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Posts Tagged ‘acs’

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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NSTEMI constitutes an important sub group of ACS. In fact it  forms the major  group. Real world data would indicate it   UA/NSTEMI could form up to 75% of all admissions for ACS in any cardiac emergency units. Risk stratification of NSTEMI is important and  is available. It is  one primarily with clinical features , ECG and troponin positivity. Classifying NSTEMI   with reference to underlying patho anatomy is not available.

Classifying  NSTEMI based on the following is  is suggested .

A.Based on the  extent  of infarct.( For example there is no entity called extensive NSTEMI  unlike STEMI)

B.Based on the Location of NSTEMI .

Currently , NSTEMI simply means there is an infarct some where in the heart ? Should we not localise it ? Is it not surprising , we have not attempted to localise  NSTEMI  so far ?

C.Based on the coronary anatomy : RCA NSTEMI vs LAD vs LCX NSTEMI.

The reason is two fold.

1.NSTEMI is often patchy , subendocardial . Some times  only islands of infarct can occur.But , .How common is segmental NSTEMI ? May not be common, still if wall motion defect occur it must be an segmental MI.Some estimate wall motion defect in NSTEMI is around 25%.

2.Is  there any clinical purpose for localising NSTEMI ?

Some would  think there is no real  purpose. That does not  mean ,  we should not attempt to do it. In fact there is an  important reason ,  we  need to  localise  NSTEMI. Triple vessel disease ,  is the common pathology underlying NSTEMI. They often have  multiple critical lesions as well. Identifying the  the  culprit lesion is not an easy task. If we know the site of infarct ,  however small it may be , it  helps us fix  the coronary artery.

A real dilemma could occur in patients  with NSTEMI , who has a  90 % lesion  in  RCA and  50 % proximal LAD lesion  . We ( tend to !)  take it as granted  ,  RCA  lesion is likely to be responsible for the NSTEMI. But  the real culprit  could be  the  recannalised LAD .  If it is so ,   the 50%  LAD lesion  could   be  more important and if you leave it free there is a strong  likely hood of recurrent UA. If we could some how located  the NSTEMI in the LAD region in this patient  , he could  get a PCI for LAD as well.

Of course , there is  an   universal approach available “Doing PCI for all suspected culprit lesion however mild it may be ”  . Unfortunately , it  increases the metal load for the  patient, which is an independent risk factor for a future ACS.

How to locate NSTEMI ?

So , it is often helpful to locate NSTEMI  . Of course ,  it needs little more efforts. A very meticulous echoc cardiography can aid in locating  the subtle  wall motion defects in NSTEMI . Perfusion studies/PET studies may be indicated in occasional patients.Myocardial contrast echo can be useful.

Coming soon

Difference between Anterior NSTEMI and inferior NSTEMEI

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When  a doctor is confronted by serious  doubt  ,  what will be the outcome for the patient  ?

Can  doubting  be beneficial for a patient ?  . It seems so ,  according to  EBM which  stresses   about statistical outcome at every turn of events in a  patient who  is critically  ill .

Is  something ,  always  better than  nothing   ?   Our  limbic  system tends to think so .  It  may not be true. But  in  dire situations ,   many  things  (Proven , unproven)  need to  be tried  however doubtful it ‘s  efficacy  may be  .This is  akin to an  emergency in an  airplane. Even here there need to be a logic.

Then ,this question  arises . How do we make  sure ,  we have a  dire situation on hand  ?

This is the key issue ,  in  the  decision making  for the   critically ill patients .  It  needs  experience ,  only experience !  Though the principle of uncertainty  is the fundamental rule in medicine ,   EBM  aims to bring some degree of certainty in medical therapeutics.

ebm evidence pci coronary

Benefits of doubting in coronary care unit.

In  a  sinking patient  with cardiogenic  shock  , try  the maximum treatment . Even if , the patient is  in severe shock  , take him to the  cath lab ,  try  open the coronary artery . Give the benefit of doubt  to him even though the chances of reviving him is less than 10%.

Risk of doubting in Coronary care unit.

A.Elderly STEMI  with SHT,(Arriving late ,  with  an unknown time  window  after an MI ) To thrombolyse or not ?  . There is  no benefit of doubt here.  Do not thrombolyse. Here , apply  the benefit of doubt against thrombolysis .

B. Chest pain with  LBBB (Thought to be new onset LBBB ) don’t ever rush to thrombolyse.  Wait for the enzyme result . Don’t try to thrombolyse your doubt , instead  thrombolyse the  confirmed thrombus !

C. Patient with persistent ST elevation following thrombolysis ,in an  otherwise asymptomatic and stable patient. Don’t  pass on  ” your doubt ” of salvaging   at least  some myocardium  by rescue PCI .Rescue  should be done before death. You can not resuscitate  dead myocytes.

Final message

The concept of   giving  the  benefits of doubt  to the patient   is a widely prevalent practice  in medicine .This concept is alive  and popular , not because it has proved effective, but because of the primitive   human perception and cognition  , namely “Something is better than nothing ” !

Common sense and logic would suggest , whenever  there is  a benefit  for doubting there would be a  equal (  or  even  more ) unmeasured  hazards and risks . This  becomes  especially  true ,  when   a   physician makes  a therapeutic move  based on doubting than on conviction .

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Primary PCI  has proven to be the   best  option for management of STEMI . But it need to be  done very early by a an experienced team in a good facility . (Note ,  it is not the individual expertise that matters !  Ronalodo alone can never guarantee a   match win  !  )

Any treatment ,  which has a great therapeutic potential also  carries a hazard .

