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Posts Tagged ‘left anterior descending’

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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                                         Coronary arteries are the major site for human atherosclerosis .CAD is considered the ultimate determinant of  cardio vascualr health of our global population.Coronary atherosclerosis has a predilection for proximal sites and branching points.Typically it occurs in leftmain, LAD ostium, LCX ostium, proximal LAD, diagonal origins, OMs RCA  and its branches .

4010940_766_gr1

Septal branches , even though divide very early  from the LAD , it  is  uncommon  to get affected by coronary atherosclerosis.  Even for an experienced   interventional cardiologist  , it  would be very rare to have  performed a  PCI for septal disease.

Why septal branches of LAD is rare to suffer from atherosclerosis ?

We don’t know the answer yet.

But , it is thought,septal branches are near perpendicular branches .The branching angle and incidence of atherosclerosis has a peculiar relationship.IAt any bifurcation  point , the atherosclerosis tend to occur ,  if the angle is more acute , and is  less common in abtuse angles .It is  almost rare  ,  if branching happens at   exact  90 degree angle or so !

The other reason for septal branches being immune to atherosclerosis is  , it runs within the muscle in its major course. The constant squeezing action(. . . and possibly bridging also)  makes it difficult for the  process of atherosclerosis to sustain and grow .

Can you still get a  septal CAD ?

Yes,  usually as  a component of bifurcation or trifurcation lesion. Some times a diagonal and septal are very close together and  atherosclerosis involves  both ostia.

What is  the implication for the  cardiologist to perform  a PCI with stenting in a septal branch of LAD  ?

PCI and stenting in the septal branches are more prone for crushing and fracture   as it is constantly exposed to the mechanical effects of muscle contraction.

Any other significance for septal branches of LAD ?

  • Isolated septal myocardial infarction can occur.This could be even a embolic manifestation.
  • Septal branches of LAD are potential target for therapeutic embolisation (By injecting alcohol)  in patients  with hypertrophic obstructive cardiomyopathy(HOCM) .This manover aims to produce a controlled septal myocardial infarction and thus paralysing the left ventricular outflow tract and reduce the dynamic LVOT gradient. This form of treatment, was glorified till recently now considered experimental !

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coronary-artery1

                                                      Coronary arterial circulation is the life line for  the human heart  and it’s survival.Typically it is supplied by two coronary arteries,  left and right coronary artery.Both, together carry about  250ml of blood every minute.( Approxinately  equal to a  cup of  coke !  ).These coronary arteries  generally divide in a predetermined  fashion , and have multiple branches . It is a  mystery , what  decides this  branching pattern

Is it like a our palmar crease  ? or the cerebral gyri ?

However , it does follow a certain rule,  one major coronary artery  will follow the  four  important grooves of heart. In the left side ,  left main coronary artery (LM) originates in the left coronary sinus (Size varying between 1mm -20mm)  and usually bifurcates into LAD and LCX. The left anterior descending artery (LAD) runs in anterior interventricular  groove while ,  the right atrio ventriculo groove carries the right coronary artery(RCA) .Left  circumflex artery (LCX) traverses the  left atrio ventricular groove.The most inconstant branch is the posterior descending artery (PDA) which runs in the posterior interventricular  groove.PDA  can arise from either RCA, LCX or both or even from LAD.

The major branches of LAD are called diagonal and septal  while the branches of LCX are called obtuse marginal(OM).There can be two to three diagonal and OMs. 

What is ramus intermedius coronary artery ? What is the incidence of Ramus ?

The left main coronary artery  instead of bifurcating into two ,  it trifurcates into three vessels.(LAD, LCX, Ramus)

The real incidence could vary betweenn (10% to 30%) depending upon the series.

ramus

What course it takes ?

It generally goes in the angle between the LAD and the LCX.It may either behave like a large OM or a diagonal branch.It supplies the lateral free wall of the LV many times.The peculiarity of this vessel is it does not run in a anatomical groove .It simply slides over the free surface of LV.Rarely, a  very abnormal course of ramus,  criss cross the aorta and pulmonary artery .

How common is atherosclerosis within  Ramus ?

We don’t know yet. But it is very likely since it is an early branch from left main, it  might  have a  predilection for atherosclerosis  as like LAD or LCX ostium.In fact now we recognise more of  trifurcation lesions involving  three branches of left main .

What would be the ECG finding if a large ramus is the culpirit vessel during STEMI ?

This scenario could be rare.

ACS in ramus could  present as ST elevation in 1/Avl /V5,V6

  • Lateral MI
  • Apical MI
  • High lateral MI

But it is realised , whenever the ECG changes are not fitting with typical ASMI or a lateral MI one should suspect a ramus lesion

 What is the significance of ramus for an interventional cardiologist ?

ramus-2

                                                   PCI in ramus is a rare opportunity for a cardiologist .The issue here  is,  if ramus is involved  adjacent LAD and LCX is also likely to be involved .So it would logically be a multivessel , complex angioplasty.Isolated ramus lesion could be tackled easily.Another issue here could  be ,since this vessel is not within  any anatomical groove  stent deployment would have a poor  support and prone for mobilisation and migration .

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Differential response of thrombolysis between left and right coronary system

  • Thrombolysis is the specific treatment for acute myocardial infarction. ( Privileged few , get primary PCI))
  • Failed thrombolysis occurs in significant number of patients ( 30-40%).
  • Persistent ST elevation  120 minutes after thrombolysis is best indicator of failed thrombolysis.
  • It has been a consistent observation  failed  thromolysis  is more frequent in anterior   or LAD myocardial infarction.

In a simple study we have documented  patients  with inferior MI  rarely had persistent ST elevation and thrombolysis  was   successful in vast majority  of  patients  ( Except in few patients associated lateral MI)

 

The mechanism of better thrombolysis in right coronary artery  is simple.The success of thrombolysis , apart from early time window , is directly correlated with pressure head  and the duration of contact between the thrombolytic agent and the thrombus. In right coronary circulation the  blood flow is continuous ,  occurs  both in systole and diastole that facilitates the maximum delivery of the thrombolytic agent . Further there is a favorable  pressure gradient  across RV myocardium  as the transmural occluding pressure across RV is considerably less then LV myocardium.

This paper was presented in the  “Annual cardiological society of India scientific sessions”

at Chennai, Tamil Nadu.India December 2000

Click to down load PPT full presentation

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                    Lateral myocardial infarction is not a common site when compared to anterior and inferior MI. But the lateral MI has some unique features, since it involves free wall of the ventricle.The laplace law mediated wall stress is more as the dyskinetic segments bulge with a long radius .Due to this,  lateral MI has a distinctly high risk for free wall rupture .Further pericardial rub is more common in thse patients.Ischemic mitral regurgitation and vulnerability to LVF is also more prevalent if the lateral wall is involved.  Generally lateral MI pateints have a turbulent and complicated course than a simple inferior or anteroseptal MI.

The angiographic correlation of  lateral MI is rarely reported in literature.

The following leisons are commonly observed.

1. Proximal  LAD with large D1  involvement

2. Isolated large D1/D2 disese

3.A left dominat LCX  with large OM1 disease

4.Large ramus disease

5.LAD total and RCA to LAD/D1 collateral pattern

Final message

If we encounter a lateral MI either alone or in combination with inferior/  posterior MI , it is better to manage these patients  aggresively with early triaging for CAG and revascularisation.

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