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Posts Tagged ‘echocardiography’

Interventional cardiology has grown leaps and bounds. We are in the era of percutaneous replacement of cardiac valves.  Mitral valvotomy for mitral stenosis is one the stupendous success  stories of interventional cardiology.

In PTMC,  we have a major cardiac valve disease ,  treated without anesthesia  in a  procedure   lasting about 30 minutes and patients  can walk  home within hours of the procedure.

The maximum such procedures are done in developing countries like India, Brazil, and many south Asian , African countries.

It is a procedure requiring continuous  fluroscopy in cath lab. This has been our traditional way of thinking. But now we learn , what we  require is an imaging    modality  for the entry of balloon into IAS and the stenotic  mitral valve .This can be Echo, MRI , CT scan etc not necessarily fluroscopy.

Why not echocardiography to guide the balloon in PTMC ?

This question was  answered successfully . Both TTE and TEE are used .Surprisingly   transthoracic  echo , by itself was   sufficient in many patients to complete  a  PTMC.

The following article in JASE (American society of Echocardiography )  opens new avenues for  echocardiography .The work was done in New Delhi India

http://www.onlinejase.com/article/S0894-7317(05)00073-8/abstract

The most surprising conclusion  from this  study is  , it is suggested complications like cardiac tamponade is less likely in echo guided PTMC !  as we are sure  where we re puncturing  and entering .

Advantages

  • Huge cost advantage.
  • Can be practiced in a wider clinical set up
  • Radiation free (Very important advantage  )
  • Live 3D /Echo and MRI are  expected to improve the  feasibility of this modality .

Caution about TTE/TEE guided PTMC.

  • Not every one can do this procedure.
  • Cardiologists who have mastered catheter based PTMC  can only understand the intricacies of  PTMC
  • While catheters can be easily imaged , when the procedure requires finer guidewire manipulations fluro is a must .
  • Currently this procedure should be done with a cath lab  standby
  • Tackling complications may be an issue , but the most dreaded complication cardiac tamponade is more easily recognised by echocardigraphy
  • Special training on this modality is to be strongly encouraged.Such thing is possible only in country like ours where RHD continues to be rampant.

Final message

Cath guided PTMC is considered  the gold standard .But ,  often  we create gold standards with impure gold ! The IAS puncture and mitral valve crossing is the most blinded  procedure in cath lab.

The same job can be done   better , with good   “ocular orientation”  by simple echocardiography

Often  in medicine , a  simple alternate technique   rarely can  compete with a proven  technique .Thus ,  these  techniques are denied wider  application and hence  fail to  prove  it’s worthiness.

Echo guided pericardial aspiration , MRI guided deep thoracic biopsy  are already established non invasive  assisted intervention , soon we can expect many cardiac intervention will be done in radiation free environment.

Unpopular treatment modalities  need not be synonymous with ineffective  and dangerous  forms of treatment.

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It sounds  to be a  simple question . But, cardiology literature is sparse  on the subject.

RV mimics a three dimensional triangular chamber .The inflow, body and outflow align themselves in complex planes .This makes measurement difficult.

What  are the measurements to be made  ?

  • RV inflow tract (RVIT)
  • RV body
  • RV outflow tract (RVOT)
  • RV Free wall thickness

How to measure RV size ?

  • Inflow diameter is assessed in inflow view ( Para sternal long axis,probe  tilted down towards lower  sternal edge (cool . . .That is were tricuspid valve is located !)
  • RV body can be assessed in long axis or 4 chamber view
  • RVOT in short axis view.

What is the normal range ?

RV Body

< 3 cm in parasternal long axis view

<8 cm Long axis ( RV apex to mid point of TV )

RV inflow(RVOT)

<  3- 4cm

RV outflow (RVOT)

1.8 to 3 cm

Note :

  • All measurements are taken in end diastole .
  • The largest diameter of RV is at its inflow(it is roughly equivalent to tricuspid annulus)
  • RVOT size can vary  , generally tapers as it reaches near the pulmonary valve .

How common is the  differential RV enlargement*?

