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A trip to Athens for EUROECHO 2012 presentation !

December 1, 2012 by dr s venkatesan

Here is some of the   highlights of my  presentation  in EUROECHO on  December 5th 2012 

At  the Mageron International Convention center  .Athens Slide1Slide2Slide4Slide5Slide7Slide3Slide6Slide8Slide9Slide10Slide11Slide12Slide13Slide14

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Essential facts about EUROSCORE

November 30, 2012 by dr s venkatesan

CABG surgery is the commonest cardiac surgery done world wide .Right from the days of CASS study the  CABG was considered a major traumatic surgery to relive a small block in a coronary artery  (Not exactly relief  . . .it  just by-passes )

However , for more than two decades  till early 1990s CABG ruled supreme.Ever since coronary stenting grew in an  exponential fashion  the outcome of CABG  needed scrutiny .Surgeons had a compulsion  to explain  the world , CABG indeed has a  acceptable risk benefit ratio in the management of CAD .

Thus came the EUROSCORE  . First developed in 1995 .The initial score used a simple additive risk next it was modified

with logistic regression .

Limitations

Can you withhold  a surgery on the basis of high EUROSCORE  ?

Is it scientifically validated ?

EUROSCORE gives us  30day mortality

What is the acceptable EUROSCORE for CABG?

http://ejcts.oxfordjournals.org/content/early/2012/02/28/ejcts.ezs043.abstract

Click to access 1749-8090-4-32.pdf

What is the major limitation for EURO-SCORING system ?

It is ironical the most important determinant of any surgery is  the surgeon’s competence and institutional expertise in handling emergencies  and financial affordability  .They are  not included in the scoring .  This makes the EUROSCORE in most of the developing countries including India a futility .

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Beware of Primary PCI : Is there a Low risk STEMI where pPCI is potentially contraindicated ?

November 30, 2012 by dr s venkatesan

This paper is to  be presented in the the Forth coming   Annual CSI meet New Delhi  December 2012

Beware of Primary PCI : Is there a Low risk STEMI where  pPCI is potentially contraindicated ?

Venkatesan Sangareddi  . Department of cardiology  . Madras Medical college

Primary PCI has proven to be the best  option for management of STEMI . But it need to be done early,  by an experienced team , in a good facility . It is not the individual expertise that matters !  Any treatment , which has great therapeutic potential  also  carries a hazard . So , these treatments  must be used with caution.  Not every STEMI patient , carry a high risk for death.  In fact , the mortality  in some of the subsets of STEMI  can be as low as 1%. If , a  STEMI patient , with a likely 1% mortality is going to get a procedure with  3 – 4 % ,risk it should (And Must !) raise a validity question  But,this issue is rarely addressed in the interventional summits.

In a case pool of 56  randomly collected primary PCIs from various institutes , the outcome  of pPCI  was analysed .It is a retrospective , observational study .STEMI was graded as high risk when one of the following features  were present and it was “low risk” when none of the feature  was  present ( Second STEMI , Extensive  anterior MI , Class 3 /4 killip, An episode of VT/VF, Complete heart block, Diabetic individuals )  High risk STEMI  constituted 22 patients .The overall in hospital  mortality  was (5/56) 9 % In high risk STEMI it was (2/22 )9.5 % in low risk  STEMI it was 3/34 6.4 % .In the corresponding period 40 patients with STEMI who were treated by only thrombolysis or heparin (If beyond time window ) was used a control . 15 patients  were in high risk In the this group the  mortality in high  risk STEMI  was (3/15 )19% and low risk STEMI  there was nil mortality (0/25) 0% .

There was an unacceptable moratlity  with  pPCI  in the low risk STEMI which fared worse than even simple administration of heparin.These data reveal a dangerous fact , that is , primary PCI does not differentiate in the procedural  risk with reference to the patient profile it deals with .While , it dramatically reduce the risk in high risk STEMI It confers a astonishing risk to low risk STEMI .The exact cause for this risk is not known . Common sense would tell , pPCI is  expertise driven driven while thrombolysis is not .Our analysis also suggest bulk of early hazard of pPCI is also logistics related.

Primary PCI could be  cautiously and consciously avoided  in  patients with  low risk STEMI even if it is technically and academically indicated. This can have a great impact in the overall outcome of STEMI management.It is suggested every STEMI patient need to be risk stratified on arrival.(It is still a mystery , why we do this for NSTEMI and not in STEMI ) . A change in the current PCI guidelines to this effect is to be considered.

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs) | Tagged , , | 1 Comment »

Right ventricle structure and function: A review

November 30, 2012 by dr s venkatesan

A one stop  solution  for every  thing you need about  right ventricle !

http://circ.ahajournals.org/content/117/11/1436.full.pdf+html

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TR jet alternans : A new marker for severe RV dysfunction

November 30, 2012 by dr s venkatesan

Here is a patient with class 3  dyspnea  who was referred  for echocardiography

X ray chest showing cardiomegaly

         Moderate TR due to dilatation of tricuspid annulus.This patient had dilatation of all 4 chambers of the heart.LV EF was 24 %

Right ventricular dysfunction is major determinant of  clinical outcome in patients with dilated cardiomyopathy. The  myocardium of the  entire heart is now known to be a single sheet of muscle rolled into different chambers . So any primary disease of myocardium will involve the entire musculature . This is the reason  , all the  4 chambers of heart goes for dilatation in  primary cardiomyopathy . Of course there can be minor variations  due to differential hemodynamic impact.

