Archive for April, 2012

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Acute rheumatic fever classically involves large   joints of lower or upper limbs  referred to as  fleeting migratory polyarthritis .But this pattern is  not  exclusive.  In fact   acute rheumatic  fever commonly  present with atypical features .The incidence can be up to 25 % in various series .The most surprising thing is ,  it can involve spinal as well as hip joints . Mono arthritis is also possible.

The only contention is , atypical features are  frequently  labelled by  some  as post streptococal reactive arthritis instead of rheumatic fever .

It is  pure  semantics at play . Whether you agree with the terminology or not  ,  never hesitate to diagnose rheumatic fever when the  joint involvement is  atypical . If  you ignore this  you are bound to  be guilty  for damaging few hearts  later.

What are the unusual joint involvement in acute rheumatic fever  ?

  • Small joints of the feet
  • Small joints of the hands
  • Cervical spine
  • Wrist
  • Elbow
  • Shoulder
  • Hip
  • Thoracic  spine
  • Calcaneus
  • Lumbar spine

The involvement of above joint can be up  to 25%

Here is an excellent paper from Brazil about the huge variation in the pattern of joint involvement in acute rheumatic fever.


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Kissing balloon is the standard technique used to tackle   branch vessel stenosis . When a vessel branches out and both branches has a lesion,  single balloon can not dilate a lesion optimally . This  is  because , the side branch  not only shares a common ostial tissue but also  shares  plaque material within the walls of main and side  vessel . Dilating one vessel alone could result in unpredictable plaque shift.

Carina is the most important anatomic structure in a bifurcation zone . It acts like a grade separator. Diverting and deflecting blood flow .The  length and angle of this grade separator determine the ostial  shape as well . A right angled side branch will have  a circular ostium .An acute-angled branch  will have oval orifice .  The plaque burden and distributions at this point becomes vital for many reasons.

When we do PCI this carinal area should be  optimally pressed and plastied  and of course covered well with the metal struts.The  simultaneous kissing with two balloons ,  one in main vessel another in side branch will reduce many of the issues . This area is a weak link for interventional cardiologists. It needs lots of efforts to protect the side vessel.

When do we do kissing balloon ?

Two broad categories.

  • Pre-dilatation and preparing a lesion ( Not routine  )
  • Post dilatation is more often done .

Look closely the layers of contention in the carinal zone. Lesion not depicted .

Kissing interface : When the balloons kiss  what lies  in between ?

  1. Simple  Balloon to Balloon Kissing with nothing intervening(Proximal to branch point )
  2. Balloon- Single layer of Stent-balloon kissing
  3. Carinal  Kissing -Balloon -Two layers of Carinal tissue -one layer of Stent -Balloon Kissing ( See above image )
  4. Twin stent kissing

When do  balloons refuse to Kiss ?

When there is a hard interface between the vessels like a severely  calcified intima /Adventia .

Eccentric /overhanging  lesions intervening.

Incomplete kiss

It need to be emphasized balloons come  into contact easily in  acute-angled lesions.

In right  angled lesions the balloons come to contact only in the proximal part.

Definite indications  for  kissing ?

Kissing is not without complications . While two guide wires are placed in all  bifurcation lesions  , kissing is  not necessary in many  lesions  .Of course it is a must in all true bifurcation lesions (Medina 111 , 011, 101, )  It may not be required in  1,0,0 if carina is away from lesion.

*Kissing can rarely aggravate the same issue which is supposed to prevent  ie plaque shift .This is due to differential pressure transmission by two balloons.

Is there a role for  twin balloon POBA  without any stenting ?

Most cardiologists would not believe  in POBA anyore (For wrong reasons though ! )

A distal RCA with a PDA ostial branch lesion could be tackled with twin balloon POBA.

Which  balloon is to be used?

It depends on whether we use the technique  as POBA, single stent or double stent technique. Non compliant balloons are  ideal  as it exerts   more pressure on the vessel wall .

Kissing   at  what  pressure ?

The pressure used is often between 8-14 ATM.

