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qt interval animation short and long002

The stretch and strain experienced by the action potential’s left shoulder region is almost similar* in both long and short QT syndromes that trigger a VT.(* Hope this explanation makes some electrical sense !)

*Click  over the image for  high resolution

What is short QT interval ?
It is a range . Any thing less than 380 ms can be considered  short.Generally It becomes important only at < 320ms.
Relationship between QTc and risk of VT .
U curve of long and short qt syndrome

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In this mean world ,most truths  exist without evidence  . . . and often  falsehoods  masquerade as truths with  overwhelming evidence !

Human  biology   has  always  been a mystery  and can express  in dramatic  ways  . While  ,  many  disorders   combine to play havoc on the body ,  few tend to  protect  each other. HT and DM can join a deadly coalition to attack the heart .Smoking  causes  extensive peripheral vascular disease ,  still  thrombo angitis of coronary arteries ( due to smoking ) is  virtually unknown. Tuberculosis does not  have the  courage to attack  the heart  valves  ,  while  it  can inflict serious injuries  all over the body . Similarly , systemic hypertension and  Rheumatic heart disease  does not  combine  well . So , it can be assumed  some unique  and hidden   protective factors  are at play  among different pathological entities and their target organs.

A  brief  account  of how COPD could be related to  CAD !  (* Mostly Imaginary !)

We know ,  COPD ,   stresses  the right  ventricle by pressure overload and in extreme situation  affects  the  LV function because of  hypoxia. It rarely impacts the coronary artery disease  . This has been  our  consistent  observation. While COPD patients often land up with LV dysfunction , investigations reveal  they are  more of a dilated cardiomyopathy and their coronary arteries are entirely normal. Diffuse atherosclerotic CAD is a rarity in  patients with  history of  bronchial asthma. Coronary micro circulation  is also observed  to be largely  intact in most people with  COPD .

We  haven’t got a call   from our pulmonology  wards  in  many decades ,  for  a true   emergency  coronary consult . Mind you ours is a  200 year old  Institution , with 3000 beds  , largest east of Suez canal !

It’ s very rare for bronchial asthma  patients  to die of  a cardiac event. Thousands of   elderly patients   throng our ER with acute severe asthma every winter  , still  extremely rare  to  precipitate an acute coronary event !

We are yet to see  critical  triple vessel disease in a patients with documented  bronchial asthma and COPD .  Even  non-critical CAD is far less  frequent  in  COPD   vis a vis  general population .  It is indeed a strange  observation  , considering both entities are rampant in the community  .

What could be  mechanism  for the perceived disconnect between COPD and CAD ?

Is it a myth ? Does it happen in all geographical zones ?  If  hypoxia is the sine qua non  of COPD  ,  one would rather  expect a close association  with CAD  , isn’t ?

One  suggestion  that  keeps  erupting  from my cortex   . It is  the  wide swinging intra thoracic pressures in COPD or  asthmatic individuals  . . .   somehow responsible . These wide swings  of pressure  are  transmitted to aortic  root . They  transform into  good coronary perfusion pressure  ,   keep the vessels  clean by pressure vacuuming effect .

We have  asked our epidemiological unit to  analyse the  25  year data from our coronary care unit  to decode the mystery .

Counterpoint

Meanwhile,  a  diagonally opposite  question was asked in UK  and found a partial proof as well . Our experience do not agree with this study  conclusions .

What is your take on the issue ?

bronchial asthma and cad

http://ije.oxfordjournals.org/content/33/4/743.full.pdf+html

Introspection

How can a opinion (rather an Imaginary essay !) based on personal observation   projected as a  scientific fact ? We need to observe , analyse and publish the data . This is what the scientific world expects us to do . Unfortunately , the journey form observation into publication has been kept  purposefully difficult . In my opinion bulk of  the international peer reviewed  medical journals with high impact factor can  convert any  junk  data  into a  scientifically palatable  recipe  !

 

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The doctrine  of  modern medicine  goes  something like this   . . .

For most medical problems ,  there  would be a solution. Keep  trying . . . till you get it !

*But , just make sure that problem on hand deserves a solution in the first place !

Modern medicine continues to  remind us  every day , the much hyped solutions  often end up in new problems and  many  times worse than the original problem !

