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Tips in femoral artery access : Rapid Fluroscopic puncture in cardiogenic shock !

July 24, 2015 by dr s venkatesan

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 %

Reference

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
Jun;65(2):205-7

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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Smiling patients and “Stunning” survival rates  with heart transplantation !

July 12, 2015 by dr s venkatesan

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 ?

HEART TRANSPLANT SURVIVAL

  • 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.

Reference

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.


2.
heart transplantation
longest survival after heart transplanation
longest survivor of heart transplant

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Iam confused with this Low flow -Low gradient -Normal LV function stuff . . . please clarify !

July 9, 2015 by dr s venkatesan

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. )

Reference

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

Posted in Aortic diseases, aortic stenosis, echocardiography | Tagged , , , | Leave a Comment »

How common is the combination of pannus and thrombus in prosthetic valve obstruction ?

July 2, 2015 by dr s venkatesan

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 .

Reference

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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How does dedicated bifurcation stents work ?

June 30, 2015 by dr s venkatesan

We know right from our pathology days in medical school , Atherosclerosis , the killer human vascular disease has a predilection for branch points. It’s no surprise around 30-40% of coronary stenosis has some degree of involvement of branch points .

PCI essentially involves palliative metal bracketing of this inflammatory cum degenerative process of the vessel wall.Tackling bifurcation lesions (BFL) requires special expertise , hardware and technique as carina and two ostia (In fact three !) are exposed to complex hemo-rheological stress de-nova and more so after the metal invasion.

The complication rate as well as long- term patency are considerably more  in BFL than regular lesions. This is why a “4S strategy “ (simple single stent strategy ) is the preferred default strategy in most BFL.

There are about dozen strategies  to tame  the BFL with  stents.One such modality is dedicated BFL stent.Various designs have been proposed in both balloon and self expansion platform.

The ACCSEES is a prototype dedicated BFL stent with DES and  a self expanding system

Reference

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Can mild Aortic stenosis trigger severe LV dysfunction ?

June 16, 2015 by dr s venkatesan

Degenerative Aortic stenosis occur with either normal  or congenitally malformed/ bicuspid valve.This contributes to the major chunk of  aortic valve surgeries and interventions (TAVR) in elderly population  . The optimal  timing of aortic valve replacement in patients with AS is debatable inspite of  well formed guidelines.

Three factors determine it .Symptoms , severity of aortic valve narrowing  and the tactness of LV function .The last parameter is a tricky one .We used to think in the past , severe LV dysfunction is a contraindication to aortic valve surgery. Now we realise ,however severe the LV dysfunction may be , relieving the obstruction will benefit  the patient and  the LV function is  also  likely to improve.

Cardiac physicians  face a dilemma when confronted with a patient  with low gradient and severe LV dysfunction .In this situation they are advised to do doubtamine stress Echo and watch for the gradient .If the gradient  increases that would  imply true fixed stenosis . (In pseudo aortic stenosis increased contractility opens the aortic valve and gradient will fall )

While this concept appears simple .There  are few  important issues that goes unaddressed  as we have not yet fully understood the  mechanism of LV dysfunction in aortic stenosis .(Link to mechansim of LV dysfunction in Aortic stenosis.)

At what degree of aortic stenosis LV goes down fighting and fail to generate the required  gradient ?

Myocardial function  and behaviour at times of hemodynamic stress can be highly  variable and most of us believe it is determined primarily by the genetic switches of myosin and other contractile elements .This is naturally proven at times of hypertensive left ventricular failure (Only in a fraction of the hypertensive population  LV is set to fail  when BP acutely raises.)

Proposed concept

Considering the complexities in cardiac mechanics , hemodynamics (and not to forget the vast control exhibited by genetic imprints over the hemodynamic behavior of LV) , it seems highly plausible even mild degrees of Aortic stenosis can inflict significant myocardial dysfunction in certain patients . Hence the phenomenon of pseudo aortic stenosis needs further critical analysis If this is proven to be true there could be a realistic indication for aortic valve intervention even in patient with low gradient / true Mild AS with LV dysfunction.
A word of caution is required .Relying too much (Which we often do ) on gradients in the assessment of aortic stenosis has skewed our common sense. Its wiser to have a  meaningful look at the valve morphology . A normal appearing  valve in 2D can never cause significant stenosis. Pressure recovery phenomenon also is to be given due respect as it over estimates gradient .This will effectively avoid surprises and guilt on table when we find a relatively good looking valve posted for AVR /TAVI

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What are the 4 components of myocardial viability ? How will you test for it ?

