Cardiology Animations : Mitral para-valvular leak

Mitral para-valvular leak

How to manage para valvular leak ? 

Does  the terms  peri  & para valvular leak mean the same ?

Coming soon  . . .

Mean while , read this article from ESC journal  for an excellent discussion on the topic .

1. http://www.escardio.org/Para valvular leak

2. The ultimate  reference on the topic of prosthetic valve assessment by Echocardiography  http://www.asecho.org/files/public/pvtext.pdf

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Essential facts about EUROSCORE

CABG surgery is the commonest cardiac surgery done world wide .Right from the days of CASS study the  CABG was considered a major traumatic surgery to relive a small block in a coronary artery  (Not exactly relief  . . .it  just by-passes )

However , for more than two decades  till early 1990s CABG ruled supreme.Ever since coronary stenting grew in an  exponential fashion  the outcome of CABG  needed scrutiny .Surgeons had a compulsion  to explain  the world , CABG indeed has a  acceptable risk benefit ratio in the management of CAD .

Thus came the EUROSCORE  . First developed in 1995 .The initial score used a simple additive risk next it was modified

with logistic regression .

Limitations

Can you withhold  a surgery on the basis of high EUROSCORE  ?

Is it scientifically validated ?

EUROSCORE gives us  30day mortality

What is the acceptable EUROSCORE for CABG?

http://ejcts.oxfordjournals.org/content/early/2012/02/28/ejcts.ezs043.abstract

http://www.biomedcentral.com/content/pdf/1749-8090-4-32.pdf

What is the major limitation for EURO-SCORING system ?

It is ironical the most important determinant of any surgery is  the surgeon’s competence and institutional expertise in handling emergencies  and financial affordability  .They are  not included in the scoring .  This makes the EUROSCORE in most of the developing countries including India a futility .

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An unpleasnt debate with a cardiac surgeon : How to manage severe mitral stenosis with Mild to moderate Aortic regurgitation ?

A 32 year old unmarried female with rheumatic heart disease   presented with class  3 dyspnea . She had severe mitral  stenosis with significant calcification , subvalvular fusion , and  a LA appendage clot . She had an aortic valve  which showed mild to moderate AR*  was  and  mild  Aortic stenosis ( Peak  Aoric gradient 30mmhg ).LV diastolic dimension was 40mm and systolic 26 mm .LA was huge 48 X 56 mm  EF was 66 % .

* The patient was having three echo reports done in various parts of the state ranging from mild  to severe  AR . I did the echo myself and I  was convinced  ,  it can at best termed as Mild AR . Let us take it as moderate AR for discussion  

To my surprise  , this patient  was   being planned for double valve replacement . (MVR  and AVR ) .

I agreed with MVR since the valve was completely  damaged and neither PTMC or mitral valve repair  is possible.

However  , I was taken aback   , how can  one  plan for a  AVR for mild aortic valve disease ? I  asked the surgeon  ?

The answer was even more a shocker to me .

Since we are  opening the chest for MVR it is better to replace Aortic valve as well . Since  repeat surgery can be avoided .

The surgeon seemed to be very much convinced about this argument .

I asked him ,   is the mortality /morbidity due to DVR is too high  to take a risk .

The LV dimension is absolutely  normal (In fact it is less than normal !)  so  the AR is definitely not significant .

The surgeon was in no mood to leave me . He argued ,  Since the mitral stenosis is severe , the AR is  probably underestimated .   ” We have quiet a few experience of AR worsening after MVR” ? he asserted !

I still fail to  understand  the reasoning of the surgeon .

How is that ,  indication for AVR could vary if it is  accompanied by  mitral valve disease . If the same patient has  isolated moderate AR  AVR is  forbidden  . Poor patient !

By the way , we have problems with our patients as well .I recall an event ,   a  disappointed  patient’s  spouse  arguing  with his the doctor for not fulfilling his Initial  promise of  replacing two valves . We are living in difficult times , I agreed with the surgeon !

Do we have  alternate solutions ?

1. Assess on table after MVR by TEE if the AR seems worsen proceed with  AVR .
2. Modern technology might answer .Let us dream  TAVR for rheumatic valve . . . not too far ?

*Transcutananeous Aortic vale replacement .

Final message

Cardiologists and cardiac surgeons should take extra care before finalizing a decision on DVR in any combined valve disease. It may seem  easier to replace two valves . Please spend few moments silently and think about these young men and women  . Valve replacements are  not like replacing  worn tires of your car.  Do not  burden the heart with multiple artificial valves without a real need for it !

