Archive for April, 2009

Heparin was invented accidentally by a 26 year old  , Jay McLean, a  pre clinical  medical student  in 1916 .It was one of the greatest discovery  in  medicine .It helped us prevent blood from clotting.Frozen blood inside human circulatory system constituted one of important mechanisms  of  human  death.This ranged from acute myocardial infarction to cerebral thrombosis  .


As we decoded the mechanism of action of heparin , it was clear it bound to the  naturally occurring molecule antithrombin 3 and effectively blocks the intrinsic coagulation mechanism and thus behaves as an important anticoagulation agent.

How heparin acts as a thrombolytic agent ?

We know , our hematological system has a powerful  natural  fibrinolytic mechanisms  to protect against unwarranted( pathological ) intravascular coagulation. This is mediated by  anti thrombin, protein C , protein S  ,  plasminogen  system etc  . Natural concentrations of tissue plasminogen activator (Tpa)  also  help in lysing intravascular clots.

There is a constant  , delicate balance between procoagulant , anticoagulant and antifibrinolytic molecules .Intra vascular  clots occur when a vascular  injury triggers  a clot formation and the clinical event occurs.

But,   once insulted ,   the  circulating blood   does not remain a silent spectator . It is  constantly  on the look out for a foe to attack the thrombus that is interfering  with its natural flow  . Antithrombin 3 is one such molecule. Success  of lysis depends on the power of natural forces. There are hundreds of episodes of microlysis that take place every day  (Which happen without our knowledge ) .In  patients with vascular  disease these episodes are likely to be further more.

What does  Intravenous heparin in high doses  do ?

Heparin immediately  blocks of powerful procaogualtion activity .One of the important heamatological principle  is “Thrombus begets thrombus “. It is  a vicious cycle. This is immediately  tackled by heparin .The powerful trigger of thrombus induced thrombus propogation is shut off .

This makes a  2 cm sized clot to remain  in  2cm . After  making sure of this , the blood in the immediate vicinity   start percolating the clot.  The heparinised blood   switches to  a pro- fibrinolytic mode as the balance of forces  is fully tilted in favor of fibrinolysis or thrombolysis.

Is there clinical evidence to call heparin as thrombolytic agent ?

Yes . Contrary to the popular scientific  principle we have only clinical evidence  . laboratory evidence is not convincing as heaprin lyses clot only in vivo . Since ,  evidnece based medicine requires  laboratory evidence  we hesitate to call this as  thrombolytic agent !

It has been a strong clinical observation ,   many  major intracardiac or  intravascular  clots  regress in size

(or totally dissolve )  with intensive heparin  regimen .The effect is seen in 48-72 hours.Some times in first 24 hours.

What are the clinical situations where heparin has successfully lysed the clots*?

  • Pulmonary embolism
  • LV clot
  • LA clot
  • Cortical venous thrombus
  • Deep vein thrombosis
  • Coronary thrombosis**
  • Portal vien thrombois
  • Renal vein thrombois

* Plenty of case reports available for each condition

** Sustained micro  thrombolysis  is the major mechanism of benefit in NSTEMI

If it is true ,  heparin dissolves thrombus , why  it is not called as thrombolytic agent ?

Why not ?  You decide yourself !

How does heparin compares with  the great thrombolytic agents*  like  Strepotiknase, Urokinase,Altepase, Retepalse , Teneckteplase (TNK TPA) ?

Many (Rather most . . .)  would consider it ,  as  foolish , to compare heparin with these agents .But the fact of the matter is except for streptokinase there is no comparison studies available. Attempting such a study  in humans will  be considered unethical. Without   a proper scientific  data  heparin  can not be ignored either.

But ,  some of the control groups in major  studies of thrombolysis  through some light !

In pulmonary embolism thrombolytic agents and heparin have similar effects on intrapulmonary thrombus

An important point to remember here is   , the powerful thrombolyic agents are administered  in as short duration (Bolus / 1  hour infusion ) .This is invariably  followed by heparin infusion . Why do we  do that ? because we know it is important . One may never know , how much of lysis is done  by the trhombolytic agent and how much by heparin .

if you analyse the  data  success rate of thrombolytic agents are infact attributable  to the follow up heparin

Thrombolytic agents  piggy packs on heparin and claims the  credit for thrombolysis *

In thrombolytic  therapy  , heparin  is considered  as an adjunct to streptokinsae but in reality  streptokinase  may an  adjunct to heparin

Importance of  heparin In Acute MI (HEAP Trial)

It should be realized  there is a time window for heparin too . . .  early administration  can have  great benefit

Early heparin prevents formation of  core  of the clot .The   importance of acute administration of  aspirin  in suspected STEMI  is well recognized  by paramedics  .  A bolus of heparin (10000 u)  immediately  could have great impact on the outcome as well  .Paradoxically we talk more  about emergency PCI,  on  transit TPA  etc . . . We have seen  number of patients  referred  with  STEMI   from   suburban areas traveling for hours with out any anticoagulants but promptly getting sorbitarate tablets ! Unfortunately prehospital heparin is rarely stressed in literature .

