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Posts Tagged ‘cardiac failure’

Medical science is  nothing ,  but trying hard all possibilities. Most innovations die .Only a fraction will survive .

That does not mean we should not try ! The greatness is in accepting the failure.  The wonder drug which was an analogue of human atrial  naturetic peptide    (BNP)  Nesiritide   , died a peacful death on July 7th 2011 .

Long before , in year 2005 ,  Eric Topal in a hard hitting  Editorial  of  NEJM  wanted to hang this drug .

But it was a case of prolonged  death sentance .

http://www.nejm.org/doi/full/10.1056/NEJMp058139

Should we  pity with the drug companies  and forgive them for delaying it’s  exit ,  enable them  recover the  cost involved  .

Meanwhile , Nesiritide might have died ,  the  concept of  BNP analogues may need to be explored further.

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As the name suggests   dilated cardiomyopathy  would imply  cardiac chambers will dilate , at least some time in the course of the disease .It can be minimal, mild or massive. A new entity called  non dilated cardiomyopathy is also gaining wider acceptance . (That will be dealt seperately )

Logic would suggest , the first chamber to dilate in DCM  should be the left ventricle because it is  facing the direct load of systemic blood. But we also know , whenever  LV is stressed , left atrium comes to it’s assistance .

Left atrium does this    by total self sacrifice ( by all  means!)  increases  it’s  force of contraction, elevating it’s  mean pressure or even increasing it’s rate (AF) .

Like most  other critical questions in cardiology  ,  the factors that determine LV dilatation in DCM ,  is  also poorly understood !

  1. Is it the after load ?
  2. Is it the  muscle mass ? or it’s turgid  or flabbiness ?
  3. Is it the interstitial integrity?
  4. Is it the blood volume ?(LVEDV ,  LV residual volume )

When the issue is complex , it is  usual  to  make the   the unknown  genetic defects  ,  the scapegoat !

As of now the most important determinant of LV dilatation  could be  the behavior of the desmins, the gap junctions and myosins the titins etc

If  the LV of a DCM patient  refuses  or  resists  dilatation what  might happen ? Is it good or bad for the patient ?

Here is a catch .  A  LV  that does not dilate  obviously should be  be good for the patient  is in’t ? Medicine is not that simple.

When   LV  fails to  dilate  it means it has become  too  stiff and rigid    and pass on the  burden to  to LA which  faces the music. And in the process it dilates.This is the reason , we  observe  diastolic dysfunction in vast number of DCM patients.( Currently it is estimated > 75% DCM will have significant diastolic dysfunction )

So , now we can imagine how complex the sequence of hemodynamic stress in DCM that determine the chamber enlargement.( RA, RV  dimension in DCM is a separate issue !)

So now answer this question :  Which chamber dilates first in DCM ?

  1. Left ventricle
  2. Left Atrium
  3. Any of the above
  4. Both of the above dilate simultaneously

The answer must be 3 .

Why  recognising this sequence of  chamber enlargement  in DCM   is important ?

  • It gives us an opportunity to assess the dominant mechanism of LV dysfunction.There are reports , where some  DCMs  have more diastolic dysfunction than systolic dysfunction  .This will have important therapeutic implication.Further , many of the infiltrative   disorders of LV can have features of both DCM & RCM .
  • When a RCM begins to dilate it is usually  a harbinger of terminal heart failure. But,  it need not be always true .  A small restrictive LV  , when  dilates ,   may acquire a  slightly improved diastolic properties , as the  LV becomes more placid . And ,  if it happens the LA size may regress.
  • The role of LV restriction devices like, Acron mesh, Dor procedure, plication  in refractory  DCM is not well defined. All these   modalities actually  adds  a small dose of diastolic dysfunction in these patients who have grossly dilated ventricles. This fact is  very important  , as presence of any preexisting  significant diastolic dysfunction in DCM makes  the role of LV restrictive devices and surgery a big question mark !

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Apart from  acute  coronary syndrome,    cardiac  failure is   the most common clinical  presentation of  CAD. Cardiac failure ,  classically present with dyspnea on rest or on exertion , while angina is the dominant presentation in ACS.  

