Posts Tagged ‘post infarct angina’

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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Up to 24 hours

  • Failed thrombolysis and persistent infarct related chest pain
  • Prolonged  Infarct pain  in spite of successful thrombolysis (Rare)
  • Dual STEMI and Dual ACS ( Combination of STEMI/NSTEMI)  *

* Generally  until   after  24 hours one should not make a second coronary syndrome  though  logically  it is possible ( Dual acute coronary syndrome)

After 24 hours -up to 2 weeks

  • Post MI angina  – IRA related (Re-occlusion, Threatened reocclusion)
  • Post MI angina -Non IRA related ( Critical  non -IRA lesion)
  • Thrombus migration /Side branch occlusion
  • Re infarction -Same territory
  • Re-infarction-Remote territory
  • Infarct extension, Infarct expansion , Dyskinetic segments  ( Acute ventricular  remodeling  has a potential to generate pain )
  • Combinations of the above


24 hour is  arbitrary cut off .There can be spill overs and over laps

*Refractory non ischemic  chest pain often atypical not relieved by anti anginal  medication   – Pericardits, Coronary dissections , myocardial /Pap muscle  tears .

After thought

Do we need to break our brain  to  find  the source of angina  following STEMI ?

Principles of scientific medicine  would demand it  . However   in this era of  hyper active interventional  cardiologists  there is little purpose  as they  tend to  open up all occluded arteries   guided by the  their  ignorance about the source of chest pain.


Video on Dual  coronary syndrome

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Post myocardial infarction revascularistation either by PCI or CABG forms the bulk of the coronary interventions world wide.There has been considerable controversy in selecting the patients for the procedure.

Certain basic rules are to be applied.

  • Never do any thing on a totally asymptomatic and fully functional patient.(Functional , means good exercise capacity of atleast( 10Mets).Just medical treatment with good doses of statins, beta blockers will do.
  • If a patient has persistent angina  following MI  ,the issue is relatively simple as  they are  candidates  for CAG  and intervention .
  • The issue becomes little complex when the primary complaint is breathlessness and echo showing  LV dysfunction.

This dilemma is due to a  simple fact

coronary revascularisation has a  great impact in relieving angina but has  less impact in reversing

left ventricular  dysfunction

So,  how do you approach a patient with LV dysfunction and exertional  breathlessness and absolutely no chest pain ?

  1. Do a  CAG
  2. Assess the lesions if any (Some times,  to our surprise there may not be any critical lesions at all ! )
  3. If there is / there are critical lesions try to corroborate with infarct segments.(Use Echo for this correlation)
  4. Don’t bother much,  if a  vessel has a lesion  that is supplying a scarred myocardium.
  5. If there is gross LV dilatation, mitral regurgitation and LV clot refer these pateints  may benefit  from surgical management

One of the rules written by the cardiology community over the past few decades has been

We must document viable myocardium before doing a revascularisation procedures on them.

This rule was self imposed ,  to prevent inappropriate revascularisation in  post MI population.

So , a  gamut of investigations (Both invasive and non invasive came into vogue) to identify viable myocardium in post MI population. Stress echo, Thallium-sesta MIBI, PET  to name a few .

Even after liberal usage of these invesitgations , we realised ,  the confusion in the  optimal selection of candidates for revascularisation has not settled.

In fact,  the correlation between viabilty and subsequent interventional benefit is  inconsistent .Not withstanding this  issue  ,cardiologists inspite of the negative results of OAT and TOAT trials ,  started  opening or by passing any occluded vessel irrespective of viability status.

Unanswered  &  Unasked questions in myocardial revascularisation ?

1.Why viable myocardium is viable even in the adverse compromised vascular  environment ?

It  is viable for the simple reason it has some capacity to be alive . By it’s inherent survival capacity (Survival of the fittest ) or it somehow gets the nutrients by cell to cell perfusion.

2. It is viable allright  ,  why it is not contracting ?

Because ,  it is biochemically and metabolically alive (Can be documented by FDG PET scan mismatch ) but it can not synthesise adequate ATPs to make the muscle contractile.

3.”Viable myocardium is viable ” what more you want from it   ?

Simple viability is not suffice . How to make it mechanically active and contractile ?

4.Is viable  myocardium    synonymous with ischemic myocardium ?.

No,  it is not (Contrary to the popular perception ) .

5. Is it not  common to find dysfunctional segments with good TIMI 3 flow ?. So what is the purpose to document viability ?

It is not suffice to simply document viable myocardium but it is an absolute necessity to prove this viable segment is also  critically ischemic .

7.If angina is  a sign of viabilty why most of viable myocardium is painless ?

This again confirms the fact , much of the viable myocardium in the post MI phase is not ischemic but” still dysfunctional” waiting for healing time. This concept  was  introduced with great fanfare* as  stunned myocardium ,  20 years ago , which was subsequently rejected my mainstream cardiologists , as this concept tend to  restrict the  freedom of interventionists. * Even though ,the concept was genuine and proven scientifically !

6.Are we  certain , the  viable ,  non contractile myocardium  (Which we painstakingly document )  will get back the contractility once the  segment is    revascularised?

Absolutely not. (With lot of PET study doumentation )  This,  we can not guarantee even in ischemic, viable segments  ,  while in the  non ischemic, viable segment it is all the more unlikely.

7. What are the chances of these viable but  non contractile myocardium  regain the contractility  by natural course ?
Very significant chances .In fact every patient recover some LV  function spontaneously over time .