But it is certain ,  RV  function will definitely be compromised  In  most patients  with  Idiopathic DCM (Less common in Ischemic DCM ) Rapid assessment of RV function is difficult  . Of course We have some clues .

2 d Features

  • Simple dilatation  of RV is suffice to say it is struggling with the  loading conditions
  • Septal bowing
  • Tricuspid annular dilatation
  • RV ejection fraction (Continues to be complex for routine usage )

TR jet

  • Dp/Dt
  • Morphology may be useful (Mainly for TR severity )

Tissue doppler

  • TAPSE
  • RV strain rate Imaging etc.

And  now  , we have observed a new echocardiographic  sign   ie  TR jet alternans  in patient with  DCM .

Note the changing TR velocity implying severe RV contractile dysfunction.

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Maude E Abbott : Mother of congenital heart disease

November 30, 2012 by dr s venkatesan

Maude -E -Abbot 

The  first book on congenital  heart disease

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Best and worst drugs to control severe neurogenic hypertension ?

November 30, 2012 by dr s venkatesan

Acute stroke /ICH/SAH/ Blood pressure is 210 /120 !

You are called in to control the BP  . . . What will you do ?

Basics

Neurogenic HT is adrenergic dependent /stress related .It is  often volume independent .Nitroglycerin worsens adrenergic  hypertension by reflex tachycardia even though it may drop the initial BP .Sustained reduction won’t happen with NTG .Further , nitroglycerine is known to elevate the intra cranial pressure and worsen  the stroke laden  cortical / brain-stem  ischemia

Best drugs

  1. Alpha methyl dopa
  2. Metoprolol
  3. Labetalol

Not best ( Worst ? )

  1. Nitroglycerine ( I guess  most  would disagree with this !  how dare you call NTG useless for   controlling HT )*
  2. Calcium blocker (It is still useful for spasm prevention in SAH)
  3. Diuretics

* IV NTG is useful in some of these patients for a instant effect. However , It has a huge risk of raising intra- cranial pressure .

Final message

Control of neurgenic HT requires correction of the primary trigger namely  the neural insult .The second best option is to stop the effects  neural signal outflow  .Adrenergic  blockers are the best way to do it . All other drugs like calcium/Nitric oxide /diuretics  are non specific  and only  provide a transient relief  and may in fact aggravate sympathetic mediated hypertension.There is no harm in giving  calcium blockers but it should always be accompanied by beta blockers to bring aggressive control .

Finally , controlling hypertension in stroke is to be done  with frequent confabulations !  with neurologists ,  as blood pressure  lowering modalities  has a competing interest with brain perfusion !

Posted in cardiology -Therapeutics, critical care ccu, Infrequently asked questions in cardiology (iFAQs) | Tagged , | Leave a Comment »

How to localise the focus of origin of VPD ?

November 30, 2012 by dr s venkatesan

Some general rules are available

RBBB -Morphology -LV origin

LBBB morphology -RV origin

Exceptions : Interventricular  septum  is electrically  RV or LV ?

Electrically it is more of  a  LV .  Septal  focus often have RBBB morpholgy . Exist points  do  matter

Three lead  approach

Rapidly looking at lead  V1 , V6 and AVR  can give us a clue

AVR +ve  will immediately tell us the VPDs are  firing  towards right shoulder .

RBBB morphology points to  a  LV focus .

Negative VPD in V5 will further confirm  LV apex is in the trailing  end  of VPD

Common  sites  for  post MI VPD

  1. LV apex and Apical septum
  2. Infero posterio MI
  3. RV origin more common

Which VPD  morphology  has better localising value  RBBB or LBBB ?

It is  the LBBB  that has more localising value . LBBB invariably fixes the right ventricle

RBBB can either be  right ventricle or left ventricle .

To be continued .

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology-Arrhythmias | Tagged , , | Leave a Comment »

Great cardiology lectures : Harvey lecture in 1918 by Kieth

November 30, 2012 by dr s venkatesan

I guess ,the art of delivering medical lectures is gradually deteriorating . This is not because of lack of young brains in teaching profession .It is primarily due to onslaught of technology  and multiple  scattered source of knowledge . I do remember some of my physiology  professors take class  in  the first year medical school  in the early 1980s  .

I wonder  I  could go back in time machine to hear the voice of Dr Kieth who delivered this grand lecture of anatomy of heart in the year 1918 .in the famed auditorium of  Royal college of surgeons . We should profusely than the BMJ for providing the text of that lecture free to us in  almost 100 years later.

By the way  . . .  for those who do not know  ,  Kieth is one of the inventor of SA node the pacemaker of the heart .

\

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2340034/pdf/brmedj06937-0003.pdf

Highlights

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Collapsing pulse collapses during . . . systole or diastole ?

November 30, 2012 by dr s venkatesan

Answer:

Your guess  was correct  if  only it is  “C”

Reference

Suvarna JC. Watson’s water hammer pulse. J Postgrad Med  ;54:163-5 :2008

 

Posted in Clinical cardiology, valvular heart disease | Tagged , , , | Leave a Comment »

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