Oh ! what a  great a quote ! When I  was boasting   myself  . . .  My wife reminded  me ,  this is just  plagiarized version of  a  2000 year old Hippocratic thought !

Primum non nocere  . . . first do no harm !

But , Hippocrates’  life  was  not  contaminated  with  drug eluting stents, I pads, and  BMWs

If   Hippocrates  arrives  in   cath lab  today  by BMW which sucks  50000 Rs EMI  ,Everolimus coated  coronary  jewellery   will  definitely  tempt him !

You  can’t  simply   compare lives separated by 2000 years

. . . I told my wife !

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Scientific studies can be fun .In our spare time we often Indulge in rapid  fire sessions. We tested 30  wide qrs ECGs from our archives  (All proven VTs)  and  asked  our  cardiology fellows to apply Brugada criteria . They could   correctly  diagnose  VT  in 18* patients.The same ECGs were shown to the staff nurses of coronary care unit . 24  VTs were correctly identified  it.They did it by  their clinical sense and Instinct. (*12 vs 6  VTs missed)

wide qrs tachycardia svt with aberrancy and vt brugada verecki  griffith002

And now , four  clinical data was  provided. (Age , sex , Blood pressure , and  past H/o  MI were given )   The Nurses were able to predict it  28/30  VTs correctly.(97 % accuracy ) and the cardiologists  were able to equal the score now. So obviously clinical sense  was far superior .

Cardiology fellows were more likely to  mistake VT as SVT. This is far more common than SVT mistaken as VT. It is a strange academic  irony ,even the junior most nurses never missed a VT !

Summary

Simple sequence of history and clinical presentation is still far more powerful than ECG data in predicting wide qrs  arrhythmias . Nurses guess work is far superior than cardiologists  in predicting a wide QRS tachycardia as VT.

In fact , the  cardiology fellows are  preconditioned to   get confused   whenever they get a wide qrs tachycardia . Why  not aberrancy ?  In my  experience I have seen this question keeps  erupting inappropriately .Even  shrewd fellows suffer  from an  oscillatory  mind between VT and SVT .This is primarily because , every wide qrs ECG  is likely to  have at least two  criteria that fulfill both VT and SVT.

The implications are  genuine  and far reaching . While nurses  show a patient centric thinking  cardiology fellows  thought process revolves around ECG . Many modern-day cardiac physicians  are disconnected from clinical reality  and are obsessed with  complex EP concepts  and end up with a miserable face in the bed side !

This is not a new  revelation in 2013 . Masood Akthar told this  three decades ago.

Caution
Never try to glorify  guess-work . EP is a great science .The  pioneering concepts have made us understand how a VT emanates, travels , and exit from myocardium . We are able to localise it and ablate it .All credit goes to science . But , when it comes to bedside recognition of VT ,  clinical  sense  is a clear winner .With a  consistently > 90 % predictive value   it  can no longer be called as  a  guesswork   and becomes a hard scientific fact. Especially so , when the  intellectual  analysis of surface ECG   could predict  it  with paltry 70 %  accuracy (Read Reference 1)
Reference
This  analysis startlingly reveal  a fact .The over all accuracy  rate of predicting the wide qrs criteria  by  popular algorithms  is   between 66-77% ,  just 16 numerals   more than  gross   guess work  of 50 : 50 ( This  . . . or  . . . that )
Link to  Masood Akthar article

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Of late many drugs are entering the  market  for human  consumption backed up by  Non -Inferiority trials (NIT ) .Few examples.

“The ONTARGET trial: Telmisartan is non-inferior to Ramipril in  New Study Results Published in the New England …”

Feb 20, 2013 – in the New England Journal of Medicine Show Dabigatran Etexilate ... daily was non-inferior to warfarin (p=0.01) in preventing recurrent VTE, …”

What is the logic behind these  Non inferiority trials ?

Why it came into vogue ? 

Do you agree with the concept of NIT ?

I have taken the  privilege  of putting my answer in the title. Believers  of NIT please excuse me.

Reference

Non inferiority drug trial

Non inferiority drug trial 2

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Cannon waves occur when Atria contracts against a closing tricuspid valve of  right ventricle .( There  would be a equivalent left atrial cannon which  goes into pulmonary vein as well  , it is discussed elsewhere !)

