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What is branch vessel STEMI ? How common it is , among STEMI population ? Can you afford to manage it less aggressively ?

Posted in Uncategorized, tagged on February 3, 2010| Leave a Comment »

STEMI is the major cardiac emergency .The acute mortality is about 20% (Both prehospital and in CCU )  STEMI occurs whenever a coronary artery is occluded  suddenly in toto .We traditionally believe that STEMI occurs only in the major  epicardial vessels. (LAD/LCX/RCA .)

The total length of   coronary tree is much  longer than the length of the three vessels put together.The diagonals , the ramus, the OMs ,the septals  run for varied  distances. The caliber of these vessels can be quite large.It is estimated the diameter  of   first diagonal ,   the first OM  or the   ramus can be as big as LAD proper in 30% of CAD population . Law of statistics tells us sudden occlusion can occur any where in the coronary tree in  ACS prone patients.

What is the real incidence of side branch STEMI ?

The  dogmatic answer is   ” We do not know”

Will we ever know ?

How will a  Diagonal / OM /Ramus   or PDA   STEMI  behave ?

It is surprising this question is not addressed by us  for  so long . Some may even question  the existence of  such an entity(Side branch STEMI ). This is most likely ,  reflect our ignorance on the issue . We know  bifurcation lesions at  the   side branch  origin is very common . Further , thrombus can migrate from a main stem to a side  branch  immediately after formation .

Clinical presentation of side branch STEMI

  • Acute presentation is identical  to  that of a major main branch STEMI . The  pain  can be severe , the primary arrhythmic threat is real . Ischemic VF , once initiated does not  modify it’s  character  according to the  quantum of insult .
  • ECG is the major variable.  You ,  don’t expect gross , ST elevation in many leads as one would see in LAD MI /RCA MI.
  • The  age old teaching that  an ECG can be entirely normal in acute MI ,  could actually imply the side branch STEMIs . When a small D2 or D3  gets occluded the ECG may not pick up the ST shifts .
  • The commonest site of atherosclerosis apart from proximal LAD is the bifurcation of PDA in RCA.  STEMI due to PDA occlusion is  the most  difficult thing to recognise. Many of them have very subtle ECG and clinical findings.
  • There has been reports of acute complete heart blocks with isolated AV nodal infarcts. Here sudden cardiac deaths are reported

It is very much possible ,  many of the  side branch  MIs   may be wrongly diagnosed as unstable angina by us , for the simple reason the myocardial necrosis is not large enough to produce ST elevation .They may actually respond to thrombolysis ,  as there is total occlusion in the coronary artery.  Since, they do not manifest ST elevation there is a lost opportunity here  . This ,   probably  is the population in TIMI 3B  trial that showed some ( statistically   insignificant ) benefit for   thrombolysis in NSTEMI.

Is primary PCI justified in side branch STEMI ?

May not be . The chances of side branch STEMI   to result in LV dysfunction and progressive adverse remodeling is considerably less . The hazards of primary PCI for exceeds the risks of  MI  due to a   septal  or diagonal branch lesion .

Final message

  • STEMI due to   branch coronary artery  occlusion is a less recognised entity among ACS.
  • Cardiologists ,  need to  look into this  issue with little more seriousness as it could represent a new  intermediate risk  category   among the much  flaunted  classification  of  acute coronary syndrome. Triaging and risk stratification of  ACS  needs  a revamp.
  • It is possible  many of the UA  patients  ,  may in fact represent total occlusion of side branches.
  • There is a  definite  case  for showing less aggression in these patient  subsets  ,  provided we are sure  about  the location of lesion.

Counter point

* Identifying  a side branch STEMI with confidence  may be very difficult at bed side in an emergency . Implication of wrongly  calling a STEMI  as benign  can be  dangerous . So it will be argued ,  one need not do this exercise of traiging STEMI into main branch or side branch .

Image courtesey

Coronary tree : http://www.southcharlestoncardiology.com/64cta.html

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Ethics in cardiology : Truths , when silent are not heard in the consultation rooms !

