Mohandas Karam Chand Gandhi ,  father of my country , India , made these observations in year 1925  about the  fundamental constituents of  violence in society . These words of monumental wisdom came when he was  addressing young Indians in a country- side rally .

mahatma gandhi quotes medical science humanity

Note, his finger points to , what  exactly is relevant to our profession ! He emphasized this  nearly  100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s  current form !

Should we include moral, behavioral and ethical classes  right from the first year of medical  school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !

Following are revered  facts  . . .  among the  “Guardians of   Cardiology” !


When false truths are synthesized to conceal a true myth . . . where will the poor myth complain ?Following are revered  facts  . . .  among the  “Guardians of   Cardiology” !

  • Primary PCI  is a greatest innovation  in modern day cardiology .Without this modality  most  STEMI patients will buy Instant  tickets to grave yard !
  • A cardiologist who intends to  thrombolyse  a STEMI is considered as a low quality cardiologist .
  • Streptokinase should have  no place in the crash carts of modern coronary care units.
  • There is nothing called “Time window” for rescue angioplasty.
  • VVI pacemaker  will convert an electrical problem of heart block into a mechanical one by depressing LV function .
  • Digoxin is an obsolete  drug even in well established cardiac failure with dilated heart.
  • Beta blockers not only fail to control  blood pressure smoothly , it often converts  a hypertensive individual into a unhealthy one  by it’s prohibitive side effects !


Here is a  video recipe  !

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Coronary  atherosclerosis is the number one killer of mankind. Many would consider it as an  essential  process of aging .Modern  life styles and habits make this appear  very early in life . There is currently an endemic (or even  a pandemic ) of   CAD due to premature  atherosclerosis. We need to recognise CAD is not a  primary heart disease  .It is an irony, heart is an  innocent bystander  to the  biological derangement  of coronary  vascular system  when  it is infested with atherosclerotic plaques .

So , when we  are confronted  with  serious atherosclerotic lesions in a coronary artery   what shall we do ?

We have three options

  1. Take on the enemy in a direct confrontation (Like war on terror ) : This is  some times called as Interventional cardiology .Caution is required as the battle  is within the human coronary artery ,  cross fires and collateral  damage  are unavoidable.

2 .Next  method  is to  find the basic cause  of  terrorism , identify  the perpetuates, facilitators    and try to correct the   root cause of it (CAD ) .This approach  also refered to as medical management  in cardiology community*  . It  aims  at regression of plaque  by statins, and life style modification and preventive cardiology. This modality is most ridiculed and  insulted by the main stream cardiologists.

*Comparable to  bilateral peace talks for a political solution to terror

3. And third option is a  real  surprise !   This  neither  confronts   the lesion   nor does it  address the initiating factors . It   just ignores  the lesion and by pass it with a LIMA /SVG  fly over ,  as if  nothing has happened in this vital high way leaving the culprit scot-free  .This option is  executed by surgeons as  CABG surgery . . . and  for mysterious reasons  this is a  well accepted one .

CABG :Here the atherosclerotic  burden is untouched by surgery . The graft can get diseased  sooner or later , native vessel disease  shall  progress some times encroaching  the ostia of distal graft site . Incidence of acute coronary syndrome following CABG is not greatly reduced for the simple reason we are not doing anything primarily to the inflamed plaques .These issues  are left ,  to be  taken care by the  medical  management .

* This article  does not want to defame these great development in cardiology(PCI/CABG) . They have a  specific role to play. CABG AND PCI remain the only option for critical  lesions with limiting angina .But please remember without  proper  medical management  ( ie Targeting  the perpetuates of  crime )  both  PCI and CABG will be a big sham !

Final  message

Avoiding   the  lesion  or  attacking the lesion  is a  primitive  method to tackle CAD  . Passifying   the lesions  in a slow and gentle manner,   preventing  further progression  or regression  of lesions is the only  “sane” method for combating CAD   . PCI and by pass surgeries  can be termed  as  21st century’s   medical  adventure sports  which  has  limited role ,  in the overall control  of CAD  for the human kind .

And  now  answer this question . . .

Cardiologists attack the lesion and  surgeon avoids the lesion ?  Who is the winner in our fight against CAD  ?

Both of them are  clear losers .The winners are  all those  humble physicians and parmedical workers (or even the responsible lay public ) who  help recognise  the early forms  of  CAD  and  counsel properly to prevent it .

This is  what  Dean Ornish   in 1991  documented in  Lancet  which was never considered scientific   for the simple reason it has no commercial value !




