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Thrombus formation  and subsequent lysis  either spontaneous or pharmacological is the key events in acute vascular emergencies .We know both STEMI and acute strokes can get aborted  naturally.

The thrombus which initially forms , triggers a natural lytic mechanism and this fights vigorously against the clotting process , and tries to get rid  of the intravascular clot.

The early  minutes are vital. (Like the T 20 cricket )  the win or loss is decided in the first few overs . The mantra is unrelented attack of the ball . . .ie thrombus !  In some patients  the clot  can never grow big to fill the lumen.These are lucky few .The mechanisms are common in both cerebral and coronary circulation. Here is were comes the role of antiplatelet agesnt .An aspirin or clopidogrel administered within minutes can prevent the genesis of  central core of the thrombus .(This is the  secret of aspirin scoring over stretokinase in STEMI in ISIS2 study done three deaceds ago !)

It should be realised,  our understanding about spontaneous lysis is very little considering explosive growth of other aspects of cardiology. It is mediated by circulating  TPA and antithrombin 3  .  Remember  every humans have it in their  blood .But how much ? How to augment it ‘s power at times of thrombotic crises ?

What could be the clinical correlates of spontaneous thrombolysis ?

  1. In brain classically it is TIA .
  2. In heart do we have TIA equivalents ?  .Yes it transient rest angina

Link to video on TIA of the heart

Read this article to get a glimpse of  natural cerebral thrombolysis  and shall we   extrapolate it to coronary spontaneous thrombolysis  .Why not ?

Arch Neurol — Nonocclusion and Spontaneous Recanalization Rates in Acute Ischemic Stroke: A Review of Cerebral Angiography Studies, December 2002, Kassem-Moussa and Graffagnino 59 (12): 1870

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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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Chest pain as a symptom in  acute MI is vitally important as it only  brings the patient  to the ER. (Realise ,silent MIs  can never reach the hospital in time ! ). Heart is  located  few  centimeters beneath the chest wall and extend up to  15 cm posteriorly.The location heart within the chest wall  , make it a  three dimensional structure .Theoretically  pain can initiate in one focus and radiate to any direction. Traditionally , when we say  chest   pain , we mean the anterior chest wall on either side .Technically , chest contains a lateral  and a posterior wall .The posterior  surface of the chest is called back of chest , or some times simply the  back .

We know , chest pain can radiate to many sites , of course the  much hyped  (May not be common yet !) being  the radiation to left shoulder , and arm.

The ischemic chest pain , even though described  as classical angina over a century ago . It applies mainly to stable exertional  angina .In    STEMI  or  unstable angina  these rules are   can not be expected to be followed  strictly.

We often think the pain of MI comes only from the myocardium ,  but there are many potential sources

  • The adjacent pericardium
  • coronary artery dissection, plaque fissures
  • Neuralgic pain from the  ischemic  nerve terminals
  • Finally dermatomal  reference pain

What is the quantum of pain signals  arise from each of these  components ?   Obviously ,  myocardial pain should be the dominant one .Here again ,  there is a dichotomy .Whether   the infarct segment elicits more  pain or the surrounding  ischemic   segment is also not clear. The  is an important difference the character of pain infarct pain is a  severe continuous  dull  aching .Some believe in   a fully infarcted segment where the nerve terminals are dead can not carry  pain  signals and pain is absent, while partially dead muscle produce maximum pain.

The somatic nervous system , that mirrors the visceral pain  into the dermatomes that the patient  feels as if the pain is originating from these sites. Heart is a huge middle mediastinal structure , primarily reflects the pain to the anterior chest wall , but  no surprise if it deflects  the pain signals posteriorly  also. Of course , the spine and the thick posterior chest muscle walls tend to  block this transmission.

But , on many occasions  patient who are admitted with ACS in CCU complain pain in the   back of chest

the following things has been observed.

  • Severe back pain in  a patient with large STEMI invariably indicate a myocardial tear .
  • Mesentric and coeliac artery occlusion
  • Aortic dissection

Back pain only STEMI

Every cardiologists would have seen atleast   few cases of STEMI presenting only as back pain.The problem here is they land up in varied departments .We have on instance of  a STEMI landing to a ortho surgeon .He was good enough to suggest an ECG and that showed an extensive infero posterior MI and later shifted to coronary care unit.