Posted in Uncategorized, tagged on February 2, 2010| Leave a Comment »

Modern medicine promises   healthy new lives  to millions. We all , enjoy  the   fruits of  great scientific discoveries.  But do we  realise , medical science is nothing but experiments done on live  human beings . All  treatment modalities   are under constant scrutiny.  A great drug becomes the most harmful drug over a short time.

A drug or a device which is banned in one country is freely used in other country , marketed by the same parent company . How on earth this can happen ?  A device  ( Eg : A stent )  which is found  inferior  can  still can  be used legally elsewhere ,  hiding the information .

  • Do we divulge all vital information to our patients ?
  • Do we reveal all our conflicts of interest to our faithful patients ?

Informed consent is  the  “greatest  invention” in medicine . That is democracy in medicine . Doctor  patient conversation is   supposed to be  most noble of all communication !

But . . . this is under  genuine threat .  In this ” New medical AVATAR ” truths  remain only as thoughts , they  rarely  come out as words or action !

One such  situation a  physician  often  faces  in his office ,   as he is compelled  to act against his  conscience

If only we  have an ability to  read  his silence it will go something like this  . . .

For the sake of  Science &  Commerce , I have to implant this device  in your heart , and  my gut feeling says  ,  you will do much better without this device as well !   But ,  I am sorry . . .  I can’t avoid it .

Doctors are not be blamed  . . . rather  , we can’t blame  any body

Patients believe in doctors , and doctors believe in science  And the irony is ,  doctors have no other option as they are  coerced to  believe ,  in whatever is published  as science even if it is  half baked , unproved,  unapproved or  even dangerous science .

Let us prey for the genuine science to prevail  at least in human health  and the mankind  reap the maximum  benefits !

Let us  recall  Mahatma Gandhi’s    “Seven Social sins”   That included one  advice for the scientific world  nearly a century ago when it  was at it’s infancy !

Seven Social Sins By Mahatma Gandhi

  • Politics without Principle
  • Wealth Without Work
  • Pleasure Without Conscience
  • Knowledge without Character
  • Commerce without Morality
  • Science without Humanity
  • Worship without Sacrifice

– Young India, 22-10-1925

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Great papers in cardiology :Understanding the blood supply of sinus node

Posted in Uncategorized, tagged , , , , , on January 30, 2010| Leave a Comment »

Sinus node which orchestrtes the rhythm of life  gets it’s blood supply by a small blood vessel arising from either RCA or LCX. (55 :45%) . The  course of sinus node  branch  is highly variable .

There are three distinct pattern observed.

  1. Posterior encircling  of  SVC .(50%)*
  2. Anterior  encircling  of  SVC(40%)
  3. Form a  “garland like ” anastomosis  on either side of SVC (10%)

* Some refer to as clockwise and counterclockwise course.

SA node is a spindle shaped structure with a length up to 20mm . Extending from cranial to caudal aspect.The pecularity of the blood supply to SA nodal artery is  , it enters the SA node either in it’s superior aspect or inferior aspect never  in  the mid part. There can be water shed area in the either ends depeding upon the entry.This can have  electrophysiological and  pathological significance .

The other consistent feature is that ,  the major trunk of SA node artery courses through the central core of SA node.In fact , many times pathologists recognise ther SA node ,  with the help of   this arterial course.

Is there a collateral blood supply to SA node ?

It is not common  . Rarely  atrial branches of LCX /RCA  can have extensive anastomosis with SA nodal branches .The hemodynamic significance  of which is  not known. 

Ischemic SA nodal disease has become an important entity . As the cardiologists are preoccupied with opening  occluded coronary arteries  in cath labs , it  is not  surprising to note, there is little  ongoing  research  in the anatomy and physiology of SA nodal  blood supply.

We have to go back in time to get some great articles on the  subject

At this point of time ,  we should realise  the 1ooth anniversary of  SA nodediscovery passed of silently  .  Kieth and Flack  found the SA node with bare eyes  in the year 1907 , when none of the present-day investigations  including ECG and X RAY were  not even conceptualised !

