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Changing definitions for massive pulmonary embolism

October 31, 2012 by dr s venkatesan

Conventionally  pulmonary embolism is classified as massive, sub massive  based on

  1. Severity of obstruction
  2. Level of  obstruction in pulmonary anatomy (MPA,Branch PA, Segmental etc )
  3. Thrombus burden
  4. Quantum  of pulmonary vascular bed  compromised

But it is always intriguing ,    the clinical outcome was not linearly  correlating with the above parameters.

Instead the outcome seemed more dependent on the following .

  1. Degree of RV dilatation
  2. Systemic hypo-tension
  3. RV shock

Image courtesy .www.smartdraw.com

So ,  whatever be the quantum of pulmonary embolism , it is the behavior of RV that is going to determine the outcome.  The current  wisdom   demands , all hemo-dyanmically unstable pulmonary embolsim may be considered as massive or high risk pulmonary embolism and  aggressive treatment  is  to be undertaken.

Counter point

There is  one major diagnostic issue  if we depend more on hemo-dynamic instability . What is that ?

There is no valid method to identify Acuteness / chronicity of   RA, RV dilatation . Consider this  example , a patient with chronic thrombo -embolic PAH presents with  acute deterioration  due to a transient arrhythmia  or  non cardiac  cause of hypotension . He is at  risk of being labeled as  acute pulmonary embolism  since he may  show   some thrombus  in his pulmonary circulation in  CT scan .  However ,  no great harm is done as long as he receives only heparin.

Reference

http://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-APE-FT.pdf

Posted in acute pulmonary embolism, critical care ccu | Tagged , , | Leave a Comment »

Can MVPS produce diastolic clicks . . . and opening snaps ?

October 31, 2012 by dr s venkatesan

Mitral valve prolapse  probably is the most common cause for  abnormal added  sounds in cardiac auscultation . MVPS occurs  when  mitral valve tissue  and its accessories  overgrow disproportionately    with reference to  the mitral valve orifice (Also referred to elongated or redundant leaflet) .The net mass  of mitral valve apparatus has an inverse relationship with  LV  cavity volume . Because of  excess motion  ,  leaflet may bulge into left atrium to different degrees and different angulations. This entity  as rule is  benign  in most people . Still ,  rampant diagnosis in the community  (With the  pathological proliferation of   scan centers  )  has raised considerable anxiety .

watch?v=esDNcqop_Ew&feature=relmfu

Hence , the criteria  to  diagnose MVPS are made stricter .Unless the leaflets are thickened and some degree of MR  occurs the  usage of the term MVPS  is  not justified .

watch?v=h6aJSuUTVb0

Unusual  sounds in MVPS

In many patients ,  AML become so nimble ,  it flexes, bends and   stretches  in both systole and diastole. These leaflets   can generate clicks  not only during  prolapse . Simple folding and unfolding of  long redundant  is known  to produce clicks.

generally folding occurs in diastole and unfolding in systole ( of course in extreme redundancy  both can occur in both phases )

This diastolic  clicks in MVPS has been reported rarely  in literature . It is   more common than we realise .The timing  of these clicks  are  not constant .Audibility is low .It can easily  be confused with opening snap of mitral stenosis .

The spatial  relationship between the sound generation and the anatomical prolapse  does not match . It is always  possible  when  PML prolapses  AML may generate a click and vise versa . Diastolic clicks or opening snaps  are known to occur in some of the severe forms of MVPS.  The first heart sound is not only loud  , the  differential  motion AML and PML  may distort  two componets of  M1  .It needs to be emphasized the loudness  of  S1  can be  preserved even in the presence of significant MR .(Even as the PML prolapses  causing MR ,  an  elongated  AML continues to generate a booming S 1)

Final message

Can MVPS produce diastolic added sounds ?   Yes . . . it can .

Mid systolic click  , and  late systolic murmur  is the classical  manifestation of MVPS . In reality , one can get a variety of noises from prolapsing mitral valve apparatus in both phases of cardiac cycle.

Reference 

These are all inferred from bed side observation . Luckily  I have found a  reference from a New york state journal of medicine .Other wise my observations would have been ridiculed .  Gone are the days   when we spend  hours together  in  clinical auscultation  of mitral valve motion  .

