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Archive for September, 2013

Right ventricle is a passive venous component of the heart .It simply acts a  transit pump for blood to reach the lungs.

It  is true  , RV is dispensable in many complex congenital heart disease as we  can connect the great veins directly into the pulmonary artery  by  Fontan , Glean and it’s clones  bye passing this chamber . Still , by no means the importance of this chamber is to be underestimated.  RV dysfunction and failure  is the key to survival  many  disorders.RV shock is is cause of sudden cardiac death in acute pulmonary embolism and RV infarction .

RV is an unique muscular chamber .It is more of a triangular shape. It has  three different parts connected by three different angle .There is no true  apex  for RV , it is   connected  to Inflow and outflow in peculiar fashion .

In the  following table I have  tired to  describe  of how different parts of RV  behave in various disorders.

what is the morphology of  RV enlargement RV inflow outflow body sinus portion of RV

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Congenital heart disease (CHD) still constitute an significant  subset in cardiology practice.The moment you ask how do you classify CHD  to any cardiologist , the answer  would come promptly as “cyanotic and acyanotic CHD “. Such is the power traditional clinical teaching .
 
There is a fundamental embryological and functional classification available put forth by Clark.It lifts  our understanding about congenital heart disease to a  different perspective. I wish,every cardiology fellow should know this.
 
 Link to embryological classification of congenital heart disease .
 
 A subset for cono-truncal anomalies is also available.
cono truncal anomalies embryology of heartReference
Clark EB. Mechanisms in the pathogenesis of congenital heart defects. In: Pierpont ME, Moller J, editors. The Genetics of Cardiovascular Disease. Boston, MA: Martinus-Nijoff; 1986. pp. 3–11.

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No procedure is  impossible in medicine    . . . but it should be useful for the patient !
Where will you ablate ? What is the purpose ?
The much  hyped*  ablation of pulmonary vein  is never going to help in rheumatic heart since  arrhythmia focus occurs at  random . How can you  locate a   focus of AF over a  huge , scarred  left atrium  ? ( which looks like a lunar surface  sprinkled with a rocky terrain ! )
Gross specimen
                                      Note the huge , scarred LA .It would
                                      be a wild guess to locate the true focus
                                      of AF . (Image source : http://www.e-heart.org)
So , the other option was disconnecting atria electrically . In the past  surgeons advocated  linear  or multiple incisions as in Maze and  Corridor procedure  after mitral commissurotomy .This  helped to a certain extent , still effective , organised atrial contraction was not restored in many.
Now , some electrophysiologists tried to do the same with catheters without much benefit.* Please realise , pulmonary vein ablation even in lone and ischemic AF is struggling  with a concept collision !
Can Right atrial focus trigger and  sustain  AF in RHD ?
Autopsy studies reveal tricuspid valve scarring in 33%  of all RHD .Since RHD is a diffuse process , RA lesions can  be very well be the focus .  It is not an easy task to identify the real culprit focus. So ,concentrating  LA  for ablation may end up in futility.
There are only few studies available on RF ablation in RHD  .This one from Istanbul ,Turkey  and it  does not favor it as recurrence rate is still significant .
rf ablation in rheumatic atrial fibrillation
Final message
Approach  to AF in RHD  : Opening up the mitral valve (or replacing it )  and controlling ventricular rate  with beta /calcium blocker along with  adequate  oral  anti-coagulation substantially reduce the risk of embolic events .One may never need to contemplate restoring sinus rhythm  in rheumatic atrial fibrillation.

//

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Normal  left atrial  (LA) volume is about  22ml/sq.meter body surfacearea  at all ages.Maximum LA volume in physiology is  about 46ml in  females and 56 ml  in males( Average 35 ml)

LV stroke  volume  for each beat is  about  70  ml . . . so where does  the remaining 35ml come from ?

Answer .

  • Pulmonary veins ?
  • Residual LV end systolic volume ?
  • Mix of the two ?

