Posts Tagged ‘pericarditis’

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


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 !


 “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 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.


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 )


  • 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


Acute pulmonary embolism

Dissection of aorta


  • 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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We know prompt reperfusion of infarct related artery( IRA) by any means  constitute the specific management of  STEMI .However, It needs  to be emphasized ,  treatment process of STEMI  is not over after  primary  PCI or thrombolysis .Early hours after a PCI or thrombolysis  is vital as well .The ill-fated coronary arteries are as  vulnerable as before.  In the setting of multi-vessel CAD  (Which usually is the case) the unpredictability is still more.

Image courtesy New york times , January 5 , 2009

When a patient complaints of chest pain  24 hours after a STEMI . Think about any of the possibilities and act accordingly.

  1. Infarct related pain ( Dull aching pain from residual neural signals from infarct zone,  till type C  un-medullated  nerve endings  die of hypoxia )
  2. Post infarct angina –From IRA zone (Residual ischemia)
  3. Post infarct angina-From Non IRA zone(New Remote ischemia)
  4. Re-Infarction
  5. Infarct expansion/ Extension /mechanical stretch
  6. Pericarditis
  7. Intra coronary dissection adjoining  a plaque (Plaque fissures  are same as dissections if they extend into media ! But plaque fissures are painless since they lack nerve endings  )
  8. Myocardial tear /Rupture (Generates  severe pain , usually transmit to back , patient often become violent and poorly respond  even to narcotics)
  9. Post resuscitation/DC shock / chest wall contusion . ( I know at least one patient  who was rushed to cath lab for a  suspected  acute stent thrombosis  ,  it was indeed   a rib fracture during an  earlier resuscitation at ER  on his arrival !)
  10. Finally ,when the  pain is refractory and atypical   non cardiac chest pain which might have been pre existing to be considered as remote possibility .

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For  a police officer who visits a crime site  every one looks like   a culprit. For a cardiologist  sitting in coronary  care unit  all chest pain  will have to look like  an infarct  !  Then only he is a cardiologist !

A rare , but costly mistake occasionally  happens . When a  patient with severe chest pain in the  retro sternal region with ST elevation in ECG , enters the ER  there is little  reason to suspect any condition other than STEMI !

This is how medical  errors takes place

Medicine is an art , we can not take it as granted .Acute MI can present with normal ECG and a dramatic ST elevation need not be MI

Here  was  a patient who presented with this ECG and one our fellows correctly diagnosed the condition .

Most  physicians would have thromolysed this patient or  might have wheeled into cath lab.  We have such events reported from primary  PCI registry .

Key differentiating points

  • Diffuse ST elevation not confining to a arterial territory
  • Absence of reciprocal changes
  • ST  segment with concavity upwards.
  • Echocardiogram and enzymes will be useful

iFAQs  in pericarditis

What is the mechanism of ST elevation  pericarditis ?

It is actually a zone of epicardial or Sub epicardial injury.

What will be the ECG finding if STEMI is associated with fibrinous pericarditis ?

Double dose of ST elevation .Mimics  a re infarction.

What are the dangers of thrombolysing a patient with diffuse pericarditis ?

It can bleed into pericardial  space

What happens

What will be the ECG finding in localised pericarditis ?

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The commonest cause of ST elevation is  STEMI .

The non infarct causes of ST elevation include

  • Pericarditis
  • Early repolarisation syndrome
  • Hyperkalemia
  • Brugada syndrome
  • CNS injury

What is the mechanism of ST eelvation in pericarditis ?

The mechanism of ST elevation in STEMI  is  injury current coming towards the recording lead. In pericarditis  we are not  sure  about the presence of  injury current  because pericardial cells are not  capable of depolarising and repolarsing .But ,  the fact that  epicardium and visceral layer of pericardium are anatomically  are almost same entities .Attempts to rip off visceral pericardium from myocardium ie epicardium is often futile .This makes it very obvious  any true pericarditis  must involve epicardial layers of the heart.

How does inflammation of epicardium  lifts the ST elevation ?

This again is a mystery .The   effect of   inflammation   on the polarity of ST segment  is  complex one. Diffuse and global ST segment elevation with concavity upwards  is the hall mark of pericarditis. This makes us believe pericarditis has to be diffuse  and involve  the entire  circumference of the heart.

Logically and realistically  this happens rarely . Many of the pericarditis are localised and regional . Even regional constrictive pericarditis are reported .The factors that determine the ST elevation in pericarditis  depend on the  spread of the inflammatory process beneath the epicardium .If the inflammation is active  andeep  ST elevation is likely to be  prominent.

The ECG is  that of a 15 year old boy  with a febrile illness .  He developed  severe myopericarditis .The echocardiogram showed  global hypokinesia and severe LV dysfunction .Patient failed to respond  with  medical therapy and succumbed  after 48 hours of onset of shock .

Can we localise pericarditis with the help of ECG ?

It is possible. But there is no clinical purpose to do it.

Can troponin be elevated in pericarditis ?