Watch the video : Heparin : The forgotten hero

Final message

  • Heparin is   an  under rated drug  as a thrombolytic agent.
  • Just because it has no direct action  on thrombus it is considered an inferior agent.( One other reason  for it to be  considered  inferior ,   it  is  very cheap  !)
  • Heparin too ,  has a time window effect in acute MI (Class 3 evidence ie   wide clinical experience)
  • It’s  usage should be early  and  liberal , especially  in out of hospital setting in vascular  emergency.
    Note of caution : This article is not meant  to  defame  the thrombolytic agents.It only stresses a point that , heparin has also a role , as a thrombolytic agent. *Whenever rapid thrombolysis is required in life threatening situations specific thrombolysis is indicated as per guidelines.

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The importance of venous system

Cardiovascular system  consists  not only of  heart  but also   the blood delivery and retrieval   system namely  the arterial and venous circulation .As  the heart pumps , 6  liters   of blood  every minute  , it  has to   traverse the  entire venous circulation promptly ,  to  complete  the hemodynamic circuit.


Source : From web. Thanks to whoever created this Image

While  physicians are preoccupied with disease  of heart there is an important  groups of disorder of venous system .The  deep vein thrombosis  (Also called venous thrombo embolism . VTE ) is the  most important  entity .This disorder even though is a cardiovascular  disease  ,  it   rarely presents to a cardiologist .

As  we tended  to ignore the  veins   for decades  now, “sudden venous deaths ” other wise called massive pulmonary embolism  is calling for our attention

What are the deep veins ?

Popleteal , femoral , iliac (External , Internal , common ) . Upper limb axillary and subclavian veins.

Clinical classification of DVT  :  Femoro popleteal  , Pelvic  ( Ilio femoral) , Mesentric DVT.

What are the high risk population for development  DVT ?

  • Genetic predisposition  constitute  the  strongest risk(Factor V lieden mutation )
  • Major orthopedic surgery
  • Pregnancy /Oral contraception
  • Disseminated  malignancy

And now  ,  the more fashionable risk factor “DVT after long distance flights”

What is key diagnostic issues in DVT ?

Key to diagnosis is clinical alertness .Local swelling  , edema legs and inflammation should alert the physician.

  • Homan’s sign(Pain on  dorsiflextion of  ankle) .
  • Louvel’s sign (Leg pain on coughing ),
  • Lowerberg’s sign  (BP cuff induced pain on affected leg at low level inflation  )

( Well’s score  is based on pre test propabilityLancet 1997 )

Many times DVT is diagnosed only after it embolises into lung.So remember shortness of breath and acute dyspnea  could be the first manifestation of DVT.

Once diagnosed  DVT  it should be  risk stratified either as low risk or high risk .

Biochemical diagnosis of DVT : DVT is a form of intra vascular coagulation and it activates fibrinolysis.D Dimer estimation has strong negative predictive value .If D dimer is negative it excludes DVT by 99% .Positive D dimer does not confirm it .

Is  it  necessary  t0 image  the venous clots ?

No . It is rarely required.  Instead we need to know the site of occlusion .Doppler and ultrasound scan can help locate the site of obstruction .

Other modalities *  may help evaluate the thrombus

Venous angiography (Filling defect, collateral )

MR angiogram

Fibrinogen tagged nuclear scan


  • Acute management
  • Long term management .

Acute management

Immediate Heparin ,  bolus followed by infusion ( 5000U, 1000U/h) followed by oral anticoagulation forms the corner stone of  management of DVT .

Once a DVT is documented should we attempt  to  improve the venous circulation or try to slow down  the venous circulation ?

There is a paradox here.The therapeutic strategy is to improve the venous circulation . A sluggish venous circulation predisposes fresh thrombus. So even though ,  it is  logical to expect some  migration of  thrombus  proximally  with the standard  therapeutic methods of DVT  ,  it is the ultimate principle of management of DVT.

How heparin infusion achieves  it’s  therapeutic goal  of clearing  thrombus burden in the venous circulation is not clear .It is believed sub clinical PE  occurs in every case with large DVT and these thrombi get   microlysed either  within focus of  DVT or in transit circulation  or within the pulmonary vascular  bed.

What is effect of intensive anti coagulation on DVT ?

  • Lyses the thrombus
  • Dissolves the thrombus
  • Dislodges thrombus
  • It can prevent only fresh thrombus

Answer : All of the above can occur

Can we track the movement of deep vein thrombus ?

It is not an easy thing to track the movement. Doppler will give an idea. Invasive investigation to track the thrombus is neither practical nor necessary.

What is aggressive management * for DVT ?

* Aggression is rarely required in DVT management.