With  tributes to those humble pathologists like  M.J Davies, R.H .Anderson, T.N. James,M. Lev ,J.L.Titus  who   followed   the foot steps  of  Kieth and Flack ,

Here is a  link to one of the great articles on the blood supply to SA node

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC514694/pdf/brheartj00203-0035.pdf

Related point : How do you  recognise  the  SA nodal artery in coronary angiogram ?

During RCA angiogram it is many times confusing  to identify the SA nodal branch . In RAO and LAO views the plane of exit  of SA nodal branch from RCA  will be determined by the  course  it is going to take .(Anterior vs posterior encircling pattern). The conal branch  which is often the first branch of RCA  ,  also behaves aberrantly  many  times. So, we can’t have a rule of thumb in identifying SA nodal branch .

When SA node branch originates from LCX it has to take a long route but once it reaches the SVC/RA junction it takes  one of the above described course. It is not clear whether LCX  fully understands it’s responsibility  , when RCA ignores it 45 % of times .  There is reason to suspect the commitment and dedication of LCX  because it rarely supply  the SA node by a   seperate branch.  It is often the left atrial CX  that comes to the rescue  and give a twig to the  SA node .

Considering the complexity of SA nodal blood supply  , one can understand  why some develop premature sinus node failure. One can never determine with evidence , how much of SA node destruction is due to ischemia and how much is due to age related degeneration and fibrosis.

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How will you diagnose ostium primum ASD clinically in the bed side ?

Posted in Uncategorized, tagged , , , on January 29, 2010| Leave a Comment »

ASD is the most common acyanotic heart disease. Clinically distinguishing  ostium primum (OP-ASD ) from ostium secundum (OS- ASD) is not an easy  task . A Wide fixed split pf S2  , a short systolic  murmur and PA pulsations  in left second space, a loud P2 and a hyperdyanmic RV occur in both .  The following features might give a clue for OP -ASD .

  • While  OS-ASD is  often an  isolated anomaly , isolated  OP- ASD is very rare.It usually occur as a part of partial or complete AV canal .
  • Early onset of symptoms
  • Early onset of pulmonary arterial hypertension( PAH )
  • Extra murmur of  1.VSD 2.MR (Cleft mitral valve ) may be present
  • Biventricular enlargement (MR/VSD)
  • ECG -Left axis deviation -Structural defect in left bundle ?

Confirmation is by Echocardiography and angiogram is rarely required today . Documentation of  classical goose neck deformity of LV outflow confirms the diagnosis.

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Tricks in echocardiography : Tachycardia a “big nuisance” to measure accurate LV function !

Posted in Uncategorized, tagged on January 26, 2010| Leave a Comment »

Assessing   LV function is the most common indication  for doing  echocardiography .Sinus tachycardia is the most common cardiac arrhythmia in humans. So, it is no surprise we encounter the above  situation  very often  in echo labs.

The principle behind echo assessment of LV function is to measure the  left ventricular wall thickening and the resultant reduction in LV cavity size.

The LV wall thickens in  systole and  returns  to baseline  thickness in diastole.When the heart rate increases the  rate of thickening has to be faster,  as do the rate of subsequent thinning in diastole. The endocardial segment of systole and thin segment of diastole tend to overlap at the base . borders are too shaggy and many times the thick So identifying true reference point  for endocardium become a difficult task.

It is  ironical  ,  inspite of  M mode echo  being termed outdated and obsolete by  most Echo schools , it remains the most utilized modality to measure LV function . It is  highly unlikely  , M-Mode derived LV EF   will be  replaced in the near future .This is because   “simplicity will always   prevail”  over  quality and accuracy .

It is all the more important  ,  the already poor index of M-Mode – LV EF %  becomes further  error prone at high heart rates.

It need to be emphasised , the impact of tachycardia in confounding  the true EF is greatest in  patients with preexisting LV dysfunction .

In a normal heart the errors are less and it can be  safely stated , tachycardias  rarely result in clinically important LV function errors

Does 2D derived EF by modified Simpson  overcome the problem of tachycardia related errors ?

To a certain extent ,  “yes ” . Here again the endocardial excursion is so fast one might have difficulty in marking the border.Automated  border detection algorithms are never corrected for heart rate related errors.

