Archive for April, 2011

Adenosine is a  purine analogue. Acts by stimulating outward K+ channel  of AV nodal tissue, more specifically  in the posteriorly   located  slow pathway in the vicinity of  coronary sinus.

Another action of adenosine is inhibition of cAMP , which is similar to beta blocking action may also help in terminating the tachycardia.

Adenosine : A 10 second cardiac miracle

  • 12mg bolus is administered , preferably in a central vein (Not mandatory  though)
  • Termination is usually abrupt . Transient VPDs are observed during termination.
  • Transient flushing may occur.
  • If the patient is taking Aminophylline group of drugs (Which are adenosine antagonists) the AV nodal blocking action may be neutralised .

(It may be apt to recall  at this juncture ,  Aminophylline is used in sinus node dysfunction or AV block to increase heart rate )


A good one from Medscape http://www.medscape.com/viewarticle/585287_2

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Coronary artery is the life line  of the  heart.The size ,  branches  and the course are  predetermined . Generally  it follows a  pattern ,  but still  it is   believed  every  human has a unique coronary finger print. (When retinal blood  vessels can do this . . .  why not the coronary  ? )

When the left main bifurcates it has to share its resources equally between the two  daughter vessel (Not exactly . . . LAD is  widow maker can’t be a daughter  !)

The logic would say LAD demands more as it has more  territorial commitment.But if LCX fights for  equality  share there is a  potential conflict here.But when LCX  is very aggressive and  demands  much more than it deserves the  issue becomes further complex

See how this LCX  gets bulk of the blood flow from Left main and no doubt this man came with  NSTEMI and  LAD region ischemia while his posterior circulation is comfortably  placed with  excess blood.

Note: The diameter of LCX even exceeds left main in certain segments.

One suggested formula (not validated ) is  diameter of   LCX +  LAD will be   at-least 150% of left main diameter .

1.5 x Left main diameter  =  (LAD + LCX diameter)

This amounts  to  50%  gain in  diameter   as it bifurcates .

Trifurcation  further increases the width conferring a hemodynamic advantage

What is the implication of unequal bifurcation  Left main ?

Hemodynamically there could be diversion  of flow into a larger orifice .But ultimately since  the blood flow is  determined  by the resistance arterioles at myocardial bed there  may not be any  practical significance . In pathological situations there could be a some impact  due to  stealing . Large LCX is more common with  left  dominant circulation  .

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Coronary atherosclerosis  can  strike  an artery  with  variety  of   lesions.It can be  any of the following.

  • Focal
  • Ostial
  • Eccentric
  • Discrete
  • Diffuse
  • Tandem
  • Ectatic
  • Multiple

  Rarely  a coronary artery  is  blessed with  all  of the  above  characters ,     added  with homo and hetero  collaterals   . . .     resulting  in  Atherosclerotic    chaos  !

What is  chaos ?


Note one such vessel inflicted with chaos lesions

How to you report the above angiogram  ? What can be done ?

We  do not treat an angiogram. We need to know the clinical background. (This  is a  50 year old man with chronic stable angina )  He also had a  lesion  in LAD and   was advised CABG with grafts to LAD  and PDA.

Is PCI possible in such a vessel ?

Most would agree , it is a crime to think about  PCI in the above vessel. Still , few hard-core  interventional  cardiologists may vouch   for success  in this vessel !

Is there any alternative management other than CABG in this vessel ?

Leaving it alone can be an intelligent strategy . (If  LAD is normal  it  may be the  best possible management)  . But , CABG will remain a default choice. But , when a person is having such a rampant atherosclerosis  he is at high  risk  for pre- mature  graft disease as well. Hence  , intensive medical management will be the key  in  such patients irrespective  of  any revascularization procedure.

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Coronary collateral circulation can be termed as one of the  mysterious  circulation in our body.Cardiologists generally do not  give much importance to it and some interventionists even ridicule it !  . But  ,  God has given it ,  with  a purpose. He adds a riddle though !  .Collaterals  grow  in  almost  every  individual  when   obstruction occurs gradually ( chronic coronary syndrome ) but only in  a few ,  it  will open up  during a real emergency like ACS !

