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Archive for the ‘Cardiology – Clinical’ Category

Why is identifying false and true lumen important ?

This helps the interventional cardiologist to plan the specific therapeutic procedure .

aortic-dissection-table

Is it really difficult to differentiate the two ?

One may wonder , why is that  difficult  to identify  the true aortic lumen by echo, after  all  , the LV empties the blood into true aortic lumen ! Yes  , in aortic root dissections  identifying the true from false lumen is rarely an issue.

aortic-dissection-4

The issue becomes  important and complicated as the propagation of dissection goes in a random and erratic way into the ascending aorta and arch and downwards.The situation could further get  complicated  by the fact there could  be multiple communication between the two lumens .Some of these communication are  hemodyanically patent others form  a simple anatomical continuity.The size and the configuration of true and false lumen are not uniform it is highly  variable.In the aortic root the size of the true lumen is usually  large and when it reach the descending aorta  as in type3 the whole thing could be reversed.

The enigma  of  these lumonomics , is that some of the native branches of aorta , would  either be, subtended by false or true lumen. This is a real tricky issue for the surgeons . If a aortic vessel branch (Say bronchial artery . . .) is perfused successfully by the  hemodynamically active false lumen should we meddle  that  at all ?


circumferential-dissection1 What are the types of false lumen ?

Usually single septae divide the aorta into two , one false lumen and true lumen.There can  be other types.

Triple lumen aorta :This is usually seen in the aortic root following dissection .Usually there is two false lumen and and one true lumen in the centre

Double barreled aorta: A circumferential   aortic dissection with a central true lumen surrounded by a  circumferential false lumen  mimicking a double barrel on within the other.

aortic-dissection

What determines blood flow within false lumen ?

  • Site of  intimal tear
  • Length of tear
  • Plane of cleavage  . Superficial  subinitmal tear with minimal  medial thickness is likey to give in easily  as the blood  dissects the plane  so it more often manifest as a flap  rather than sustained  dissection
  • Number  of exit points (It is often assumed  aortic dissection  there is typically one entrance and one exit point .

but  more  often  multiple exit points can occur. Some points can have both two and fro flow as it may act as both as entry or exit points

What  is the importance of identifying  point, exit point , true  lumen false lumen etc ?

  • This is vital for planning   repair  of  the segment
  • optimising side branch blood flow
  • some time one may require to create an exit point  for providing useful thermodynamics   of false lumen that could give branch to a vital area.

Why false lumen is  prone for thrombosis ?

  • Sluggish flow within false lumen
  • Plane of cleavage of intima  and media  create an  irregular surface that  trigger  tissue factor mediated thrombus.
  • Free floating cob webs   intimal  remnants may accelerate thrombus formation

What is the clinical significance of  finding  a thrombosed false lumen ?

Large thrombus can occur within false lumen.The presence of which , sometimes an advantage as

it limits further progression of false lumen (An organised thrombus is sort  of  natural  stent graft !)

many of these patients do well with medical management.

C J Sanderso Thorax 1981;36:194-199;

Can thrombus occur in true lumen also ? How common it is ? If so what is the mechanism ?

Yes , but it is rare  as the velocity  is  more .But it can occur in following situations.

  1. Preexisting atherosclerosis can be  a milieu for  insitu thrombus
  2. Thrombus in true lumen  can occur at the entry point where there is intimal tear ,  which  projects  into true lumen. that can  deccelerate the  flow(Rare)
  3. Thrombus in the false lumen may project into true  lumen  through another tear.
  4. Migration of false lumen thrombus may occur distally and reenter the  true lumen.

What is a cobweb ?

Cob web are the residual ribbons of dissected internal elastic lamina of aorta .
They are variably called as aortic bands, strands ,  septae, flaps etc.

What is the significance of the junction between false and rue lumen ?