The complex shape and architecture of RV  make  the  direction , sequence  and magnitude of  RV enlargement less predictable .

  • Diastolic loading of RV generally have more uniform enlargement of RV .(Inflow, body, outflow )
  • In dilated cardiomyopathy RV enlargement  common in short axis > long axis
  • Pressure over  loading may not result in uniform enlargement as the pressure points on RV surface is not homogeneous.
  • In congenital heart disease , RV shape and size  depend more on the morphology(location of VSD, infundibular  anatomy, muscle bundles, extent of trabeculations etc)
  • In arrhythmogenic  RV dysplasia (ARVD) outflow  tract enlargement is more dominant.

* The fact that ,  RV can enlarge  in focal and localised manner make it mandatory to measure RV dimension in multiple views and in all possible diameters.

At what  pressure RV begins to enlarge ?

RV is believed to enlarge at > 60mmhg .Hypertrophy is usually precedes dilatation  .

At what volume overload RV begins to enlarge ?

Our experience with ASD indicate when the pulmonary  blood flow  is twice that of systemic blood flow RV is distinctly enlarged. May be it begins to enlarge at>  1.5: 1 shunt

RV begins to enlarge horizontally or longitudinally ?

this aspect is not studied much.  Generally volume overload causes more uniform enlargement.

How does acute RV enlargement differ from chronic RV enlargement ?

Dilatation is more conspicuous in acute RVE ( Pulmonary embolism, RV infarct ) associated wall motion defects and thinning favors acute RVE.

Normal or increased thickness is expected in chronic RV enlargement

Here is a  five-star rated  article on RV dimension

Published in 1986 , still considered a  land mark paper  . . .

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Echocardiography is about 50 years old tool.It has evolved from simple M mode to sophisticated tissue Doppler and 4D imaging. Color Doppler imaging was a great revolution ( One  can  consider it  as big as invention of ultrasound itself  !)

Even though , we could code the pulse Doppler samples into color coded pixels (Called auto correlation computed by Fourier algorithm) the full potential of color Doppler is yet to be explored. Accurate assessment of regurgitation  lesion severity continue to trouble  us  .

The PISA concept fizzled out due it’s complexity and   inaccuracy.It  exhausted  thousands of  cardiology man  hours  and  precious  academic time ! (Not really waste . . .it stimulated our intellect !)

I wonder we have a method to predict  early  “The would be failed concepts”  in medicine !

Vena contracta* Who named it     http://en.wikipedia.org/wiki/Vena_contracta

Suddenly common sense struck us . . .  simplicity replaced complexity . The concept of vena contracta came in to vogue.

It is a  simple estimate of the  narrowest part of a regurgitant  jet.It  is good enough to assess the severity of regurgitation .The diameter is measured  in the   zoomed up view of  the  leaky valve  aided by color flow. If it is > 6mm it is severe regurgitation .(Both AR/MR)

Please note ,it is  one of the measurement  we  take in the  dimensional regurgitant  shell of (blood dome )  in the PISA method . The harrowing exercise of calculating ERO  with all those radius and velocity etc  may be fresh in many  minds !

Can’t we extend the simplicity of  the concept of vena contracta further ?

As usual ,  we assume  many things in medicine .

Here the concept of Vena contracta(VC)  requires

  • The orifice is near circular. (Very unlikely , considering the complex shape of mitral valve especially in diseased state)
  • The vena contracta applies only to single jet MR
  • Central jet (Eccenticity increase the chances altering the shape of ERO )

but, the major advantage is VC is not much  influenced by loading conditions .And the parameter used as such without amplifying the error.

Why vena contracta  is not used to  assess mitral stenosis  severity ?

I wonder why it shoudn’t ?  The same principles apply, the flow through  narrowest point of mitral  valve  will reflect the degree  of narrowing. In fact ,the inter-leaflet distance  could be   same as  vena contracta  in mitral stenosis.

If we assume !   the orifice as a circle,  then  50 %  the vena contracta is   the radius  the orifice  and ERO  can be easily arrived .