It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

  • 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
  • The medical  world started looking for options to manage CAD.
  • 1970s : CABG was  a major innovation for limiting angina .
  • 1980s: Plain balloon angioplasty a revolution in the management of CAD.
  • 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
  • Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
  • Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
  • 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
  • 2002: BMS are too notorius for restenosis and may be dangerous to use
  • 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
  • 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
  • 2007 : The drug is not  the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
  • All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
  • 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
  • 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we  look back in time and “constantly scrutinize”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

NSTEMI  constitutes a  very heterogeneous population .The cardiac   risk   can vary  between very low to very high .  In contrast ,  STEMI patients  carry  a high risk for  electro mechanical complication including   sudden death .They all need immediate treatment  either with  thrombolysis or PCI to open up the blood vessel  and salvage the myocardium.

The above concept , may  be true in   many situations  ,  but what we fail to recognize   is  that ,   STEMI   also  is  a heterogeneous clinico pathological  with varying risks and outcome !

Let us see briefly ,  why this  is very important  in the management of STEMI

Management of STEMI  has undergone great  change  over the past 50 years and  it is the standing example of evidence based coronary care in the modern era ! The mortality  ,  in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15%  in 1960 /70s . Early use of heparin , aspirin   further improved the outcome .The inhospital mortality  was greatly  reduced to a level of  7-8% in the thrombolytic  era. And ,  then  came the interventional approach, namely primary PCI ,  which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence   for the   superiority  of PCI  , it is only a fraction of  STEMI patients get  primary PCI   even in some  of the  well equipped centers ( Could be as low as  15 %)

Why ? this paradox

Primary PCI   has   struggled  to establish itself  as a global  therapeutic concept  for STEMI ,   even after   20 years of it’s introduction (PAMI trial)  .  If we  attribute ,  lack of   infrastructure  , expertise are  responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world ,   reluctant to do primary PCI  for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI  patients !

All STEMI’s are not  same , so all does not require same treatment !

Common sense and logic would   tell us any medical condition should be risk stratified before applying the management protocol. This will enable  us to avoid applying “high risk  – high benefit”  treatments in low risk patients . It is a great surprise,  the cardiology community has extensively researched to risk stratify NSTEMI/UA   ,  it has  rarely  considered risk stratification of STEMI before  starting the treatment.

In this context , it should  be emphasized  most of the clinical trails on   primary PCI  do not address  the clinical  relevance and the  differential outcomes   in various  subsets of  STEMI .

Consider the following two cases.

Two young men with STEMI  , both present within  3  hours   after  onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL   ,  Low blood pressure , with severe  chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal  or no  discomfort .

In the above example,   a  small inferior  MI by a distal RCA occlusion  ,  and a proximal LAD lesion jeopardising entire anterior wall , both  are  categorized as STEMI !

Do you want to advocate same treatment  for both ?  or Will you  risk stratify the STEMI and treat individually ?  (As we do in NSTEMI !)

Current guidelines , would  suggest PCI for both situations. But , logistic ,  and real world experience would clearly favor thrombolysis for the second patient .

Does that mean,  the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a  random basis  by  not so well experienced cath lab team.

(Note : Streptokinase  or TPA does not  vary it’s action ,  whether given by  an ambulance drive or a staff nurse or even a  cardiologist !  .In contrast ,  the infrastructure and expertise have the  greatest impact on the success and failure  of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc)  need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

A land mark concept , that changed our understanding about the mechansim of genesis of Atrial fibrillation happened  in the year 1998 .( Haïssaguerre ,Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins N Engl J Med 1998; 339:659-666). He proved AF originates in specific focal points from the pulmonary vein ostia at its draining point in LA.Even though there only few selected focal points it was difficult identify those and hence empirical RF ablation of all 4 pulmonary vein became a standard practice. 100s of thousand of these invasive procedure were carried out in patients with chronic AF.

Now, in a span of 10 years , we realise many of these patients require second or third siting of ablation.The irony is , there are many non pulmonary connections  that require repeat ablation.

Common mechanism for recurrences are

  1. Inadequate first ablation
  2. Reconnections
  3. Inflammation and fresh scars
  4. Additional venous focal  sites (coronary sinus  ,SVC, Vien of marshall)
  5. Multiple mechanisms /*Non- focal , systemi AF mediated by neurohumoral triggers ?

A study from the prestigious JCE in May issue of 2015, reveals a starling fact , that about 50% of AF patients  have additional connections  other than pulmonary vein that require ablations at a future date.

If proven right ,  just wonder how much of knowledge and its dissemination  , efforts from  EP industry , technology transfer  over the years is threatening to become redundant .Let us hope,we will somehow conquer the AF either electrically or pharmacologically.

pulmonary vien ablatioan atrial fibrillation carto non pulmonary vien connection

A strong message comes out from this. In modern science, one need not be unduly excited about a new breakthrough.Proof of concept will have to overcome the ultimate test , ie time .

