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 )





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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 .



obesity paradox

obesity paradox 3

obesity paradox 4

obesity paradox 3 jama archives of internal medicine


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



Counter to the  concept

obesity pardox does it exist


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.


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

sexual activity in cardiovascular disease  circulation 2012

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While many of us are preoccupied with wires and balloons ,( coronary  myopia ! )  , our radiology  colleagues are making rapid strides . Let us spend some  time  to understand  how  the myocardial segments  are inflicted the  final insult . We need to realize , there is a pattern  to  this myocardial  end game of scarring and fibrosis.

MRI is the  gold standard to assess the myocardial architecture . It has a role in both assessing the anatomy , function  , perfusion and viability .

how to differentiate ischemic dcm from idiopathic dcm myocardial scar epicardial transmural

  • LV function is assessed  by cine MRI
  • Viability  stud by  delayed enhancement MRI (DEMRI , also called as  LGE- Late Gadolinum enhancement  )
  • Myocardial scar best assessed by DEMRI*
* Why do you require DEMRI to identify scar ?
One can detect scars in plain MRI but contrasts make it better .Hence delayed enhancement in by DEMRI is used  to detect scars.
Is it ischemic  DCM or Non ischemic DCM ?  ( That is the question we commonly ask  
We rely too much on CAG anatomy for this. It can be misleading. Cine MRI with DEMRI  gives the answer straightway with high degree of accuracy  .  CAG is required in all  ,  but if it is normal , or  has insignificant lesions  , the dilemma  of ischemic DCM would continue !)
**Note ,there is one   simple algorithm proposed by the author   to  differentiate  Ischemic DCM from Idiopathic DCM  without MRI – Click here to  Link
Following  scar patterns in DEMRI help us to arrive a diagnosis.
Favors Non ischemic  DCM
  • Mid myocardial scar
  • Epicardial scars
  • Global sub-endocardial scars
  • No scar(Ironically if  no delayed  hyper-enhancement is noted it is likely to be non Ischemic DCM )
Favors ischemic DCM
  1. Regional transmural scars
  2. Localised sub-endocardial  scars
* Ischemic DCM will always involve subendocardium as ischemic wave front goes from sub-endo to epicardium.
examples for Non Ischemic DCM
  • Amyloidosis (Can be restrictive as well )
  • Chagas
  • Fabrys

Why is  scar localisation and Quantification important ?

Apart from differentiating various cardiomyopathies  it has  few clinical implication .

  • Since scar indicates irreversible damage , if extensive  it will  argue  against any re-vascularisation .
  • Scar location becomes vital if we plan CRT .It will be futile  to place a CRT lead over a scar.
  • Scars are often  form a macro re-entrant circuits for VT .Help us localize or zeroing in VT focus.
  • Scar quantification is helpful risk stratification of patients  with HOCM .and their family.
Final message
Myocardial scar location and quantification  is the new mantra in a  patient with dilated heart with cardiac failure.
It may be more important than even a coronary angiogram .MRI  will prevail over   any of the available echocardiogram modalities to assess the scar pattern.
myocardial scarring mri

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I know ,there is a VSD out there !  but I am  unable to  get the gradient across it.This situation can be quiet  common .The reasons could  be technical, anatomical or  hemodynamic.

As a rule ,  if we hear  a  pan-systolic murmur clinically ,   one must be able to catch  a good  Doppler spectrum somewhere by  echocardiography . However , If  the murmur is restricted to  early or mid to late  systole, VSD  jet is often attenuated in echocardiography .

In the  following situations ,  VSD  jets  may not  record a distinctive Doppler spectra. Invariably the velocity is low , spectrum is short,  less intense ,  lacks good shape and borders are hazy !

  • A closing  VSD
  • A Small muscular VSD
  • VSD with  Severe pulmonary hypertension
  • VSDs with muscle bundle criss crossing
  • Double chambered right ventricle (DCRV, where VSD usually drains to high pressure chamber.)
  • VSD  associated RVOT obsruction  (Note: classical TOF VSD will never generate a murmur)
  • VSD with sinus of valsalva aneurusms (  Doppler  jet  can be really  difficult to record )
  • Inlet VSDs are missed because  convectional  views of echo are perpendicular to these inlet jets.(Short axis better  )
  • Another common situation  is post STEMI VSR.Both a small apical VSD or multi tract  VSD associated with  infero posterior  STEMI   gradients are  difficult to obtain.

What is   inference ?

Doppler spectrum will help detect  small VSDs and color doppler will not miss even a tiny VSD.Doppler spectrum across VSD  is dependent many  factors other than the presence of VSD. However some large VSDs are detected better by 2D echo rather than doppler signals.

Final message

Presence of a Anatomical  VSD does not  imply it should generate a noise.The murmur as well as Doppler signals  are  primarily  determined by the pressure difference on either side of VSD. After all , one of the  largest VSD  that  we encounter

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Syncope in CHB is due to unsafe escape rhythm, changing focus of VPDs,  extreme bradycardia, (<20 /minute),  pause induced VT, (Usually polymorphic and torsades is quite common .)  ultimately may end with convulsions,  ventricular fibrillation, and death.

Syncope in SND is due to extreme slowing of SA node . Sinus pauses or even arrest can happen resulting in ventricular standstill. Fortunately, a stable escape rhythm ensues more often than in CHB. (It may just be around 20 or 30/mt. still, ventricular arrhythmias are uncommon. ) This implies an important fact that stability is more important than slowness.Fatality is rare in SND.However, the mechanism of syncope in  SND is influenced by the integrity of AV conduction also. If it is severely impaired it can trigger ventricular arrhythmias as well as the escape focus becomes unstable infra hisian location.

Paradoxically, in patients with SND, an episode of palpitation due to AF  or sinus tachycardia precedes the episode of syncope. An intelligent patient may recognize this as a warning and can take lying posture after runs of palpitation.This is because of tachycardia-induced suppression of  SA node prolong the sinus node recovery time still further.

How to differentiate cardiac syncope from simple vasovagal syncope?

Cardiac syncope  is differentiated by common vaso-vagal syncope (VVS) as the latter occurs during erect posture . It may be entirely due to vascular component and hence it may simply represent hypotension without a true cardiac limb .(Vasodepressor syncope)

Hence the pulse rate and volume may take some time to recover in VVS, while Stokes  Admas of CHB  usually have a well-formed bounding pulse in the recovery phase, as the rate is low and systemic hypoxia is a consistent feature.

How is the respiration during Stokes – Adams syndrome ?

Intact. Oxygenation in the lungs goes on for time being. The pooled pulmonary blood gushes after the termination of syncope and causes  the classical flushing. Since the hypoxia causes systemic vasodilatation the flushing is more obvious.(Unlike vasovagal syncope where they are often pale)

History of stokes Adam’s syndrome Morgagni is the  one who gave credit to their  discovery

Though Morgagni first described the clinical picture of this syndrome in 1761,  It was published much later by Two Irish Physicians  Stokes, Adams. Wish this entity is referred to as Morgagni-Stokes-Adam’s syndrome


1.R. Adams. Cases of Diseases of the Heart, Accompanied with Pathological Observations. Dublin Hospital Reports, 1827, 4: 353–453.

2.W. Stokes. Observations on some cases of  permanently slow pulse. Dublin Quarterly Journal of Medical Science, 1846, 2: 73–85

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