The classic false lumen is crescent shaped. True lumen is either round or oval(Gibbous moon)
Tunction between false and true lumen has some characteristic feature.It mimics  the letter Y. The mainstem of Y correspond to main(  Normal full thickness)aortic  wall of the true lumen.The  oblique lines represent the outer wall of the false lumen and the septae dividing true (Fig 3)

dissection-41

What is the natural history of false lumen after surgical correction ?

Surgeons often leave the false lumen insitu , especially beyond the arch in type A dissection.

If false lumen is large  >70% of aorta , secondary dissections may occur in the long term.

Which is the best imaging modality  for  assessing dissection of aorta  ?

Even though MR angiogram and CT scans are shown to be good imaging tools in the evaluation of  dissection of aortamany practical issues creep in doing MR or CT angiogram.Many of these patients are too ill and will be on multiple arterial and venous lines Doing an MRI is  too dificult a task .Further these imaging modalities require a another arterial access .Requires contrast injection and  CT has in addition , radiation hazard.

TEE is a simple investigation can be done even in unstable patients in the bedside .Further also help us  us evaluate the aortic valve function and associated complications of dissection. TEE will be very useful peroperative also in assessing the repair.

*But MRI  and CT can give a long axis , saggital cuts of aortic dissection depicting the entry and exit points in a single image

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Coronary stents have revolutionised the management of CAD. Stents are metallic scaffolding devices that help keep the atherosclerotic plaque  plastered within the coronary arterial wall.Thus it gained the name angioplasty. Stents have aradial strength that  exerts a constant force on  the plaque . Since metals are unfriendly partners for coronary artery , we need to have minimum metal within the coronary artery.The stent struts weave around the lumen generally the stento/ artery area ratio should be as less as possible (15%).

But this has a trade off .The uncovered area of plaque tend to project into the lumen .This is many times not significant.But can be a problem if the plaque is very soft and bulk of the lipid core may reenter the lumen.this event is called plaque prolapse.

plaque-prolapse

What is the time taken for plaque to prolapse ?

Generally it is late event.But it can happen immediately after the procedure also.

Which type of lesions are more likely to have plaque prolapse ?

Eccentric and complex lesions especially with overhanging edges are prone for prolapse

What is the sequale ?

It can be benign.If there is a erosion due to stent struts can precipitate an ACS.It progresses into instent restnosis in many.

What is the angiographic appearnce ?

Angiographically it often appears as luminal  irregularity withi stented segment .

Many times , it may appear as a filling defect also.

Is there any specific issues in plaque prolapse in drug eluting stents ?

Coornary artery is not drugged uniformly by the drug eluting stents.In fact contact  lines of metalic struts  , through it’s micropore oozes the drug with polymer.Pathological studies have revelaed non homogenous drug penetration and resultant irregularity on the plaque surface.This could amplify the plaque penetration preferentially in few areas.

How to manage plaque prolapse ?

It should be managed as any other instent restenosis.Plaque resection with atherectomy devices has not solved the problem to the desired levels.A second stent is the most common approach advocated by the cardiologists.(Whic is not ideal though !)

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Prosthetic valve obstruction is an important complication of artificial valves.The incidence of prosthetic valve obstruction  is  estimated  to  be  4% per year.

  • Pure thrombus 75%*
  • Pure pannus 10%
  • Combination of pannus and thrombus 12%

Data from Deviri (J Am Coll Cardiol, 1998; 32:1410-1417 )

pannus-2

*Note statistically you are going to be right 3 times out of 4 if you diagnose thrombus over pannus

Pannus  literally means a hanging flap of tissue. It is is a membrane of granulation tissue as an response to healing.It can  occur anywhere in the body. When it occurs in the prosthetic valve tissue interface it has important consequences.It  is  same  as excessive scarring , ( something similar to keloid formation ) .

pannus

How do they clinically present ?

Prosthetic valve thrombosis is usually a acute or sub acute event as thrombus formation rapidly deteriorates the clinical situation.Pannus brings a patient with the complaints of chronic progressive dyspnea.(This rule is very subjective  but . . .)

What are the determinants of pannus growth ?