The rate of progression of Aortic valve disease following MVR  can be slower than we think . With surgical techniques and  expertise   improving every year ,   repeat aortic surgery may be done safely in selected few ,  in case it becomes necessary !

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This PARTNER would give sleep less nights to our cardiac surgeons !

Cardiologists are  closing in ,  trying to capture the final frontiers. The  trans-cutaneous Aortic valve Implantation now has  a two year follow up. (NEJM March 2012  Issue) . The results are encouraging .

While two companies are fighting for the supremacy in TAVI ,   the real  threat is for the cardiac surgeons. Currently Edward  Sapiens  has an edge over Medtronic core valve as it  has a provision to redeploy or fine-tune the  final geo- position.

Reference

PARTNER 1

PARTNER 2

Medtronic core valve

Open access  article  by Martin Leon

http://www.rmmj.org.il/userimages/22/1/PublishFiles/25Article.pdf

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When LIMA terminates with multiple branches . . . Is there strong reasons for surgeons to rejoice ?

I recently came across an unusual LIMA  arterial  branching pattern .

Random thoughts

• A naturally dividing LIMA faciliates multiple sequential grafting of LAD or diagonal branches.
• As branches steal the LIMA flow it is not good for the patient
• Surgeons struggle to clip the branches.
• A branching LIMA has tendency to have  small diameter (As in the above patient )

I need a surgeons Input here.

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The “Grand -father” of interventional cardiology

Who is the father of interventional cardiology ?

William Rashkind a cardiologist from Children’s hospital, Philadelphia in 1966  probably is the first person who thought it was indeed possible to use a wire and balloon as cardiac therapeutic intervention .When surgeons were groping in dark with  sick cyanotic new borns with dTGV , He along with Miller executed their idea.

It was published in JAMA

How the Rashkind  has revolutionized  our approach to congenital  heart disease  is evident from the current guidelines in 2011.

The procedure has since evolved with improving hardware and we are able to ferry a blade into the IAS for cutting .

Current  recommendations for Atrial  septostomy

It is primarily useful

1. Atrial septostomy  to enhance atrial  mixing (eg, transposition of the great vessels with restrictive/intact atrial communication) or to decompress the left atrium
2.During Extra corporeal membrane oxygenation (ECMO)   to decompression   of left atrial hypertension

3.If there is poor cardiac return from ECMO  circuit  low venous saturations  (Class 1 Evidence  C)
It may also be tried in  (Class 2 )
1.  Hypoplastic left heart syndrome  with  restrictive atrial communication.

2.  Static balloon dilation of  l synthetic / bioprosthetic  IAS  (eg, Gore-Tex)

3. Tricuspid atresia with restrictive atrial  communication

4 .Pulmonary atresia with intact IVS

5. TAPVC with  restrictive atrial communication.

6. Primary pulmonary hypertension / Eisenmneger VSD/PDA .(Occasionally useful )

Reference

http://circ.ahajournals.org/content/123/22/2607.full.pdf+html

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Mechanisms of rheumatic mitral regurgitation

Mitral regurgitation is  one of  the most common lesion of rheumatic heart disease .Mechanism of MR in acute rheumatic fever is different from chronic rheumatic heart disease.

Acute Rheumatic fever

The following mechanisms contribute to MR of acute rheumatic fever

1. Edema of leaflets (Carey Coombs murmur )
2. Valvulitis
3. Small verrucous  vegetations (See Image )
4. Acute LV dilatation in fulminant cardiac failure.

* Note  : Acute rheumatic fever in its first episode can never  cause stenosis  however fulminant the fever may be  .There is no acute mitral stenosis .But ,  during recurrence and reactivation some amount of stenotic process may occur.  Still ,  recurrence and reactivation are more often related to significant MR rather than MS. ( Isolated mitral stenotic lesions  rarely  give h/o recurrent rheumatic fever )

Chronic rheumatic  heart disease

As the mitral valve gets progressively damaged  any combination of MS or MR occur .The following mechanism are involved in  the genesis of MR. (Pathology of Mitral stenosis is not discussed here)

1. Chordal shortening, tethering , pulling , prevent proper co-optation
2. Chordal lengthening
3. Chordal disruption (Minor > Major )
4. Prolapse of either AML or PML (Not both ,unlike myxamatous MVPS)
5. Infective endocardits  of  leaflet
6. Perforations of  leaflet
7. Annular  dilatation
8. Fibrosis of posteromedial/Antero-lateral   pap muscle(Rare )
9. Left atrial pathology

* The direction and the  width of MR jet is  related to the mechanism of MR.

