Archive for July, 2015

Beta blockers(BBs)  have become  key drugs in  management of CHF .It helps by blocking  toxic effects of inappropriately  elevated   catecholamine  , which is actually a  compensatory response(A fight and survival reaction )  from the sympathetic system  to a failing  heart . This process becomes a liability in the long run  as the  adrenergic receptors either down regulate or even promote apoptosis and cell death .Along with  RASS-ACE  it affects every cell in the body promoting neuro- humoral catabolic state.

By trial and error  methodology we have found blocking the sympathetic system by BBs confer  consistent benefits in CHF .This is in contrary to the days we were ignorantly stimulating the beta receptors with positive inotropic  agents and  wary to give BBs in cardiac failure .This is one the most dramatic 180 degree turn around in the annals of clinical cardiac therapeutics last century.

Is all BBs  same ? Is it the class effect ?

It is tempting to think  all  BBs are  equal and to conclude they simply represent a class effect.But carvidilol  seems to be the flag bearer , for whatever  reason . (Apart from the outcome of  landmark studies , there is a pharmacological basis for it’s superiority COMET/COPERNICUS)

What is the secret of carvidilol’s superiority in CHF than other BBs ?

We know CHF is a systemic syndrome as do the  sympathetic activation .Hence , In CHF , it would require a non selective , systemically acting beta blocker to reverse and reset the adverse  effects of  catechlamine.surge.(Does that mean Propronolol (Inderal ) could be the best ?)

Carvidilol being a non selective BB  fits  perfectly  for the job . Of course , additionally  it has alpha blocking action that reduce the  after-load  reliving he LV wall stress during systole enabling further lowering of MVO2 and   promoting  regression of LV size as well.

Having said  that  prototype cardioselctive agents  like  Metoprolol , Bisoprolol are also  backed by robust evidence  for survival benefit in CHF . How to explain this paradox ? (CIBIS/MERIT )

“Thinking wildly(Evidence  would come later ) it is possible the benefits  from cardio selective agents are  accrued much  later as the dosage is titrated upwards . I would believe the  “inflection point”  of benefit could be same time they lose the cardioselectivity”

Final message

Cardioselectivity is  boasted as a gifted property of BBs .It may be true  in HT, arrhythmia and angina , but  in cardiac  failure it plays a different  ball game .The simple logic is the target  receptors need to be blocked  in systemic fashion.


2. http://www.jfponline.com/fileadmin/qhi/jfp/pdfs/6402/JFP_06402_ClinInq1.pdf

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Syncope is a classical feature of LVOT obstruction especially with valvular aortic stenosis.The mechanism of exertional syncope in Aortic stenosis is traditionally attributable to the fixed obstruction .This fixed obstruction is not able to cope up with increased cardiac output as demanded by the exercising muscles . But exercise  induced reflex as well as local vaso-dilatation mechanism is intact . The consequence is predictable. A critical fall in SVR amidst a obstructed LVOT precipitating a syncope.

However , If the above mechanism is the sole reason for syncope in Aortic stenosis , we have a problem to explain why syncope is  rare even in critical mitral stenosis which is also fixed LV inflow obstruction ?

Is there some thing unique in LVOT obstruction that causes syncope ?

No, it is nothing to do with LVOT .To generate a true pathological syncope, reduction in cardiac output per-se may not be enough . It appears there should be an inappropriate systemic vasodilatation as well to precipitate a syncope.This can happen only if the parasympathetic system gets activated by some means . The trigger is located in the mechano- receptors of left ventricle . Hypertophied left ventricle with high Intra cavitory pressure (Often above 200mmhg) generated due to LVOT obstruction activates the syncope circuit.The same rule may apply for RVOT as well .One could get syncope with critical valvular PS or severe pulmonary hypertension when RV mechanical receptors get a triggered.

What happens in mitral stenosis ?

In mitral stenosis , LV is under- filled ,  wall thickness is normal .There is little likely-hood of LV mechno-receptors to get stimulated as the LV wall stress is normal. This is the reason syncope is less common in mitral stenosis. However , this is not  absolute rule , syncope can still occur in severely narrowed orifice of mitral valve due to low flow state alone or a ball valve thrombus and paroxysms of arrhythmia .

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Femoral artery puncture is still the default technique for cardiac catheterization even as the radial access has gained huge popularity in recent years.Though patient  comfort and access site complications are clearly low in radial approach, complex procedures still demand femoral access. The true draw-back of  the obsessive  adaptation of radial access could be the  gradual loss of expertise in the fine art of femoral artery puncture.

It’s true femoral artery puncture can be troublesome at times by palpatory method .How to get into a difficult femoral artery with a poor pulse either due to anatomical reasons, extreme obesity or a compromised hemodynamic status ?