Time is the major determinant. minimum period required is 12  months. It is a avascular mass.It should be noted  a  injured pannus can predispose  a thrombotic process and a chronic thrombus  can trigger intravascular   growth factors  that promotes pannus growth.

What is the direction of growth of pannus in prosthetic valve ?

The pannus grows , usually in the tissue valve interface.It tracks and creeps along the suture lines .Generally this does not encroach the valve orifice or chamber sapce  , but occasionally the hanging edges can hit upon a leaflet.This is more common with tilting disc on the side of minor orifice. When excessive it can make a valve leaflet almost standstill.

How common is pannus formation in starr edwards valve?

Is relatively uncommon as the dynamic ball periodically interrupts the process of pannus in growth within the orifice.

Final message

Why is recognition of pannus important ?

Prosthetic valve thrombois is amenable to thrombolysis and it should be proptly differentiated for pannus.This is many times a difficult excercise, but the above observation will be helpful.

Further reading

http://content.onlinejacc.org/cgi/content/full/32/5/1410

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To further understand women's heart click on the title

SCD  continues to be  the major mode of  death of  our  population . Millions of men die every year instantly .The commonest mechanism is due to primary ventricular fibrillation following an abrupt closure of coronary artery due to a thrombus.Most die , within few minutes of the event, some  before reaching the hospital , few within the ambulance  and an  unlucky few die on the CCU bed  or cath lab table even after getting the best treatment.

If we analyse the data, there is a  surprising fact !  Men form the bulk of these SCD victims.In our experience , out of 100 cases of consecutive  in hospital primary VF only  6 were females , indicating  an important  biological phenomenon to be studied.The data for out of hospital primary VF is more difficult to get , but the  log records of EMRI and emergency rescue team consistently confirm the male preponderance of primary VF .

How  does the female heart enjoys this relative immunity from primary VF even as the blood supply is acutely compromised ?

The answer  is  not known . If we are able to  decode this , one can replicate the same  model in male .

The QT paradox and incidence of primary VF

QT interval represents a combination of  electrical depolarisation and repolarisation .It is a well established   scientific  fact  that  women have   relatively  prolonged QT interval .This  is determined by evolutionary biology and  inherited characteristics of  potassium channels  during myocardial repolarisation

In simple terms, the female heart  knows how to relax slowly and prolong the electrical relaxation time.(Not mechanical)

It is also a well known  fact ischemia mediated a prolonged  QT interval is a trigger for dangerous ventricular arrhythmia.This ischemia induced QT prolongation is less pronounced in females than males as the baseline QT itself is slightly longer in women.The percentage increment of QT interval during acute ischemia is significantly higher in male .This could be one reason for the preponderance of VF in men

The billion dolor question and a real challenge for the cardiologists is

How to make a heart electrically inert during ongoing ischemia ?

  • Pain is also trigger for primary VF due to high adrenergic tone.Prompt control of chest pain make VF less likely.
  • Lignoacaine a myocardial anesthetic if administered quickly can prevent many of the primary VF.

And now , shall we  think little wildly !

What if , if  we administer lignocaine spray straight over the (or sublingually ) in every patient with  chest pain

as like a sport injury and try calm down the heart electrically !

Also read

1.Lignocaine  the forgotten hero .

2.View this video -Ignorance based cardiology !

Reference

Arrhythmias and sex hormones


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Post myocardial infarction revascularistation either by PCI or CABG forms the bulk of the coronary interventions world wide.There has been considerable controversy in selecting the patients for the procedure.

Certain basic rules are to be applied.

  • Never do any thing on a totally asymptomatic and fully functional patient.(Functional , means good exercise capacity of atleast( 10Mets).Just medical treatment with good doses of statins, beta blockers will do.
  • If a patient has persistent angina  following MI  ,the issue is relatively simple as  they are  candidates  for CAG  and intervention .
  • The issue becomes little complex when the primary complaint is breathlessness and echo showing  LV dysfunction.