If there is chordal shortening due to fibrosis  of mitral valve  co -optation plane is altered . The degree of chordal shortening , pap muscle fibrosis (rare)  symmetry of chordal involvement determine the MR.

Rheumatic mitral valve prolapse

• This could be  more common than we realise.
• It can be true or pseudo.
• True prolapse occur due to chordal weakening or lengthening .
• In chordal disruption the leaflet tips usually become flail

Since rheumatic process fixes the PML first , the AML   appear to overshoot the plane of PML and   appear as prolapse.(Pseudo )

The sail like AML commonly  directs the jet posteriorly and laterally .(Murmur conducted to axilla and back )

It is rare for PML to prolapse in RHD , if  it does occur ,  it directs the jet anteriorly (murmur conducted to aortic area mimic AS !)

It is rare to see a  perfect  central jet in RHD  . presence of  Central jet is a good sign to consider mitral valve repair.

Myocardial involvement in RHD.

Even though rheumatic fever is a classical  example for  pan-carditis , it is surprising   to note (Of course fortunately !)   how  myocardium escapes in the  chronic process of RHD.

Is it really true  ,  myocardium do not get involved in chronic RHD ?

Clinical cardiologists rarely discuss this issue. Pathogists indeed have documented significant lesions within myocardium  . Involvement of left atrial myocardium and  rarely  ventricular myocardium in the sub mitral  zone  can influence the  degree of  MR

* Even in acute rheumatic fever with fulminant carditis , myocardial involvement is  disputed by many  ! . My belief is ,  there will   definitely a subset  in   both acute and  chronic  forms of   RHD   , in which myocardium  gets  involved . In our institute LV dysfunction associated with RHD occur in  up to  5 % of  RHD population .

Importance of knowing the mechanism of MR

Two aspects  appear important

1. Is there a potentially  reversible component in pathology so that we can  wait  before intervention  ?

I have seen children referred for mitral valve replacement due to severe MR  . In due course   MR regress by the time they reach the tertiary center (waiting period included ) At least one child i remember,  the MV surgery was canceled  due to spontaneous regression MR.

It was later found the MR was  more of valve inflammation than degeneration .

* Always think about the possibility of reversible rheumatic MR  in every severe isolated  MR in children (Do not apply this rule in adults or in combined MS or MR  )  Do a ESR, ASO and start an  intensive anti inflammatory therapy  , aspirin with strict penicillin prophylaxis .With this  one can definitely postpone the surgery  in few cases  and  may avoid it altogether !

2. Surgical implication

If we could delineate  the  exact pathology of MR   it will facilitate  the   repair . Annular  reduction and  neo  chordae  etc . Of course ,the surgery could be  very  difficult in scarred mitral valves ,  Dr Sampath kumar *of AIIMS  New delhi , India  would  feel other wise !

*A pioneer in mitral valve repair in chronic  RHD (See reference 2 )

Questions  that need  answers

How is balloon/Surgery  related injury different from rheumatic process ?

Why is  rheumatic  mitral vale  prone for bacterial infection ?

What is the relationship  between  extent of  aortic valve involvement and  degree of mitral valve involvement in RHD ?

Reference

1.http://circ.ahajournals.org/content/94/1/73.full?sid=10599470-3563-4c38-b688-c5fc8c032f96

2. http://icvts.ctsnetjournals.org/cgi/reprint/5/4/356

Books

There two popular books exclusively  for cardiac pathology

1.Silver

2. Renu Virmani

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Proximal LAD means what ?

Proximal LAD lesions require  specific and early Intervention.Hence we need to know what exactly  we mean by proximal LAD disease.Unfortunately , it means different things to different cardiologists .There is no dispute regarding the  origin of  LAD since it begins with bifurcation point  .The problem comes with  this question !

Up to what distance LAD can be termed as proximal ?

1. Bifurcation  to   “First   diagonal” of  any size
2. Bifurcation  to   “First Major diagonal”
3. Bifurcation to     “First septal”  of any size
4. Bifurcation to    “First  major septal”
5. Bifurcation  to   “Any major  first branch ” (Either septal or diagonal )

Answer : I think  4 is the correct answer . But many believe  5 can be correct as well !

Why  there is  confusion in the  definition of proximal LAD ?

This is because the first branch of LAD itself is not a  constant one  . It can either be a septal  or  uncommonly  a diagonal.