Other issues in LV function assessment  during tachycardia

In the presence of CAD  , the coronary arteries  often have varying degrees of obstruction.  Hence ,the  myocardial  segments  also exist  in varying degrees of ischemia.

In patients with significant CAD ,tachycardia due to any cause (Compensatory /Non compensatory -Fever, anxiety etc) can be considered a stress to myocardium . (By all means ,  can  we  consider it   an  equivalent of  dobutamine   stress echo! ?)

We know , dobutamine stress echo , has a variable effect on the contractility of LV. It can either  depress , argument, or  have neutral effect .Different lesions have different response depending upon the baseline viability of myocardium . For example  a 70% lesion  subtending a infarcted  –  viable segment may improve , while a 90% lesion supplying a normal LV segment may either worsen or hypercontractile .

What is poor man’s viabilty test ?

Grossly differing LV EF % in two different echocardiograms at two  different heart  rates may be an indirect clue  for the presence of viable myocardium.(Poor man’s PET or Thallium !)

The final message

The above concepts remind us the complexity of measuring the true EF in the presence of CAD. Purists,  may even question the existence of  a ” true normal  EF” in  a given patient

So, in the presence of marked tachycardia what is the ideal advice ?

  • Aviod measuring EF % during tachycardia , atleast in patients with CAD.
  • Use simpson method whenever possible
  • Atleast attempt it  few times,  you will overcome the laziness !

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What is the significance of biphasic T waves ?

Posted in Uncategorized, tagged on January 25, 2010| Leave a Comment »

T waves  are the most enigmatic waves  in clinical electrocardiography  . This is not a surprise , when you consider a tall T wave  and   a   markedly  inverted T wave both can be normal in  at least in 6 leads out of 12 lead  standard electrocardiogram ( V1 V2 V3 , 2 ,3 AVF, ofcourse the AVR  )

Common T wave patterns that can either be physiological or pathological

  • Tall T wave
  • Inverted T WAVE
  • Notched or Bifid  T wave
  • Biphasic T wave

* T wave polarity is strongly determined by the direction of QRS vector. Generally it should be on the same direction as QRS. In the presence of conduction defect or chamber hypertrophy  this gets  altered and is refered toa s  secondary repolarisation changes . This has to be differentiated  from primary biphasic T waves.

What is a biphasic  T wave ?

A T wave which is inscribed on either side of baseline is called biphasic T wave .

Many of the normal persons can have a biphasic Twave.

A typical biphasic wave can be two types

  • Terminal positivity
  • Terminal negativity

Terminal negativity is more significant than terminal positivity , especially in CAD.

A terminal negativity especially in mid precardial leads would suggest ongoing ischemia in LAD territory .

This happens due to dispersion of repolarisation between endocardium and epicardium.

The other mechanism could be the altered ventricular  gradient between QRS vector and T wave vector.

Why biphasic T waves are important ?

The biphasic T waves are known for dynamic change in polarity . It may either pull down the or pull up the  adjacent ST  segment . Prolonged QT interval is a closely related to the biphasic T wave.

Some times a U wave can be inscribed in such a way it may mimic a biphasic T wave. This is especially common in baseline bradycardia.

LVH is one of the common cause of biphasic T wave (Usually terminal positivity )

Biphasic T wave as mode of presentation of NSTEMI

Even though , ST depression is considered the dominant and classical theme of NSTEMI  , It is now recognised NSTEMI  has another  mode of   common presentation as biphasic T waves.

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Pleuro – Pericardial effusion

Posted in Uncategorized, tagged on January 24, 2010| Leave a Comment »

A combination pleural and pericardial effusion is more common than we realise .

Here is a patient with  both  effusions.

  • The etiology was tuberculosis.
  • Twin pressure effect   increases the chances of tamponade
  • Careful echocardiography is required to identify both .
  • Large left  pleural effusion can mimic a pericardial effusion some times . A useful clue is looking at  the LV  apex.It is invariably free in pleural effusion.

Unanswered question

Is there a anatomical continuity between pleural and pericardial spaces ?