How and why , only  few of us can  recruit  coronary collaterals   during   acute occlusion ?

God  blesses acute coronary collaterals only in selected few  , who  are on the right side of his good books .This can be  the other name for our  destiny !

Role of coronary collateral circulation  in acute coronary syndrome.

  • Limits  infarct size and volume
  • Promotes salvage
  • Converts q  MI to non q  MI
  • Prevents Unstable angina from becoming MI
  • Prevent primary VT and VF*

All  of the above can be vital  in saving a life  . Even as  we realise 30 % of STEMI do not even reach hospital  , it seems certain men and women with early collateral recruitment  will never  fail to reach the hospital alive

Is there a simple  method to identify  people who are blessed with acutely recruitable   collaterlas ?

I am afraid it is  almost equal to  asking   for a glimpse of GOD   !

Wait . . .  when we were on cath lab  few  days ago a  stunning  phenomenon happened  that could pave way for identifying  potential acute  collaterals  in any human being.  Follow this site  . . .the details will be posted !

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 Hypertension  ranks  number one  in the risk for future  stroke . Surprisingly this is true  for ischemic  as well as  hemorrhagic strokes.

 What  causes  thrombosis or  rupture of small cerebral arterioles ?

 It is somewhat similar to coronary events . ( With one major exception,  coronary vesels  are   not prone for rupture ) .It is  believed   sudden spikes of   blood pressure  and the resultant endothelial injury are responsible. Atherosclerotic plaque fissure and inflammation  also  contribute. 

Is embolic stroke related to hypertension ?

The vast majority of embolic stroke are believed to  arise from heart .This belief is getting gradually eroded , as we now know aortic arch and carotid arteries vie for this honour . .(This was indirectly proved in AFFIRM trial  when rhythm control failed  to reduce the incidence of  stroke inpateints with AF ,   implying much of the strokes arise  in the upstream rather than within the cardiac chambers )  

Meanwhile , there is no controversy  in  SHT  promoting  both cardiac  and non cardiac embolus to brain

Systolic ,  Diastolic or Mean pressure   which is  important  in the genesis of stroke  ?

All parameters  are  important , but the   systolic blood pressure  is vested with more  vigour  to damage the  cerebral arterioles. The reason  systolic pressure is more important lies  in the  fact ,  it  can  attain  high pressure peaks instantly ,  unlike diastolic or pulse pressure which  slowly builds up. Further , systolic BP  carries  leading edge of the pressure  curve with high Dp/Dt and hits  the target  first !

At what pressure the cerebral artery becomes  uncomfortable ?

We do not know  the answer as yet , but any systolic pressure above 180 mmhg is a huge stress for the cerebral arterioles.The rapidity with which the BP  raises  (Dp/Dt) also becomes  important  . High blood pressure increases the shearing stress .It  interferes with nitric oxide synthesis and promotes endothelin release which precipitates  cerebro vascular event.

How do you identify people who are at risk for stroke ?

While  cardiac physicians are obsessed with exercise stress test to predict CAD  very  few  are worried about  stroke . In fact the same exercise stress test can be used to stratify stroke risk. The exercise induced systolic blood pressure  raise  is a useful risk stratifying  tool. This concept is there for more than a decade without reaching the clinical domain.

The following paper was  published in stroke journal (2001)  from the picturesque university of  Kupio Finland.(See below )  It is a wonderfully done study and throws great insight into the  new  emerging  science of  Intra cerebral hypertension .


The following can be summed up as risk factors for stroke during EST  (Derived from   various sources  and  . . .  with   liberal dose of personal  logic !)

  • Raise of 20 mmhg  SBP  at  2  minutes .
  • Increment of >  20mmhg in SBP any subsequent minute.   
  • Any  SBP  above 200mmhg during  EST
  • Failure to  reach baseline SBP  at 6 minutes recovery .
  • SBP  or DBP remaining high  even  after  the heart rate reaches baseline.


 Final message

For the kind attention  of all  cardiac physicians . . .  whenever you do an  EST for a cardiac indication ,  please spend the first  few  minutes  carefully ,and   look at the  blood pressure response . It is encouraged ,  to  specifically mention about the  behavior of  SBP  and write a remark about the propensity for  stroke in  every EST/TMT report .   Let us grow our brain  sense as well   . . .  for   the sake of our patients !