We essentially live in our blood vessels and age in our arteries.CAD is the principal  cardio vascular disease, which  God has created in Homo-sapiens to ensure they  do not stay more than “allotted life span” in this planet. Of course , the current generation cardiologists equipped with scientific weapons , have since decided to take the fight directly in the Almighty’s domain .Contrary to the popular medical doctrine, treating an established CAD seems to be easier task than preventing a new onset CAD.

While , arteriosclerosis is a normal aging process, atherosclerosis could be an  aging as well as a distinctive pathological process. However , athero-thrombosis  is a definite pathology of vessel wall .We know at any time atherosclerosis  can transform into  athero-thrombosis  and result in  clinical event depending upon the  triggers and other associated conditions, which we refer to as major or minor  risk factors.

In scientific terms ,

  • Primary prevention  of CAD is preventing first episode of  Coronary  event*(Typically , CSA, STEMI/UA,NSTEMI/SCD,)
  • Secondary prevention  is  prevention  of  second  or subsequent episodes following the first clinical event.(*What if , if  the first event is silent and never known ? )

For all practical  purposes CAD and  coronary atherosclerosis is synonymous. Can we  prevent atherosclerosis in human biological system ?  What are we  supposed to refer to  such a preventive measure , if any ?

We are biased towards obstructive CAD as we often  think it is the  the only form of CAD .Then , how do we diagnose , treat and prevent a minimal non flow limiting plaque , coronary endothelial dysfunction , or  acute coronary erosion that can occur in very early stages of atherosclerosis, in other wise healthy persons.(Routine IVUS ,OCT ? Futile isn’t )

  • Preventing  sub-clinical  CAD  from manifesting  as clinical CAD , is technically   primary prevention”  but still  patho-biologically  secondary prevention.
  • Preventing a CAD in a patient  with peripheral vascular  disease  or preventing CAD in a patient with TIA or stroke is secondary prevention for cerebrovascular disease but  falls within the definition  of primary prevention of  CAD.
  • Then  comes the new semantics :Primordial prevention .This could be same as primary (or another  version of primary prevention ).Primordial prevention is preventing development  the risk factor  itself (Like DM,HT, Dyslipidemia )

So ,whenever , we talk about primary prevention of CAD by Aspirin or Statins ,realize the complexities involved .Before i finish, let me make you  dizzy further with this quixotic one . In a multivessel CAD, as the  atherosclerotic  plaques are scattered across the coronary arteries in various stages of  maturity  , long term Aspirin  following  anterior STEMI has to secondary prevent an event  in LAD territory  . . . but   primary prevent a plaque disruption in RCA territory !


1.USPSTF Guidelines : Aspirin for the Prevention of Cardiovascular Disease: Preventive Medication

TAVR is the new state of the art Aortic valve replacement procedure done by cardiologists .Nearly 200 thousand implants have been done , and it is
backed up by major trials TAVI TAVR valve dislodgement embolism partent a b What keeps the Aortic prosthesis in situ in the aortic root/Annulus  ?

The valve is not actively fixed but passively positioned in aortic root by either self expanding or balloon expanded valve  system .It retains the position by two different forces acting on the valve in two difffernt directions , but work coherently to keep the valve static .The radial force of the hardware is centrifugal and the elastic force exerted by annulus is centripetal .It may appear mysterious how these oppose each other in a balanced way and arrest the valve in the desired site. Fortunately, there is little  supero- inferior force operating and hence the chances of dislodgement is low .It should also be mentioned we are not yet clear about the best site for TAVR. Annular , supra annular ,or is it at lower virtual annulus , all has some advantages and disadvantages.

Is progressive aortic annular dilatation possible in these degenerative aortic valve ?
Aortic stenosis is chronic degenerative disease. Generally we expect the annulus is narrow and fixed. However for some reason if the aortic annulus loses it constricting force or the root dilates or fresh calcium deposits, there is definite risk  (Not theoretical :See Reference ) of valve destabilisation  , dislodgement and embolisation . *It is vital to understand the para-valvular leak could be a  remote precursor of such potential dislodgement as it represents  micro gaps  in the prosthetic / tissue interface.

How many such  embolisation of valves  are reported following TAVR ?

While the incidence of para valvular leak is common ,(up to 20%) fortunately valve embolisation is reported between .3 to 7.5% (Ref 2). Stastically , subclinical   destabilisation, malpostion  and dislodgement should be more common. The timing of displacement is not clearly reported in literature .It can occur  at any time between few hours after implantation to a much delayed (months after ) complication .

Final message

TAVR is a major break through in Interventional cardiology .It gives us hope for possible TAMR (mitral) and other valve repair modalities .Though dislodgement of prosthesis appear a rare event it is tempting  to ask ,  whether we should work towards a actively fixing valve in aortic root ? That remains a open question !