Logically yes. We need to validate the data ,comparing with a gold standard .When there is no gold standard , and what  we are testing is  better than gold standard what shall we do ?

Final message

Complex  measurements  lead to  complex errors (Lesson learnt from PISA) , with simple parameters  errors do not get amplified.

Do not ditch any investigation just because it is simple  . . .

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The greatest  adverse effect of modern medical science is the  notorious phenomenon  of  amplifying  medical trivia .We rarely realise how much of anxiety this causes to our patients. We can’t complain either, as many of the medical professionals make a living out this.

For  cardiologists and echocardiologists , there is  often an  issue  in  reporting  some of their findings .Doppler is a great tool , especially the  color Doppler  which can pickup even few clusters  of RBCs that leak into atria  every time the AV valves closes. Ideally this  has to be  labeled as physiological MR or TR .If the arotic root is obliquely aligned with it’s leaflets one  may even  get a physiological AR .

While  it is better to ignore these lesions , some call it as Trivial MR / TR/AR .

This can be detected up to 40 % of individuals.

What does trivial regurgitation  mean to a doctor ?

It means nothing . Few may  use  it as  a weapon to advice further visits to their  clinic and do serial meaningless  follow up scans .The irony is   some of these  patients  enjoy this  . . . and it  becomes a different matter altogether.

What does it mean to the patient?

Anxiety for the majority  ,   for the modern net educated public. No issue ,  for the ignorant and the take  it easy men !  We have seen number of patients getting cardiac symptoms after reporting the physiological MR or TR.

So, should we report physiological events in routine echocardiogrpahy?

We need not . But we do it often .Why ?

There are few  reasons for this phenomenon ( Which  I believe are true  , after observing as many echocardiography centers for more than few decades)

  • Doctors and Imageologist are often self suspicious and worried about missing something and getting exposed among their peers and public. They do not want to miss any abnormality. So even a trival abnormality of negligible importance is also reported.
  • In the prevailing  Geo commercial medical world there are issues other than  academic  creeping in..
  • Many get bored to  report normal reports  as they  want to add spice to their report hence they fill it up all fancy terminologies . This sort of spice reporting adds self esteem the medical  professionals .It makes some sense to report and reveal what they know to the non specialists.
  • Finally, the present day high IQ patients also do not expect a bland ( normal ) report.They often relish  some scribblings in their master health check reports. They tend to  question the authenticity  if we simply say  everything is normal.

The following can be termed as Echo trivia in otherwise healthy individual

  • Mild LVH
  • Age related impaired relaxation of LV without LA enlargement.
  • Mitral valve prolapse without MR
  • Minimal pericardial effusion
  • Patent foramen ovale  without any shunting

When does a trivial lesions can be important ?

In a patient with established heart disease  , a trivial valve leak could become important. For example  in dilated cardiomyopathy, COPD, MVPS dilated aortic root etc .Here regular  follow ups may be necessary.

Aortic and mitral valve degeneration with calcification in the elderly is now implicated in many of the unexplained strokes .Hence  even though it is  age related physiology it need to be given importance.

Can trivial regurgitant lesions be a risk for infective endocarditis.?

No one knows. Logic would  imply a risk ,  as micro jets are  the norm here . But the potential for it to cause a endothelial damage is negligible. Some sinister thinking cardiologists    Many of the native valve endocarditis in otherwise normal hearts may be attributed to this physiological MR/TR .(Evidence less cardiology !)

Clinical use of physiological TR and MR ?

The physiological TR,MR jet helps us to estimate pulmonary arterial pressure and LA mean pressure. Systemic cuff pressure minus MR jet pressure give us LAP.TR jet plus RA pressure give an estimate of PA pressure .

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Left ventricular dissection is a rare complication of STEMI .A case report

Click on the slide to see the video  hosted in  youtube

Slide 1

Slide 2

Reference

http://www.ingentaconnect.com/content/bsc/echo/2009/00000026/00000003/art00006

http://resources.metapress.com/pdf-preview.axd?code=g4kqby7wnkjepetx&size=largest

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The LV ejection fraction ,  is  the most revered medical parameter for both physicians and cardiologists.There are anesthetists and surgeons , who  do not  operate  a  cardiac patient  without knowing it.There are  physicians  who  do monthly assessment of EF in their patients  with dilated  cardiomyopathy.