Thanks again  to Dr S.Kurl et all from Finland  for their  nice article which  stimulated  me to write  this post .




Further queries

How common is stroke following a EST procedure ?  Can high blood pressure dislodge a carotid plaque during a stress test ?

The answers will be posted soon once I  get it . ( Of course you can do it if you know !)

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Left bundle branch block (LBBB)   has a curious but important relationship with  STEMI . LBBB inflicts a dramatic change in qrs morphology   with  a diagonally  opposite   polarity of ventricular activation . This masks    the initial qrs vector  and  makes it a difficult task  to diagnose acute MI in this setting. The ST segment which is of primary importance  in STEMI is   lifted  up due to altered repolarization .

LBBB can be associated  with  STEMI in the following ways

  • Acute necrotic LBBB  with massive myocardial damage – Impending shock
  • Chronic LBBB with acute STEMI
  • Transient ischemic LBBB during STEMI
  • Rate dependent  LBBB (Usually tachycardic  ,  rarely bradycardic  )
  • STEMI in pacemaker rhythms

While every one of the above can be experienced ,  the most common diagnostic conundrum  occurs ,  when a patient   comes with acute  chest pain and LBBB . There has been many criterias  suggested to diagnose STEMI in the presence  of LBBB.

The criteria  proposed  by Sgarbosa  (A  GUSTO   off shoot )  in 1996  caught our imagination .One prime reason for this is ,  it came from the prestigious NEJM and Duke university combine. Suddenly this became the de- facto standard to diagnose  STEMI 

In the  past 15  years  ,  our experience in one of largest coronary  care units in India , we have   found this criteria   to have  little utility value  in STEMI and LBBB  . Most of the time  a correct diagnosis was made  by   simple clinical guessing .

Next to  clinical assessment, we found cardiac enzymes (Troponin and CPK ) were reliable in diagnosing  STEMI with LBBB.

Surprisingly ,echocardiography  was as unreliable as ECG .( The paradoxical  septal motion invariably confuses the already  confused  cardiology fellow who usually does the emergency echo  !) 

Even as our  CCU documentation was  far from satisfactory  , now this article from Mayo exactly reflect  our observation.

Sorry   Sgarbosa . . . the criteria was  based  on  sound observation and a  good  electrical principle  . . . still LBBB is able to beat   it convincingly ! ( Very low sensitivity !)

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WPW syndrome remains as  a   fascinating ECG entity ,  ever since it was described by Wolf , Parkinson and White in the year 1930.It is  primarily a  disorder of cardiac embryology . Heart is an organ made up of  tissues from mesoderm and neuro ectoderm.The muscle which comes from mesenchyme has to be incorporated with specialized conducting system. This is a complex  process .It is determined by the bio-genetic forces. When errors happen in the embryonal  tissue  flow  congenital anomalies occur.

In  WPW this  error   happens  exclusively in the conduction  tissue movement  . Normally the specialized conducting system    pierces  the  entire  AV ring and connect atrium  and ventricle  .Later ,   it regresses in  all areas  except in the AV nodal zone  . When  It  fails  to regress ,  these  remnants of  conductive  tissue act as AV accessory tissue  and create electrical  short circuiting .This is the reason , all these pathways are located in the close vicinity of AV ring.

Accessory pathway shows   varying conduction velocity , but generally devoid of  decremental conduction properties .  The presence of such pathways make these individuals prone for variety of cardiac arrhythmias .It can range from  simple AVRT  to  malignant antidromic  AVRTs  that can end up in  VT /VF.

Resecting  these  pathways surgically was once popular.  Effective blocking  of  the pathways with  drugs  is a good option. Currently ,  it is possible to  locate and  ablate  most of these  pathways   successfully.

Even though there are many protocols to locate accessory pathway the one that is very popular is  simple   Type A and type B  WPW , which locates the pathway either in the  left  or  right  ventricle  respectively.