There are times, blind puncture based on anatomical guess could work. Alternate ways do exist. One can access the femoral artery by ultrasound guiding  with or without  smart needle system . More practical is the empirical  puncture based on surface anatomy  over the head of femur in fluoroscopic screen.The later method is not really crude as some would  think !. It was suggested by Grossman and popularized by none other than father of Interventional radiology Dr Dotter in 1970s .(Radiology Apr;127(1):266-7.Fluoroscopic guidance in femoral artery puncture.)
By fluroscopy , in AP view the head of femur can be divided into 5 zones.(Huggins) Zone 1 and 5 or superior and inferior to head of femur.The zones 2,3,4 are divided into upper, mid and lower third.
Where does common femoral artery bifurcate ?
The bifurcation of the CFA occurred in zones 2, 3, 4 and 5, which was 1%, 9%, 43% and 47% of the time, respectively, and thus occurred within the lower third of the femoral head or below the lower border of the femoral head in 90% of patients.

femoral artery puncture by fluroscopy

Image source Cardiovascular Intervention and Therapeutics January 2014, Volume 29, 18-23 Madjid Chinikar

femoral artery puncture by fluroscopy 2

Image source Cardiovascular Intervention and Therapeutics January 2014, Volume 29, 18-23 Madjid Chinikar

How to approach ?
A 18 G needle could be ideal
Puncture the skin at zone 5 inferior border of head of femur. Enter the artery at mid point in the Zone 3.
The chances of hitting the femoral artery is near 95 %


1.Fluoroscopic localization of the femoral head as a landmark for common femoral artery cannulation. Garrett PD1, Eckart RE, Bauch TD, Catheter Cardiovasc Interv. 2005

2.Fluoroscopy vs. traditional guided femoral arterial access and the use of closure devices: a randomized controlled trial. Abu-Fadel MS1, Sparling JM, Zacharias SJ, Catheter Cardiovasc Interv. 2009 Oct 1;74(4):533-9
3. Fluoroscopy guided vascular access: asking the right question, but getting the wrong answer? Turi ZG. Catheter Cardiovasc Interv. 2009 Oct 1;74(4):540-2

4.Imaging or trusting on surface anatomy? A comparison between fluoroscopic guidance and anatomic landmarks for femoral artery access in diagnostic cardiac catheterization. A randomized control trial. Madjid Chinikar, Azam Ahmadi, Abtin Heidarzadeh, Cardiovascular Intervention and Therapeutics January 2014, Volume 29, 18-23

5.A Prospective Randomized Clinical Trial of the Use of Fluoroscopy in Obtaining Femoral Arterial Access Chadwick E. Huggins, MD, Michael J. Gillespie, MD, *Walter A. Tan, J INVASIVE CARDIOL 2009;21:105–109

6..Puncture of the popliteal artery using a Doppler-equipped (SMART) needle in transpopliteal interventions.Kluge A1, Rauber K, Breithecker A, Rau WS, Bachmann G.Eur Radiol. 2003 Aug;13(8):1972-8. Epub 2002 Nov 22

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Heart transplantation  as a treatment modality was conceptualized  by Christian Barnard in 1967 . Still considered as an  “Act of God” this  surgery is regularly performed worldwide by dedicated  transplant team consisting of cardiac surgeon , physician , Anesthetist , pathologist and others .Unlike other organs , heart transplant cannot have a “live donor” .Though  started  half a century ago, the real  pace has  picked up only in last 2 decades .Currently it is  “globally accepted  standard” intervention in terminal cardiac failure (Including pediatric heart conditions)

How are the survival rates ?


  • Now, many centers  are able to reach the  bench mark Stanford- statistical rates with a consistent  five  year survival rate crossing   75% .
  • The median survival rates is 10.5 years
  • One of the estimate indicate , If they cross first year, median survival reach 13.5 years
  • There has been many living survivors who have  crossed 30  years.

Looking at these numbers  , there is dramatic impact  in terms of global disease burden and the life gained.Statistically  speaking  successful treatment by heart transplant is equivalent to overwhelming  many  cancers in a human body !

Can these  results reproducible in all centers ?

These excellent outcome is  the reward to highly dedicated teams with  pioneering work culture . One should be cautious to start new transplant center without proper facility and expertise.Unregulated heart transplant  centers is vested with risk of pulling down the excellent  statistics of this unique form of human organ exchange.

Newer developments

Patient  selection criteria and  strategies to prevent rejection is being streamlined .The major  issue is availability of donor heart and how to optimize organ procurement and increase transport survival time .Transmedics has deviced a state of the art organ transport system . The other exciting thing expected to happen is potential (Ironical though !) heart donors from  even cardiac  /circulatory deaths . (Dhital KK, Iyer A, Connellan M Lancet. Adult heart transplantation with distant procurement and ex-vivo preservation of donor hearts after circulatory death: a case series.2015 Jun 27;385(9987)

What about artificial hearts ?

As of  now biological heart has definite edge over  artificial heart.Meanwhile rapid development of LV  assist  device and near total artificial  hearts may  end up with destination therapy rather than bridge to transplant. The “INTERMACS ” data are very promising and let us wait for the day artificial heart  can  score over the biological  ones.