Final message.

  • Revascularisation is non controversial in patients with angina
  • In patients with  primary symptoms of dyspnea  ,  it is less effective and documentation of myocardial viabilty per se will not guarantee successful outcome following revascularisation.Out come depends on  multiple factors .

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                                        Angina pectoris , classically occur on exertion and gets relieved on rest .This is called typical chronic stable angina as described by Heberden (CSA ) .  Unstable angina(UA), the term originally described by Noble O Fowler in early 1970s. ( Also being referred as  intermediate coronary syndrome , preinfarction angina etc).The definition for unstable angina has evolved  over the years  and currently  refers to .

 1.All new onset angina of any degree* Some include severe angina only ! New onset angina of very mild degree on exertion could be the onset of the first episode of  stable  angina. 

 2.Rest angina of more than >30 mts not relieved by taking sublingual nitroglycerine.

 3.All Post MI angina

 4.Any angina in patients who have been stented by PCI.

How to recognise a patient  who is shifting from  stable angina to  UA ? 
UA is  to be suspected when  a patient develops. 
5.More frequent episodes than usual
6.Angina occurring at lesser level of exertion than before 
7.Angina radiating to new site ( Example : Chest pain radiating  to jaw rather than to the usual left arm or vice versa)

Why the first episode of angina is given a special status and often considered critica ?

Angina is the  clinical expression of   myocardial ischemia.The course of  the  first  episode of angina , can not be predicted.It could be a the beginning of a chronic disease process, or it could be a progressive coronary occlusion as in unstable angina /NSTMEI , or the onset of even a STEMI.
In contrast a patient with chronic stable angina  has a predictable chest pain , at a particular level of exertion, radiation to same site, same character, and the patient knows for sure the pain  would promptly dissappear  when he takes rest or nitroglycerine  tablets.

What is the underlying pathology in UA ?  

Generally it is very rare for  a stable plaque to produce a  serious episode of unstable angina .It  requires  an unstable plaque* to  precipitate an unstable angina !
Unstable plaque refers to any plaque which is eroded, fissured, ruptured or  hanging  eccentrically ,  with
an active thrombus.

What is the significance of post PCI angina?

It is an irony, any angina following PCI is to be considered unstable as sudden occlusion of stent is quiet common.This is a paradox of sorts as one would wonder in a patient  with CSA who undergoes PCI with stenting  of left anterior descending coronary artery  (LAD)  all his subsequent episodes of angina  will be labelled as UA  even if a stable angina occur in his other coronary artery.And these patients would go for early invasive approach and potentially inappropriate interventions even if they are at low risk !

Is all angina at rest can be termed as unstable angina ?

No, but many times ,  rather most of the times  cardiologist believe all rest angina to be unstable.

What are the situations where stable angina can occur at rest?

An episode of angina during mental stress, or post prandial* state are very common in patients with CSA. This gets relieved after the stress. Some times  patients with CSA during episodes of fever may get angina at rest .These are considered variants of stable angina.
Post prandial angina , may be considered by some as unstable

How often a diagnostic confusion occur between CSA and UA ?

Generally, this issue is rarely addressed in cardiology literature , for the  simple reason it is never considered an  issue at all !
According to Canadian cardiovascular society grade 4 stable angina  is almost similar to unstable angina , as it denotes angina occurs with minimal effort or even at rest. In fact CCSC grade 4 should be termed as UA.

Can ECG be useful to identify stable angina from unstable angina ?

                                    ECG will some times  come to our rescue when one is confused between stable and unstable angina even though resting ST depression can occur in both stable and unstable angina . Statistically , if ST depression is noted during an episode of angina it is more likely to be UA rather than CSA. . Apart  from ECG , Troponin T or I levels may be elevated in some of the patients with unstable angina. Rarely stable angina can also show elevated troponin.

In patients with systemic hypertension and LVH or cardiomyopathy resting ST depression may not indicate UA 

So differentiation between, stable and unstable angina even though appear simple and  straight forward, it requires a diligent appraisal of history , physical examination (Aortic stenosis /HCM  may cause stable angina)  and ECG, enzyme evaluation.

Final message

In any coronary care unit ,  admissions with initial diagnosis of  ACS/UA/NSTEMI , subsequently turn out to be simple stable coronary artery disese . This error happens because the chest pain  or ECG changes  are aggravated by non cardiac factors like a mental stress or a post operative stress  or fever etc.
There could  be another school of thought, that is to err on the side of  safety, and manage all  rest angina as UA  .But the hazards of unwarranted therapy might exceed the risks of leaving these patients alone.
In this context ,there is a need for a new definition for unstable angina .
One ideal version could be . . .
  • Any angina , of any degree  which is caused  mainly by the supply side defect (By a acute thrombotic /disruptive plaque   occluding the  coronary lumen  with a imminent danger of myocardial infarction is to termed as real UA.
  •  All post MI and post PCI angina are unstable angina
  •  Rest angina which occurs due to increased demand situations need not be  labelled  as unstable angina for the simple reason  there is neither an active plaque nor a  fresh thrombus likely  in these patients. They rarely develop  recurrent angina or MI . The mechanism of angina at rest here is most often due to a tachycardia and resultant increase in MVO2 .(myocardial oxygen consumption) .Currently they are called as secondary unstable angina.In fact , anti thrombotic drugs are misused in these situations as they satisfy the criteria of UA/NSTEMI.

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