So , these treatment must be used with caution.  Not every STEMI patient , has a high risk of death.  In fact the mortality  in some of the subsets of STEMI ,  can be less than 1%. If , a  STEMI patient with a likely 1% mortality   is going to get a procedure with  3-4% ,  risk it is bound to raise a  validity  question ?

primary PCI PTCA STEMI CORONARY ANGIOGRAMS

What are the situations in  STEMI , where primary  PCI could be dangerous*?

* The  term dangerous here  means ,  Risk > Benefit .

Side vessel STEMI : STEMI in  branch coronary arteries. Main vessel STEMI(LAD,RCA,LCX ) has higher risk than side vessel STEMI( Diagonals, OMs, Septal) .

Side vessel  STEMI is not easy to diagnose in ECG ,  but an MI with ST elvation restricted to  only  2 leads  could be a side vessel STEMI.

The following could be some examples.

  • 1 /AVL , High lateral
  • V2 V3 ,   Septal
  • 3 AVF ,  PDA/RV/ Acute  marginal
  • V5 V6     OMs/Ramus

A spontaneously evolving  STEMI , with  ST segment   returning   towards  baseline  and T wave  getting inverted .This indicates IRA is either partially patent and  the coronary blood flow is in the salvage mode. Here , thrombolysis is going to be very effective .

Final message

In the management of  STEMI  , primary PCI could be  consciously avoided in some of the patients   to improve the overall outcome .

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04_16

How good is Troponin T or I  to rule out acute coronary syndrome in the emergency room  when a  patient presents  within two to three hours after the onset of symptoms ?

  1. Very useful
  2. Useful
  3. Rarely useful
  4. Not useful
  5. Not at all useful

The answer is  5 , can be 3 or  4 , never 1 or 2 !

If you are surprised with the answer

Findout why , read further

troponin-i-troponin-t1

19_trop-t-sen1

troponin-i-troponin-t-2Final message

Troponin has a definite diagnostic  and prognostic value in  STEMI or NSTEMI  but relying on a single normal troponin level very early after an ACS can be . . . futile.

Realis,   diagnosis of ACS , especially  STEMI , is primarily by ECG and clinical features . Even in NSTEMI biomarkers help primarily to risk stratify the event. Bio markers come into picture only in borderline  ECGs and in baseline ECG defect like LBBB/Pacing rhythm .

It should be recognised , the major draw back of cardiac markers is , it  does not represent real time cardiac myocyte  events. (But the good old ECG has this unique property !) .The myocyte secretion & release  kinetics , the effect of  native (and pharmocological ) reperfusion make it a unreliable  marker.Apart from the time lag  , the  laboratory methods to detect these  molecule needs further refinement.

For the current day cardiologists ,  it is  required to finish off the entire treatment  of MI  within 6  hours by doing a primary PCI . It is an irony , troponin begins to appear only by  then to be detected in the blood !

Further reading

A .All about troponin

http://www.annals.org/cgi/content/full/142/9/786

B.Troponin In aortic dissection

http://www.ncbi.nlm.nih.gov/pubmed/15887472

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pci-ptca-ebm-stent

Scientifically ,  the  indication for coronary revascularisation   should be  based on following

  1. Patient’s  symptom ( more specifically angina , dyspnea is less important !)
  2. Prov0kable  ischemia  ( A significantly positive stress test )
  3. Signifcant LV dysfunction with  documented  viable myocardium &  residual ischemia
  4. A revascularisation eligible coronary anatomy * TVD/Left main/Proximal LAD etc ( *Either 1, 2 or 3 should be  present  in addition )
  5. All emergency PCI during STEMI /High risk NSTEMI

Practically ,

A CAD  patient  may fulfill  “Any of the above 5 or  “None of the above 5” ,  but ,  if   a coronary obstruction  was  revealed  by coronary angiogram  and if he  fulfils The 6th criteria , he becomes  eligible for  revascualrisation

6th criteria

If the patient has  enough monetary   resources (by self  ) or by  an  insurance company  to take care of PCI /CABG *

*The sixth  criteria overrides all other criteria in many of the cath labs .Of course , there are few genuine ones still  fighting hard , to keep the commerce out ,  from contaminating cardiology !

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First and foremost is

Avoid the procedure if  not really indicated.A lesion which  has more thrombus load  than a plaque and it is ,  subcritical and not limiting the flow  , PCI may be inappropriate  especially if the ACS is stabilised.

  • Adequate anticoagulation  along with  2b 3a blockers should be used
  • Predilatation should be minimally used or to avoided.Direct stenting preferred.
  • In primary PCI suction devices (Export etc may be useful)
  • Distal protective devices  are  “hyped up devices” rarely useful in an occasional patient with good distal vessel diameter.
  • Pseudo stent approximati(fig 1) may occur. A Layer of thrombus may get plastered between stent and the vessel wall.In the post PCI  phase , with intense anticoagulation and antiplatelet regimen this layer may get dissolved and stent  may lose it’s grip and may dislodge or migrate.Another possibility is the dead space  beneath the stent  becomes a potential site for future  thrombus and ACS.

thrombus-and-pci

Fig 1

  • To prevent this complication , high pressure inflations and Post procedure IVUS (Intra vascualr ultraound may be done to ascertain lack of thromus between stent/vessel wal  interface)
  • Drug eluting stent evoked a special concern , when used in thrombotic milleu.This , has now been  proven to be  safe

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