Archive for August, 2013

Anterior mitral leaflet  has a classical M  shaped motion. Infrequently , M mode echo will record a triphasic pattern .

Triphasic AML motion

The exact  answer is not known . I guess it is a normal variant.

Often  it is recorded  when there is a long  and redundant AML , especially if the M-mode cut is too close to  the tips.

Though it is not common , I have seen in few the triphasic gets converted into classical M shaped pattern if the cursor is moved slightly away from the tip of AML.

Relationship to Heart rate

Some times it appears in slow heart rate and tends to disappear with tachycardia .

Triphasic Doppler filling vs Triphasic M-Mode

We do not know yet ,  how  the  triphasic AML motion  correlate  with triphasic Doppler filling pattern which  is considered a fairly good evidence for  LV dysfunction.

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The pericarditis  of acute rheumatic fever is not a true infective pericarditis.It is more of inflammation .It is primarily  T cell mediated  reaction . Neutrophils rarely take part  in this inflammation and hence  no significant  exudation . Hence , there is less  sticky and adhesive molecules inside the pericardial space .The most inflamed layer is epicardium which a nothing but visceral  pericardium .This layer lacks the tensile strength to constrict the underlying myocardium.

why rheumatic pericarditis does not go for constrictionFor constriction to occur the fibrinous  ( thick ) layer of pericardium need to be involved . In rheumatic fever  even though it is  pancarditis ,  fibrous layer is not  involved. Further the inflammatory gradient is thought to spread from within  (Unlike tuberculosis )

Note :  In chronic tuberculous pericarditis,  diffuse inflammatory process  invade from the exterior surface . Very often ,  one can not differentiate  layers. In extreme cases even myocardium and pericardium can not be separated .


The peri-cardial effusion of acute rheumatic fever

  1. Is transient ,non infective and resolving (Unlike valvular inflammation !)
  2. Less of neutrophil activation  (Less adhesion)
  3. It does not involve the thick , tensile  fibrous layer of pericardium hence lacks the contractile force .

Other lingering  questions

1.How common is tamponade  in acute rheumatic fever ?

2.How important is the mass of the effusion (Viz  a Viz  Intra pericardial pressure !) in causing tamponade ?


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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 .


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



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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Platelets are humble blood cells that  roam  in clusters and guard  against  any  bleeding in internal organs. Though it has natural powers to regulate itself  against aggregation at inappropriate sites , certain high risk individuals need to take these drugs to prevent cardiac event. Patients  who harbor intra-coronary foreign bodies like stents  need more intense antiplatelet  regimens.

We have variety of antiplatlet drugs. Aspirin does it  by blocking  COX. It is irreversible .Clopidgrel does this differently by inhibiting  P2 Y12 receptors .Clopidogrel has been used extensively in India. Some brands of it are many folds costly as well !

A curious encounter

A certain patient with a stable CAD,  from higher strata  of society was offended when I replaced his long term  prescription of Plavix(Clopidogrel)  with Aspirin.His major humiliation was  this  new drug costs just  50 paise ! He suggested  to me  ,  it is huge insult to him  as his driver also takes the same medication !

What does pride  do in platelet inhibition I tried to explain him  ?

He was amused !

I asked him to go elsewhere , to any star-rated , upscale health suit  nearby to fulfill his wishes !

The above event happened few years ago . I am just posting it from by diary .

Final message

In this unequal world , prestige comes to play even in illness and the drugs they take ! I wonder, how prevalent, is the issue of pride  in our patient’s mind that decide  the treatment modality  in modern day medial care !

Your comment.

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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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Inter atrial septal aneurysm is a benign disorder of IAS where the flap  of fossa ovalis bulges on either to right  or left atrium. It may be associated with fine fenestration or even a classical  ostium secundum  ASD.

atrial septal aneurysm 002

An unusual buckling motion of IAS aneurysm.

Though the pressure within the atria is one of the determinant of this  bulge.The morphology of the flap is such that it more often prolapse into LA than RA. Rarely it can be dynamic and  moves 180 degrees , buckling between RA and LA .This unusual  motion is real stress to IAS and can trigger atrial  ectopic beats. and atrial tachycardia .

Read  related article  IAS aneurysm 


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Human physiology can dramatically surprise us.Here is a situation regarding K+ ion and cardiac function.

Low potassium level is a well known cause for skeletal muscle  weakness and paralysis.While,in cardiac muscle usually the opposite happens.It is the high potassium levels that depresses and cause paralysis.(That’s why,it is used in cardioplegic solutions. )

But,the classical differences between skeletal and cardiac muscle need not apply in critically  low levels of K +

What happens when K + is critically low ?

We know, K + is the vital  ion that maintain not only the membrane potential ,(Recall Nernst potential ) but also keeps the action potential floating and dipping with every beat.

Imagine the intracellular chaos when these ion levels changes in dramatic fashion . (Of course,God has ensured very tight regulatory controls at various levels within each cell ! )

However , ECG changes are expected 100 % of time with falling K +  especially below 3meq.Surprisingly , low K + levels have little  mechanical impact.(Or is it our ignorance,considering the fact , cardiac electrical mechanical activities are tightly coupled?)We have to find answer from patients like this .

A  30 year old women came with breathlessness and fatigue and her ECG.

hypokalemia STEMI ECG changes

Can we afford to miss a diagnosis of STEMI ? With all our collective wisdom STEMI was diagnosed promptly . . . of course wrongly !

She was adviced  streptokinase.A shrewd fellow who reviewed  the old records spotted the past  history  hypokalemia , and Inj streptokinase was put on hold.(Lucky patient  . . . she was not shifted to cath lab )

Her  K + was 2.3 Meq. The LV function was significantly impaired with global hypokinesia, which  improved with correction of K+.

hypokalemia STEMI ECG changes 001

She was later referred for  nephrology work up , they had made a possible renal tubular disorder for the Hypokalemia.

Clinical Implication.

When potassium levels are critically low myocardial  function may deteriorate.Here is a patient with dramatic STEMI like ECG with extreme hypokalemia.

Our ignorance regarding electrolytes and myocardial function  remains unexposed .In critical care units  wide swinging metabolic and electrolytic  parameters are common.ECG is just a marker  for these .Similarly all LV dysfunctions are not primary myocardial disorders (Sepsis, Hypoxia, Extreme acidois , Uremia ,drugs,toxin  can lead to myocardial dysfunction.)

Experienced  physicians  do not form hurried opinion.Wait . . . allow things to settle down and assess again.After all ,there is long list of causes for ST elevation other than STEMI !


1.Chest. 1979 Feb;75(2):189-92.Cardiac dysfunction in a patient with familial hypokalemic periodic paralysis.Kramer LD, Cole JP, Messenger JC, Ellestad MH.
2.Acta Neurol Scand. 1978 Dec;58(6):374-8.Hypokalaemic periodic paralysis and cardiomyopathy.Schipperheyn JJ, Buruma OJ, Voogd PJ.

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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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