It is logical to assume about 35 ml of fresh  blood  from 4 pulmonary vein*  rushes into LV with every diastolic cycle  .It  never stays in LA  .It just uses LA as a transit  route ,

*In diastole the four PVs,LA  and LV all act like one single chamber .

 

Is this reasoning correct ?.

If we believe the continuity equation this explanation is correct . However still what  we need to know the fate of residual  LV volume (End systolic LV  volume which is also  about 35 ml that would be  in queue for ejection into Aorta  for the next beat !)

Further , we know the LV end systolic volume is not constant .During exertion it  can reach  negligible levels (<10 ml) .At times of vigorous contractions  it can touch near zero as well . Then , It become vital for the  pulmonary venous reservoir  to be act as a  major donor for  LV blood volume for  every ensuing beat.

If the hemodynamics of pulmonary vein LA interface is tricky even in physiology ,  one can imagine the complexities  if the LV diastolic function and left atrial compliance  is affected

Debit and credits of  LV end -diastolic volume .

Let us assume LVEDV is about  1o5  ml .LA blood volume is  roughly one third of LV volume .For every beat equal amounts of fresh blood  from pulmonary vein . These two (LA+PV)  adds to the  residual  blood in LV  to make LVEDV 105   ml . From this 70 ml is ejected as stroke volume leaving behind 35 ml.


lvedv lvesv stroke volume wiggers cycle left atrial volume pressure volume loop residual diastasis

Image template from http://www.cvphysiology.com

 Further questions

LA Chamber volume and blood volume need not be same .What  I struggle to understand is , total anatomical  LA volume  measures  35ml , while the amount of blood it is supposed to hold is also about the same .Does  it mean the LA is completely filled with blood . . . air tight !

Will the LA compliance make it accommodate twice or thrice the blood volume during exercise ?

What is quantum of residual end diastolic  LA volume ?

 

Reference.(Normal LV and LA volumes )

echopedia

 

 

 

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Obesity is a major cardio vascular risk factor.We earnestly  believe  this  by  evidence from Framingham and other studies.However , epidemiological  truths   can be dissociated from individuals .

We now understand  some  of the obese  patients fare better in CHF outcomes  apparently because of the obesity ! Even patients who undergo PCI show some benefits.This concept  is being proved in large data base of  > 200,00 patients.

Possible mechanisms

The lay man’s logic may apply (Science hidden somewhere !) Obese persons  have basically a  large heart with better cardiac reserve and  muscle mass .These hearts are  pre-conditioned to extra burden of MVO2  in it’s life time . So it  is able to tackle  hypoxia better, takes more time  to get fully exhausted .After all heart can consume fatty acids for it’s energy requirement.

Adipose tissue may also  secrete favorable anti-inflammatory  chemicals , though majority of adipocytokines are detrimental  except adiponectin .Paradoxically  the tumor necrosis factor TNF  (Same as cachectin or Interleukin 6)  is less  in obese patients .

 

Reference

obesity paradox

obesity paradox 3

obesity paradox 4

obesity paradox 3 jama archives of internal medicine

Reference

The landmark Lancet article that first raised the question of obesity paradox

http://www.ncbi.nlm.nih.gov/pubmed/16920472

http://care.diabetesjournals.org/content/36/Supplement_2/S282.full.pdf+html

Counter to the  concept

obesity pardox does it exist

http://science.howstuffworks.com/life/human-biology/obesity-paradox.htm/printable

Obesity   paradox applies in stroke too ! This study (TEMPIS) from Berlin  Germany  suggest controversially though

 

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Pacemaker lead implantation is basically a blind procedure .We are supposed to pace the RV apex . It is akin to anchor a ship in the sea bed. Screwing leads are preferred in permanent pacing  ,but tined leads have few unique advantages as well .

Can we combine the advantage of both ?

pacemaker lead in rv apex anchoring how to

It is believed displacements are more common with tined leads . May be yes . . . or  is it really so ?

