Archive for July, 2009

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 ?

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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Total coronary artery occlusion is a common finding in CAD  especially in chronic stable angina. Normal coronary blood flow is 5 % of cardiac output  that amounts to 250-300ml/mt.At an average  heart rate of  70/mt  , each  beat  injects  about 5cc blood into the coronary circulation.This is shared between two coronary arteries.  This means , only few CC (2-3cc) of blood enters  each coronary artery with each cardiac cycle .

When one of coronary artery is totally occluded what happens to the coronary

blood flow ?

A.Total coronary blood flow  can be be  maintained   normal  at rest  as it  forms  only about 5% of cardiac output  (or it is only  slightly reduced )

B. It is believed , the unobstructed coronary artery  could receive the blood meant for the contralateral coronary artery. This  possibly explains the increased coronary artery diameter in the non obstructed artery.

C. It’s nature’s wish ,  that the  contralateral  coronary artery  shall share  50% of  it’s  blood through  collaterals if available.

D.If collaterals are not formed it , the unobstructed coronary  artery  may be over perfused with double the amount  of blood flow.

E. Some times , the collaterals steal  much more than what  the  obstructed coronary artery  deserves and make the feeding coronary artery ischemic. This is many times observed in  total RCA occlusion with well formed  collaterals  from LAD/LCX.

F.The collateral flow  in CTO also depend on whether flow is directed from LAD system to RCA or from RCA -LAD system. The LAD is better placed to assist RCA than vice versa.This is for two reasons.1.LAD blood flow is higher than RCA so it can share it.2.The driving pressure is more  from LAD -RCA , as RCA can receive  blood flow even during diastole .

F.During exertion , the coronary hemodynamics become further complex.The collateral’s are traditionally thought to be less than adequate during times of exercise.But it is more of a perception than solid scientific data.This rule  may be applicable in only certain group of patients. We know CTO patients with very good exercise tolerance who have documented collateral’s.

G.Collaterals can be either  visible or invisible by CAG. The strength of collateral circulation is not in it’s visibility but it’s capacity to dilate and  respond to neuro humoral mediators at times of  demand.  Currently  , there is lot to be desired  regarding  our knowledge about  the physiology  of visible collaterals , no need to  mention about invisible collaterals !

Final message

The above statements  are based  on logics and observations .

Is it not a  irony  in cardiac literature ,  where  thousands of articles  are coming out every month  to tackle  totally occluded coronary artery(CTOs) ,  there is  very little data   regarding the coronary hemodynamics in chronic total occlusion .   How  does a patient with CTO can manage a active life with only one functioning  coronary artery ?

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Thanks to wordpress.This  blog has caught the attention of some professional sites.

I was interviewed   by Jodie Elrod on behalf  of   EP lab digest July 09 Issue

dr s venkatesan www.drsvenkatesan.com

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Contrast induced  nephropathy (CIN)  is potentially a serious problem. The following precautions are useful in the prevention of CIN.Patients with  serum creatinine>1.5mg carry a  progressive  risk .Diabetics and elderly are more prone.Protienuria is a added risk.

  • Adequate pre procedure hydration is a must . Normal saline (.45%NaCl) infused over 6 hours on the day prior  to flush the kidneys  of protiennaceous  substances.
  • Low protein diet in the days prior to procedure could be useful.
  • Ionic contrast to be  avoided.
  • Among noninionic  low osmolar , monomeric Iohexol may be avoided . Use of isoosmolar , dimeric Iodixanal has some advantage.
  • Oral antioxidant N-acetyl cysteine  600mg twice a day pre and post procedure along with .45% NaCl infusion  is found to be  useful.
  • Sodium bicorbonate infusion . Three  ampuoles of normal saline .9%  in one  litre normal saline infused 3ml/kg per hour started i hour prior to procedure and continued at 1ml/kg for 6 hours post procedure has a renoprotective effect.
  • There could be a role for combination of N -acetyl cystiene and sodium bicorbonate

