. The ECG changes  can be very minimal or  some times simple bradycardia is the only clue. One should be able to recognise this entity (Non dominant  RCA STEMI)  as the outcome is  excellent and these patients  would never require procedure like primary  PCI

** A inferior MI due to a dominant LCX and a large OMs have comparable outcome as that of extensive anterior MI. The ECG will reveal ST elevation in both inferior and lateral leads.

***In patients with prior CAD  and collateral dependent  multivessel disease  the  inferior anterior sub classification does not make much sense as  entire coronary circulation can be mutually interdependent.

Final message

Inferior STEMI  generally lacks the vigor  to cause extensive damage to myocardium in most situations .Further they respond better to treatment. Risk stratification of STEMI based on the location of MI has not been popular among mainstream cardiologists. This issue needs some introspection as  the costly and complex treatment modalities like primary PCI  is unwarranted in most of the low risk inferior MIs.

Related posts in my blog:

1.Why thrombolysis is more effective in RCA?

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