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I know ,there is a VSD out there !  but I am  unable to  get the gradient across it.This situation can be quiet  common .The reasons could  be technical, anatomical or  hemodynamic.

As a rule ,  if we hear  a  pan-systolic murmur clinically ,   one must be able to catch  a good  Doppler spectrum somewhere by  echocardiography . However , If  the murmur is restricted to  early or mid to late  systole, VSD  jet is often attenuated in echocardiography .

In the  following situations ,  VSD  jets  may not  record a distinctive Doppler spectra. Invariably the velocity is low , spectrum is short,  less intense ,  lacks good shape and borders are hazy !

  • A closing  VSD
  • A Small muscular VSD
  • VSD with  Severe pulmonary hypertension
  • VSDs with muscle bundle criss crossing
  • Double chambered right ventricle (DCRV, where VSD usually drains to high pressure chamber.)
  • VSD  associated RVOT obsruction  (Note: classical TOF VSD will never generate a murmur)
  • VSD with sinus of valsalva aneurusms (  Doppler  jet  can be really  difficult to record )
  • Inlet VSDs are missed because  convectional  views of echo are perpendicular to these inlet jets.(Short axis better  )
  • Another common situation  is post STEMI VSR.Both a small apical VSD or multi tract  VSD associated with  infero posterior  STEMI   gradients are  difficult to obtain.

What is   inference ?

Doppler spectrum will help detect  small VSDs and color doppler will not miss even a tiny VSD.Doppler spectrum across VSD  is dependent many  factors other than the presence of VSD. However some large VSDs are detected better by 2D echo rather than doppler signals.

Final message

Presence of a Anatomical  VSD does not  imply it should generate a noise.The murmur as well as Doppler signals  are  primarily  determined by the pressure difference on either side of VSD. After all , one of the  largest VSD  that  we encounter

Time is muscle. This quote  became  sort of ” cardiology sermon”  in the last  few decades .Cardiologist think  they stand  on a 100 meters sprint track once a patient with STEMI arrives .This is indeed true ,  if we  agree  time is  muscle and  our urge is to reduce the door to balloon time .Please  remember ,  this rush matters  much ,  only if the patient comes through very early  when the muscle is really getting damaged . (No issues  . . . even if the fire engine comes in  slow motion if the  house is burnt fully !)

Time is muscle agreed  . . .  but  muscles are  kept alive by  factors other than time  !  So muscles can  defy time if God  is willing !

Time is one of the important components of management of STEMI.  Other things matter too !  Age , baseline co-morbidity ,  underlying extent of CAD, collateral support of IRA territory , and finally  individual variation in hypoxic damage in myocyte is (Rarely  been studied in detail.)

Door  to balloon time for a patient  who lands up within  1 hour window need  to be  much  different from a patient who comes at 10 th hour .The issue is important  because  we use a procedure which requires delicate decision-making ,(IRA-Non IRA issues etc)  the results can be  sub optimal ,  and even be hazardous in low risk STEMI . So , door to balloon time  may be a less  important  component of  time window in a patient who comes after 6 hours .This is the reason  overall outcomes are not changing in a large cohort  of rapidly performed PCI.

The presumed  absolute  relationship  between  “Time  and  muscle”  concept is  always been a suspect . This  is proven by a flawless study from  NEJM .

nejm stemi most important article

http://www.nejm.org/doi/full/10.1056/NEJMoa1208200

This study should infuse more sense to  us ,  time and again, we are  hijacked and sedated by high dose of  pseudo scientific concoction .In fact ,  indiscriminate rapid PCI may not be in  the good interest of  all  patients with STEMI ,  if it is not properly done  .Without realising this fact many developing countries are indulging in extravagance of  costly STEMI programs wasting  the exchequer.

This landmark NEJM  paper convincingly underscores a fact  that  achieving  rapid door to balloon time  is not  going to be the game changer in  conquering  the Global   STEMI  championship  . We have to take the coronary care into the streets  or to their homes as well .This is where the pre-hospital thrombolysis will  emerge in a big way in the future .

A slow and steady thrombolysis beats a fast and furious primary PCI on any given day in all uncomplicated STEMI .This we have proven for over three decades in  one of the India’s largest coronary care unit .( Where is the data man ?  Genuine experience is data . Why  we require , the act of publication to convert an experience into evidence . Often times ,  I  would feel , data is the most unscientific word in medicine . Many Truths  lack evidence , false hoods come with plenty !  For all those  scientific  homo sapiens  , please recall  70 % of ACC/AHA class 1 recommendations are backed by level C evidence ie simple opinion from  perceived experts! )

Final message

A fast and furious primary PCI may not be  the answer in all STEMI population

Thrombolysis  can be  done  with near  zero time delay , it does not require special expertise where an ambulance driver can reperfuse   a myocardium without much fuss and glamor ! He does not have to  split his hair to identify which is the IRA in a complex multivessel STEMI as well ! The streptokinase and TPA will home in  to the target site  smoothly and swiftly .

If indeed ,  time is the major factor in STEMI , we have many other ways to tame  the time . If muscle is more important than time ,  pPCI is  rarely  the answer !

Some India specific  thoughts

Is it not a shame  , we talk about primary PCI  for all  our patients  who do not even get timely Aspirin* after a STEMI! .It is something akin to what we witness every day ,  as our country folks  wield touch screen  Androids  . . . conversing  in open air toilets !

* While the importance of  Aspirin is undermined , It is different story altogether , these patients  get sorbitarate promptly whenever they get chest pain  (mis-placed and  dangerous priority ! )  prescribed by the  roaring  GPs ,  who suffer from discontinuous medical education ,  propelled  by the deeply penetrated 1000 crore oral Nitrate market .

And STEMI workshops are conducted by self-proclaimed experts  every few months in posh  7 star hotels all over India .

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.

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 .

Summary

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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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.

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 !

Reference

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.

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 .

https://drsvenkatesan.wordpress.com/2012/05/27/in-extreme-mental-stress-left-ventricle-becomes-a-banana/

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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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 ?

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 .

greenlane

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.