No it should not happen in pure isolated pericarditis.But , epicardial involvement can result in inflammatory damage  to muscle and troponin can be elevated. When pericarditis occurs as an accompanying manifestation of pancaritis troponin  is bound to elevate (Fulminant pan carditis of acute rheumatic fever)

Final message

Pericarditis need not be diffuse and global infact pathologically it is rare to have global pericarditis  . Localised pericarditis especailly adhesive type , which involves the  posterior  /anterior  epicardial layers can mimic an  either inferior  or anterior  STEMI  . This has important clinical implication as unneccssary coronary interventions can be avoided.

Do not expect  text book descriptions for any ECG pattern in clinical cardiology .

We will be rarely  correct . . .

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Logic would suggest  any two structures  in close proximity can have  some sort of anatomical , physiological or sometimes pathological relationship .Esophagus and heart  share a strategic  anatomical  space within the mediastinum  . The left atrial wall  is abetting the esophagus with only few millimeters separating the two. Trans esophageal  echocardiography has utilised this proximity for it’s  advantage . With the probe in esophagus we can get a  100%  interior view of left atrium . Both these structures can mutually compress one another at times of pathology . ( LA compression on esophagus in mitral stenosis , Esophageal compression of LA in hiatus hernia or esophageal growths) . Now ,  we also  realise , esophagus  a   functionally unrelated structure  to  cardiovascular system  can have a impact on cardiac functioning.

Hiatus hernia of gastroesophageal junction can mechanically compress the posterior aspect of heart and result in atrial  arrhythmias and pericarditis  ?


1 Duygu H, Ozerkan F, Saygi S, et al. Persistent atrial fibrillation associated with
gastroesophageal refl ux accompanied by hiatal hernia. Anadolu Kardiyol Derg
2008; 8(2):164-165.

A case report from South africa


Read further for esophagus- heart  stories.

  • Esophageal ulcers , spasm can trigger electrical activity that can mimic cardiac event  or rarely precipitate a real angina  , what is often referred to as  linked angina .
  • A rare case of pneumopericardium due to rupture of esophagus into pericardial space
  • ST elevation in ECG due to esophageal spasm


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Heart is externally covered by two layers of pericardium .  Pericardial space is formed between parietal and visceral layers of pericardium . It is a narrow space which is normally lubricated with pericardial fluid up to 25ml. When these two tissue surfaces  come into contact ,  pathological  rub takes place.It is heard  whenever the pericardium is inflammed . Pericardial rub is a distinctive but uncommon  clinical sign .

Common clinical conditions

  • Acute pericarditis
  • Uremic pericarditis.
  • Rheumatic pericarditis
  • Post myocardial infarction

Pericardium has two layers .

There are four  possibilities for pericardial rub to take place.

The rub can occur

1.Between the two layers of pericardium

2.Between the visceral pericardium and the epicardial layer of  heart*.

3.Between parietal pericardium and the  chest wall

4.Pericardium can rub with the adjacent pleura( Pleuro pericardial rub )

The second and third mechanisms are very rare.

An update

We have realized one more possibility . Diaphragm forms the floor of the heart on which the hanging heart  rests . Rubbing of pericardium over diaphragmatic surface is a beat to beat affair that lasts the entire life !. In inflammatory states of  diaphragm especially  the contagious  ones from abdomen  , can result in pericardio- diaphragmatic rubs .These rubs are almost impossible to hear clinically.

pericardial effusion rub plural pleuro pericadial

*The anatomic mystery : Is epicardium same as visceral layer of pericardium ?

Some anatomist feel that both are same entities. If that is the case myocardium can never split its relationship with visceral pericardium.But it is also a anatomical fact visceral pericardium engulfs the coronary artery and  are located sub epicardially.

How many components of pericardial rub are clincally heard ?

Pericardial rub  classically has three components. Systolic, mid diastolic, and pressytolic atrial components. Pericardial rubs are typically described as to and fro rub. Systolic component is most consistent. In atrial fibrillation mono component pericardial rub is heard.


Superficial , scratchy, high pitched ( Can also be low pitched)


Left sternal border , left 2nd or 3rd space  .Best heard in  sitting , leaning forward in inspiration. Many times the rubs are transient and evanescent . Since it has multiple components it may be mistaken for added heart sound like S 3 or S 4.

What is the mechanism of pericardial rub in the immediate post MI phase ?

Presence of pericardial rub post MI indicate a transmural involvement or atleast significant epicardial involvement . Recognition of this is important as presence of pericardial rub increases the risk of rupture  and hemorrhagic effusion if anticoagulants are used.

What is the  relationship between  pericardial effusion and  pericardial rub ?

Generally it is said with the onset of effusion pericardial rub disappear.But this is not necessarily true.

Rubs after contusion chest and fracture ribs can be with the chest wall and may have  no relationship with effusion.

Is pericardial rub a painful condition ?

Pericardial  rub associated with acute inflammatory pathology is severely painful (like a pleuritis).But pericarditis associated with chronic inflammatory conditions are less often generate pain.The exact reason is not known.

What is pleuro pericardial rub ?

This  clinical entity is poorly defined , often taught by veteran professors  in clinical auscultation classes.It can be heard in the mid segment  or diaphragmatic pleuritis with or without pericardial effusion in patients with  atypical pneumonias.

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