  • Thrombolysis : Systemic/local catheter based
  • Venous angioplasty/Stenting
  • IVC filters


Indication for thrombolytic therapy

Surprisingly,   thrombolytic therapy has limited role in the  management of  DVT. There  is absolutely no role for routine thrombolysis in DVT (Heparin does the same job , more consistently with less risk )

It is used only when there is limb threatening or lung threatening situation .

Pulmonary embolism already occured

Massive iliofemoral thrombosis .

When will you call a vascular  surgeon ?

Thromboembolectomy as a treatment for DVT is rarely advocated .

The 2004 American College of Chest Physicians consensus statement on the treatment of thromboembolic disease recommended against the routine use of venous thrombectomy in acute DVT except in cases of phlegmasia cerulea dolens . ( Severe necrotising venous edema )

The issues against surgery are

  • Generally these patients are more sick and co morbid conditions
  • Complex nature of surgery in deep iliac veins
  • Blood loss  from deep friable veins
  • The surgery further traumatizes the vein, recurrence  of DVT is  very much possible
  • Primary cause is not addressed by surgery

What are the indications for IVC filter ? What  are the types of filter available ?

The indication for IVC filter in the acute management of DVT * has been ( Rather continues to be  . . .) controversial .The major reason for the controversy is the risk  ( The wasted effort  too !)   to benefit ratio and  is not clear.


There are three types of IVC filter available

  1. Temporary venous filters
  2. Temporary retrieval IV filters ( Gunther tulip ) Nitinol recovery filter Bard
  3. Permanent IVC filters

*In long term prevention of PE the indications are fairly established.

Differential diagnosis

Is there an entity  called  superficial venous Thrombosis (SVT)

Superficial venous thrombosis and thrombophlebitis are more common than DVT and should not be confused with DVT. ( Easier said, some confusion is bound to occur !especially ,  when it occurs  over  thighs ) .This is common  following IV line  and  varicose veins in lower limb Present with pain, tenderness, or an indurated cord along a palpable  superficial vein  with erythema. It is less likely to propagate into pulmonary circulation.

How often a superficial venous thrombosis convert into deep vein thrombosis ?

Patients with superficial phlebitis above the knee have an increased risk of deep venous thrombosis and should probably have ultrasonography.They may require  warm compression , NSAIDS and  local thrombectomy.

What is the post-thrombotic syndrome? How to differentiate it from recurrent  DVT ?

Post-thrombotic syndrome is  due to the damage  to the  valves in the veins  that leads to chronic venous edema of extremities. It may mimic like an DVT . usually occur within 2 years of DVT.

Unanswered questions

1. What will happen to  the thrombus following filter insertion ?

Large thrombus gets trapped in IVC .The problem gets shifted form the legs to the vena cava .This makes it mandatory  for these  IVC  clots  to be cleared either manually or  pharmacologically. Small thrombus and embolic showers continue to cross the filter without  difficulty.

2. IVC filters are recommended in DVT , if a patient has an absolute contraindication to heparin but , is it not a fact ,  filters also demand  anticoagualtion ?

It is true , filters demand anticoagulation. So ,  oral anticoagualtion should be given whenever possible in all  even after IVC filter. This is  , not only to make sure filter does not get clogged but also prevent further  clot formation in the legs and also   distal to the filter in   (Procoagualnt )  individuals .Further , anticoagulation forms the mainstay treatment in patients with chronic thromboembolic PAH ,  which the filter does not address to.

3. Is there safe venous clots that the pulmonary circulation can effectively tackle ?

Typically PE occurs  as

  • Massive acute PE
  • Sub acute PE
  • Chronic pulmonary thrombo embolism (Showers of microemboli lead to PAH )

Consider the following pulmonary  vascular anatomy : MPA 2.5cm ,  RPA,  LPA 1cm segmental pulmonary artery 5 mm ,  pulmonary arteriole 3  mm ,  pulmonary capillaries 200 microns . The  deep venous thrombus typically has  a diameter of  up to 1-1.5 cm . It needs a at least  2. 5 cm   diameter  clot to occlude the main pulmonary artery.Micro thrombus may get cleared by pulmonary vascular bed.There can be safe venous clots.

Final message

  • DVT and PE are the common venous emergencies.
  • Prevention of PE is the major aim of acute managment.
  • Identifying the underlying cause and prevention of DVT per se is the long term aim.
  • Aggressive local approach is largely  unnecessary except in leg / lung  /life  saving situations

Intensive Heparin protocol  followed by long term oral anticoagualnats (1 year or more)  is  an excellent approach in most patients.


The most important point to remember is the treatment for high risk DVT and suspected  or established PE is exactly same

*Only 10% of PE  are candidates for thrombolytic or surgical  therapy so at times of real dilemma , there is nothing wrong in administering  heparin in all patients with suspected  high risk  DVT/PE  even without confirmation.

All those hi fi stuff of V/Q scan , pulmonary angiography may be a misadventure .Remember empirical (Some call it as unscientiifc ! )  therapy  too , can save many lifes

Further reading

Best Link for  IVC filters   http://www.tigc.org/eguidelines/VenaCava.htm


  1. Decousus H, Leizorovicz A, Parent F, et al. A clinical trial of vena caval filters in the prevention of pulmonary embolism in patients with proximal deep-vein thrombosis. N Engl J Med 1998;338:409-415.