June 14, 2015 by dr s venkatesan

An attempt is made to look for individual components of cell viability .See the table below. It is a generalized statement for understanding purpose only. Various imaging modalities assess the overall physiology of myocyte function (however  they test  an individual component of a cell more than the other) We may believe an unit of cell would die in “one-go” at times of ischemic injury.Reality is much complex.There is considerable variation in intracellular survival mechanisms . A cell can die in a regional fashion with residual signs of life scattered across among the different organelles. The quantum of damage to Nucleus /mitochondria may appear determine the recovery . The reverse can also happen .What is the purpose of mitochondria respiring if contractile element is totally damaged ? It becomes a “vegetative cell”. The gross discrepancy we are witnessing in myocyte cell function recovery with reference to both acute and chronic reperfusion is attributable to this gap in our knowledge.

myocyte viability demri spect thallium dobutamine contrast echo 2

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Medical Ignorance : Just Ignore it . . . move on , lets live the moment !

June 9, 2015 by dr s venkatesan

It is believed  (assumed ?), medical science is propelled by constant quest for knowledge and improvement in basic and clinical science that eventually would transform into better patient care and favorably impact  global health standards. We know the field of medicine is growing in an unimaginable pace.It’s obvious  any growth if uncontrolled or not properly guided is at risk of deviation from the main goal and ultimately  turn malignant and destroy the system which it’s supposed to guard.

How many times we realise the current treatment we administer would soon become obsolete and  even become dangerous ? What is the point in replacing treatment A by B , and  then  B is pulled over by C or D   and suddenly finding A is better than either C or D (and still we hesitate to fall back on A because its an oldie!)

Still ,this is what we call  as practicing ” State of the art medicine” How about a person who defies state of the art ,  and able to fore- see the futility which is threatening to be the  norm in modern medicine. Then,who is really Ignorant ?

I stumbled upon this  wonderful writing on this issue by ex BMJ editor by Richard Smith. Mind you , this was published way back in 1992, when the boom of  futile  ” Human  Health shopping”  was just about to explode !

medical ethics ignorance based mediicine

Link to The ethics  of  Ignorance

Post-amble

Don’t get confused .Noble professionals are  licensed to  practice  with whatever is published as science as long as their intentions are deemed to be genuine .Harm arising out of  practicing what’s considered best as on today is acceptable in the court of law.

Meanwhile , its a tragic truth, If you do not follow the herd , you are at risk of being punished even for goodness committed by you. Wisdom and conscience  can never win a legal battle ! If you have the courage try practice them !

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A new marker and prognosticator for uremic LV dysfunction

May 30, 2015 by dr s venkatesan

Heart and kidney work in tandem and share a close functional relationship  during health and disease.Progressive cardiac failure causes kidney function to deteriorate,what we call it as cardio -renal syndrome.Similarly, progressive renal disease inflicts either a reversible /irreversible LV dysfunction .The mechanism of  LV dysfunction has not been fully decoded. It is primarily biochemical mediated but at later stages it can be irreversible and structural damage can occur.

We believe uremic  micro molecules leaking from plasma  into cardiac Interstitium  (Myocardial proteinuria ?)  are somehow responsible for the progressive LV dysfunction. Now ,  we have new evidence for albumin – carbon interaction  possibly at myocardial level due to formation of carbamino albumin (C-alb) .

This paper from  Kidney International (2015) 87, 1201–1208;  highlights this new finding .

C-Albumin carbamylationElevated C-albumin is a new  marker for this unique , still not fully understood  entity  “Uremic cardiomyopathy”.

Further reading

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A Radial Trick : Strictly for advanced Interventional cardiologists !

May 20, 2015 by dr s venkatesan

Radial coronary interventions has become a global norm .Even complex procedures are being accomplished with ease adding on to the patient comfort and low risk for access site complications.However !occasionally we need to have multiple access sites to know the detailed real time  contra lateral coronary  anatomy is desirable .This becomes  vital in the retrograde approach for CTO.

Want to  have a quick glimpse of  RCA flow while one is attempting LAD PCI without additional puncture ?

How about doing a contra-lateral  angiogram with the same guiding catheter and wire in-situ within the ipsilateral ostia ? Here is an Innovation.

Of course ,the same concept can be used in femoral angiogram as well.It could reduce procedural time, adds more  efficiency of the hardware system handling.  One can’t ignore the idea as well as the comment of the  author, who says the trick is only for an advanced Interventional cardiologist.

Reference

1.Ferdinand Kiemeneij Simultaneous Transradial Coronary Angioplasty and Contralateral Coronary Angiography With a Single Guide Catheter for Total Coronary Occlusions ,J INVASIVE CARDIOL 2014;26(2):87-90

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