This dilemma is due to a  simple fact

coronary revascularisation has a  great impact in relieving angina but has  less impact in reversing

left ventricular  dysfunction

So,  how do you approach a patient with LV dysfunction and exertional  breathlessness and absolutely no chest pain ?

  1. Do a  CAG
  2. Assess the lesions if any (Some times,  to our surprise there may not be any critical lesions at all ! )
  3. If there is / there are critical lesions try to corroborate with infarct segments.(Use Echo for this correlation)
  4. Don’t bother much,  if a  vessel has a lesion  that is supplying a scarred myocardium.
  5. If there is gross LV dilatation, mitral regurgitation and LV clot refer these pateints  may benefit  from surgical management

One of the rules written by the cardiology community over the past few decades has been

We must document viable myocardium before doing a revascularisation procedures on them.

This rule was self imposed ,  to prevent inappropriate revascularisation in  post MI population.

So , a  gamut of investigations (Both invasive and non invasive came into vogue) to identify viable myocardium in post MI population. Stress echo, Thallium-sesta MIBI, PET  to name a few .

Even after liberal usage of these invesitgations , we realised ,  the confusion in the  optimal selection of candidates for revascularisation has not settled.

In fact,  the correlation between viabilty and subsequent interventional benefit is  inconsistent .Not withstanding this  issue  ,cardiologists inspite of the negative results of OAT and TOAT trials ,  started  opening or by passing any occluded vessel irrespective of viability status.

Unanswered  &  Unasked questions in myocardial revascularisation ?

1.Why viable myocardium is viable even in the adverse compromised vascular  environment ?

It  is viable for the simple reason it has some capacity to be alive . By it’s inherent survival capacity (Survival of the fittest ) or it somehow gets the nutrients by cell to cell perfusion.

2. It is viable allright  ,  why it is not contracting ?

Because ,  it is biochemically and metabolically alive (Can be documented by FDG PET scan mismatch ) but it can not synthesise adequate ATPs to make the muscle contractile.

3.”Viable myocardium is viable ” what more you want from it   ?

Simple viability is not suffice . How to make it mechanically active and contractile ?

4.Is viable  myocardium    synonymous with ischemic myocardium ?.

No,  it is not (Contrary to the popular perception ) .

5. Is it not  common to find dysfunctional segments with good TIMI 3 flow ?. So what is the purpose to document viability ?

It is not suffice to simply document viable myocardium but it is an absolute necessity to prove this viable segment is also  critically ischemic .

7.If angina is  a sign of viabilty why most of viable myocardium is painless ?

This again confirms the fact , much of the viable myocardium in the post MI phase is not ischemic but” still dysfunctional” waiting for healing time. This concept  was  introduced with great fanfare* as  stunned myocardium ,  20 years ago , which was subsequently rejected my mainstream cardiologists , as this concept tend to  restrict the  freedom of interventionists. * Even though ,the concept was genuine and proven scientifically !

6.Are we  certain , the  viable ,  non contractile myocardium  (Which we painstakingly document )  will get back the contractility once the  segment is    revascularised?

Absolutely not. (With lot of PET study doumentation )  This,  we can not guarantee even in ischemic, viable segments  ,  while in the  non ischemic, viable segment it is all the more unlikely.

7. What are the chances of these viable but  non contractile myocardium  regain the contractility  by natural course ?
Very significant chances .In fact every patient recover some LV  function spontaneously over time .

Final message.

  • Revascularisation is non controversial in patients with angina
  • In patients with  primary symptoms of dyspnea  ,  it is less effective and documentation of myocardial viabilty per se will not guarantee successful outcome following revascularisation.Out come depends on  multiple factors .

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Why PCI  in   left main CAD is considered  an inferior modality than CABG ?

CABG is superior to PCI for the  simple reason it provides complete revascularisation virtually in all  patients with LMCAD , while PCI is possible only in a fraction of patients with LMCAD.