What is new in catheter thrombolysis in DVT ?

dvt thrombolysis


A interventional catheter based clot lysis for  DVT

For the comprehensive  ACCP 2008 guidelines of managing DVT  reach the following site

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Sick sinus syndrome  or sinus node dysfunction (SSS, SND ) is one of the common cause of  symptomatic bradycardia .The other cause for  pathological bradycardia is complete heart block.Together , these two entities share 99% of indications for permanentpacemaker implantation.

The sinus node can get affected in various diseases . The commonest cause for SND is age related.This is manifested  as inappropriate bradycardia .The  other common presentation of  SND is exaggerated bradycardia to betablockers and calcium blockers.In fact , some consider drug  induced bradycardia  is  nothing but  , unmasking of underlying SND.Pathological states that result in SND include  hypothyrodism , infiltrative   and inflammatory diseases . (Surprisingly ,  ischemic  SND  is a lesser  clinical problem when considering  the  rampant CAD in our population )

What is  is a fundamental difference between SND and complete  heart block* ?

Sinus node is the proximal most pacemaker of the heart. When it fails the chances of  a  subsidiary pacemaker coming to the rescue is far greater than  a complete AV block. Further the quality and stability of the escape pacemaker is better in SND. In fact , in pure SND  ( With out AV nodal disease)  a sinus arrest is rarely fatal as escape rhythm  occur without fail.

* It should be emphasised  ,  there can be associated AV nodal disease in  significant (10%)  number of patients with SND .This may be present either at the  time of diagnosis or it can develop later in the course .This has important implication in the selection of   pacemaker .The discussion here is confined to isolated SND .

How common is ventricular escape rhythm in SND ?

It is very rare. the ventricle never gets a chance to come to the rescue as invariably junctional pacemaker takes over at times of extreme sinus pause/arrest.For the same reason , pause dependent VT (Brady dependent ) is also less common in SND .

What is  stokes Adam’s attack ? How  common it is  seen in SND  ?

It is the cardiogenic  syncope due  to extreme bradycardia. This classically occurs in complete heart block , when

the the escape rhythm becomes either very slow or temporarily goes for sleep .This results in a huge  pause (unlike sinus pause  of   , the pause  here is  ventricular pause  , this is  actually an  asystole  )  it  can  immediately trigger an VT or VF .

If  SND is not life threatening why pace maker is indicated in them ?

The pacemaker is primarily indicated for prevention of dizziness , near syncope or syncope.So primary impact is on improving quality of life  , not reduction in mortality. While in CHB  pacemakers improve  symptoms and survival.

Which form of SND can be dangerous ?

When SND is associated with rapid atrial fibrillation  some times it can trigger a VT/VT if ,  these patients also have

a fast accessory pathway with short refractory period. (<250msec)

Final message

If you have only one pacemaker at your disposal , but there are  two patients ,  one with SND and other with CHB please put the pacemaker to  the patient with CHB , even if the later has insurance coverage and the former is not .You are justified in  diverting  the pacemaker !

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LV dysfunction , perhaps  is  the most common  medical term used by  physicians  world over.But surprisingly , It is not easy to infer what they mean by it ! The term literally means left ventricle is not functioning all right .

LV dysfunction can be classified by many  ways.

  • Symptomatic vs Asymptomatic
  • Global vs  Regional
  • Reversible vs Permanent
  • Systolic vs  Diastolic
  • Ischemic vs Nonischemic
  • Primary vs  Secondary ( Muscle vs valve  etc)

If you analyse the above classification LV dysfunction can mean different things to different people , at different times.Though systolic dysfunction ,  as reflected by low EF % ( Less than 50% ) is the major cause of LV dysfunction  the issue is not simple.

Is coronary artery disease ( CAD  ) a must for LV to  become dysfunctional ?

No , not at all .CAD  is the leading cause of LV dysfunction .Primary muscle disorders -cardiomyopathy is an equally common entity. Valve disorders especially  aortic valve stenosis is   another common cause for LV dysfunction. Further ,  systemic hypertension, diabetes mellites, renal failure, can result in serious impairment of LV function .Some drugs ( Adriamycin ) can either precipitate or aggravate LV dysfunction.

If  physicians themselves are confronted with such complexity , how are ,  our other medical  colleagues  (Forget about the patients !   ) will understand  the concept of LV dysfunction.

But , the  crux of the matter is every doctor believes  LV dysfunction is synonymous with low ejection fraction. A surgeon or an anesthetist is quiet happy to operate  if the ejection fraction is above 60% .

Can a patient  have significant LV dysfunction with normal Ejection fraction ? (EF )

Yes , this can occur in advanced degrees of diastolic dysfunction, where cardiac contractility is normal but

fails to relax adequately .