1. A survivor of late prosthesis migration and rotation following percutaneous transcatheter aortic valve implantation. Pang PY, Chiam PT, Chua YL, et alEur J Cardiothorac Surg 2012;41:1195-6.

2.Thirty-day results of the SAPIEN aortic Bioprosthesis European Outcome (SOURCE) Registry: A European registry of transcatheter aortic valve implantation using the Edwards SAPIEN valve.Thomas M, Schymik G, Walther T, et al. Circulation 2010;122:62-9.

3.Migration of the transcatheter valve into the left ventricle Christopher Cao , Su C. Ang , Michael P. Vallely Mart Annals of Cardiothoracic Surgery Vol 1, No 2 (July 2012 4.Delayed Transcatheter Heart Valve Migration and Failure Vuyisile T. Nkomo, Rakesh M. Suri, ,J Am Coll Cardiol Img. 2014;7(9):960-962.

TGV is the most common cyanotic heart disease to present at birth.The outcome is dismal unless it is intervened at the earliest .It becomes a real  emergency if the dTGA is associated with intact IVS and IAS. (Though foramen ovale /ductus  may help for a while prolonging the survival . Often times , it is restrictive and demands immediate septostomy if primary arterial switch correction is not attempted )

Presence of VSD provides vital time interval to plan  surgery in a less emergent fashion. Otherwise , arterial switch if  contemplated one has to do it before 2-3 weeks (Rarely up to a month ) .The principle is to reverse the circulation before the  systemic left ventricle regress its myocyte function as it is exposed to low pressure pulmonary circuit .


We know , dTGA  has two parallel circuits in a bizzare hemodynamic disconnect .The right sided  pulmonary circuit sustains  the systemic blood flow with deoxygenated blood.The left sided systemic circuit recirculates oxygenated blood into pulmonary circulation again and again.

Survival depends upon , the anatomical communication between two circuits and the effective quantum (Deoxygenated)  of blood flow to the lungs .

Which communication is best for survival d TGA ?

The key is to understand   what we mean by “mixing  vs  shunting”  and the effective pulmonary blood flow (ie quantum of truly deoxygenated blood reaching lungs  vs oxygenated blood recirculating  the lungs in a hemodyamically wasted loop

It appears both atrial  ventricular level  mixing is good for maintaining adequate O2 saturation than PDA .

What does PDA do ?

Ductus is expected to persist in  dTGA  when  IVS and IAS are intact  . It is not clear  what determines the persistence of duct  in dTGA with intact IVS. Principles of natural  hemodynamic adoption would argue , all patients with dTGA should never close their ductus and foramen ovale. While , In reality it may be true for PFO to persist, ductus often gets closed on schedule* , aggravating  the hypoxia .(Both flow mediated myogenic resposne, O2 content of ductal blood and size are the determinants of ductal closure)

The ductal circulation in dTGA can be complex . It initially  acts as a channel to mix both arterial and venous blood flow .It can become a liablity  if its large , as the pulmonary vascular resistance falls,  blood is shunted from aorta to pulmonary circulation and potentially precipitate failure .Please note,  this shunting  also can  improve  the saturation as it diverts aortic blood into lungs ,still the ultimate usefulness will depend upon intermixing  at some other level  other than ducuts , ie either atria  or ventricle .One should  realise  ductus can never bring  good admixture as it happens outside the heart .It is obvious intra cardiac  mixing  with ASD and VSD  is always better and devoid of providing differentially saturated blood  to the extremities  , which is an inherent feature  PDA mediated  mixing .If ductus  is the only means of mixing and shunting  the lower half of the body has  an advantage as it is perfused continuously by oxygenated blood .This  may manifest as  reversed differential cyanosis in few combinations of TGA physiology. (Relatively pink  lower limbs and cyanosed upper extremity )


Ductus can be a double edged friend or single edged foe  in dTGV . It depends upon the size , quantum of shunt and associated  channels of mixing like ASD and VSD . If it occurs with  intact IAS and IVS it plays a role of  life sustainer.

Presence of ductus is definitely useful  initially.It can either help by mixing, intermittent bi-drectional shunting  or committed left to right shunting .This is why we attempt to  preserve its patency or even recannalise it by stenting  in such situations .The later can be used to buy time and train the regressing LV .However ,large ductus can be counter productive  if additional shunts are also present where one should even contemplate closing it .



pda in dtga ductus ductal flow in tga2.Transposition of the great arteries with intact ventricular septum and patent ductus arteriosus. Waldman JD, Paul MH, Newfeld EA, Muster AJ, Idriss FS.Am J Cardiol. 1977 Feb;39(2):232-8.

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

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 .

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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