Now ,every one is interested to know what is their EF ?  Thanks to the global  information highway .We witness ,   patients who are extremely delighted when their  EF increases from 45% to 48% . Similarly , they get depressed when it falls by 2% .

Why this hoopla around the LV EF ?

Every one knows EF is nothing but a LV contractile force at a particular  beat of the heart . It is possibly a crudest possible way to screen for   LV function.( Of course it can still be useful  in patients  with established myocardial disease to follow up  LV dysfunction)

The  most important caveat in  EF is it’s dependence on the loading conditions  of heart .It is   also  heavily influenced by the  heart rate.We now, even a severely dysfunctional LV can contract vigorously with inotropic stimulation  like dobutamine  or whenever local catecholamines.

Our obsession with EF is complete and it is not expected to get cured in the near future.

There are many hundreds of articles in cardiology literature  which  ridicules the EF as sole parameter for assessing LV function. Still ,  it is the number one parameter to asses LV function  in real world as well as in  vast number of land mark clinical  trials .  Are all those trial  results to be doomed ?

Even as  the  LV EF is   being labeled as  futile index  ,   we  also  realise we have not traveled  far from our great clinical   ancestors . Thousands of  years ago   the Chinese  yellow  emperor  of medicine  found  the cardiac contractility  by pulse volume  and predicted death accurately  ,  probably  better  than the live 3d echocardiography   derived EF   guided by LV volume rendering algorithm !

The purpose of this article is to tell the current generation physicians  there are some simple and probably  accurate  clinical tips  to rule out significant LV dysfunction.

One can confidentially tell  the LV  EF  would  be > 50%  in 99% of population if they have the following !

  • A brisk upstroke of carotid pulse.*
  • A well palpated tapping apical impulse**
  • A Loud  first heart sound(S1)
  • A  totally normal ECG (Even a normal QRS complex  is suffice !) ***
  • Normal CT ratio in Xray chest
  • A  comfortable brisk walk of  at 6 km/hour for 10 m .

* A brisk central arterial pulse is nothing but the reflection of LV DP/DT a sophisticated echo parameter assessed  with much hype ! A good thumb with an   alert brain can accurately tell a given patients dp/dt is within normal range.

** A loud S1 and tapping apical impulse indicate the velocity of closure of  anterior mitral leaflet.Which is in turn reflect the force of contraction of the antero lateral  papillary muscle of LV .So what you hear a loud s1 is nothing but the contractile function of the most important  part of LV namely the pap muscle of LV.

*** A normal ECG ,  generally tells us  all is  well with LV myocardium . Finally,  it makes  immense sense to correlate the functional capacity to EF. (90% correlation)

Final message

Mind you ,  all the above modalities come either  free of cost or a fraction of  echocardiography  . It is estimated up to 90% echocardiography scans to R/O LV dysfunction can be avoided . The global health care costs can be saved and be utilised for some better purpose like protecting our atmospheric shell  from the  hazardous   gases

Note of caution

While ,one can rule out signficant LV dysfunction by above mode  ,  it can miss  other forms of LV dysfunction like relaxation defect etc . (ofcourse the EF also misses it !) .Judicious use of functional  imaging modalities are adviced in those who require it.

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The most famous and popular view in clinical echocardiography is para sternal long axis view.It gives us an instant information about the status of left atrium , left ventricle and aorta.Left atrium appears to be seen in full. Still , one should realise it is far from truth.There is a huge blind spot  for left atrium in this view .

For a complete imaging of LA one need to do a short axis view at aortic level, and of course a 4 chamber view . All these three views put together , can at best give a 80%  exploration of LA .The rest of the  20%(  some times vital !) can be seen only be transesophageal echo .

Why para sternal long axis fail to give even glimpse of the 4 pulmonary veins ?