Today we are  in the era  , working in hi- tech cath labs ,  aiming  to  capture those same  redundant  mitral leaflets  with catheters  and clip its wings to reduce the mitral regurgitation  .

Asking for a phon0-cardiographic  documentation of diastolic mitral click in MVPS    would be a laughing stock among current generation cardiologists  !  Still I would argue for such a study !

Posted in Cardiology - Clinical, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), MVPS | Tagged , , , , | Leave a Comment »

Simple tips for operability in Eisenmenger syndrome ?

October 31, 2012 by dr s venkatesan

Is this child with Eisenmenger operable or not ?

The answer to this question is  debated for many decades . The old school of thought was  grown with meticulous cath study (Pioneered by Paul wood and his team ) .Calculating PVR is academically fascinating . With  so  many  variables,  assumptions and too much dynamism in a circulatory system , It has never been proven as a  gold standard .

The presence of following  factors points to  possible advantage for  shunt closure .

  1. Pink Eisenengers ( Complete  lack of   clinical  cyanosis   )
  2. Clinically mild cyanosis  but  Oxygen saturation   nearing 92 %  (We  have seen an occasional  patient  with 98 % )
  3. If Echo shows  a dilated left atrium and left ventricle (VSD,PDA) it indicates a significant L-R shunt.
  4. Lack of septal bulge towards  LV (This Indicates  RV has  still  some  useful life in it ! )
  5. Pulmonary  flow velocity > 1.5m/sec indicates fairly good flow across RVOT (Qp/Qs calculation is  almost impossible in bi-drectional shunt )
  6. Pulmonary artery diastolic pressure  <  3o mmhg
  7. Pulmonary artery pulse pressure > 50mmhg

*Oxygen, Tolazoline test in cath lab has  limited value.

**Temporary balloon occlusion and watching  for reversibility is not useful (As fall in PAP and  PVR is a long term affairs )

Final message

Scientific cardiologists may feel awkward  to read this message .

  • With mortality for shunt closure in   Eisenmenger  reaches  nearly 50 %  ,  it is essentially a 50-50 guess game !
  • We  often depend on our collective  clinical acumen (Also called as  Gut  feeling   . . .”I some how feel  this child will do well ! “
  • Most  importantly  surgeon’s  experience and expertise would  finally prevail  over cardiologist !

Posted in Cardiology - Clinical, cardiology congenital heart disese | Tagged , | Leave a Comment »

And now . . . An “Intra coronary ECG” during primary PCI from within the IRA !

October 31, 2012 by dr s venkatesan

Failed thrombolysis is a well debated concept, while failed primary PCI is a conveniently neglected phenomenon .

How to assess successful reperfusion following PCI or thrombolysis?

I do not know how many  of us know this vital fact !

Coronary angiogram is squarely beaten by the humble  ECG in assessing the effectiveness of myocardial  reperfusion . This is not hard to understand as  coronary angiogram *  can  tell us only  about epicardial  patency ,  while ECG  sends vital perfusion  data from within the  myocytes ! Which do you  think is superior ?

And now  interventional cardiologist have realised this fact . they  measure the ST segment  regression instantly once the primary  PCI is  completed . How ?  An ECG is recorded from  right inside the infarct  related artery .

*Of course myocardial blush score , TIMI frame count are poor alternatives !

This paper just published in CCI is  a fascinating revelation .

http://onlinelibrary.wiley.com/doi/10.1002/ccd.23455/abstract

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Clinical cardiology, STEMI-Primary PCI | Tagged , , , , , , | Leave a Comment »

What is the mechanism of dyspnea when it occurs as “Anginal” equivalent ?

October 31, 2012 by dr s venkatesan

Anginal equivalents are distinct  (often vague  ) symptoms that occur in response to myocardial Ischemia , instead of angina. Dyspnea or shortness of breath  is the commonest anginal equivalent . The incidence and exact mechanism  is not clear. Both angina and dyspnea are sensory  events . Both are  perceived  at the level of cortex. Angina occurs when ischemic  muscle  triggers pain signals from the   nerve  twigs engulfing the myocytes membranes  and the vasavasorum.