What if  ,  both these  occur together in an acute fashion ?

Yesif it occurs  together it is called ischemic cardiac failure . Fortunately , this is quiet uncommon . It has   an adverse outcome,  especially if it occurs  as a companion of NSTEMI . Let us see how . . .(  Most of the episodes of cardiac failure  in CAD  means only  LV failure )

For cardiac failure to occur , there need to be a mechanical contractile dysfunction or defect . In CAD population , this can  occur in  one of the following way.

  • Loss of LV muscle (Acute  Myocardial infarction as in STEMI)
  • Mechanical defects (Mitral regurgitation/VSR etc)
  • An arrhythmia (Commonly VT or AF / CHB )  can precipitate  cardiac failure

Apart from these three , there is  an important mechanism of acute LVF, namely ischemic stunning of major part of LV resulting in severe mechanical dysfucntion.This is a dangerous form of cardiac failure (Pathologivcclaly it is thought to represent  contraction  band necrosis !) this occurs in global ischemic situations manifested as gross global ST depression.

So,  there are two types of  ischemic LVF  .  STEMI   occuring due to infarct( ± ischemia ) Other  one (NSTEMI)entirely due to ischemia.

Logically ,  one  may n’t   refer  STEMI related LVF as  ischemic LVF at all  , as infarct has already occured. While , NSTEMI related LV could be the ” True ischemic LVF “


What are the differences between cardiac failure that occur in  STEMI and NSTEMI ?


lvf in nstemi stemi

Is post infarct failure  ( The commonly used terminology  , now out of vogue ! )  a type of ischemic LVF ?

In the strict sense , it is not . Here the dead myocardium , is responsible  for the   failure .To label a  LVF , as  ischemic , ongoing ischemia must  be  documented and further it  should  be shown to  contribute   for the  mechanical dysfunction .

This is of vital importance ,   if you wrongly attribute ischemia  as a cause for  the LVF , the patient may be taken up for emergency  revascularisation .It is not going to help much (Infact , it may  worsen !) as  this cardiac failure is not going to be corrected  .What we require ,  here is an  aggressive medical management  protocol .


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Ventricular remodeling  follows large myocardial infarction .This term denotes to  change in size , shape  and function  of the ventricle   due to altered  myocyte geometry .It is now believed  , this  process begins to occur very early  following a STEMI.(less than 24hours)

lv-remodeling

In which MI remodeling is more common ?

Any MI of large size , especially  anterior  and lateral MI.  Inferior and posterior MI are less affected by adverse remodeling.The incidence is up to 20% of all myocardial infarction ,  if left untreated. Ventricular aneurysm formation and dyskinetic segments can be termed as the worst form of remodeling. The old terminologies of infarct extension and expansion could by synonymous with ventrilar   remodeling .(Note : Every patient with STEMI undergoes some form of physiological remodeling that should not be confused with progressive pathological remodeling , we are discussing  here ! )

What is the clinical impact of remodeling ? How to prevent it ?

Progressive cardiac failure and a  poor outcome .  It may provoke ventricular arrhythmias. ACE inhibitors (CONSENSUS study 1992 )  has since revolutionized  the pharmacological  prevention of adverse remodeling.

How to recognise left ventricular remodeling ?

Many methods are available .

  • 2 D Echocardiography
  • Tissue doppler
  • LV angiogram
  • MRI

These imaging methods diagnose remodeling  only after it manifest* .We know remodeling is a cellular and molecular process .The earliest trigger for remodeling is the mechanical stretch and wall stress on the ventricles.Large areas of necrosed myocardium and  the adjacent normal myocardium sets a perfect stage for eccentric pulling of myocardial segments and unregulated slippage of myocytes.

* Diagnosing fully established  ventricular remodeling  serves ,  no great   purpose as it is very difficult to reverse it by pharmacological methods.it requires complex surgery.

What is the effect of mechanical stretch on cellular function ?

It is well known  myocyte granules secrete Type B  -Naturetic peptide  in response to stretch. It could be a very early sign of adverse remodeling. So monitoring of  BNP may give us an opportunity to intensively treat those patients who are likely to land in progressive cardiac failure.