Back pain as marker of impending rupture

Severe back pain in an established STEMI is a ominous  sign as it is often a  marker of impending rupture. Here the patient is in extreme distress, and may become violent and restless .(Hypoxia adds to woes!)

Does posterior  MI  more likely to produce back  pain or posterior chest pain ?

Not proven  but distinctly possible.  ( posterior MI -Posterior pericarditis- Back  pain .)We emphasize  posterior  chest leads  in  ECG V7  to V10 in inferoposterior MI .  We  expect  the injury current to  flow to  the back , is it not logical  some of the neural signals would  also  reach the back.

Final message

Never underestimate back pain. We are tuned to think chest  has only one surface that is anterior .This is a gross missense .After all , there is a huge area(> 30X 30 cm )  of chest wall located behind us .

Take an ECG in all patients with  acute  pain  in the back of the chest . Even though this may look a  funny advice   . . . it is  an  important clinical tip   for all those  budding physicians  of this world. If  one life   is  saved per 100 innocent back pain cases ,  this article  acheives it’s purpose !

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Drug eluting stents are liberally used  worldover .

It is very unfortunate ,while the jury is still confused about the role of DES  “even”  in chronic coronary syndrome ,

There has been widespread use of DES in  the   potentially hazardous    thrombotic milieu  of STEMI  . It is well known  the DES ( polymer and drug)   has a dangerous liaison  with the thrombus.

Even as the evidence base was about to accumulate against the DES in STEMI , there was  an undue haste in the use of  this stent in STEMI .

Now in 2010 the results are out the DEDICATION trial

  • The culprit is out
  • The truth exposed
  • DES kills more life than bare metal stents   during primary PCI

Read this article  ,just released in Atlanta 2010

http://www.cardiosource.com/clinicaltrials/trial.asp?trialID=1618

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Management of  atrial fibrillation has been a  big puzzle for cardiologists  for many  decades  till  it became a corporate game , and  now in the era of recession it has become  medicare’s  night mare !

So , we  were  made to dance to the tunes of the so called evidence based cardiology . . .

  • From only rhythm control to . . . in 1990s
  • Either rhythm or rate control  . . .       in early  late 1990s
  • Then cost control  was found  more important than rate control  . . .
  • . . . So rate control became superior to rhythm control in early 2000s

In 2010 , even the  rate control  became  a luxury ,  here comes the  real ace !   ” Casual rate control may be  suffice in most cases of AF “

Read this article  from  NEJM , which tries to  make  sense out of nonsense  and judge for yourself

Probably the most influential  article  in electrophysiology over  the  next decade

Click  below to reach Nejm article

http://content.nejm.org/cgi/content/full/NEJMoa1001337?query=TOC

http://content.nejm.org/cgi/content/full/NEJMe1002301?query=TOC

Gist of the trial

Technically and literally it  means a  “Take it easy attitude” as long as patient is comfortable , even a rate  of  more than 100 is allowed . Few years back the above concept could be termed a “non sense”

Final message

In this  perennial  management issue  of AF  ,  Whether ,   we were successful in  restoring   sinus rhythm or not , we have restored  the common sense*  Thanks to RACE 2 investigators.

* Do not unnecessarily trouble a  asymptomatic  patient with those powerful  and costly  antiarrhythmic drugs .

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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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Hunting for  treasures in medical jungle is no easy job

There are  thousands  of websites for learning  radiology  and then ,

This one  . . .

Hats  off  to   William Herring, MD,

http://www.learningradiology.com/toc/tocorgansystems/toccardiac.htm

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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 , best visualised in  Para sternal  long and 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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Are the drug eluting stents really better than bare metal stents ?
A million dolor question ? , No . . . a billion dolor question
A study which answered most convincingly with a huge data base  published in LANCET 2007.
  • 38 trials  , Metaanalysis
  • 18 023 patients with
  • 4 year follow-up of up to 4 years.
  • No mortality difference from bare metal stent vs DES
But unfortunately there is  no takers for this  study . The usage of DES continue to  surge ahead  .
The problem facing the medical science in the current era
It takes years  of research to get  into  the truth    and  still   longer time  for  us  to  accept it ! Ironically  falsehoods have immediate patronage and there is no incubation period !

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