Huge data base  has been accumulated over the past 80 years  regarding WPW syndrome,  still   many questions are unanswered.  One of the important clinical issue is  multiple  accessory pathways , scattered  at  random  across the  tissue planes of atrium and ventricle  .

The other issue is intermittent pre-excitation and shuffling  of path ways during tachycardia  .

It is very rare to see a patient who manifests both Type A and type B pattern during sinus rhythm .Here is an  article from  unexpected  quarters  , Colombo Sri-Lanka in the year 1972  candidly  describes a patient with classical  combination  of  Type A and  B  WPW . It is great to see such an interesting  observation in the pre  EP/Echo era from a remote island nation.

Now , let us ponder over  these questions

    1. Can a pre-excitation  happen simultaneously in both right and left free wall pathway ?
    2. How will the ECG look like  when impulse travels over multiple pathway ?
    3. When dual pre-excitation combines   with  normal AV  conduction  ,     will  it not make  a  triple AV pathway ?
    4. How does a supra-ventricular impulse decide ,  which pathway it is going to travel  when confronted with a choice of  three or  four pathways ?
    5. How do you plan ablation for such a patient  ?

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What do you advice a patient with single vessel  CAD  with milder forms of angina or no angina ?

Medical management ?  May be you are right . But most of us do not  follow this  correct advice.  Why ?  We have a inherent bias against  medical management  . Cath labs exude  unmatched glamor and  attraction in various forms  to both cardiologists and their patients.   Now , here is a   surprise  finding  , unpalatable though , for many of  us !  Simple jogging or bicycling can have equal if not  more relief  than even a angioplasty . This study which came in 2004  was made sure , not to  gain a prominent place in cardiology literature.


Let me pedal faster . . . cardiologists are after me !

The circulation article

How does exercise help in reversing CAD  ?

We know the prerequisite for plaque formation is the endothelial  injury along with lipid accumulation. Further ,  high local adrenergic(vasomotor) tone ,   growth factors and inflammatory activity would accelerate the plaque formation.

Regular exercise  has been  convincingly  shown to improve  the endothelial function. It  restores  the optimal adrenegric tone in the coronary micro circulation so the blood flow is brisk and pro-coagulant  activity is reduced .

It is easy to accept  the fact ,   exercise  can  prevent   progression of plaque   . . .A question that lingers in many including  many  cardiologists is this   . . .How  is it possible   for exercise to  regress well  established plaques ?

When   exercise  can   dissolve  huge  fat loaded  abdominal  tummy  in matter of weeks ,   there need not be any doubt  about the efficacy  of   exercise  in regressing   minute  lipid laden  coronary tummies (also called as plaques) .

(Of course , the  above statement  is supported by  documented  angiographic evidence  as well !)  Read below and  also the AVERT study .

Final message

Attention  all CAD patients ,  empower yourself , you  can become your own  cardiologist . You can perform angioplasties with bicycle  at zero  cost ,  of course  you have to pay for the bicycle !

This article “hypes up” the importance of physical activity in the management of CAD. But , it has to be  combined with optimal anti anginal drugs, good lipid control , blood pressure and diabetes  control  if present  , stress reduction  and good  sleep  to keep the CAD and cardiologists  at bay !

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We know  acute coronary syndrome  presents* with  either  STEMI or NSTEMI. (*It actually doesn’t present , it is our understanding and interpretation ).  Bifurcating  ACS into two is more by convention and convenience .Does  the intra-coronary  plaque  dynamics  really  permit us to divide ACS in to two distinct ECG  entities ?

Are we oversimplifying it ?  Probably yes.

The following paper was presented in the cardiological society annual scientific session in New Delhi few years ago (2006)

It generated an intense debate  , finally the chair person  reluctantly concluded such events are  possible. . .

but need more proof   . What is your take on this issue ?


S.Venkatesan ,G.Gnanavelu,V.Jaganathan,

Department of cardiology . Madras Medical College. Chennai

Acute coronary syndrome (ACS)  is  classified into  STEMI  and NSTEMI and has gained universal acceptance. The classification was done by   clinical & electro physiological   findings    with   some   pathological basis. The   classification   came into vogue primarily to simplify the decision making process of thrombolysis. ( STEMI –Thrombolysis eligible .NSTEMI  Thrombolysis ineligible.) The limitation of this classification is well   exposed   as   we   now know,    STEMI can evolve into NSTEMI and NSTEMI can evolve into STEMI .   Identifying the culprit artery in ACS is   not straight forward especially in NSTEMI. Adding further complexity   is   the newer   observations that diffuse vessel inflammation,  and  multiple active plaques(MAP) are responsible for many of the episodes of  ACS.