Experts may use differential pressure inflation depending on the lesion characters.

Which  is the Most complex form of kissing ?  

Two stents, two balloons . Here the interface contains two metal layers . At carnia the two metals engulf   two layers of  tissue as well .

Final message

Bifurcation lesions  are being  conquered with more success in recent years.

The techniques have refined. Stent designs and drug eluting stents  are  helping us in many ways.

We have learnt  from our  mistakes and accepted the limitations.

Wisdom  prevails now , there is a universal consensus  for less  metal in the notorious  carinal  area.

Still, ignorance  remains*  as  a major  guiding force   . . . when  we  navigate  the difficult atheromatous terrains  in  live human  coronary arteries !

*With due respects to IVUS, OCT and FFR .

**Forward looking IVUS, and camera tipped guidewires may change the scenerio.


Further reading

What-is-the-simple-approach-to-bifurcation-pci ?

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Here is an X-ray of classical rheumatic mitral stenois with a mitral orifice of  .8 square cm.

Why the left heart border is straight in mitral stenosis ?

It is due to 4 factors.

  1. Hypoplastic aorta
  2. LAA
  3. PA
  4. Under filled LV

Note :

  • This straightening occurs   only  in  isolated , severe forms of mitral stenosis  as it requires under filling of left  ventricle   and Aorta.
  • Significant mitral regurgitation will lift the lower end of straight line .
  • In associated aortic valve lesions especially in aortic regurgitation the straightening can not occur as LV and  Aorta continues  to be conspicuous.
  • If mitral stenosis  causes severe PAH and tricuspid regurgitation , RV  can  become  huge  and form the left heart border and distort the straight line.

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Amiodarone acts  by

  1. Correcting the  rhythm  to sinus .
  2. Controls  ventricular rate  alone
  3. Does both ?

Answer is 3

How can it correct the rhythm alone ?  If  the rhythm is corrected ,  rate will automatically be controlled,  unless Amiodarone converts AF into Sinus tachycardia  which is very unlikely !

Of course  Amidarone  is not a  magic drug .The success rate of  Amiodarone  restoring  sinus rhythm is far . . . far less . . . than our expectations ! . It fails to  convert to sinus rhythm in a significant chunk *. Interestingly ,   it may still  control the  ventricular response  by its beta blocking action .

*Our estimate is , the failure rate Amiodarone  is  between  30-40%  or even higher ,  as   bulk of AF we witness   is due to Rheumatic heart disease.

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Which is the best drug  for  “ventricular rate  control” in atrial fibrillation  ?

  1. Digoxin alone
  2. Diltiazem alone
  3. Atenolol alone
  4. Digoxin +Atenolol
  5. Digoxin + Diltiazem

The answer is 4.

This is based on a study  done by Bramh N  Singh  and his team  from California published in 1999 . (http://content.onlinejacc.org/cgi/reprint/33/2/304.pdf  )It  was  a wonderful study   involving  just  12 patients ,  still good enough to prove a  point . It was a sequential cross over study a rare theme in medical trials !  where same patients act as control .Hence bias and host variations are  nil. Few excerpts from the study .

It is very clear, for optimal rate control we need a combination regimen , Digoxin must be one of them .Atenolol combined well with Digoxin , even as though Diltiazem resulted in maximum dip in nocturnal heart rate.

Digoxin + Atenolol is clear winner in rate control during exertion as well ! Note Digoxin has absoutely no control over the heart rate at times of exercise !

Few thoughts about this study

This study has clearly documented superiority of combined drug regimen for rate control in AF .

Still it leaves a  lingering question !  Why verapamil was not used as an agent in this study  ?

If only ,  verapamil was used (As we do in our hospital )   Digoxin -Atenolol  combination would have  faced a  really  tough competiton.

Another  curiosity is  ,  what would  have  been the power of a unique combination   of Atenolol  and Diltiazem  in controlling  ventricular  rate in AF ?

Any way , it was a wonderful cross over study  . Such studies are a rare breed ,  always welcome in this world  of  funny  pharma trials  wherein  a new drug is  compared with a dud drug called placebo !

