Archive for August, 2013

Takotsubo cardiomyopathy is an  unusual response  of the left ventricle to extreme emotional stress .The catecholamine  surge  has  a profound stunning  effect of LV apex  and  a paradoxical hypercontractility of basal LV.

The exact mechanism is not clear , Following factors may contribute.

  1. Multi-vessel coronary artery spasm,
  2. Cardiac microvascular dysfunction.
  3. Abnormal myocardial fatty acid metabolism,
  4. Reperfusion injury  after an ACS *

However , the most accepted mechanism is Endogenous catecholamine-induced myocardial stunning and microinfarction

Why is LV apex alone affected  ?

The adrenergic receptor distribution is high in LV apex .They are exposed to high concentration  and gets stunned easily . Basal LV has less adrenergic innervation  , so it shows less of catecholamine toxicity , instead  it exhibits.  hyper-contractile mode. However, this rule is not absolute.

One more suggestion was apical balloons correlated with wrap around LAD.(Báñez B et all 2004)

what is the mechanism of apical ballooning syndrome 2 takotsubo cardiomyopathy

Image courtesy Circulation December 16/23, 2008 vol. 118 no. 25 2754-2762

*Some consider ACS should never be  linked to  Takotsubo.But it is not easy to differentiate.(Carrillo JACC 2009(Kosuge JACC 2010)

Reference from this site

A link to related article -Ischemic Takosubo  from this site .


Reference from other journals
what is the mechanism of apical ballooning syndrome takotsubo cardiomyopathy

1.Báñez B, Navarro F, Farré J et al. (2004). Tako-tsubo syndrome associated with a long course of the left anterior descending coronary artery along the apical diaphragmatic surface of the left ventricle.]”. Revista española de cardiología (in Spanish; Castilian) 57 (3): 209–16

2.Carrillo A, Fiol M, Garcia-Niebla J, Bayes de Luna A. Electrocardiographic differential diagnosis between Takotsubo syndrome and distal occlusion of LAD is not easy. J Am Coll Cardiol. Nov 2 2010;56(19

3.Dorfman TA, Iskandrian AE. Takotsubo cardiomyopathy: State-of-the-art review. J Nucl Cardiol. Jan-Feb 2009;16(1):122-34

4.Kosuge M, Ebina T, Hibi K, Morita S, Okuda J, Iwahashi N. Simple and accurate electrocardiographic criteria to differentiate takotsubo cardiomyopathy from anterior acute myocardial infarction. J Am Coll Cardiol. 2010;55(22):2514–6. doi: 10.1016/j.jacc.2009.12.059.

how to differentiate takotsubo cardiomyopathy from anterior stemi


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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 !


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.

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)
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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A 25 year man ,  hotel  manager  who had a documented DVT , since 2011 was on tablet warfarin . He discontinued  the drug by sheer miscommunication as he was told he should stop the  drug  beyond INR 3 by his general practitioner.He stopped it permanently  instead of titrating the dose of warfain .Six months later he landed  in August 2013 with an episode of minor hemoptysis . Clincally he was normal .His lower limbs were fine.

He was investigated and  his image file showed .

pulmonary embolism  3  total occlusion of LPA

pulmonary embolism  3  total occlusion of LPA

pulmonary embolism total occlusion of LPA

Living with one lung

  • He is comfortable with one lung function (Akin to  Pneumonectomy )
  • His saturation was 100 % at room air
  • Pulse -80/mt .BP 110/80mmhg
  • His physical activity  did  not show any significant limitation (At worst class 2)

One of the cardiac surgery consultant wanted to do pulmonary embolectomy and endarteriectomy .

In fact , he was admitted in the critical care unit driven by the dramatic CT images.

One enthusiastic cardiologist wanted  thrombus aspiration and pig tail catheter based thrombolytic  irrigation within LPA !

How did we manage ?

  • The risk of major vascular surgery was considered high in an absolutely asymptomatic individual .
  • Intervention was considered too adventurous.
  • He was  put on oral anticoagulant with target  INR 2.5-3.(After a 1 week Heparin overlap)
  • We hope the thrombotic CTO will open up gradually but for surely .As the power of  natural lytic  molecules should not be underestimated as we have witnessed in LV and LA clot disappearing over months.
  • However the option of putting IVC filter was strongly recommended for him , as he has only  functioning  lung  which  is threatened by a potential  embolus from DVT . The patient wanted to come back for IVC filter next month.
  • He was also worked up for all those protein C, S,  Lieden mutation stuff.
  • The patient was discharged in stable condition (By the way he  was never unstable either !)

* Meanwhile the hemoptysis  did not recur. CT scan showed a small wedge infarct in left lung that was in the healing mode.

Final message

This is a perfect example of  CTO of pulmonary artery being  managed conservatively* .We will let you know the follow up .

Link to related topics in this site.

Deep vein thrombosis-Therapeutic dilemmas

What do we mean by conservative management ?

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I wish to  be in New Zealand , not only because of the stunning  natural beauty but also to pay tribute to one of the great  cardiac surgeons  of our time from Auckland .
An alluring  country side cricket ground  abutting the runway  . . . Queenstown I think !

Sir Brian Gerald Barratt-Boyes (1924-2006), Who pioneered all forms of  heart surgery that  specifically included  complex congenial heart disease . Thousands of Kiwi   children are alive and leading a  magnificent life today  because of this  man from Green lane an alumni of Mayo .

barret boyce tof intra cardiac repair cardiac surgeon

Many heart surgeons from India and Asia pacific have trained under him .


Green lane Hospital Auckland.

This is the  hospital where Barrat Boyes worked headed the department of cardiac surgery .He had to over come large bureaucratic hurdles before becoming world ‘s leading cardiac surgery center. And , he lives everyday  in all cardiac units   through this book .

barratt boyce kirklin

Here is a link to pay tribute to this extraordinary man.

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I’m trying to get  a right  answer for this question for quiet some time. The literature on lipids is so vast  , one can never finish reviewing it.There are   nearly two dozen journals that  deal with lipids ,Atherosclerosis, obesity ,and vascular biology .

Yet  , the answer to this simple question is elusive to us .The Irony is complete when we have evidence for   two diagonally  opposite responses 4 and 5 .

My interpretation of the issue

Any lipid molecule if exceeds a critical  level ( Only  if   . . . associated with hypertension, or diabetes or smoking ) can penetrate the vascular endothelium. ( HT-pressure injury , Smoke- Endothelial dysfunction  due to Nitric oxide depletion) DM -Glycation of cell membrane  , finally some  unknown inflammatory component )

Though evidence  for direct endothelial  injury is more for LDL ,  less for TGL (Almost nil  for VLDL , but  TGL has more VLDL in it !)

Strangely ,these molecules , express a mob psychological behavior .In isolation they appear innocuous. But ,in an  unfavorable   setting it shows signs of  revolt. If a group of  LDL molecule start attacking a  dysfunctional segment  of endothelium , the other molecules  like TGL and VLDL fractions would love to join the crowd  and inflict further  damage . (Of course ,the lonely HDL may watch the chaos silently !)

Questions to ponder

If LDL is a sharp knife like molecule  trying to injure the blood vessel , every normal human being is potentially threatened  by this  lipid fraction . Mind you,  this is a physiological molecule  traversing the human vascular system  at concentration  of 130mg/dl  at the  velocity of blood .

So it is  foolish  to blame this  physiological molecule for all our ignorance.

I recall one recent definition for hyperlipidemia

The lipid levels at which a patient develops vascular injury is considered high for him !

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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.


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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