Is diastolic dysfunction less dangerous than systolic dysfunction?

May be , that is the dominant opinion   , but  there are sufficient evidence  emerging  that opinion is wrong.The main reason for diastolic dysfunction  to send a ” not so sinister signal ” is over diagnosis of  grade 1 diastolic dysfunction in the general population  . The echocardiologists considered it fashionable for a quiet a longtime (Many have changed since then !)  to report all patients  with reversed E :A ratio in the mitral inflow doppler profile as diastolic dysfunction. This has resulted in  thousands  of  asymptomatic , healthy people getting  labelled  as grade 1 diastolic dysfunction  undermining the importance of this entity.

The fact of the matter is true diastolic dysfunction is indeed dangerous , if not more dangerous than systolic dysfunction  for the simple reason ,  there is  no specific treatment for this condition

To improve the specificity to diagnose genuine LV diastolic dysfunction it is suggested to remove grade 1 diastolic dysfunction from the literature .

Other causes of LV dysfunction with normal EF

  • Some times , there can be wall motion defects  and   mitral regurgitation but still the EF can be normal .
  • Mitral valve dysfunction can be a part of LV dysfunction .The EF is either  not affected as ischemic damage  might be confined to papillary muscle.
  • Vigorous compensation from non ischemic areas  can normalise an EF

What is the difference between LV dysfunction and  LV failure ?

Many times  both these terms are perceived  to convey the same meaning .But it  can  never be used synonymously .Cardiac failure is a clinical entity while LV dysfunction  is  a  derived  technical parameter  by and large an echocardiographic enity. Cardiac failure   is defined classically as a clinical syndrome .(elevated jvp, edema * S 3 rales etc)  Neuroueohormonal activation  can occur with both.

A patient with   LV dysfunction    when destabilsed  develops   LV  failure and after stabilisation of   LV failure he is brought  back to  the baseline  LV dysfunction

*What is the link between LV dysfunction and RV dysfunction ?

RV can not be silent companion when the LV fails  . There always have been link between the two.

LV dysfucntion begets RV dysfunction   and LV failure can trigger a total heart failure

Apart from the classical concept of ventricular interdependence  ,  where  inter ventricular  septum plays a pivotal role , now there is strong evidence  to  prove  both LV and RV myocardial muscle  bundles are interwoven . In fact failing LV drags the muscle bundles over RV also (Friendly pull , let us die together !)  and this is classically seen in idiopathic dilated cardiomyopathy where all four chambers of the heart dilate. There is also biochemical  evidence the RV myocytes deplete thier norepinephrine stores  in LV failure.

Is there an entity called transient  or temporary LV dysfunction ?

The classical chronic reversible LV dysfunction also called hibernating myocardium is a different topic shall be discussed later.

Can acute ischemia cause LV dysfunction  ?

Yes .This can occur during ischemic stunning of myocardium during NSTEMI .This can result in acute pulmonary edema* at times.This can be termed as ischemic LV dysfunction  as there is no myocardial necrosis .

* The pulmoanry edema mentioned here is the  flash pulmonary edema carries very dis prognosis.

What is the cause of LV dysfunction in critical aortic stenosis ?

Is it fibrotic ?

Is it necrotic ?

Is it ischemic ? (Associated CAD )

Or is  it simply  a mechanical inability* to contract  as the outflow is closed ?

There is no specific answer . All the above factors may contribute .*But the fact that  most patients recover full normal LV function  following aortic valve replacement would make the last explanation more likely.

What does the term LV  dysfunction mean to a  cardiac surgeon when he plans  for  a CABG ?

LV dysfunction becomes an important determinant of overall  outcome   in  patients who  are  going  to receive a CABG .The surgeon will have contingent strategies  during peroperative and post operative phase while operating  in hearts with severe LV dysfunction.

How much  of LV function  is going to recover after CABG  ?

This  can not be predicted accurately but CABG  may not  resucitate all dying myocytes and bring life in them .The buttressing effect of blood within the dysfunctional segement can improve contractility and  reduce the wall motion defect(This is an indirect mechanism of improving EF )

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The answer to this question  is not  easy  , as   one  would tend to believe . In fact this question , takes it for granted     revascularisation  will  improve the LV dysfunction in patients  with severe LV dysfunction.

The truth is , we  are not sure   about the mechanisms . How   revasculariastion  will have an effect  on  chronically dying or dead myocardium  ? (Acutely dying myocardium is a different story, where revascualrisation has a profound effect , that is called salvaging the myocardium )

This  issue is  of great clinical significance  in end stage ischemic heart disease  .A typical  myocardial segment in ischemic cardiomyopathy  has millions of  the dead cells  interwoven with dying cells  with  occasional  clusters if live cells scattered all over .Once the process of myocardial apotosis sets in ,  myocardial cell death does not result  in segmental destruction  instead  an universal cell death.(Paracrine signals of  cell death that spills over to adjacent segments  )  The current standards of revascualrisation (PCI and CABG) aims to provide blood flow  in a segmental fashion. Even if the blood flow is restored in an obstructive vessel it is not clear , how it is going to enter the chronically atrophied myocytes.