Dyspnea during myocardial  ischemia  is multi-factorial

  1. Signalling error .( Mismatch between respiratory /Cardiac  receptors  neural traffic)
  2. Cortical perception disorder.
  3. Autonomic neuropathy (Blocks pain signals  but still may carry  myocardial stretch response)
  4. Coronary sinus lactate –  Biochemical /Chemo receptor stimulation
  5. Isolated  Ischemic LV relaxation defects  , and resultant elevation of LVEDP
  6. Ischemic systolic stunning  and secondary  diastolic dysfunction  (elevated PCWP  pulmonary stretch receptors stimulation )
  7. Ischemic MR . Eccentric MR jets and regional and segmental elevation of pulmonary venous pressure has been reported. (Unilateral and segmental pulmonary edema)
  8. It is possible  ,  Ischemic wall motion defect per-se  can induce myocardial stretch and create a feeling of dyspnea.

Out of the above eight factors  which is  most important  ?

The most popular and easy to comprehend   mechanism   is number 5 : Ischemic diastolic dysfunction .

(Fellows will be appreciated if they  know this !   )

Posted in Cardiology - Clinical, Cardiology -unresolved questions, Cardiology-Coronary artery disese | Tagged , , | Leave a Comment »

How to manage an Asymptomatic , 90 % LAD lesion with FFR .9 and TMT positive at 9 mets ?

October 31, 2012 by dr s venkatesan

How to manage an  asymptomatic 45 year old man with  90 %  mid  LAD lesion  , with  FFR  .9   who is  stress test  positive at 9 Mets  ?

Six  cardiologists and six responses   . . .  and the elusive seventh sense

  1. FFR is most scientific test to assess  physiology of coronary stenosis  . I will  go with that  and put this patient under  medical management.
  2. I agree with FFR, still the  patient has no symptoms  , but why the hell is EST  + ve ?  I am confused  .
  3. I would definitely stent the lesion irrespective of the symptoms .
  4. I would order a stress thallium . I do not believe in FFR
  5. The data provided  is insufficient. I would like to this patient in my clinic , and if necessary  may  order a fresh CAG.
  6. For a 90 % LAD  lesion FFR should not have been done in the first place .That is the root of the confusion. He should have received a stent long back .

Final message

FFR is  a terrible concept   for two reasons . One ,  it never bothers about flow across  a lesion. It simply  relies upon  pressure drop. we all know  there  is an intricate relationship   between pressure and flow . Simple pressure drop can never be  expected to translate into incremental flow in biological systems .The  second major limitation is  it  ignores the  morphology of the lesion . We know an eccentric soft  lesion with a  good distal   FFR  is  live  coronary explosive .

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Coronary artery disese | Tagged , , , , , , | 1 Comment »

Do you know this man ? . . . . Who enters your cath lab every day !

October 31, 2012 by dr s venkatesan

This man enters your cath lab  every morning !  . . .  He is Mr Stent !

“

Endo-prothe`ses coronariennes autoexpansives.”

    “Endo-prothe`ses coronariennes autoexpansives.”  This is the official name given to coronary stents  when it was first used in man in 1986 in France . The first  stent in human coronary artery was implanted by Puel . Followed by Sigwart  ,Puel combine .

Later on  , the name Stent came into vogue . Surprisingly stent is not a technical name . It is a name of British dentist. To know more about the historical aspects of coronary stents read the following review from Circulation.

References

http://www.fauchard.org/history/articles/jdh/v49n2_July01/charles_stent_49_2.html

1 .Puel  J, Joffre  F, Rousseau  H;  et al.  Endo-protheses coronariennes auto-expansives dans le prevention des restenoses apres angioplastie transluminale, Arch Mal Coeur 8 1987 1311-131

2. Sigwart U, Puel J, Mirkovitch V, Joffre F, Kappenberger L. Intravascular stents to prevent occlusion and restenosis after
transluminal angioplasty. N Engl J Med. 1987; 316: 701-706.