Apart from the above measures the following general rules are vital

  1. Use minimal amount of dye .<30ml. Dye volume  is more important than the type.(50 ml of isoosmolar dye is more likey to cause CIN than a 30ml of ordinary dye !)
  2. Minimal views to delineate anatomy.
  3. Whenever possible utilise biplane angiography.
  4. Do not  give in to the  temptation of injecting a renal shot.( Although you could miss a renal artery stenosis (RAS), which is likely in these patients .Some may argue  for it ,  as  it gives us an opportunity to cure the RAS )
  5. Stage the  procedure and post it on different day if intervention is required.
  6. PCI for discrete straightforward lesions may be attempted
  7. Avoid complex PCI in renally compromised
  8. Review all the drugs for the potential renal offenders.
  9. Manage the diabetes , cardiac failure meticulously
  10. Have nephrologist always on a  standby mode

Post procedure follow up .

Hydration to continue

Follow up biochemistry

How often we require dialysis   in these patients  ?

It can be avoided in most if we have taken sufficient precaution. In severely compromised renal  function peri procedural dialysis is often used.

Finally , before doing a CAG in renally compromised patient always ask this  question and answer it genuinly . Is the CAG/PCI is really indicated in the given patient ?   Does it going to make a difference for the patient ‘s life ? If the answer is  – No – please avoid it !

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Common causes

  • Left atrial appendage clots
  • Left atrial  clots
  • LV mural thrombus (Post MI, DCM)
  • Mitral aortic valve infective vegetations

Conditions that could be commoner than we think!

  • Aortic valve  calcific debri
  • Aortic arch atheromas
  • Paradoxical embolism through foramen ovale.*

If we consider incidence of patent foramen  ovale in general  population is up to 20%  the problem of paradoxical embolism could be really significant.PFO is a potential  right  to left channel of more than 5 square cm .

Unusual causes

  • Mitral annular  and posterior leaflet  calcification
  • Tumor embolus (Myxoma etc)
  • Prosthetic valve thrombus.

Cause never known and identified.

There are times a cardiac source can never be identiifed.This can very well happen , as a transient arrhytmia can trigger a thrombus formation and subsequent examination are totally normal .The incidence of such group can never be known !

A brief  account on cardiac embolus

Cardiac  embolus constitute an important cause for stroke or TIA. There are number of important conditions that can result in cardiac embolism. The embolus could be a  thrombus(95% of times ) , Vegetation, tumor, calcific debri, cholesterol , atheromatic particles , rarely chordal and subchordal structures following it’s rupture.The size of the embolus could vary between <.5mm to 1-2cm in diameter.The average size is 1cm . The clinical presentation depends upon the size, content of the emboli(Thrombus vs non thrombus) )  site of trapping, freshness of thrombus, natural lytic process.

The common  sites  of trapping is middle cerebral artery.The average diameter of MCA is around 2 mm.So one can imagine almost most of the cardiac emboli can not traverse it, and hence a  dense stroke .But , micro thromboemboli , can safely cross cerebral circulation.they usually present as TIA or a chronic lacunar infarcts and many times vascular dementias. Cardiac thrombus rarely gets struck within the carotids.This is especially common if there is associated critical carotid stenosis.The situation is a dire emergency.(Inspite of the fact there is circle of willis for

How do you investigate ?

A complete physical examination with well documented clinical history

A meticulous echocardiography with possibly a TEE (Transesophagel echo)  may  done .

Underlying disorder to be tackled.

When a emboli is released from the heart , what determines  it’s entry into carotid ?

The aortic ejection force is such that whatever particle that exit from the heart , tend to hit on the carotid first.Only if it fails to accept it , it is pushed across the aortic arch into the descending aorta.This result in peripheral embolism .Some times a emboli gets struck within the carotid .This  especially happens  if there is associated with critical  carotid obstruction .This can result in massive stroke and sudden neurological death( The threat is real  inspite of the presence of circle of willis which supposed to come to rescue in cases of sudden unilateral carotid obstruction)

What is the relationship between atrial fibrillation and cardiac emboli ?