It should be noted , the septal and  the diagonal  branches  neither respect   seniority  nor follow a  hierarchy .The first diagonal may be diminutive while the   second or third diagonal may be major one  and vice versa .Further  ,  there can be a trade of  in length and caliber of   septal and diagonal branches  .This  phenomenon is also  common between  diagonals  and   OMs  . All these confound the picture .

Cardiologists even though they are  primarily physicians they are  pro-anatomy  like surgeons when it comes to coronary interventions .

                                  In the strict sense ,  we  need to differentiate a  lesion  from being   physiologically proximal  or anatomically proximal  !

Is there a proximal LAD equivalent ?

There are three  situations  this can occur .

• Some times a lesion  by  definition may not fit in  as proximal  LAD  but physiologically  few major diagonals  will arise after the lesion.
• Other situation is , LAD lesion may be  mid or distal but  a major first  diagonal may be diseased  , making it  equivalent  to proximal LAD in terms of physiology.
• A mid LAD  with a large OM lesion which is running in the D1  territory

Final message

It is ironical  millions of cardiology interventions happen  for proximal  LAD lesions  every year without  even  proper understanding of what we mean by  it ! Youngsters are argued to ponder  over this issue whenever  they indulge in  such cases for revascularisation!

Reference

Text books differ in their definition about proximal LAD. Currently , the  SYNTAX  scoring system  has defined the coronary segments in a practical way.

http://www.syntaxscore.com/index.php?option=com_content&view=category&layout=blog&id=1&Itemid=32

Definition from SYNTAX

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A two minute video lecture on one of the great prosthetic heart valves !

The prosthetic cardiac valve which saved so many lives  in the later half of 20th century is no more. A valve which is not only  known for its excellent durability  but also  devoid  of sudden  mechanical  occlusion , unfairly  lost its place  by the rival  mechanical  bileaft valves. (Supposedly superior hemodynamics !)

Here is a nice video  from Indian surgeon  which  describes the hardware of  Starr Edwards valve .

Please read a related article from my site

Who killed Starr Edwards valve ?

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Which is the commonest type of bicuspid aortic valve ?

Bicuspid aortic valve (BCAV) is  one of the common  congenital abnormality of heart . Incidence can be 1-2% of population . It can result in premature aortic degeneration with Aortic stenosis/Aortic regurgitation or both .

The normal development and arrangement of three cusps is altered ( rather interrupted )  during fetal life.

There can be two ways BCAV can occur. One is due to the   fusion* of two leaflets to covert a  tricuspid  valve into  bicuspid  ,  and the other is    two cusps develop de novo .The former has a raphe , while the later has no raphe.

The  fusion* occurs between  either

• Right and left (R +L)
• Right and  non coronary cusp  (R +N )
• or Left and Non coronary cusp (L +N)

(* The fusion is embryological , not acquired )

Most often the  fusion is due to lack of division in the valve  analgen .Hence a raphe (A conjoint remnant) is noticed .

90% of BCAV has raphe  ,only 10 % lack raphe . Aortic root is also structurally abnormal in many .(Little clinical sequale though !)

Coronary artery origin anomalies  are more common with  BCAV. We also know co-arctation of aorta has a embryological link with BCAV.

The commonest type of BCAV is

The most hemodyanmic stressed BCAV is R +N type fortunately it is rare

R + N fusion is a high risk BCAV as degeneration occur fast

The least common type is

The coronary artery origin anomalies are common

BCAV in the absence of raphe is classified separately (This constitutes 10 % of all BCAV)

The nomenclature  is

• Antero posterior (Common type ) AP
• Lateral (L )

What is  the pathological significance of raphe ?

Many  believe presence of raphe accelerates degeneration as leaflets have  rough surfaces . Still , BCAV with raphe has less coronary anomalies and aortic root pathology .

Presence of raphe  indicate relatively  a minor embryological defect  , as the fault is in the failure to divide after the formation of analgen , while BCAV without raphe  imply  lack of development of analgen itself . This is expressed in the coronary sinus anatomy and aortic root dimension and orientation .

So currently it is  welcome  to spot  a raphe in the patient point of view  .Echo cardiogram is notoriously  unreliable to diagnose raphe. Once degeneration process sets  in ,  it is almost impossible to recognize  the  presence or absence of raphe .

* Please note ,tricsupid aortic valve with eccentric leaflet closure  shares  a close pathological relationship with BCAV. Premature degeneration ,  (AR more common than AS here ) .This entity will be discussed separately later.

 

Image courtesey

Part of the Image (The valve) is adopted from Yale university Image Bank .

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