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.
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 ?
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 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 colud 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.
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 .
- 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.
- 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.
- Presence of mechanical complications of ventricular septal rupture , ischemic MR can brings the mortality on par with large anterior MI.
How different is the clinical outcome of inferoposterior 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.
Inferior STEMI generally lacks the vigor to cause extensive damage to myocardium in most situations .Further they respond better to treatment. Risk stratiifcation 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 unwarrnated in most of the low risk inferior MIs.
Related posts in my blog:
1.Why thrombolysis is more effective in RCA?