For long ,the two conditions were thought to closely linked entities.AF slows blood flow across the atria, predispose to left atrial clots and possibly increased stroke.So vigorous means to restore sinus rhythm were attempted. But to our surprise, the incidence of stroke was not greatly reduced between optimal anticoagualtion and sinus rhythn restoration. This indicated many of the cardiac source of embolism could be distal to left atrium aortic arch atheromas, carotid etc (AFFIRM study)

Restoration of AF into SR can possibly prevent thrombus  formation  only in one chamber , while systemic anticoagualtion can prevent thromboembolism virtually any where from the high risk zones across the LA, LV,  Valves, Aorta, arch, carotids etc. So , it defies scientifc logic , to attempt AF restoration by all means (The exotic pulmonary vein isolation etc !)  to  eliminate one of the cause of stroke.

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Ventricular ectopic beats are the most common cardiac electrical abnormality for which cardiologist’s consultation is sought.VPDs are one of most benign observations in ECG and  and almost every  heart experiences it. In 24 hour holter recordings it was reported up to 25% of healthy  individuals .

In spite of this ,  the fear of  noting a VPD in a given tracing of ECG is genuine both for the patient and his physician.This is because  VPDs  can be  a forerunner of dangerous ventricular arrhythmias.

  • VPDs are often graded according to the count and morphology and frequency.(Lown’s ,Bigger’s grading)
  • VPDs that occur in single are less fearsome.( It may not be so . . .)
  • VPDs in couplets and  triplets raise considerable anxiety.( Again it need not be . . .)
  • A series of VPD lasting for 30 seconds is called non sustained ventricular tachycardia(NSVT)
  • If it exceeds 30second it called sustained VT.
  • VT may remain as VT in many.
  • VT may degenerate into VF  ventricular fibrillation in minority( ie cardiac arrest)

The importance of VPDs do not lie  in the number ,  morphology or frequency  but most importantly  in  the underlying etiology. If it occurs in a structurally normal heart it is largely benign.

New onset VPDs should be investigated thoroughly. The commonest symptom is palpitation.

vpd ectopic

Friendly VPDs : Some of  situations where VPDs are  commonly observed and has little significance are.

  • Exercise induced VPDs
  • Pregnancy induced VPDs  (PIH /Peripartum DCM are  rare possibilities)
  • Thyroid associated VPDs
  • Alcohol /Smoke related

What are the VPDs that could be clinically  important ?

VPDs with chest pain(Ischemic etiology )

VPDs in patients with dyspnea.(CHF , COPD)

Drug induced VPDs(Digoxin etc)

Renal failure associated VPDs

VPDs due to hypoxia/Hypokalemia

In patients with pre existing heart disease.(Congenital, valvular, myocardial disease)

What prevents a non sustained VT from becoming sustained ?

No one really knows the answer.Most of the NSVT self terminates.A healthy heart some how gets the capacity to self terminate the arrhythmia.The normal  LV  fails to sustain the abnormal electrical circuit . A diseased heart may not be able to do so . Further if there is electrolyte abnormality (low potassium), or lack of oxygen it may maintain a VT.

What are the most dangerous forms of VPDs ?

  • VPDs that occur during  acute coronary syndrome.
  • VPDs associated with cardiomyopathy( Ischemic , nonischmic,)
  • Some forms of primary electrical disorders of heart( Brugada syndrome, ARVD , CMVT etc)

How do you investigate patients with VPDs?

General medical work up in all.

Echocardiogram is usually necessary in most.

Holter monitoring in occasionally.

Coroanry angiogram rarely

Electrophysiological study in high risk category

How do you manage  patients with VPDs?