Meanwhile , many studies are available   suggesting  coronary revascularisation does indeed improve LV dysfunction. These  evidence has never been  conclusive .Real world experience would also  confirm this  simple fact , that   angina relief is definite following revascularisation but not dyspnea  relief  in patients  with LV dysfunction .

So ,  when seeking the  guidelines  for revascularisation  ( PCI or CABG )  in patients  with CAD one need to ask  this  specific  question

Does the patient has

A.Angina alone

B.Angina and dyspnea

C.Only  dyspnea

If the answer is C ,  assess the patient again , rule out systemic causes of dyspnea (Anemia, renal function etc)  rethink  or postpone  revascularisation.If primary  or secondary LV muscle dysfunction has set in revascularisation has little value.

Also read

Viable myocardium

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Coronary collateral circulation is the God’s gift to mankind.It has potential  benefits  ( and  of course real benefit !)  both during acute and chronic coronary syndrome.

Collaterals in CCS

The classical role of coronary collateral is in patients with chronic stable angina.It is quiet common to see patients with totally occluded  LAD or RCA with normal  LV function maintained  by extensive collaterals .

Collaterals during ACS.

An intact and functional  collateral circulation can prevent an NSTEMI  from converting into STEMI.In fact many of the patients with unstable angina patients carry on with viable myocardium just because thaey have good collaterals.It gives us a time window to intervene .Some times the col laterals are good enough and help us avoid a revascularisation in toto.

Collateral’s in  STEMI.

This is not well understood. Some  researchers  reported opening up of collateral channels very early after a STEMI. Logic would suggest , anatomically patent functionally closed collateral channels are  always available at time of crisis. But not every one is blessed with such rescue mechanism.

What determines  the native collateral channel development in human cor0nary circulation ?

When  the answer is unknown , it moves to  the  genetic domain also called  – God’s domain .

Our ignorance in decoding coronary collaterals is vast.

The chief cause of this ignorance is we always  tend , not believe things which we don’t see.

Coronary collaterals channels need to atleast 1mm  to be visualised by CAG.There could be a vast network of micro collaterals out there within the myocardium invisible to current imaging methods. (In fact , this has a link with outcome  of the COURAGE study )

Is coronary collaterals have all the three layers of an artery ?

Yes .But the media lacks muscle.

Is coronary collateral less prone for spasm ?

May be.

The drugs we give , Calcium blockers , betablockers, and nitrates have same  hemodyanmic effects  as in native coronary circulation ?

We don,t know as yet. Nitrates are supposed to improve collateralisation

How common is atherosclerosis to involve the coronary collaterals ?

How often is an ACS precipitated by an collateral occlusion ?

May be more common than we think.

Can we stent a  2mm wide  collateral to maintain  the patency in case of a CTO  ?

A question need to be answered by current generation interventional cardiologists.

Is coronary collateral gives protection against primary VF ?

In one sense ,  the number one killer of mankind is  in fact not STEMI but the VF that follows it .

Why only a few develop a VF following an MI ? What determines the arrhythmic response to ischemia ?

Some anecdotal observation  of     suggest a role for early coronary collateral  opening in the prevention of VF .

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Diagnostic issues in cardiac failure : A  febrile pleural effusion in a patient with LV dysfunction .

Is it a transudate or exudate ?  How to confirm the pleural effusion is primarily cardiac failure related ?

When the classical protein criteria is inadequate or prone for errors

Try this more specific marker  within the pleural fluid

N-Terminal Brain naruretic peptide

Pleural fluid NT-proBNP is very useful in establishing the diagnosis of HF-associated effusions, and it confirms this diagnosis . The measurement of NT-proBNP rather than serum to pleural protein gradient is recommended for identifying mislabeled cardiac transudates.

Reff :Biomarkers of Heart Failure in Pleural Fluid. Chest. 2009 Apr 10.

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Radial access  for both diagnostic  coronary angiogram  and  PCI has been increasing steadily.Many centres have adopted an  exclusive radial approach. Newer ,  radial specific  hard ware  is  being produced.(Link) .It is surprising , radial approach has  gained momentum  primarily outside  USA (Europe , Japan, India ).The advantages of radial access is primarily , patient comfort, less local site complication.

Prerequisite for radial approach.

The importance of  pre procedural Allen test to document dual blood supply is  well established but the less  appreciated  concept is  preprocedure  radial artery size  assessment . It  could be as important as Allen test .

The normal diameter of radial artery lumen is 2.4mm (Range 1.8-3.0) .Some population have still smaller radial lumen(India KA.Sambasivam et all mean 1.8mm). Compare femoral artery (8.5mm diameter, 4 times bigger )

Imagine this  situation ,  a 1.65 mm (5 F) diameter catheter trying to enter a 1.7mm radial artery !