1. The Registry of the International Society for Heart and Lung Transplantation: Twenty-eighth Adult Heart Transplant Report–2011.Stehlik J1, Edwards LB, Kucheryavaya  J Heart Lung Transplant. 2011 Oct;30(10):1078-94.

heart transplantation
longest survival after heart transplanation
longest survivor of heart transplant

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Aortic stenosis is diagnosed by 2D valve morphology, area ,and pressure gradient across the aortic valve.Though anatomical 2D images and indices are good enough to diagnose severe AS , we are obsessed *  with pressures  which are subjected moment to moment hemodynamic and contractile variables. To record a good gradient we need a normally contracting ventricle and good flow across the narrowed LVOT. If any one of the is critically compromised  gradients can’t be picked up by Doppler.(A new entity of AS was recently included , which fails to generate the gradient in spite of good LV function and the AS being significant.)

So ,whenever one records a “Low gradient AS” there are 4 distinct possibilities.

  1. Truly mild AS
  2. Technical inadequate Doppler alignment , with possible true moderate /severe anatomical  AS .
  3. Low gradient AS due to LV dysfunction, with true moderate /severe anatomical AS
  4. Low gradient AS with Low flow but normal LV function, with true anatomically moderate/severe AS

Echocardiographer should rule out 1 and 2 before going to the complex world of low gradient severe AS.In my personal opinion , the entity of Low flow , Low gradient with Normal LV function appear  redundant ( or is it beyond my understanding ) .One should look at the valve morphology and decide in such situations.

Then , one will shortly bump into this query  is it 2 or 4 ?

How to differentiate a  technically defective  recording  of low gradient AS  from  true low flow due to narrowed LVOT.(Low gradient for me , high gradient for my professor !)

Now, basic readers  may please leave ,

Few inquisitive may ask   ( naturally though)

Does the ” low flow -low gradient AS”  is an exclusive phenomenon  that can occur only with normal LV function  or can it  occur in  dysfunctional left ventricle as well ,  who also have small cavity size and narrow LVOT  ?  (Within the low gradient AS due to LV dysfunction subset ,  How much is attributable  due to anatomial low flow  and how much is related to depressed LV contractile force ?)

Another googly . . .

Why can’t  Doubutamine* stress test  routinely  undertaken in the subset of patients with  with subjects with Low gradient /normal LV function to augment the anatomical low flow and find whether it is true  low flow or not ? *This would mean , a most impractical situation wherein every patient  with even mild AS should need to undergo dobutamine testing to rule out significant AS.

Final message

As of now ,this new concept   “Low flow , Low gradient, with Normal LV function” appears an  intellectual excess with little impact on patient outcome.The proposed new entity ultimately increase the likelyhood of over diagnosing  severe AS.Iam still expecting  more clarity  on the issue. ( or else for the moment forget the pressures and  simply fall back on  a meticulous assessment of 2D valve morphology and take a call , you will be surprised how often we get into man made scientific traps. )


1.Low-flow, low-gradient aortic stenosis with normal and depressed left ventricular ejection fraction.Pibarot P1, Dumesnil JG.J Am Coll Cardiol. 2012 Nov 6;60(19):1845-53

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Prosthetic valve obstruction is becoming a common clinical issue .It can be either acute, sub-acute or chronic . The pathology is usually thrombus formation , scar tissue growth (Pannus) or rarely a mechanical defect. Echocardiographic differentiation of thrombus from  pannus can be difficult .Generally , pannus is smaller , linear (less round) ,encroach from the periphery to central , mean gradients are consistently lower  than thrombus mediated obstruction. Clinically  pannus related obstruction present less acutely and occur in-spite of good compliance of anticoagulant medication and a well maintained  INR .

Trans thoracic (TTE)  , Trans-esophagel (TEE ) echocardiography , and real time 3D TEE are useful imaging modalities .The value of cine fluroscopy should be never underestimated and it is probably still the the best way assess the struck metallic leaflet.

Though the pathogenesis of pannus and thrombus are considered different there  is no reason they can’t  occur in a given patient at the same time.We know at least  one patient who had been referred to surgeon for mitral valve obstruction due to failed thrombolysis  had showed heavy load of thrombus  attached over a well formed pannus originating in medial sewing ring.

FInal message

However intelligent one may be , human brain often  tends to get skewed when confronted with a sudden query like  “What is your diagnosis , This or that  ?  Pannus or thrombus ? .Most will  go with  any one of it ! However, cardiac physicians must be aware  both pannus and thrombus can occur overlaid simultaneously in a given patient .The exact incidence  of such “combined thrombo-pannus”  is not known  but bound to be higher as we look for it. In fact , many of the residual gradients after lysis is attributable to undiagnosed pannus.  There is also a  suggestion scarred  , injured  ,  rough surface of the pannus could be the initial trigger for thrombus formation .


1.Differentiating thrombus from pannus formation in obstructed mechanical prosthetic valves: an evaluation of clinical, transthoracic and transesophageal echocardiographic parameters  John Barbetseas,  Sherif F Nagueh,  Christos Pitsavos, ;J Am Coll Cardiol. 1998;32(5):1410-1417. 

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