  1. Generally do not require any specific drugs in vast majority of individuals .
  2. Reassurance is the key
  3. Ask them to avoid potential triggers like smoke, alcohol, coffee, tea and related bevarages.
  4. If palpitation is troublesome beta blockers( Propronolol, Atenolol, metoprolol can be used.)
  5. Anxiolytic may also be given.

*If the patient has  systemic disorder like hyperthyroidsm , anemia  or underlying heart disease he has to get the specific treatment.

Caution:It has become fashionable for the physicians  to use powerful antiarrhythmic drugs like amiodarone (Cordarone) liberally in patients with asymptomatic VPDs with structurally normal hearts.this practice must be absolutely avoided as amiodarone is one of most toxic  cardiac drugs known  with great pro arrhythmic activity.

When to refer a patient with VPD to a electrophysiologist ?

Physicians   can  treat   most of these patients. But the following will require EP consultations

  • Patients with syncope
  • Patient who have LV dysfunction(Low ejection fraction EF%)
  • Has had an episode of ventricular tachycardia
  • Cardiac arrest

What will the Electrophysiologist  do ?

These patients will be evaluated for inducibility of VT/VF and if the LV function is poor (EF<30%  MADIT 2 criteria ) many would receive implantable cardivertor defibrillator(ICD) or life long anti arrhythmic  drugs.

Some times radiofrequency (RF ablation)  waves are used to ablate the focus of VT.This is possible only if it occurs close to endocardium as  intracardiac catheters do not have access to epicardial  focus. Among  ICD and RF ablation later could be preferred whenever feasible as it eliminates the arrhythmia , while  the former only tackles it only after it occurs .( Hence ICDs  , even though a technological marvel can not be labelled as curative ! )

Final message

VPDs are the   most common cardiac arrhythmia .Most of them are benign. Few of them require extensive investigation.

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How will you refer to a ventricle which is not dilated but still has severe global contractile dysfunction ?

Traditionally cardiomyopathy is classified as

  • Dilated (DCM)
  • Hypertrophic(HCM)
  • Restrictive (RCM)

But there is large group of pateints who do not show any of the above features and still have global hypokinesia  contractile dysfunction. this group has been largely ignored .It could constitute up to 25%of all cardiomyopathy.there can be some overlap between non dialted cardiomyopathy and RCM.

We report our experience here with

non dilated cardiomyopathy click to download PPT

non dilated  cardiomyopathy

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Infective endocarditis (IE) continues to be a dreaded  medical problem. The clinical outcome has not improved much , in spite of  availability of powerful antibiotics. Early surgery in eligible patients  could provide the best possible results.

One of the major determinants of morbidity and mortality  in IE  is the renal involvement.

Kidney gets affected in almost all the patients  with IE.  As IE is a  a systemic illness and  immunological activation is  the  norm ,  some degree of renal involvement is universal. Microscopic hematuria confirms this. This is due to clogging and  globulin mediated  damage to glomerular membranes. There is a linear co relation between  the size of the vegetation and degree of renal involvement.

The following  mechanisms are attributed   for  rapid deterioration of renal function in patients with IE .

  1. Renal arterial emboli-occlusion-renal infarct
  2. Immune complex mediated  focal nephritis .
  3. Diffuse ,  rapidly progressive glomerulonephritis
  4. Drug induced renal dysfunction, especially with  aminoglycosides, vancomycin etc
  5. Finally &  most importantly , the underlying cardiac condition, which result in refractory cardiac failure  may either be primarily responsible for the renal compromise or aggravate the situation.
  6. Combination of each of the above can occur

How to manage renal failure and IE ?

This forms a deadly combination.  Aggressive  planning  & implementation  is  required. Cardiologists, cardiothoracic surgeons, nephrologists  should  discuss the strategies  together.  A microbiologist  is also welcome !

