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Archive for February, 2015

I was recently asked to suggest a topic for debate on STEMI in  a major Indian cardiology conference. I wished , this is what we  should be mulling  over, with a set of  virtual  guest lectures and special invitees from heaven ! Plenary  session : State of the Art  STEMI care             Time :  11.AMSpeaker : Dr Hippocrates Topic : Aren’t  we erring   on either side of the  Noble profession ? Moderator:  Dr. William Osler Chairperson :  Dr .Harvey Cushings, Dr,Sir Thomas Lewis ,Dr Paul Wood , Excerpts : “While , vast number of  our country-men’s  culprit artery doesn’t even get that  mandatory  Aspirin on time . . . an urban rich  man’s  distal non-culprit artery  is decorated with a fancy  bio-vascular scaffold making  that innocuous lesion vulnerable in the process as well !  Aren’t  we erring   on either side  in the  Noble profession ?

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Atrial fibrillation is the most  common arrhythmia we encounter in clinical cardiology .Ironically it is  uncommon during ACS and extremely rare in association with UA/NSTEMI. Surprisingly , an entity ” Ischemic AF” is not to be found in cardiology literature.

The incidence of AF in STEMI is less than 5%. Occurs more often due to factors other than primary ischemia of atrial musculature. Of-course , AF in association with Infero posterio MI and RVMI is an important trigger for AF.LCX disease is more often associated with AF as it gives up a consistent branch to left atrium.

Though it is tempting to implicate ischemia as a trigger for AF ,most often it occurs , in elderly ,associated COPD ,hypoxia preexisting atrial disease .Acute elevation of LVEDP and stretch of left atrium could be a more logical mechanism.

Hemodynamic impact

  • AF can bring down the blood pressure.
  • Worsen ischemia by increasing the MVO2
  • Could be very destabilising in RV infarction
  • Surprisingly it is well tolerated in many STEMI patients.

AF in STEMI- Is it an emergency  ?

It would appear so. But , if hemodyanmicaly stable one need not panic.Many times they are transient .Correcting  hypoxia, optimizing beta blocker would help.

Role of DC Shock  , Precautions before shocking  & Post shock events

  • DC shock is done only if there is hemodynamic instability  or ongoing ischemia .(Very difficult to rule out the later )
  • Mural LV clots can form even within 24 hours and DC shock embolic strokes may ensue .
  • Hence it is mandatory to do an echocardiogram prior to shocking.

Drug of choice

  • Betablocker
  • Class 1c -Flecanide.
  • Class 3 -Amiodarone./Ibutilide/

Role of Digoxin

There used to be a concern about usage of Digoxin in the setting of ACS as it pro-arrhythmic , but it remains useful in the management of AF .There is no other  anti-arrhymic drug available to control, the heart rate without depression of  the LV  function

Rate control vs rhythm control

Always aim for rhythm control in the setting  of ACS.Rate control is may not be a  logical concept in acute settings though Amiodarone does both.

Wide QRS Atrial fibrillation

As we know , AF in STEMI can conduct with aberrancy , and we have a traditional teaching all wide qrs tachycardia are VT in the setting of MI making our patients statistically vulnerable.

After all , both entities lack discernible p waves. At high rates it may be difficult  to identify irregularity  RR interval. However , one would shock such patients  and both AF and VT would respond .All is well that ends well.

Summary

AF during STEMI is a risky arrhythmia and needs urgent intervention , but one need  not be alarmed .There is a set of protocol . Only hemodynamically unstable AF require DC shock .Many times it is just transient.There has been instances of  physician panicky that has resulted in more adverse events .

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Cardiologists do magic inside the human coronary artery , that too in a  live beating heart , unlike the surgeons.Blocks are removed , holes are closed, valves are inserted ,  scars are burnt, new electrical connections  are laid .They do this with relative blind vision with good degree of success. Still, as we aim for more precise interventions we require excellent imaging  modalities to assist us.

In  PCI of CTO(Chronic total occlusion)   the critical element to know  is  the morphology of the  tissue plane , what  exactly  we burrow ?  as we navigate  through complex, often hard shapeless tortuous tissue tunnels  . Our patients will be  surprised to know we are currently doing this with our eyes shut. If only we have a camera guide in the tip of the wire it give us tremendous advantage .

CTO pathology

The CTO morphology .Image source : Kenichi Sakakura ,Eur Heart J. 2014 Jul 1;35(25):1683-93.

The exiting IVUS technology can only look sideways . Now a new vision is added by annular array of transducer at tip with CMOS sensor .The technology is just coming out it would be  use for us in the near future .

Anatomy of the forward looking ultrasonic eye

ivus forward loooking cto intervention

Reference

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In this era of synthesized evidence base,  one of my  intellectually aberrant  student asked  How can we indulge in  a popular coronary procedure   with  class 1 indication backed by level C evidence  ?   (As defined by  the seemingly invincible  guideline committee  of various  International cardiology organizations .)

medical ethics silence guidelines

I told him ,

  • Institutional protocols are to be followed
  • Guidelines are to be respected
  • Recommendations are to be considered
  • Please be reminded  all of the  above can be rejected  outright !