Cannon waves  happen only when P waves fall within QT interval in ECG as QT represents the electro-mechanical systole of  ventricles.  (Since P wave represents atrial systole , it is simple to understand when it falls within QT both atria and ventricular contractions collide to produce a cannon wave into the neck or pulmonary veins.)

The following two images of cannon waves  taken from the legend  Dr Paul woods own tracing  .

irregular cannon waves in jvp  complete heart block

regular cannon waves in jvp  svt avnrt  11 va conduction  002

Regular cannon waves

Occur during SVT  with 1:1 VA conduction.*

1 : 1  VA conduction  can be considered as  absence of  AV dissociation  (Rather  disciplined  VA association with every beat ) This is essential to create a hemodynamic  milieu for regular cannon waves.

* In AVNRT , VA conduction in strict  sense  is a misnomer  .It is simply a retrograde conduction thorough  the AV node .

Irregular cannon waves 

  1. Complete heart block .
  2. Multiple random VPDs
  3. Some patients with VT.*(Who are those patients ?  Those with AV dissociation when retrograde “P” wave falls  within QT interval cannon occurs. As expected this occurs in random fashion  which makes  the cannon fire irregular.

Can we get regular cannon in VT ?

Yes , but rare . As explained earlier this can happen only if AV  association occur on a retrograde fashion.

Further reading in this site

What-is-a-cannon-sound  , how is it related to cannon wave ?

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Rheumatic fever and RHD is still a major cause for  cardio vascular morbidity and mortality in India .It seems , improving quality of life  has little  impact on the incidence .(We could realise  this as  we sit in the cardiology OPD of a 200 year old hospital !) There is no country wide data on the true prevalence .  Our understanding of rheumatic heart disease is based on isolated  studies on localized populations .

Of late , cardiology   resources  in our country is diverted towards  much glamorous CAD the poor continue to  suffer with  RHD.

Just Imagine many   hospitals indulge in 1000s of PTCA every year  but hardly do  a  hand full of PTMCs.

How our cath  lab resources  are used   across the breadth and length of country needs some introspection (Currently , I believe we have about 750   labs ) .I think there should  be a binding legislation  in every cath lab .For every 10 PTCAs done   at least one PTMC must be done to heal the poor .( Like the Air-craft license  .You can’t fly only the lucrative metro sector is given only if IT  services less developed areas )

In this scenario ,  it is a pleasant  surprise  to find a  wonderful review article on RHD from the two pioneers ,  in lesser known medical journal IJMR  .

Review article rheumatic fever  Indian journal of medical researchEspecially heartening  is  the fact ,  it is a collective effort  from two  distant  regions of India ( Kochi from down south and  New Delhi In the north) . While politicians keep the divide , it is a great  work  of the authors , which  would help  youngsters  who  would like  to go on a national mission on eradication of RHD. .

Reference

http://www.icmr.nic.in/ijmr/2013/april/centenary%20review%20article.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2840767/#CIT12

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asd-closure-device-www-drsvenkatesan-com

The following  factors are critical determinants of the success of ASD device closure

  1. Location of the defect ( Only ostium secundum )
  2. Size of the defect (<35mm .Never forget  simple truth , larger the defect shorter would be the  rim )
  3. Shape  of the defect (Please note ,none are strictly circular but most devices are ! )
  4. Eccentricity of the defect (RA aspect of ASD need not match LA aspect)
  5. Length of the rim ( 5mm said to be adequate)
  6. Thickness of the rim ( Least respected parameter .Thin filament like rims are notorious  in sagging the device into RA)
  7. Pre and Per- operative TEE (As Vital as the procedure)
  8. Technical expertise . (This includes extreme patience  of the primary operator .Most sub optimal results and complications are related to this.
  9. Good team ( Not every  interventional  cardiologist should  attempt this !)
  10. Courage to abandon the procedure
  11. Device brand (Probably less important )

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Hypertension is  probably the most   important clinical entity for physicians
for decades .With the advent of modern interventional cardiology management of HT with  drugs have become a  less glamarous job for us. Still , the quantum of the problem and it’s impact on the  risk of CAD and progression   remain a major issue.
There many  different bodies periodically coughing  up guidelines  to manage HT.
  1. JNC from USA
  2. British Hypertension society from UK
  3. European society of cardiology
  4. World hypertension league
  5. Finally WHO guidelines* ( It is not a regular exercise ,WHO releases it  as and when it feels like !)

