Archive for July, 2009

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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It is the  embryological remnant within right atrium  often observed as , mobile strands within RA extending fromIVC orifice to IAS. Some  times  it is difficult  to differentiate from eustachian valve  of IVC.The network is formed by collagenous material  and mimic valvular tissue

chiary network echo


2% of general population . ( Means 10 crore persons  in our world ! )

What is considered  a benign echocardiographic observation for long  ,  may not be innocuous  . It  can predispose to certain clinical events , although rare.

  1. Mistaken for right atrial mass
  2. May produce  innocent murmur
  3. Catheter entrapment within RA
  4. Infective endocarditis of the network , and tricuspid valve
  5. Abnormal P waves and trigger for  atrial tachycardia
  6. Disrupted chiary network  prolapsing into RV
  7. Associated  foramen ovale  may induce  streaming  .This maintains  an embryonic right atrial flow pattern into adult life and directing the blood from the inferior vena  cava preferentially toward the interatrial septum





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The right ventricle  is a unique  chamber of the heart . It is the anterior most chamber and  triangular in shape.  Even though  the walls of RV are  not  clearly demarcated ,   it does  have  anterior ,  posterior, and lateral free surfaces   . Anatomically it has a inflow  body, apex and outflow portions . The apex of right ventricle , blends with the lower IVS at an acute angle.

How does RVH occur anatomically ?

The anatomy of RV is such that  it does not allow  it  a concentric  RVH ( like LVH ) . In fact , there is a  disproportionate free wall , anterior  wall   hypertrophy  many  situations  like  PHT/Pulmonary stenosis. The  infero posterior aspect of RV rarely show hypertrophy.

Since RV is the anterior most chamber, located just beneath the left border of sternum   RVH brings the RV  further closer to chest wall .This makes the V1 lead to show  tall R in V1.

What happens in RVMI ?

Unfortunately, when we  refer to RVMI , we generally do not make any efforts to locate or estimate it’s  size.  Since RV has , anterior , lateral and posterior surface  , the site  and  the  extent of the  mI will have a major impact  on the  ECG  features .

Most often  the RVMI occur as a  part of infero posterior MI  .Hence ,  it is uncommon for the anterior surface of RV to get involved.  But ,  it can be involved if  RCA gives of a   large RV branch  that reach the anterior surface of RV.

Anterior RVMI can occur as a part  of LAD MI  , if a large conal branch cross the RV surface.

What prevents the lead V1 from showing the  ST elevation of RVMI ?

  • Most of the RVMI do not involve the anterior surface of the RV so , less chances for ST elevation
  • Further , if a true posterior wall  MI  occur as a part of  RVMI (Which is often the case !)  V1 can never  show ST elevation  as the  posterior MI  tend to have a ST depressing effect in the V1, V2 leads.
  • Extensive IWMI , can have reciprocal ST depression in V1-V2.This again , prevents V1 lead to show the ST elevation

So many times , even though V1 lead is just sitting over the chamber RV it fails  to  pick  the  ST elevation forces of RVMI

Advantage of V4 R ?

V4R records remote RV forces , as these  signals are not contaminated by the inferio posterior ST forces. Hence  a  1mm ST elevation in right sided chest leads have good sensitivity  and specificity to diagnose RVMI .

When can V1 show ST elevation in RVMI ?

If the RV anterior wall is predominantly involved (Ie Anterior RVMI ) ST elevation can occur in V 1 like a anteroseptal MI.

rvmi ecg

Rarely a q RBB can occur in V1 in isolated RVMI.

Final message

V1 lead , though anatomically proximal to RV has less value in diagnosing RVMI since this lead picks up  Infero posterior  negative ST forces  and  the anterior  forces of RVMI get neutralised . So relying on lead V1 to diagnose RVMI is not adviced , except when  the anterior surface of RV is predominatly  involved.

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