  • Pulmonary veins are probably ,  the most vital structure  in LA . There are 4 veins , generally  arranged in 2 pairs
  • Unfortunately all these 4 veins does  not  interrupt the ultrasound beam in this view .The beam in para sternal view crosses  the anterior and lateral surfaces and to a  very small area of inter atiral septum(  IAS )
  • These enter  the posterior surface of the LA in an oblique angle . The angle of entry is widely variable .Some times they need to run a parallel course with LA posterior wall . This makes recognition and delineation  of PV from LA very difficult ..
  • Since all   4 pulmonary veins are located in the posterior aspect of LA ,  they  are best visualized either in apical 4 chamber (Right pulmonary veins) or short axis views(Left pulmonary veins)

When can pulmonary veins visible in PS- LAX view ?

When PVs take an abnormal course like in TAPVC or when they enter coronary sinus etc .

Rarely ,  huge LA enlargement may pull or push the PVs and make them visible in LAX view.

See the link

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Even though it is a great vein , often the imaging pulmonary veins by echocardiography is a not a pleasant excercise.

This is due to the following facts

  • The pulmonary veins are posterior structures
  • They occupy the far field of echocardiographic window
  • The pulmonary veins often enter obliquely into the LA
  • The course of PVs are highly variable ( Like RCA origin !) especially in ASDs ,where identifying PVs becomes all the more important

Hence no fixed imaging angle can be advised . But generally a pattern is observed.

  • Right pulmonary veins are best viewed in apical 4 chamber or 5 chamber or in between (Especially RUPV is  seen best in 4.5 chamber view !)
  • Left pulmonary vein , can be seen in apical 4 chamber but best visualised in  Para sternal short axis view.

Other modalities for imaging pulmonary veins

TEE : Can be  very useful since it is brings the vein closer to the probe .But needs more expertice.

Contrast echo :Probably a simple and best modality often underutilised.

Very useful to clinch the diagnosis when PVs take abnormal course as in PAPVC .

MDCT , Spiral CT, MRI  are the new age modalities that can provide us  with dramatic  3d images of PVs.

The  echocardiogram will always prevail over these sophisticated gadgets for its simplicity and also it’s ability to give us the physiology of pulmonary venous flow which is vital in many diseases(Constriction, Diastolic function etc)

The following illustration is a gross attempt to simplify the imaging of PVs.Please note the rules may not be applicable in all.

Left upper and lower pulmonary veins in short axis view will be posted shortly .

Reference

The images are  based on  personal observations and  an  excellent insight  on the topic from  Department of Cardiovascular Medicine, Guangdong Provincial People’s Hospital, Guangzhou , China

http://ejechocard.oxfordjournals.org/content/9/5/655.full

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Internet is  a  wonderful gift for  for mankind   but  only  occasionally we find great resources .

Hats off to Dr .Pybus from Australia for his efforts

A must read for  all cardiologists rather  everyone involved with echocardiography

Click on the Image to reach the site

http://www.manbit.com/ERS/ERSAZ.asp

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Imaging  coroanry artery is  generally  in the   domain of interventional cardiologists. MDCT has helped us to change that.

The  humble echocardiography can   identify the origin* of   coronary arteries   in  most   persons. The resolution power of modern day echocardiography is  2mm and the left main  ostium is >3.5mm in 99%  of population . If some body says one can’t  visualise the coronary artery by echo ,   it can only reflect their ignorance or lack of patience to get an optimal image. Of course technological limitations are there.

*  To be emphasised again , only the origin can be identified.

Can we identify ostial leftmain or proximal  left main disease  by echocardiography ?

It should be possible in  few .

Can we place  a doppler sample volume  within  the left main and measure coronary flow velocity ?

When obsterticians are able to  assess the  uterine artery flow  in a bulky uterus ,  it should be possible to do the same in  a coronary artery . Motion artifacts is the issue in the heart.  Micro sample voulme (<1mm) are expected in the future  that will make a non invasive coronary flow assesment a distinct possibility.

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