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Posts Tagged ‘sgarbossa criteria’

Top 5 conditions that closely mimic and often mistaken for STEMI !

  1. Early repolarisation syndrome
  2. Left bundle branch block(LBBB)/ Left ventricular hypertrophy(LVH)
  3. Hyperkalemia
  4. Pericarditis
  5. Brugada syndrome

ERS

The repolarisation is due to  K + efflux . The  K channel porosity  is subjected to high degree of genetic  variations .If the repolarisation starts even by 10 milli- second earlier,  it would have early take off from descending  limb of R wave  and  the J point  ST segment appear elevated.

  • Common  in young  males . Especially in vago-tonic persons with relative baseline bradycardia
  • The ST elevation in ERS is often global .
  • Concavity is upwards .
  • ST elevation can be dynamic ( Further  confusing the picture ! )
  • On EST it  is expected to the  touch the baseline .
  • Benign entity in most . ( False alarm of STEMI is the major risk !)
  • There is some evidence ERS may confer a risk  of  primary VF ,  if they  experience a true STEMI  (Michel Haïssaguerre 2008  NEJM )

* STEMI in ERS :  The issue becomes too delicate ,  if  a  patient with ERS  develops  a true ACS .   ERS being a common ECG pattern in general population , it is not wise to label  every  chest pain in  ERS patient as benign . Suspicious  ones demand observation in step down units , at least !

LBBB

 “Any patient with  LBBB & chest pain . . . suspect  MI”  .

Unfortunately,  this rule is  too reverently followed by  physician community.  In fact ,  ACC/AHA guidelines  reinforced this behavior ,  as it  added a key word  in  their STEMI guidelines   “New onset”  or   “presumably new onset ”  LBBB is  an  indication for PCI/Thrombolysis    .( Physician presumption is a too delicate thread  to hang  our concepts !   )

               Every LBBB is new onset unless you have  a  documented proof otherwise  . . .   it seems to suggest !

Probably , this  is the reason many of the LBBBs are thrombolysed when they present to ER in an acute fashion . Of course , we can apply criteria of  Sgarbossa  to differentiate !  however flimsy it may appear . It  help us to exclude few benign LBBBs. Still ,  Sgarbossa will  struggle to  differentiate  an acute STEMI  in Chronic LBBB  from an  acute LBBB in  old AWMI .

Simply put . . . even old MIs  are at risk of  acute intervention if they have LBBB  and vague chest pain !

How to overcome this ?  Always rely on clinical  features  . If  STEMI is causing the LBBB ,  it  should be a large extensive one and you can not  expect the patient to be  comfortable .(Logic  would suggest necrosis of  large  parts of IVS is necessary to cause LBBB ) Chronic  LBBBs  are relatively comfortable  .

Of course , there  is one another  issue to comprehend  ie  transient ischemic LBBB .We do not know the true incidence  and long-term significance of this entity . Here , LBBB is  not due to necrosis of  the bundle but due to ischemia . (Almost impossible to differentiate it from  rate dependent LBBB  with  aberrancy  )

Role of enzymes and Echocardiogram in LBBB  and suspected STEMI .

You can always ask  for   Troponin  T / CPK MB .(They are helpful only  if 3 hours have elapsed , can we afford to wait ? ) . LBBB  due to STEMI  will  purge  a large quantum of cardiac enzymes from the infarcted zone . (So a marginal elevation is not going to help!)

Unfortunately,  LBBB  can induce wall motion defect in septum that may awkwardly simulate an ischemic wall motion. Even experts have erred in this . One clue  is,  the motion defects  can  not  extend   into anterior wall . It  is confined to septum ,the second clue  is a little delayed  post QRS  thickening of IVS (Septal beaking sign will vouch  for benign LBBB with fair degree of success  )

LVH

  • LVH can mimic a STEMI due to secondary ST/T changes . (Secondary to tall R wave )
  • LVH with incomplete LBBB  – A very common association that can further elevate ST segment in v1 to v3 .
  • Left ventricular hypertrophy  mimics old MI as poor R wave progression in V1 to  V3.
  • Contrary to our belief even Inferior  leads can  show q waves due to  inferior  septal hypertrophy.