The stakes are high for the drug industry .Anti hypertensive drugs are the  major source of revenue  to them . Any dip in per capita consumption will have direct impact on their health ! ( WHO bothers about public health ? )

The so called scientific  guidelines,  are generally made balancing patients health vis a vis drug companies health .I have found more often than not it was tilted towards the industry .

The fact that there are multiple guideline with varying impact factors makes sure the confusion among the global physician intact . This is one of the aims of the pharma companies as they influence heavily  when to initiate the treatment ,  and what we are  supposed to prescribe.
Some of the guideline are notorious for insinuations . One example was about the definition of pre hypertension  few years ago .It has since been removed  from the literature after a critical debate .

* One may wonder why I’m focusing always  on non scientific  issues more than academics .(I some how feel non scientific factors are going to impact our health more than any other factor in the coming  generations  )

Now is the beginning of a balance .

European society of cardiology 2013 guidelines for hypertension
Among these guidelines  I would  think  ESC is close to reality and fairness.
Even    it was carrying dubious advices till recently .Now they have come out with new one in 2013.Most changes are  welcome.
  1. It is essentially about cleansing the contaminated guidelines
  2. Removing unnecessary medications
  3. Unified definition.
  4. More efforts to identify true secondary HT
The salient  points
There are  18 point update in the ESC 2013 . All of them are great . Essentially they are about the basics we have been  taught as we learnt in our final year MBBS. (The rest of our life we have to unlearn  the junk we have accrued over the years  from various CMEs )
I can modify it and  short list
  1. Do not start too early .Have universal definition (Now 140mmhg)
  2. Respect non drug treatment ,( However attractive the  gold tipped pen the  representative leaves  in your consulting suit !)
  3. Avoid using multiple drugs
  4. Never miss a secondary HT .( If  diastolic BP> 110mmh almost always a renal component would be there .Remember Conn syndrome (Primary aldosteronism )  is 10 times more common than much hyped pheochromocytoma ! Just do K+ levels to detect this )
  5. In CAD patients never treat HT in isolation .( Measure blood pressure with sugar and  lipid 120 /70 mg of LDL )
ESC 2013 is a commendable Initiative . It has  tried to remove most errors of the past .obviously  the pharma industry will be unhappy as it will definitely bring down  total drug consumption the  population.
Final message
HT  is an important target  for prevention and management of CAD
Thanks to the much maligned pharma industry  .
We have good drugs.Use it judiciously . Try to reduce the number of drugs .
If possible make them drug free.
If a patients taking   beta  blocker for associated  cardiac condition do not add another anti HT drug . (Recall  from your distant memory , beta blocker is a anti HT drug too !)
Simply follow common sense . (* If you think you  lack  it  ,  get  it from your learnt patients .Many  of them have in plenty . I often do that . One  question they keep asking  “Should I take this drug  life long doctor ?”  is a definite common sense booster!  )

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A Cardiologist will never accept  the diagnosis ,  if a technician reports   a  ECG as normal in a  patient with chest  pain   . . .

While , the same cardiologist  gleefully  accepts  an  echocardiogram   done by a technician  and  treats  the patient without  verifying the veracity of the finding !

Why ?

Some where along the cardiology training  , we have been made to believe Interpreting  Echo Images does not require serious medical knowledge . . . but we strongly believe  ECG  cannot be read by technicians however well they are trained .(In-spite of the fact , Echo images are highly dependent on the person who does it , while ECG wave forms are  totally independent of the person who record it ! )

ECG, still has a  prestigious place  in cardiologist’s mind ,  while Echo is often considered  an inferior  Investigation.  Many of us consider ECG interpretation  as a  brainy work while Echo image acquisition and  interpretation is perceived a dumb job* !

Lastly , probably most importantly ,  performing  Echo  is   a time intensive process for the  present day cardiologist  who’s hands are tied with  catheters and  guide-wires  .He has little time for  the meanly echo . .  . hence  ready to compromise on the quality .

* With due respects to all non invasive cardiologists (That includes the author !)

Final  message

I would think it is  fundamentally inappropriate  for technician  to  report Echocardiogram (Of-course they may record it  ) . Unfortunately , for some reason this practice is continued  in many  parts of world .

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