Posted in Cardiology -Interventional -PCI, Cardiology quotes, Cardiology-Land mark studies, history of cardiology | Tagged , , , , , , | Leave a Comment »

DES fails in the all important STEMI – EXAMINATION !

October 31, 2012 by dr s venkatesan

DES is  a revolutionary coronary support device ,   but it was always a suspect  when it came to STEMI and primary PCI .

How good and safe is DES in STEMI ?

Cardiologist were always beating around the bush for a specific answer to this question.

The general  principles and background

DES was thought to be unsafe in a thrombotic milieu .(DES was notorious for acute stent thrombosis) .Still ,first generation DES ( Sirolimus and Paclitaxel ) were thought to be unsafe in STEMI .However anecdotal evidence suggested DES reduced stent thrombosis  . .Then came the 2nd generation DES (Zotarolimus and Everolimus ) . There was a  excitement every where .The logic  was   “If first generation of DES is not good . 2nd generation  must be good”   What a way to think scientifically .Wisdom  did not prevail  . Many started using ZOTA /EVERO  in STEMI  .(Medtronic and Abbot were silently enjoying the scenario !)  And now finally Everolimus was tested with BMS in  STEMI .

That is EXAMINATION trial for you  . . . Published in Lancet  September 2012

It  has found  2nd Generation DES are not superior to BMS in STEMI in terms of  patient outcome . The study broadly concluded  that  the patient related parameter did not show any significant difference  while  stent related outcome seemed  fare better.

Why this patient – stent dissociation ?

How can large group of patient who  have more stent thrombosis and TVR ,  still  no correspondingly increased ACS or deaths

Does this mean  these stent thrombosis are safe events ?

The answer lies in the fundamentals. The  stents  represent  anatomical  correction  , while  the patient  outcome depend   more on physiology ( flow )  so we are back to square one  to the fundamental  coronary conflict  ie  improving anatomy need not impact physiology.

Critical comments

After reading the EXAMINATION  trial  I asked my third year fellow .

What was  the re-stenosis rate  in DES vs BMS  at 6 months ?

He said this study never analysed the issue of re-stenosis  .

I asked him , Are you sure ?

He confirmed it with a firm Yes.   And then , I found this

                                   A shocking omission for a study which is supposed to answer a   critical question whether
                                   DES is good for   STEMI in the long term
Final message
What a way to conduct a large  land mark study ?
This  study   never bothered to find out the re-stenosis rate  with DES  after  primary PCI and compare it with BMS  .
In fact they have conveniently mentioned ,  follow up angiogram was not part of the study protocol .
I concluded  at the end of journal  review meet   , that  this  EXAMINATION  was not properly conducted   and DES may come back with a vengeance   in the near future !

Posted in Cardiology -Interventional -PCI, Cardiology-Coronary artery disese, STEMI-Primary PCI | Tagged , , , , , | Leave a Comment »

A near “foolish” attempt to correct Anemia by emergency angioplasty !

October 31, 2012 by dr s venkatesan

This is a true story  . . . happened  many years  ago under my direct  vision.

A  48 year old women came with significant breathlessness and catchy  sub -sternal chest pain .

“I  was exerting too much in recent days  doctor” , she said .

Her ECG  showed  a tachycardia and dramatic ST depression in most leads .

The ER in charge promptly texted the cardiologist .

The moment he saw the ECG ,he  had no hesitation , to order for an emergency angioplasty  (  How can he plan a angioplasty  , without even  knowing the coroanry anatomy . some one murmured  . May be   . . what he probably  meant was emergency angiogram   the other explained )    Further , he was telling his    fellows  . . . that  this is going top be  tough case and a possible  left main PCI .

An emergency  angiogram was done .  On table  it was a huge  surprise for every one ,  it was a  a classical  text book   look alike normal coronary arteries !

The moment normal CAG was  visualized  the consultant  concealed his momentary  surprise    and went on to say  it is classical case of syndrome  X   with severe micro- vascular disease causing ECG changes !

As  the patient did not give any opportunity to poke her coronaries   she was wheeled out of  wheeled out of cath lab.

Meanwhile ,  first year  fellow came rushing with the blood reports and biochemistry .

Is everything  alright ?   Yeh sir ,  except her Hb %  . . .  it is  5.6  Grams !