It is not the tines  or screws that is going to  determine the early displacement , rather ,  it is the expertise , commitment and the time spent during the implantation that matters . I have witnessed equal number of  early lead dislodgement in both .

One issue often goes unreported is that , when screwing lead is used operator is subconsciously complacent.While cardiologists who implant  tined lead is more cautious , make sure it is well trapped in RV.

Screwing leads.

  • Screwing leads should not be positioned in the same place as tine leads.
  • This is because , RV apex is rich in trabeculae. Screws can enter one of the trabeculae or it may even enter  inter  trabecular  space. or poke  thin trabeculae which may  break in near future.(Realise ,how blind we are !)
  • Screwing  should be done in area where there is least  trabeculae  ideally in  lower end of septum. Since we do it blindly , we can’t be sure where exactly we have screwed .
  • Please note , pacing parameters are less  reliable than anatomy One may get surprisingly good pacing threshold even in trabecular pacing.
  • RV non apical pacing is possible only with screwing leads . However , the superiority of RVOT, para hisian pacing is yet to established in patients with normal LV function (Note  90 % of individuals who require PPM have normal LV function )

Tined leads

  • In contrary,tined leads are best placed where there is dense trabeculae.
  • It is natural entrapment.
  • The expertise of screwing  in a best place of RV is not required.
  • Whether screwing  predispose   to septal perforations in long term follow up is not known. Logic would suggest it may  !  (The Initial of few mm  of IVS tunneling  is done by us ! )
  • Diaphragmatic twtiching is more common with screwing leads.
  • Explantation  issues  is similar in both .

What does experienced cardiologists say ?

Cardiologists before the era of EPs were using  only tined leads  without any major hitch . I know electrophysiologists rarely use tined leads now . In our institute ,  with a  cumulative experience of over 3000  pacemakers  over 30 years( 99% are with tined leads ) , we  have no reason to believe they are vastly superior technique.

However there are few definite Indication for screwing lead

  • Abnormal RV anatomy
  • Loss of RV trabeculae
  • Marked Tricuspid regurgitation
  • Pulmonary hypertension
  • Second lead in RV
  • LTGV

* Note all atrial based pacing are screw based as atria lack trabeculae.

A suggestion

pacemaker lead in rv apex anchoring how to tined vs screwing lead   003

Final message

I would believe ,there is no major difference in both short and long term outcome between these two system of leads.Each has it’s own advantage.

After thought

Why can’t  we accrue  the benefits of both ? I think we have good scientific reason to request the pacemaker industry   to  design  a lead which  can have both tines and screws to  provide  double safety .Simple isn’t ?

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Cardiologists are  not  single organ  specialists . They are supposed to  be sincere guardians of the  the entire vascular system .Sexual dysfunction in  males  is almost synonymous with erectile dysfunction(ED) .The male sex organ is equally  dynamic organ like the heart . It demands a sudden gush of blood  to the tune of  500 ml  during complete  erection  .This  conveys an important  message . The penile macro and micro vasculature is as important  as coronary mIcrovascular bed. Atherosclerois of  LAD  can be as common as atherosclerosis  of pudendal artery .It can precede or follow the coronary lesion. Penile insufficiency is a early marker of endothelial dysfunction. All patients with CAD should be screened for  ED and vice versa.

This  is not a  sexual  intrusion in academics , but I am sure , a sustained  erection  that  completes  a normal sexual act  may very well  rule out a proximal LAD lesion 99 % of times .

Do you know , > 7  Mets  on a tread mill  will  rule out a  significant left main disease with high degree of accuracy   !  Sexual acts require more than that (One may do a study on this !)

There has been  some interesting guidelines for managing   issue of sexual dysfunction in CAD. .Princeton consensus conference is  the famous one.

References

princeton consensus conference sexual dysfunction in cardiology princeton 3 sexual dysfunction in cardiology

sexual activity in cardiovascular disease  circulation 2012

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