Hyperkalemia.

With aging population and rampant  acute and chronic renal disorders it is becoming  a daily affair to get calls from medical units for ECG changes .We know  the rapidity of  efflux  potassium is responsible for ventricular re-polarisation .Phase 2, and 3 are K + exit zones. This is the same phase ST segment and T wave are inscribed.In hyperkalemia  K + accumulates inside the cell and keep  ST/T  segment  elevated .T wave also  becomes tall . It can mimic  both as hyper acute  STEMI .

Read a related article (Dialyisable current of Injury )

Pericarditis

  • ST elevation is not confined to an arterial territory
  • Can be global .(Regional ST elevation  does not exclude pericarditis)
  • ST elevation is concave upwards as in ERS

Link to Read regional pericarditis
Brugada syndrome

Brugada syndrome  is  an ECG -Clinical complex in which ST elevation in pre-cardial leads is associated with  ventricular arrhythmia. The defect lies in sodium channel . It reflects  a mis -match between RV and LV epicardial repolarisation forces .It keeps the RV epi-cardial current afloat and  the pre-cardial leads  facing the RV records ST elevation that  mimics  STEMI. It often  shows  a RBBB pattern and varying patterns of ST morphology  . The  ST segment is  also  subjected to dynamism  , due to change in autonomic tone and myocardial temperature  .(Febrile VTs)

After thoughts

Other close contenders for the top 5 slots

Myocarditis

Acute pulmonary embolism

Dissection of aorta

More

  • Acute stroke (Neurogenic ST elevation )
  • Stress cardiomyopathy (Takot Subo )
  • Acute abdominal conditions mimicking inferior STEMI.
  • Panic attacks /Anxiety states / chronic anti psychotic  medications which are known to elevate ST segments.
  • Contusion chest

(Cocaine hearts / Coronary arterial spasm / LV dyskinetic segments  and  LV aneurysms  were not nominees ! )

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Left bundle branch block (LBBB)   has a curious but important relationship with  STEMI . LBBB inflicts a dramatic change in qrs morphology   with  a diagonally  opposite   polarity of ventricular activation . This masks    the initial qrs vector  and  makes it a difficult task  to diagnose acute MI in this setting. The ST segment which is of primary importance  in STEMI is   lifted  up due to altered repolarization .

LBBB can be associated  with  STEMI in the following ways

  • Acute necrotic LBBB  with massive myocardial damage – Impending shock
  • Chronic LBBB with acute STEMI
  • Transient ischemic LBBB during STEMI
  • Rate dependent  LBBB (Usually tachycardic  ,  rarely bradycardic  )
  • STEMI in pacemaker rhythms

While every one of the above can be experienced ,  the most common diagnostic conundrum  occurs ,  when a patient   comes with acute  chest pain and LBBB . There has been many criterias  suggested to diagnose STEMI in the presence  of LBBB.

The criteria  proposed  by Sgarbosa  (A  GUSTO   off shoot )  in 1996  caught our imagination .One prime reason for this is ,  it came from the prestigious NEJM and Duke university combine. Suddenly this became the de- facto standard to diagnose  STEMI 

In the  past 15  years  ,  our experience in one of largest coronary  care units in India , we have   found this criteria   to have  little utility value  in STEMI and LBBB  . Most of the time  a correct diagnosis was made  by   simple clinical guessing .

Next to  clinical assessment, we found cardiac enzymes (Troponin and CPK ) were reliable in diagnosing  STEMI with LBBB.

Surprisingly ,echocardiography  was as unreliable as ECG .( The paradoxical  septal motion invariably confuses the already  confused  cardiology fellow who usually does the emergency echo  !) 

Even as our  CCU documentation was  far from satisfactory  , now this article from Mayo exactly reflect  our observation.

Sorry   Sgarbosa . . . the criteria was  based  on  sound observation and a  good  electrical principle  . . . still LBBB is able to beat   it convincingly ! ( Very low sensitivity !)

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