Mechanical complications are not rare following acute MI .In fact , it closely competes with electrical deaths . Many times it is not recognised and get wrongly labeled as simple pump failure .
Echocardiography has revolutionised the way , we approach these deadly complication.(Of course , many deaths could not be prevented still !)
The early days of STEMI is critical . This is the time the infarcted muscle softens and invaded by blood components like neutrophils etc. The biochemical events in the infarct zone is a least studied aspect by current generation cardiologists. Some , especially women tend to lyse their interstitial collagen faster. This minute break ups coalesce to form a tear , When this tear is subjected to hemodynamic stress and mechanical stretch a rupture is all too likely.
The rupture site is predetermined by the patients fate !. If the tear occur in free wall of LV , in all likely-hood ,we are going to lose the patient. If he is blessed , the rupture take place in the interventricular septum .Here , the issue is less disastrous as the blood is simply shunted to a different chamber .In fact , some consider VSR puts an ailing ventricle at a slight hemodynamic advantage which is referred to as decompression . The LVEDP has a biphasic response to VSR .An initial raise bfollowed by a flat response.This has a clinical correlation too with a temporary deterioration and subsequent stabilisation.
The issue of thrombolysis and ventricular rupture was controversial for decades .It never got a correct answer and finally we have our own conclusions .
Thrombolysis as such reduces the net incidence of ventricular rupture even though late thrombolysis do increase the risk of rupture. What does the above statement mean to you ? confusing is isn’t ?
For population based approach thrombolysis has a no negative impact , but in a given individual one has to weigh the risk vs benefit .
How to manage ?
Unstable patients (Real shock or impending shock . . .please note every one with 90mmhg pressure is not unstable !)
- Emergency coronary angiogram , VSR closure , CABG
- VSR closure only , without angio /CABG (An useful option if your surgeon )
Four approaches available
- Treat as emergency as above
- Wait still instability begins (Yeh . . .I really mean it !)
- Sort out a elective plan.
- Send the patient home with VSR * ( we have two patients attending our OPDs for >5 years )
* Exceptional case not to be taken as a model for management.
There is rarely an agreement between surgeon and cardiologist in timing intervention in VSR patients. Treatment protocols vastly differ in various institutions with the common theme being early surgery .
Cath based therapy for VSR closure is still considered a cardiology adventure sport .
Some observations about VSR
- The doppler VSR jet if reaches 4-5 m/sec (65-100 mmhg) the prognosis is often good , as it indirectly reflects the native LV function .A ventricle which could generate 100mmhg pressure head, even after a supposedly large MI is great by any standards.These are the ventricles that fight till the end and patients do well in the adverse circumstances.
- In the other end of the spectrum we have a VSR with a faint murmur and 3m/sec jet .They will be hypotensive and end up in shock soon.
- Infero posterior VSRs do badly due the complexities of tears.
- Medical management do have an important role in stabilising these patients.
- LVH if present is again a favorable sign
- Tissue friability could be an important issue why many surgeons fear early surgery.(Some deny this and some say it is never an issue .I am yet to get clarity on this aspect .I expect an answer from cardio thoracic surgeons .)