  • If it is purely a pre -renal failure due to CHF, there is no major worry.The  patient should  do well with cardiac failure management.
  • The role of CT surgeon is always vital, since 75% of times , IE patients require  valve replacement or vegetation/abscess  removal  in  an  emergency or semi emergency basis.
  • Pre operative and peri-operative dialysis will  improve the results.
  • Renal replacement therapy , combined with valve  replacement may be the ultimate therapy .It  could be the most heroic way to save a patient but carries near death mortality.

If ,  there is strong  evidence  to suggest  immune activation ,there could be a role for steroid administration. Literature  does not address this issue . Long term follow up of renal function is required in these patients .

Final message

Renal failure in IE is common and the underlying mechanisms are often complex.Early intervention is the key as there is  almost  “no  option” for   conservative management in this situation.

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Aortic stenosis is one of the commonest valvular heart disease.Degenerative, calcific aortic valve is the underlying pathology . Many of the degenerative aortic valve is thought to be  a sequel to bicuspid aortic valve .The exact incidence of BCAV  contributing to degenerative aortic  stenosis is difficult to determine as many of these leaflets  lose  it’s  identity  . Rheumatic aortic stenosis continues to be a problem in developing world.Though ,primary aortic stenosis  is the  dominant theme , some amount of aortic regurgitation is commonly observed in all these conditions.

Apart from the severity of aortic stenosis  there are two  other important factors that determine the long term outcome.

  • LV function
  • Associated CAD.
  • Timing of surgery

Left ventricular dysfunction is a common  companion in severe aortic stenosis .Once the LV dysfunction sets in , there is a rapid decline in the clinical outcome.Some  of these patients have very severe LV dysfunction (EF< 30%) .

LV dysfunction  ,  underestimates  the true gradient across LV .  Cardiologists are  often  preoccupied with assessment of  true severity  aortic stenosis  in the presence of LV dysfunction .Sophisticated dobutamine stress echo, is supposed to help us.

Unfortunately cardiology literature has  little to offer  regarding the mechanism of  LV dysfunction in critical aortic stenosis

Some of the possibilities are

  1. Sub endocardial  contractile dysfunction   due to long standing high wall stress.
  2. Diffuse myocardial fibrosis , scarring , apoptosis.
  3. Associated CAD and ischemic cardiomyopathy
  4. Finally it could be a “Pseudo LV dysfucntion”  ie , simple mechanical stunning due to high afterload.This is a distinct possibility as some of  these   patients with  worst   LV function  recover fully following AVR.
  5. Combination of the above mechanisms  can occur

How will you determine  whether , the LV dysfunction of aortic stenosis is reversible or irreversible ?  Is viability an issue in LV dysfunction associated with aortic stenosis ?

Even though it is logical to think  LV dysfunction of CAD and LV dysfunction of aortic stenosis  are similar it  may  not be so ! ( Unless the LV dysfuntion  due to obstructive coronary  disease coexists)

Following rules need to be applied in patients with AS and severe LV dysfunction.

  • Every patient with critical aortic stenosis should undergo CAG.
  • The question of reversible vs irreversible LV dysfunction generally need  not arise.
  • There is no better way to predict the recovery of LV function other than the trial of relieving the obstruction.
  • So ,all patients* irrespective of  any degree of LV dysfunction shall undergo AVR
  • If there is obstructive CAD they need to be taken for AVR with CABG

*AVR  is  probably contraindicated , in  systemically ill &  co morbid patients , with grossly  dilated  ventricles. Here balloon aortic valvotomy  and  possibly PVR(Percutaneous valve replacement)  could be an answer.

Final message .

LV dysfunction of aortic stenosis is a poorly understood phenomenon. Since it is very difficult  to predict whether it’s reversible or irreversible , real world clinical experience  would suggest there is no need to predict it at all !  and every one should have AVR  irrespective of their LV function.

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The valve replacement surgery is one of the great innovations in cardiac surgery. The common disorders that require mitral and aortic valve replacement are

  • Degenerative , calcific  aortic stenosis and regurgitation.
  • Rheumatic mitral, aortic valve disease.
  • Ischemic heart disease -Ischemic MR
  • Some cardiomyopathies

The mortality in valve replacement surgeries vary  between AVR, MVR, and DVR.