Now  . . . Try this  one


  1. Corrects  rhythm
  2. Controls  ventricular rate
  3. Does both ?

How can it correct the rhythm alone ? If rhythm is corrected ,  rate will automatically be controlled unless Amiodarone converts AF into Sinus tachyardia !

Of course  Amidarone  fais to  convert to sinus rhthm in many , still it may control the rate  by its beta blocking action.



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Ventricular tachycardia is  a major cardiac electrical disorder. Even though it  connotes a deadly meaning the prognosis and outcome vastly vary.It can be a benign arrhythmia in  structurally normal heart that present as occasional fasicular VT  or Exercise  induced RVOT , to dangerous ischemic polymorphic VT which rapidly degenerate to VF and SCD if not reverted . It is ironical we are  trained  to put all VTs in a single basket and  propagate fear psychosis among   physicians and patients .

Management of VT has certain broad principles.

  • Identify the cause
  • Whether  specific structural heart diseases present or not
  • Identify the mechanism if possible
  • Rule out transient metabolic cause as a trigger

Therapeutic targets

  • Stabilising the cell of origin
  • Passifying the scars
  • Interrupting bundle branches in  BBR  mediated tachycardia
  • Ischemia related  Focus – Re-perfusion
  • Reversing LV dysfunction



  • Correct Cell hypoxia /Acidois
  • Pharmacological ( Class 1A/1B /1C , class 3 and Beta blockers , Magnesium  )
  • Role of  beta blockers for VT management is largely under recognised.It has an important role to play in both acute and chronic  VTs)

Electrical (DC shock ,Ablation and ICD)

  • DC shock is treatment of choice  all emergency VTs
  • Ablation  aims  at preventing episodes of VT .Ablation needs EP study and  expertise of  an electro physiologist.
  • ICDs  revert it only after the VT emanates from the focus . ICD can be implanted without knowing the focus .May not require a EP consult.


CABG + Surgical scar excision , Aneurysectomy  might help in certain refractory VT.

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I  wonder  this  question is being  asked  over many  generations in medical schools ,  yet to be answered clearly. The traditional explanation  given is   ”  mitral valve is  kept  open wide till onset of systole and it closes with a bang due to a long excursion it has to make ”   This concept is no longer tenable and acceptable ( For the simple reason  if the valve is wide open  . . .  hemodynamically significant  mitral stenosis  cease to exist !)

There are  two major factors that determine the loudness of S1 in mitral stenosis

  1. Hemodynamic
  2. Valve structure and morphology

Mitral valve closes whenever the ventricular pressure  curve crosses above the LA mean pressure . This is the pressure crossover point (LV/LA) .

In normal persons it happens very early after the onset of  ventricular contraction  .(ie  the LV pressure has to raise only to  about 8-12mmhg . At this point the LV pressure curve has  certain  force of contraction (Dp/Dt) .Since in mitral stenosis the mean pressure is raised well above normal  (Often 20-30mmhg)  the LV pressure cross over point is slightly delayed  and more importantly occur at a higher  slope  of LV pressure curve  . Even this slight delay adds a punch in the ventricular contractility .The impact of LV contractility on mitral valve closure especially the  AML is forceful .

(Imagine the force of  impact of a  stone hitting you  from a distance of 1 meter from above ,   is different from a stone hitting you from 10 meter above   as it gains the momentum )

The second phenomenon is  probably  more important as it involves acoustics the final step in the genesis of loud  S1  .

The mitral valve need to be  not only pliable  but also the conduction properties should be intact.

Acoustic principles state that even a speck of calcium in the AML  can dampen the sound that is generated  by leaflet motion.

(Try touching a speaker cone while it is playing  .The sound immediately drops and dampens.)

Similarly for S1 to be loud  the valve should pliable without any significant calcification or extreme rigidity or subvalvular  fusion .)

