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Posts Tagged ‘ventricular septal rupture’

Ventricular septal rupture is a major mechanical complication of STEMI . Excruciating  chest pain ,  is the sine qua non of  any myocardial tear , dissection and rupture . It is surprising ,   VSR  following STEMI  is rarely a painful event . I can recall number of  such events  , when a  stable   patient with persistent ST elevation  in the  coronary care unit ,   wakes up next morning  with a systolic murmur.And echo reveals a septal defect promptly.

Three  reasons  can be  proposed  for relatively  pain free rupture of IVS in STEMI.

  1. Typically  VSR  occurs in 3rd or 4 th day of infarct . By this time myocardium  can be as  soft as an ice cream ! . There is not much stress and strain at the site. The necrotic  debri just gives way to spikes of   LV systolic pressure .
  2. For rupture to occur there   must be  transmural infarct  .The pain nerve terminals also die in the process .
  3. Further , it is a cavity to cavity rupture  (LV to RV ) . Direct pericardial  stretch  does not occur .

* Ventricular free wall tear   is a near fatal event is extremely painful .This  often occurs  in the first 24 hours when  the nerve terminals are  alive . The free wall rupture is more of  a  tear in the plane of  myocardium . The  pericardial  (epicardium)  layer has  rich   somatic  nerve supply .

In summary

Early  myocardial  tear   involving the epicardial  surface can be severely  painful  .  Late giving way  of softened  , necrotic  often  hemorrhagic muscle ( especially in the IVS ) is less painful or totally painless.

Coming soon   . . .

By the    . . .  what happens  to  pieces of  septal myocardium as it  gives way  and enter the right ventricle   ?

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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 .

An irregular tear in the mid ventricular septum

This patient did well with initial medical support and referred for surgery electively

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 )

Stable patients

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 .)

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We know,  electrical deaths constitute the bulk of sudden cardiac deaths in MI.  Mechanical deaths due to pump failure, muscle rupture , valve leak , also cause significant deaths   .(Surprisingly many of the mechanical deaths   may also   fulfill  the sudden death criteria !)

Free wall rupture is  invariably a fatal event. Papillary  muscle trunk  rupture  leads to severe LVF and unless intervened sure to result in fatality.

The ones who tear their interventricular septum  are some what blessed ! Here ,  the rupture does not result in instant death as there is  no loss of blood ,   instead , there is an  volume over load of right ventricle  followed by the  left ventricle  after a  few beats. Hypotension is the  rule. Even though this is a major complication there is something about  VSR which makes it unique.

Sudden giving way of IVS has  a decompressing effect on the ailing left ventricle.This many times  bring a  temporary relief to LV and if the patient survives the first few hour he is likely to stabilise  further . In fact , sudden deaths within 24hours after the onset of VSR is an exception.This defect always gives the cardiologists and surgeon some time to plan the management. We need to use this time judiciously.

The natural history is delicate . Five themes are possible

  1. Very unstable Instant death( Fortunately a  rare theme )
  2. Unstable – Deteriorating further
  3. Unstable to Stable * fit for discharge even without surgery
  4. Stable from the onset and  continue to be stable* .
  5. Stable to Unstable (Probably the most common theme )

* Pleasant themes occasionally witnessed !)

Here is 55 year old women came with extensive anterior MI with lower septal rupture.(She belonged to type 3 of the above scheme)

)

Note the septal rupture is visible even in 2D Echo

 

Color flow showing significant shunting from LV to RV.This shunt depends upon the LV contractile function, LVEDP and ofcourse the RV pressure

 

If there is severe RV dysfunction or bi ventricular dysfunction flow across the defect is inconspicuous.Brisk left to right shunting may be an indirect marker for good LV systolic function and absence of significant pulmonary hypertension.Both imply a better outcome.

The main determinant  of survival is the  underlying LV dysfunction and associated co morbidity(Renal function ) and complications .

Infero -posterior ruptures tend to be complex and  may have multiple irregular tracks  that makes it difficult to repair.

Investigations

Echo cardiogram is the mainstay .Serial echos should be done to assess the mechanical function and the progress of VSR.Hemodynamic monitoring may be done without injuring the patient .

Medical management

  • Often supportive , but  effective . Dobutamine infusion can maintain a life for few days.
  • Paradoxically , LV dysfunction and elevated LVEDP restricts volume overloading of VSD.
  • Associated MR, Arrhythmias  need to be taken care of .

Surgeons role

  • Very Vital.
  • Experience counts.(Individual as well as  Institutional )

Timing of surgery

Continues to be a controversy . Surgeons love to operate in a stable patient. But they need to realise , surgery is often needed to stabilise  many  patients. . The issue of tissue friability  is blown out of proportion in the literature .When a  life is  is at danger we can not worry about  friable tissues !

The rule of thumb could be

  • Operate as early as possible in unstable patient.
  • Post pone surgery in stable patient as late as possible ( Late here means . . .elective non emergent surgery )

Surgical options

  • Simple VSR closure without  knowing coronary anatomy
  • Simple VSR closure after knowing coronary anatomy
  • VSR closure with CABG ( total revascularization)
  • VSR closure with partial revascularization

In our experience  each of the above , has a role in a given patient depending upon the logistic , financial , social and even  the available expertise. (A good surgeon in bad Institution !)

Is coronary angiogram mandatory  before attempting to close VSR ?

Logically yes. If it is not available  just do not bother .  But, many times , when issue is saving lives , we can not afford to be too scientific , many lives have been saved by not following  such strict  protocols .A simple emergency  thoracotomy and closure of rupture site (Without even touching the LAD ) can be a distinct  and viable option in  a selected few .

Role of cardiologists

Contrary to the popular belief the role of cardiologists is minimal , except  to prepare  the patient and hand over to the surgeon.

Interventional approach to close  a VSR  is currently  be termed as an  adventurous option ! The VSRs  can assume unpredictable shapes  and the  tears can be multiple  in  different planes. The devices , catheters and  other hard ware are not specifically made to tackle these  issues  .An acquired VSR  should never be compared with congenital VSD.

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