The bewildered  consultant *  realized   the  high  coronary drama , that is  been enacted  over the  past 2 hours !  and  learnt  (and taught) a most important  lesson to their fellows !

Hi guys , this is neither  a NSTEMI nor  a microvascular syndrome X  . . . this is simply anemia related  extreme  ECG changes !  We have erred in our reasoning and  our pre cath clinical scrutiny has  gone awry ! 

He went on to say  ,  don’t worry  many times medicine is learnt in  hard ways  . After all nothing adverse has  happened here .

The women was subsequently investigated and handed over to  gynecologist for a probable hysterectomy .

Final message

Please be reminded  , anemia  can produce  variety  of  ECG changes.  In extreme anemia  global ST depression is  common especially if  tachycardia is associated .

The lesson here  is ,  whenever  gross  ST depression is witnessed  with vague chest pain  check the hemoglobin first . This is an unusual story of a women  ,  with simple  anemia  (due to   chronic mennorhagia )   landed in cath table in an acute fashion .  Luckily  she  did not have any  incidental coronary  lesions  that prevented her becoming a  greater cath lab  victim !

* The bewildered consultant is none other than the author  of this blog.

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , , , | Leave a Comment »

Why FFR is a terrible concept ?

October 31, 2012 by dr s venkatesan

Fractional flow reserve is  a new coronary hemo-dynamic para meter used to assess physiological impact of border line lesions in coronary artery disease. The calculation is simple

FFR is  a terrible concept * for two reasons .

One ,  it never bothers about flow * across   a lesion. It simply  relies upon  pressure drop. We  know  there  is an intricate relationship   between pressure and flow . Simple pressure drop can never be  expected to translate into incremental flow in biological systems .

(FFR anology  in co-arctation of aorta . Can you take difference between upper limb  BP and lower  limb BP as a most accurate   Index of severity of co-arctation of aorta ?  )

How crude it would be   . . .  to  believe so ?

Two   it  ignores the  morphology of the lesion . We know an eccentric soft  lesion with a  good distal   FFR  is  live  coronary explosive .

The  FAME 1 and FAME 2 studies  glorified  FFR  !  I differ in many ways .

Some of  the  observations made about FFR.

  • FFR is to be  done only in discrete ,  safe looking  , intermediate lesions .(Do not ever attempt it in a eccentric lesion )
  • FFR wire is a  stiff ( stainless steel ) wire .  Careful maneuvering is necessary . Lesion crossing  and pull back  FFR wire require some expertise.
  • FFR / OCT  combo,   increase  not only the  fluroscopy time  ,  this procedure can be  more complex than  the intended   PCI .
  • My colleagues tell me FFR measurements are not often  reproducible .(I have little experience in this )
  • Adenosine induced vasodilatation  is not natural physiological model . Further it has  a potential for  a coronary steal if there is near critical lesion in contra lateral artery.
  • There are many occasions   FFR wire has caused  dissection  and  subsequent stenting was necessary  .(The very thing  the cardiologist wanted to avoid !)
  • Bifurcation lesion FFR measurement is prone for errors
  • FFR in two tandem lesions cannot be assessed   accurately
  • Post PCI FFR is not practiced routinely in may centers  the fear of  status quo of FFR.

Final message

This post is not to defame the FFR as a concept . Just to make you think  . . .  how often ,  we  are entrapped  in a  pseudo -intellectual  game in  the cath lab ! FFR  as a tool , can still  be valuable to assess coronary hemo-dynamics in a selected lesion population especially,  discrete,  single vessel ,  or left main disease  with around 70 % narrowing . But never go with FFR alone .Consider the morphology , location   of the lesion .

Finally do not forget  ,  the   good old  EST  can  give a stiff  fight  for supremacy over FFR  in terms of assessing physiological impact of a coronary stenosis (Especially in single vessel disease ) 

Reference

Fractional Flow Reserve versus Angiography for Guiding Percutaneous Coronary Intervention . http://www.nejm.org/doi/full/10.1056/NEJMoa0807611

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Cardiology-Coronary artery disese | Tagged , , , , , , | Leave a Comment »

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