It is important to realize the PML  contributes less to the intensity of S1 . Hence even if some calcium present in PML it won’t  affect the intensity of S1

Other important factors that affect the intensity of S1 include

  • LV function ( Onset of LV dysfunction elevates LVEDP reduces the net gradient across mitral valve )
  • Presence of  mitral regurgitation .
  • Aortic valve disease (Especially AR )
  • Heart rate
  • Rarely associated Tricuspid stenosis make T 1 component of S 1 louder

Final message

The loud S 1 is due to both physiological and anatomical factors  of mitral valve   .The condition of valve may be  more important  for the simple reason , whatever be the hemodynamic  predispoistion  for loud S1 ,  the  prevailing  valve morphology  has a potential to nullify it !


The image modified from  http://www.texasheart.org

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A 55  year old man came with a BP of  1o0/70 with vague symptoms of back  pain to our ER.

Troponin T  was positive

Can we thrombolyse ?

There is a minimal ST elevation in inferior leads  but not amounting to  the required criteria 1 mm

Technically No , Academically yes , scientifically No , logically  yes

*I wont thromolyse but i will take him to cath lab maybe the modern answer

 What we did ?

We did neither !

Just observed in CCU with heparin infusion , Aspirin and clopidogrel .

Note: The ECG becomes almost normal .The initial suggestion of inferior MI is stands questionable

Serial ECGs  were taken .

And now . . . after 24 hours a new complete heart block appear with classical evolved pattern of inferior MI.The most interesting feature is patient has been comfortable all along even as his posterior aspect of heart is experiencing terrible electrical earth quakes.

Is troponin Guided thrombolyis  an accepted  concept  ?

Yes ,  only in few situations like , posterior MI ,   LBBB  , pacemaker rhythm, re infarction .(Note , true posterior MI do not elevate the ST segment but depress it ) .

One may be surprised why we shouldn’t lyse a patient  whenever  troponin is elevated in acute coronary syndrome  (After all it denotes myocardial necrosis and infarct !)  The point here  is ,  troponin can raise in all forms of MI (NSTEMI, even in some cases of chronic stable angina )  Read in this link Why thrombolysis is contrindicated in UA/NSTEMI

The benefits of thrombolysis  is not proven in small and micro infarcts.  ECG  ST  eelvation   remain the  sole criteria for thromolysis for STEMI because  of  high degree of  correlation with total coronary occlusion .

In this era of rapid interventions the treatment concepts has blurred as we tend to do PCI and stenting  most cases of ACS including UA/Unstable angina

OK , what happened to this patient ?

Temporary pacer  was kept stand by with a sheath and catheter in situ.

Next day  morning  AV block disappeared .Patient was comfortable .

To our surprise , in the same  evening his ECG showed a complete heart block with AV dissociation . Still the heart rate was good . The demand temporary pacemaker didn’t take over .

On the third day , every conduction disturbance disappeared and  patient was sent to the wards. He is being discharged in a  stable condition with std drugs .there was  a minimal wall motion defect in infero-posterior segments with an ejection fraction of 50 % . He is  scheduled for coronary angiogram  2 weeks later.

What is the pathology ?

Pathologicallyit could be a small focal area of Infarct  incidenataly invloving the AV node .(This is alss refered to as vital area Infarct”  )It is hard to differentiate whether AV block is due to revrible ischemia or necrosis  , simple tissue edema ,  high vagal tone . or combination of above .If the block recovers it can be concluded necrosis is not the dominant theme.


Final message

STEMI presenting  primarily as heart block is less common .  When such a presentation occurs extra caution is required.

Many  of these patients  may not show a classical ST elevation  and hence do not permit us to thrombolyse   as per criteria.

It is  the  individual physician’s discretion to do so ( or not to do  ! ) . No body is going to fault. After  all  5 % of thrombolyis world over is for  benign early  repolarisation syndromes.

The above description is  an example of complicated inferior MI  . . .  still managed effectively by conventional methods.

Further reading

Why inferior MI is considered Inferior ?


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      After  years  of   of experience  I  realised  knowledge and  Ignorance  share  an     intimate relationship !  


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