Is it not a futile excercise ?   Many of the failed radial access is due to  radial artery /catheter mismatch .


There has been occasions , when the radial sheath is larger than radial artery itself !

So the size of the radial artery becomes vital in planning radial CAG.

What are ways one can estimate the size  of the radial artery ?

  • Volume of pulse (Still Useful , but can fool us some times!)
  • Thick radial walls (Monckeberg,s sclerosis)
  • Ultrasound imaging

Radial artery spasm

Radial artery has more medial  smooth muscle and further the fibres  criss cross the artery. Further , the radial artery is richly innervated by sympathetic  nerve terminals.

The major factor that determines likely hood of spasm is

  • Pain  intensity.
  • Amount of free space between sheath and vessel wall
  • The frictional force between sheath and artery wall is the powerful trigger for spasm and pain.

What is the biochemical mediators of radial artery spasm ?

It is logical to believe all  vascular  spasm are due to calcium .But it is not. Calcium blockers have  no definite relief for  spasm.Nor adrenaline mediated alpha receptor stimulation  has a major contribution for RAS. Phentolamine is useful

Is there a objective and quantitative method to assess radial artery spasm ?

Removal of the radial  requires some force.  Kiemeneij ( Measurement of radial artery spasm using an automatic pullback device. Catheter Cardiovasc Interv 2001;54:437–441.) demonstrated if one require > 1kg force to remove a sheath it correlates with clinically significant spasm.

What are the serious sequel of radial artery spasm ?

Radial artery rupture and radial artery avulsion has been reported when attempting to remove the sheath from spastic arteries

Management of radial spasm

There are two aspects to this problem

  • Prevention of  spasm
  • Treatment of established spasm

How to prevent or reduce  radial artery spasm ?

Radial artery is a very sensitive artery .The incidence of spasm can be up to 20%  The spasm can be due to

Hardware, technical ,anatomical factors.

Apart from  above  three factors,  the most important is anxiety related .The key principle is ,   sedating the  radial artery is as important as sedating the patient .

Sedating the patient

Explaining to the patient about the procedure can allay the anxiety. It is a fact , the tactile perception of catheter movement  in radial route is more than the femoral .In very anxious patients (Some centres use it routinely )  IV sedation (Midazolam)

Sedating  the radial artery.

Local anesthesia : Subcutaneous lignociane , though widely used has a drawback.It can aggravate pain, induce spasm , accidental entry into lumen may cause a hematoma  .All can potentially make the pulse feeble. So care should be taken in giving minimal lignocaine ( At a specific  point needle entry) with a short needle . One should watch , the grace with which experienced radial interventionist give the local anesthetics !

Arterial cocktail

The arterial cocktail consists of combination of Nitroglyceine (200 mcg) , Xylocaine (50 mg) Verapamil (5 mg) an. Heparin(5000 IU). Sodium bicarbonate (4%) is optional to neutralise the acidity of the solution

How to administer ?

Ideally spasmolytic cocktail should be given before the sheath is introduced immediately after puncture . As the drugs has to get in contact with the arterial wall .if cocktail is given after introduction of sheath one of the following may be done.

  • Give the drug as it enters the artery.
  • Pull back the sheath when injecting the drug.
  • Use a side holed sheath.

Technical issues to prevent radial artery spasm

Try to puncture in single prick . If the first puncture is not successful , don’t attempt to cross a spastic radial artery Remember (Unlike femoral ) successful puncturing of a spastic radial artery may be the beginning of a vexing and tiring procedure.So if we have lot of difficulty in getting in ,  please avoid the procedure and switch to femoral . (Spastic signals may spill over to left hand also !)

Remember unlike femoral cathetrisation , in radial access,  getting out the catheter could  be more tricky   than getting in !

Avoid procedures that would  require  multiple catheter , guide wire exchange .Complex lesions and in emergencies.( Some experts do Primary PCI through radial !) .Now  dedicated radial hardware are available.

Sheath selection (Visit :  Arrow International )

Long sheaths have been used in the past. It makes the spastic segment lengthier.Now short sheaths are increasingly used. Long sheaths (20-25cm ) give better suppport during catheter manipulation. Side holed sheaths  is a newer innovation. This maintains the  blood flow on the sides of sheath and reduces friction with vessel wall .Further, it can deliver the arterial cocktail to vessel wall and effectively prevent or reduce spasm.

Catheters : Use 5 F/6F. Rarely 7f are used.

Guide wires :Hydrophilic guidewire are radial friendly.

How to manage established severe spasm ?