Finally , realise  Individual  decisions based on sound scientific understanding with zero non academic intrusions  will be revered forever !

*Caution : If you  think  you haven’t  yet reached that the level of  individuality , come what may ,  you are  expected follow these  advisories  which are primarily aimed at  providing quality care and  you will be pardoned of any adversaries as well  !

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ecg pulse deficit biventricular bigeminy

 

Answer : Most probably  B .

What we feel in peripheral pulse ,  is one weak and the one strong beat in sequence .The later is due to post VPD potentiation. Since there is a compensatory pause , ECG rate (Number of QRS complexes /mt)  and pulse rate are same .

Ironically , heart rate and ECG rate are not same as VPDs impact mitral valve more than aortic valve  and cause additional  S 1 than S 2 making heart rate considerably more than pulse rate and logically it must be  double the pulse rate . This may be difficult to  appreciate by auscultation, but can be documented by phono-cardiogram or by M mode echocardiogram.

 

 

 

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The gradient across coarctation  is not  simply (& solely ) determined by degree of obstruction , as one would believe.Understanding the hemodynamics and various factors that can influence the gradient is essential Relieving the  obstruction /gradient by stent or surgery  may not be synonymous with successful treatment as we understand now the entire aorta right from the root to abdomen can influence the gradient ,along with systemic factors.We also know , some of these patients harbor histological abnormalities in the entire stretch of  Aorta , what is  being  referred to as pan aortopathy  , that may influence the long-term outcome.

coarctation gradient collaterals002

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A cardiologist  is  a physician who has  trained himself  in a special  way  to deal with any problem of heart.Ironically , it exists only on paper.The field has developed so vast  no one can master everything .There is no such  “Pan or global cardiology expert” .In fact it would be shortly become unethical to try to become one !

Pediatric cardiology  has developed into such a big field , doing a echo in newborn or  infant has become a comprehensive job and  requires  special talent .This unique  and excellent study from Narayana Institute , Bangalore published in the  prestigious Annals of pediatric cardiology   throws up interesting realities about the quality of echo report done by adult cardiologists in children .The error rate  appears  huge and stands at  prohibitive 38%. While many errors were minor , major  were also not insignificant (23%)

pediatric echocardiography by adults cardiologist

With bulk of the pediatric echo  involves  in the critical decision making  process of device closures and interventions the  data required  becomes vital .The commonest cause for  error is probably not due lack of  knowledge and but to due to lack of commitment and  continuous  exposure in doing echocardiograms in  those age group.

While this paper  decently skirts the issue of quality of pediatric echo done in medium sized hospitals without pediatric cardiology service ,I can say the error rates or inadequate reportage could be significant  in such hospitals  with apparently good ranking .

Final.message

Of course ,we have many  adult cardiologist who do  excellent  pediatric work , It looks like , as a general rule  performing pediatric echocardiograms  by non -institutionalized  adult cardiologist  may not be appropriate ! It may be wise for them to avoid doing echocardiogram in small infants with  truly complex disorders (even perceived  complex) till they gain the required expertise and confidence.

I recall an  adverse  issue happened years ago ,  when I had  missed an associated    PAPVC  in ASD that made my surgeon anxious on table .In a country like ours there is no one to audit our work , “our conscience remains the only option” to deliver the best for our patients  especially so, when they are tiny lives in distress.

After thought

Who am I to suggest  who should do echocardiogram ? , after all every cardiologist is licensed  to do that . One simple  suggestion  would be , if  not confident  they can at least mention in their report it is only  preliminary evaluation and need to be followed up with  an expert . I do that whenever its required  and gives me peace of mind as well !

More controversies* to come

Can adult cardiologist do pediatric intervention ?

* Controversy : One of the meaning for this word  is  “It is a thought  process  set into motion , that aids digging up hidden truths ”

Reference

 

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We know aortic regurgitation causes  a deluge of   hugely popular peripheral signs of aortic run off  , which are taught  right from 2nd year medical school.

aortic runoof

When the aorta  leaks it reflects in the entire vascular tree .How is that a  leak in the remote aortic valve cause a quincke’s to and fro pulsations in the finger pulp ?

aortic-insufficiency

Is the blood in the finger  trying to follow  the regurgitant  jet  that  go back into left ventricle ? Does the to and fro murmur of  Duroziez over the  femoral artery imply  there is reversal of  blood flow in femoral artery ?

Things are  little complex than it appears

It is true the initiating event of collapsing pulse is the regurgitant jet , however the mechanism that amplifies and sustains it , lies in the altered peripheral hemodynamics.