AVR – 2-5%

MVR 4-12%

DVR  6-15%

Source CTS.net

Determinants of outcome

General factors applicable for both valves

Elective vs Emergency

LV function

Associated CAD /CABG

Co morbid conditions

The following observations  can be  made  in valve replacement surgery

  • Mitral valve function is closely linked to LV function while Aortic valve  is not .
  • AVR  patients always do well than MVR in  the  immediate post operative period
  • Aortic stenosis patients do well than aortic regurgitation .
  • Mitral stenosis patient do well than mitral regurgitation
  • In   DVR  the excess mortality is due to  the addition of MV , not by  AVR .

Aortic valve replacement has better post operative outcome when compared to mitral valve replacement ,Why ?

Aortic valve has only two components namely a  annulus  and leaflets. The prosthetic  aortic valve  replaces both these natural components . Mitral valve has 6 components , prosthetic mitral valve has only two components . Hence  , any prosthetic mitral valve is far inferior to natural mitral valve . The  pap muscle, chordae, and LV muscle fail to assist the artificial  mitral valve.  So , between AVR and MVR   AVR is far perfect  prosthetic surgery and  the hemodynamics   mimic as closely to the natural valve.

Why aortic stenosis patients do better than aortic regurgitation ?

Aortic stenosis  results in severe  LV outflow obstruction .The LV struggles to pump across the obstruction.So , once it is relieved by a prosthetic valve , there is great relief for LV .We know the the aortic valve orifice becomes <1cm2 in critical AS . (Like a pin hole !) .Prosthetic aortic valve at least doubles or triples this orifice and the LV enjoys this sudden relief  and  becomes active or even hyperactive in immediate post operative phase , later  it    settles to a near normal LV function. It has been observed even very severe LV dysfunction associated with aortic stenosis recovers well .

What happens  in AVR done for  dominant or isolated  aortic regurgitation ?

Here the situation  is dramatically opposite.The purpose of  prosthetic aortic valve is  reduce the  aortic valve orifice .

In AR ,  the  left ventricle  is  used to eject  the blood  with ease  across LVOT   without  much  resistance  ,  only to find part of the blood returning  back into the chamber . In  the next beat it does the same and  the cycle   continues for ever .This in due course , dilates the LV  and increases  wall stress and afterload.  LV dysfunction follows .This  takes long time to set in.That’s why chronic asymptomatic AR patients  do so well and they do not require surgery until after the onset of LV dysfunction .(End systolic LV >55mm)

After the aortic valve replacement , the LV suddenly finds  the newly introduced prosthetic valve  a hindrance !. As all artificial  valves  have  less than the natural orifice. LV   takes some time to adapt to the new environment . The EF initially may slightly fall and recovers later.

If pre- operative LV dysfunction was significant the immediate post operative period can be critical.As even a slight fall in EF can result in prolonged hypotension.Many of these   pateint may  require  prolonged inotropic  support.

What are the differences between MVR done for mitral stenosis and MVR done for mitral regurgitation ?

Here again ,  the same principles apply.The Mitral stenosis patients do well following MVR than MR patients.This is because of two reasons .  MR patients  have dilated LV  and may also have associated impaired LV function .A chronic MR is  some   what  a stress reliever  for the LV  ,  as  with every contraction it can decompress a little   bit  . It is an important hemodynamic  fact  ie  ,  presence of   even a  trivial  MR helps the LV to tackle the  it,s  afterload  easily by increasing the dp/dt and also the EF.

So when we introduce a a fully competent prosthetic mitral valve all of a sudden the LV again struggles for some time.

Final message

MVR  patients has less favorable  clinical outcome than AVR .

Coming  soon

How  different is the anticoagulation  protocol difference between AVR  and  MVR ?

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