For severe  spasm with sticky sheath / catheter

  • Increase the analgesia with morphine
  • Repeat NTG and Verapamil
  • Warm compresses over the forearm
  • Never pull with force
  • Wait for an hour and try pulling again (Often successful )

Last resorts

An axillary block

Vascular surgery

Reference and further reading

For excellent collection of radial access resources  please visit  www.radialforce.org

(Much of this blog’s content is based on this article )



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Ectopic beats or premature depolarisations are the commonest  cardiac arrhythmia encountered . Human heart , is a  non stop  electro mechanical organ ,  and it is not surprising   ectopic beats are so common  and can literally originate  from every cell of heart. But , generally it   emanates  primarily from  the special conducting cells . At times  ,  even  other cells (Myocytes, interstitial cells )  can generate abnormal electrical potential.These ectopic electrical potentials  can be compared  to  electrical load shedding when there is excess electrical strain .

Vast  majority of ectopic are benign  in human population. When this occurs ,  in the milieu of underlying heart disease or during ischemic  episodes they become clinically important and initiate a sustained arrhythmia.

Classically and traditionally ectopic beats are described in the

A.Ventricle :      Ventricular premature beats, (VPD)

B.Atrium:             Atrial premature beats(APD)

C.AV junction : Junctional premature beats.(JPD)

If you note , one important structure is missing from the list.

Yes , it is  SA node.  Can it result in premature depolarisation ?

When do you suspect a SPD(Sinus premature depolarisation)

  • It manifests a  an sudden unexpected , sinus beat exactly as the previous sinus beat. Followed by a pause.
  • The P wave morphology exactly is similar to prior p wave.
  • Many times we miss this entity as we tend to over  diagnose APD than SPD.
  • SPDs tend to occur in bigeminy rhythm.

Differential diagnosis

  • Sinus arrhythmia and pause
  • APD
  • SA node echo beats (Part of SA node reentry)
  • SA blocks

How do differentiate  a sinus arrhythmia from sinus premature depolarisation (SPD ) ?

Sinus arrhythmia occurs in a baseline bradycardia environment.

It does not not come as   “on -off ” pattern . It has a gradual onset offset dynamics.

Clinical significance

This is a clinically unimportant arrhythmia* .This  is probably the reason , it is not a popular concept .

*But it can confound in the diagnosis of  , other important rhythm  disorders.it could be a expression of  sinus node dysfunction and a precursor of  inappropriate  sinus tachycardia The significance could be substantial in atrial triggered  based  pace maker rhythm

Final message

When you confront an unexpected , early , sinus beat not accountable to sinus  arrhythmia  or APD

suspect SPD.It is  not rare , it is a  grossly under diagnosed entity.


Sinus premature systole  http://www.chestjournal.org/content/64/1/111.full.pdf?ck=nck

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Pacemaker rhythms  result in classical ECG with  LBBB morphology.It is a universally understood  fact that  RV pacing would  produce LBBB and LV pacing a  RBBB pattern in surface ECG.As with any other rules in medicine , it is not 100%  perfect .(May be 70%)

In the process of oversimplification of rules  we have forgotten a simple fact , that is, interventricular  septum is  shared by both the ventricles . ( functionally and electrically )

In due course , cardiologists and electrophysiologists  have  recognised this fact. A pacemaker lead hitching on the IVS  can behave independently and disobey this  golden rule of pacing.(RV-LBBB,LV-RBBB). Depending upon the orientation of the lead and the pressure it exerts  on the tissue  and degree of penetration of the screwing lead into the septum, the resultant   ECG can  either have a complete RBBB pattern ,  partial RBBB or partial LBBBB or combination of both.

Can RBBB pacing be stable ?

Yes.,  provided the the fixity of the lead and other parameters like impedance and pacing threshold are good.

Before labelling RBBB pacing as safe one should rule out pathological RBBB pacing like septal perforation and

accidental entry into LV through foremen ovale.

Is coronary sinus pacing an acceptable alternative  for  long term permanent pacing ?

The answer is generally ” No ” ,  but it needs rethinking.

A coronary sinus pacing may happen accidentally.The leads get located  either in the main stem coronary sinus or it”s tributaries.the morphology of ECG depends upon the branch it enters.Leads when they reach LV aspect result in RBBB morphology.

Can  we do intentional coronary sinus  pacing for complete heart block ?

There are many accepted  references in literature  that terms   RV pacing as unphysiological and has high risk of precipitating or aggravating cardiac failure. So currently , alternate sites of pacing are explored.( Septum, his bundle , biventricualr etc)

It is an irony , in this era of cardiac resynchronisation therapy where we do coronary  vein pacing  , the same concept is not being tried for regular  permanent pacing in special and difficult situations.( Severe TR, Left sided SVC, AC canal defects etc)

Final message

  1. RBBB morphology following  permanent pacing  need not elicit a panic reaction provided all parameters are stable.
  2. In patients  with difficult RV anatomy* ,  who need permanent pacemaker implantation a modified  coronary sinus pacing can be a solution .But as of now no such speciifc leads are available.EP Industry should take a note on this .

*Epicardial pacing is an option in such situations .But it requires surgery.


Safe right bundle branch block pattern during permanent right ventricular pacing Journal of ElectrocardiologyJanuary 1, 2003   Yang, Yung-Nien ; Yin, Wei-Hsian ; Young, Mason Shing

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