The systemic arteriolar resistance is  dramatically low in chronic  severe AR  by a reflex phenomenon ,  as cardiac out put is increased and vascular tree adopt to it. So, with each  beat when blood is ejected two things happen in diastole .While a small fraction runs back into LV , the rest of  blood runs off , as if it goes in a free way  making all peripheral pulses dynamic , bounding and collapsible.

Hence as the name suggest all the peripheral signs of AR  are due to the peripheral mechanisms rather than primary event of aortic run off  into left ventricle.

Why carotid pulse does not show the collapsible nature of  pulse in AR  ?

If aortic leak into LV  is the dominant mechanism ,  carotid  artery should obviously manifest a collapse ,but it doesn’t  ,as carotid has no direct continuity with the  peripheral low resistance circuit

What is the hemo-dynamic  correlates of    descending  aortic flow reversal  in  severe AR ?

The central vascular tree  manifest  some  reversal till the regurgitant  velocity fades off . This can occur in severe AR, extending into certain length of aorta. This can be picked up by Doppler probe. Please realise  it is only  the wave form that get reversed  not the actual blood stream.( The momentum gained in systole  continues to push forward in-spite of the pulling back forces of regurgitation)

Why peripheral signs are  absent in acute AR ?

Acute AR even if it’s  significant does not cause a collapsing  pulse because it takes time for the peripheral vascular tree to go for vasodilatory mode.Further ,LV is also less compliant keeping the LVEDP high and regurgitant fraction low.

Summary

Answering  the title question ,the mechanism of  Aortic run off  in AR is both central and peripheral.  However  clinical  signs are largely due to high cardiac out put and the resultant   adaptive  response  of the  vascular tree due to low  systemic   vascular  resistance  triggered by  reflex  dilatation of small arterioles of the  peripheral vascular bed.

 

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In the last few decades  we have  understood a major concept in the genesis of cardiac arrhythmia.Slowing in the propagation of cardiac impulse is a key  trigger to precipitate a reentry circuit and initiate a tachy- arrhythmia.Still , many conditions like first degree AV block, chronic RBBB or even LBBB are  benign entities  as along as the heart is structurally normal .They seem never increase the incidence or life time risk of  cardiac arrhythmia . Longevity is unaffected.( Or do we assume many things ?)

How is this possible ? or is the theory of slow conduction triggering reentry is flawed ?

Think again . . . if these patients who later on develop a structural heart disease , with an episode of ACS , myocardial or valvular disease,  the original slow conduction substrates these people were harboring ,  will it become important ?

Surprisingly , we have no answers in literature.When Haissaguerre et al found preexisting ERS pattern could be a trigger for primary  VF in case they develop ACS  , he opened up a huge debate as it involved converting  a vast number of normal population electrically anxious.

Now ,is it possible the so called  benign  blocks of heart like first degree AV blocks , RBBB , LAHBa , would be important  at times of ACS  and possibly make them prone for for primary ischemic arrhythmia .

Is bundle branch re-entry possible in structurally normal heart ?

We need answers. Some one , (Any EP fellow) somewhere  could take up the issue and enlighten us !

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ICDs are one of revolutionary devices , invented last century  that can defy “death & fate”  in high risk cardiac patients who are threatened with ventricular tachycardia or fibrillation .A decade long hard work by  Mirowski  and team from John Hopkins culminated in the dramatic  the first AICD implant in 198o. ( In my opinion, this medical invention can be compared to an event of such  significance as moon landing by Armstrong and team ! ) Ironically , in the last decade such a revolutionary device was sort of misused and thousands of devices were explanted for inappropriate indications.

Fortunately , better sense prevailed recently .The indications are getting  refined. I am sure ICD will go a long way in prevention of  both expected and unexpected sudden  electrical deaths .We are into  the 4th decade of its evolution.While the electrical circuitry has been mastered , power supply remains an issue as they require continuous power supply like a mobile phone. Current technology allows about 6-8 years of battery life.

EL-ICD boston scientific longest life icd smallest profiale dynagen inogen madit indication for icd

Now , Boston scientific  has come out with new technology which make its  battery life extend  by 100%  to 12 years.  It is a major break through , expected to evolve  further  until probably we have rechargeable  batteries or biological power sources .Stretching a wild thought , the days couldn’t be far off  when the smart phones which are omnipresent in every human-being  , could not only power the ICD  remotely and control it too !

 

Indications (ESC/AHA 2012)

CAD

  •  Post MI* /LV dysfunction  ≤ 35% /NYHA   class II or III  (*  > 40 days)
  •  Post MI* /LV dysfunction ≤ 30% /NYHA Class I (* > 40 days )
  •  With non-sustained VT due to prior MI, LVEF < 40%, and inducible VF or sustained VT at  EP study

Non ischemic structural disease ( Idiopathic DCM, ARVD etc)

  • With structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable.

Primary electrical disease

  • With syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at electrophysiological study

 

Reference

Link to Product manual form Boston scientific.

Boston scientific

 

 

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