If  we take 100 patients  with left main  disease may be ten (At best !)   would be  suitable for PCI ! In other words PCI is contraindicated in vast majority of LMCAD  by technical criteria alone , while there can never be a contraindication for CABG in patients with LMCAD.(Except  when , comorbidity precludes surgery )

Why  PCI in  LMCAD difficult ?

It is  dependent on  technicalities

CABG does not tackle a lesion,  it simply avoids it  and by passes it ” No great brains required”

while PCI takes on the plaque frontally ,  in the dangerous  terrain of  left main artery  itself !

so,  much caution,  planing ,  logistics are required . Further ,  if there is a complication there is a potential

for catastrophe  as the only  supply line is cut off . This is the reason , cardiologists were worried to try this on

unprotected left main. (Protected LMCAD refers to left main disease following CABG  wherein atleast   LAD or LCX is  grafted )

Points to ponder in LMCAD

  • PCI is suited for isolated discrete LM disease.In realty  this is seen in less  than 5-8 % CAD.
  • LMCAD is very often associated  with  critical and multivessel distal CAD . So these patients will be candidates for CABG.
  • Left main ostium or LAD ostial  involvement makes PCI a tougher exercise
  • Calcification is more common in LMCAD that  again makes PCI difficult.

The following article in Feb 2009 is a major blow for proponents of  PCI for left main

http://circ.ahajournals.org/cgi/content/extract/119/7/1013

left-main

http://content.onlinejacc.org/cgi/content/abstract/51/5/538?ijkey=84c977d189e84327c3abbd4c1228de17dd99048a&keytype2=tf_ipsecsha

Final message

  • Conquering left main disease is an interventionist’s  ultimate dream.
  • But, before that they have  to tackle the bifurcation lesions .This is of vital importance, because 2/3 rd of left main  patients have  some form of bifurcation lesions. Current techniques , hardware  and outcomes are far below the idealistic solutions in bifurcation lesions.
  • Till that time ,  CABG would  remain the only choice for all , but for  a small fraction of isolated  left main disease where PCI may be possible.

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Lignocaine , probably has saved more lifes  world over  than any other cardiac drug .

It was the only choice for ventricular tachycardia  till 1990s, both in pre and post  thrombolytic era.Every coornary care unit has reverted tens of thousands of  unstable VTs with this simple and cheap intravenous drug.the utility value of lignocaine is not limited to ischemic VT alone it is effective in in almost all forms of VT.It was classically administered in two or more boluses followed by an infusion.

What happened to this wonder drug  with great performance record ?

The  power of   statistics , and inappropriate interpretation by the scientific community  has left a serious blow to this wonder drug .Now the drug has been made redundant, and mainstream cardiac literature has made everyone feel  guilty , if  anybody  uses this drug for VT .

Why did lignocaine lose the battle ?  The reason is three fold

  1. The advent of  much fancied Amiodarone
  2. One negative study  for antiarrhythmic drugs in post MI period (CAST) 
  3. And two so called  positive studies  for Amiodarone (ALIVE & ARREST) has sounded the death bell for this drug  which has resuscitated millions of life !

CAST study http://content.nejm.org/cgi/content/abstract/321/6/406 

All , CAST  said was routine suppression of  asymptomatic ventricular arrhythmias  in the post MI period is unwarranted. But you know , how this  world interpreted it  “Lignocaine  has no role in ventricular arrhythmias in post MI setting ”  The most funny thing  was  lignocine was never used in CAST study .

The  studies involving one to one comparison  of Lignocaine and Amiodarone (ALIVE and ARREST study) was also not interpreted  properly.These studied only shock resistant VTs. What about the role of lignocaine where defibrillator was not available ?