In this scenario   there   could be two are more pathological processes   one   resulting   in  a total occlusion   and other sub total occlusion resulting in both patterns of ACS simultaneously .(STEMI & NSTEMI  Dual ACS)

We   describe two  patients  who had   presented to our CCU  . Both had STEMI one in  lateral  other in anterior wall . They   were thrombolysed   as per  criteria. Both patients had gross ST depression (>4mm)  elsewhere. In one patient it  corresponded  to the reciprocal  leads .The outcome of  thrombolysis  was turbulent .Both patients worsened and one developed  recurrent VT . Paradoxically the ST elevation   regressed   indicating a successful   thrombolysis  in the STEMI  territory  even as the ST depression  was worsening in the other leads. Angiogram   revealed   multivessel CAD with   recannalised  LAD  lesion with eccentric , thrombus containing  lesion in RCA/LCX. One patient expired and other was referred for revascularisation.

We   believe   both of our   patients  experienced  Dual ACS.

When to suspect dual ACS ?

Dual ACS is likely , when  STEMI is associated with ST depression  in at least 5mm in any two leads  or   when there is disproportionate  reciprocal ST depression ( > 2mm of primary). The reason for the poor outcome could be due to a therapeutic conflict between   STEMI & NSTEMI as the former  is  thrombolysis friendly while the later is not . Role of   thrombolysis in  such situations were ACS wanders between STEMI & NSTEMI is not defined. Another possibility is the concept of reciprocal ST elevation,   where in the index event  could be NSTEMI and STEMI is a secondary response  and  thrombolysis is apparently  contraindicated.

We conclude that in patients with ACS,   two or more   plaques can simultaneously get  activated  and  present  as a combination  of STEMI / NSTEMI   in the same  patient  in two different coronary arteries.(Dual ACS) .We suggest   that in every  patient who present with  STEMI  a possibility of   dual ACS  is to specifically considered,  as  thrombolysis could be disastrous  and  instead  they  should  reach   the  cath  lab directly.  .

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Hurricanes  are ocean’s  reaction to the climate change  especially  in subtropics.  When low pressure  zones  form over the ocean surface  the nidus for hurricane is sown .It   gradually intensifies to form deadly cyclones.The maximum damage is done when it  encounters the land . The following image  depicts how the hurricane Katrina caused havoc in the southern US coastline .

Hurricane katrina .Click to view animation


When the human blood stream is interrupted  by any pathological hurdle  it  gets  agitated . It encounters both turbulence as well as  a  slow flow phenomenon . Virchow taught us centuries ago  , slow flow , a vessel wall defect and  an abnormal blood combine to create a  clot. This is what happens in mitral stenosis . What appears as a mild turbulence  gathers momentum  and becomes a storm .The eye of the storm has the  least velocity and it  forms  the core of the future clot.

Left atrial strom visualised by TEE


What is left atrial jelly ?

A  pre- clot stage with impending clot formation may be referred to as a jelly . The exact  duration for  a contrast to get converted to clot is not known.It depends host of factors from hemodynamic and rheological factors. It  is  believed every clot   must be preceded by at least a brief period of auto contrast.

Is there a intrinsic  defect in blood in those patients who have spontaneous contrast ?

Yes , there has been  excess  fibrinogen  in these  patients. http://www.ncbi.nlm.nih.gov/pubmed/11744141

Can we dissolve  spontaneous  contrast ?

It  may be  possible with intensive anti coagulation. Ultrasonic dessication may be a modality that could be developed in future.

Is  the presence of  spontaneous echo contrast a contraindication to do PTMC/CMC ?

Some centers do believe so. Currently intensive anticogulation ,   meticulous preparation   with  special  precautions  during procedure will reduce embolic  manifestation.


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