A baseline level of NT-proBNP >120 pmol/L identified patients  prone for adverse remodeling .Serial measurements showed further increase. It is possible to identify adverse remodeling of LV by documenting fresh elevation of BNP following MI .

Reference :

1 )Nilsson JC, Groenning BA, Nielsen G, et al. Left ventricular remodeling in the first year after acute myocardial infarction and the predictive value of N-terminal pro brain natriuretic peptide. Am Heart J 2002;143:696-702.

2)http://content.nejm.org/cgi/content/full/352/7/666#R24

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Diagnostic issues in cardiac failure : A  febrile pleural effusion in a patient with LV dysfunction .

Is it a transudate or exudate ?  How to confirm the pleural effusion is primarily cardiac failure related ?

When the classical protein criteria is inadequate or prone for errors

Try this more specific marker  within the pleural fluid

N-Terminal Brain naruretic peptide

Pleural fluid NT-proBNP is very useful in establishing the diagnosis of HF-associated effusions, and it confirms this diagnosis . The measurement of NT-proBNP rather than serum to pleural protein gradient is recommended for identifying mislabeled cardiac transudates.

Reff :Biomarkers of Heart Failure in Pleural Fluid. Chest. 2009 Apr 10.

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Dopamine and dobutamine are  the most commonly used inotropic agents in clinical cardiology.

The following table represents a simple comparison of the two drugs.

dopamine-dobutamine

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                                    Competence of mitral valve is vital  for proper hemodynamics of  heart .A trivial mitral regurgitation ,is observed in nearly 10-20% of normal population detected by doppler echocardiograpgy .This is other wise clinically insignificant. In fact , it is expected  , the sonographers do not report this,  as it might increase the patient anxiety.

Can a mildly incompetent mitral valve be a hemodynamic advantage ?

Left ventricle , physiologically can have only one exit, namely LVOT and aortic valve.If there is normal  impedance , at this level (LV after load )  it  is refered to as  physiological .In disease states , as in cardiac failure there is raised after load or LV wall stress.this makes the LV struggle to pump blood into aorta.The more the dilatation the more the wall stress (Laplace law). more the wall stress more the after load.

 The  main principle of management of cardiac failure  for decades  has been promoting  LV inotropism .Now we have realised this is fundamentally a wrong concept, (Except in acute heart failure). Hence the main option available now is to reduce the after load , ACEI do that most effectively and proven to improve survival.

What is the effect of  trivial or mild MR on LV after load  ?

It is a hemodynamic fact for MR  to increase LV contractility  and Dp/Dt  due to a relative reduction of after load.

In patients with cardiac failure , even a mild improvement in LV contractility can give a  symptomatic improvement .

 

09tmr1

Can mitral valve act as controlled safety valve allowing only a trivial or mild MR ?

This may be difficult . But it happens naturally in many of our patents in cardiac failure .

Probably , these are same  patients who come under the 20% incidence of physiological  doppler  MR .Other group could  form the  functional MR*

We have found, patients with  DCM  with mild mitral regurgitation tolerate excercise better than patients who have very competent and rigid mitral valve.It is presumed a mitral valve which gives in a little bit , decompresses the LV with a symptomatic benefit.But if the MR , is occurs in an eccentric path or it results in significant volume burden the potential advantage becomes a liability.

Related issues

*Functional mitral regurgitation. Functional MR is said to occur , when patients with cardiac failure, and resultant dilatation of mitral annular ring, and lack of opposition of leaflets

While milder forms of MR are well tolerarted  , when it occurs  acutely ( even if it is mild) ,  it can be dangerous and result in sudden pulmonary edema  .This usually happens in acute MI or infective endocarditis etc.

 Final message

  • Minimal or mild  mitral regurgitation without any significant volume overloding  in some of the patients with dilated cardiomyopathy  could bring  a hemodynamic advantage .
  • So one may not unduly worry about , a mild MR (central jet) in patients with DCM.It could be after all a safety exit for overstrained LV

We will report the results of the ongoing study about the impact of presence /absence    of  mild MR on the 6 minute walk test in patients with dilated cardiomyopathy.

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