Link to ALIVE and ARREST  read and make your own conclusion.

http://content.nejm.org/cgi/content/abstract/346/12/884

http://content.nejm.org/cgi/content/full/341/12/871?ijkey=8fa241f3cebb86a177632ec6ccadfb5a3ded7bc2

 Final message

  • Lignocaine is not  only a topical anesthetic  , it is powerful and gentle myocardial anesthetic when administered in post MI period.
  • With this property it  successfully cardioverts and prevents dangerous ventricular arrhythmias.
  • Time tested and worthiness proven.
  • While , we are made to believe  the success rate of  Amiodarone in VT is far superior than ligncaine .It is a falsehood.
  • Any experienced cardiologists will recognise ,  many times even  Amiodarone resistant VTs often respond to Lignocaine .
  • The fact of the matter is , without a good quality  one to one study  , lignocaine was ditched. One reason for this could be  Lignocaine ,  is a generic drug and has no market value.

Let us take home , the message (scientific or unscientific ! ) Lignocaine still has a great role to play in the management of dangerous ventricular arrhythmias .The only caution is ,  it should not be used routinely and indiscriminately in all asymptomatic patients with  VPDs or nonsustained VT . (Acknowledging CAST conclusion.)

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Cannon waves occur classically, during  ventricular ectopic beats .(Commonly irregular) regular cannon waves occur during Junctional tachycardias with 1:1 VA conduction

Cannon like wave may appear  in the jugular vein if the VPDs is timed in a such a fashion ,the atrial systole occurs with a closed AV ( Tricuspid and mitral valve ) so the atrial  contractile wave is reflected back into the veins.This not only happen in right atrium but also  in the left atrium , but the cannon waves are sent into the pulmonary veins , which is not visible. As by  tradition  cannon waves are  meant to be seen only in neck veins , we rarely realise   the importance of such waves in the pulmonary veins.

There must be some significance for this  abnormal pulmonary venous waves  which  travel  in a retrograde fashion.In fact , with  the advent of echocardiography, we realise  pulmonary flow reversal is an important contribution for raised PCWP.

The dyspnea during multiple  VPDs can be due to

1.Transient Mitral regurgitation and resultant elevation of PCWP.

2.Pulmonary venous cannon waves and  it’s effect on  J receptors.

3.Many of the intermittent  episodes of  dyspnea  (Especially paroxysmal nocturnal dyspnea ) , other wise unexplained could be due to this pulmonary venous cannon waves.

4.It also need to be studied how this pulmonary venous cannon waves distribute themself into the 4 pulmonary veins.

//

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Angina is classified in many ways .The most useful , clinical classification is stable and unstable angina . While  ,the former generally is considered   innocuous  the  later conveys a sinister  signal to the patient as well as  the physician. 

Why stable angina is  stable ?

In stable angina

  • The patient knows how the pain is going to behave by his past experience.
  • Very predictable .The patient knows at what distance it’s going to come
  • He also knows when  it will disappear.(For some , with rest for others with nitrates)
  • He also knows where the chest pain will radiate.
  • If some thing is unusual it is unlikely to be  stable angina , also any  first episode of angina is considered unstable as one wouldn’t  know how the angina is going to behave !

How is that stable angina has such a learned behaviour ?

The main reason for  the beningn nature of  stable angina is the coronary artery has “stable plaques”

Stable plaques produce stable angina  ,Unstable plaques cause unstable angina

Stable plaque s restrict blood flow only at times of  increased demand( ie supply side ischemia.) There is no thrombus in these plaques.As soon as the exertion ends the angina is relieved.So in chronic stable angina, the patient is stable, the angina is stable , the palque is stable , the coronary blood flow is stable.

Unstable palques have erosion and thrombus , and it interferes with blood flow even at rest .So in  unstable angina, not only the angina is unstable , the plaque is unstable  ,coronary blood flow is unstable. So it is obvious unstable angina , may not be relieved by bed rest.It needs intensive treatment.

Is there a overlap between stable and unstable angina?

Yes. In fact it is more common than we realise.

Read this post https://drsvenkatesan.wordpress.com/wp-admin/post.php?action=edit&post=2177

Related topics

How is a stable palque converts into a unstable plaque ?

How do you identify these vulnerable plaques ?

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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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