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Strongly positive exercise stress test is equivalent to a brief episode of unstable angina

Posted in Cardiology - Clinical, Cardiology -unresolved questions, Uncategorized, tagged , , , , , , , on January 20, 2010| Leave a Comment »

Exercise stress testing(EST)  is one of the common investigation modality in the evaluation of CAD.he indication for EST  generally fall into two broad categories.

  • Diagnostic in patients suspected to have CAD
  • Prognostic evaluation in patients with established CAD .9Many times after a coronary angiogram)

Currently there is a major shift in our thinking,  patients with  classical angina  may undergo coronary angiogram  directly .This is understandable as the stress test  has little to   improve  diagnostic  sensitivity and specificity in patents with clinically obvious CAD.

So , it is now becoming clear , the diagnostic  value  is  increasingly  restricted in the evaluation of  o atypical chest pain .

What is a strongly positive response ?

  • Gross ST segment depression > 2-3mm
  • Occurring in stage one
  • Fall in blood pressure
  • Prolonged angina into recovery

What is the angiographic  correlates of strongly positive EST?

  • Critical left main disease
  • Near total proximal LAD /LCX
  • A severely compromised bifurcation lesion

Morphological correlation

  • These patients  often have eccentric lesions with irregular margins.
  • unstable  lesions
  • Lack collaterals

What is the effect of vigorous  excercise on a critical flow limiting lesion ?

The shear stress over the plaque  increases  with  exercise  and  the  transcoronary gradient can reach a theoretical 60-90mmhg .One can imagine the what this stress can do to the  unstable lipid core .This is the reason unstable angina is an absolute contraindication  to EST.

What does a strongly positive EST imply for the patient ?

  • It indicates he needs urgent CAG and  most likely an immediate revascularisation.
  • Often , these patients have prolonged angina , and mandates admission in a coronary care unit.
  • there has been many incidence of ACS in these  patients  within 24hours of EST.
  • Lives have been lost  on their  way back    ,   as  these patients are sent home , as EST is a  OP procedure .

Final message

  1. It need to be realised a strongly positive response to EST  could  be a  clinical equivalent of  unstable angina .
  2. The common response  from a   physician or cardiologist    after witnessing  a  gross ST depression to EST  would be   “Had  I known this  I would have sent him straight into cathlab instead of EST ”
  3. If only , we give little ear to our patient’s  history we can pick the high risk clue in 9 out of 10 cases !
  4. It can be argued ,  a strongly   positive  EST  by itself  is  “A  clinical diagnostic  failure”  ,   ie  failure  of the physician  to recognise  the likely hood of strongly  positive EST ie a left main disease.
  5. These patients  should never be sent home immediately  after the EST .This is fraught with a risk SCD
  6. Most of them will require observation in step down unit for 24 hours  and if feasible they should be posted for coronary angiogram in the earliest available slot.

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Foundations in Echocardiography : It is only occassionally , “A great article ” that comes free of cost !

Posted in echocardiography, Great websites in cardiology, Top ten in cardiology, Uncategorized, tagged , on January 19, 2010| Leave a Comment »

A  humble  tribute to  Mr. Doppler : Let us  remember this  man ,  every time you hear that hissing  Doppler  signals   , as  we  put the Doppler probe inside the heart.

Doppler ‘s brief encounter with life

Gave us one of the greatest diagnostic tool .

Born in  1803 in Salzburg, Austria,  died  in Venice, Italy 1853

Click over the portrait to learn Doppler’s life

Read and enjoy yourself !

Doppler and his principle  : By Richard J. Bing, MD Professor of Medicine – USC (Em) – Director of Experimental Cardiology – Huntington Medical Research Institute Visiting Professor in Chemistry – California Institute of Technology – Calif – USA

http://www.dialogues-cvm.org/pdf/51/DCVM51_04.pdf Courtesy  Servier

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More bad news for drug eluting stents , as new dangers emerge in the form of “late stent malapposition”

Posted in Uncategorized, tagged on January 17, 2010| Leave a Comment »

Drug eluting stents have  taken the cardiology community by storm . Millions of drug eluting stents are implanted every year. Sudden stent occlusion without  any warning has been the major threat of DES. Dependence of these patients , on meticulous dual anitplatelet  therapy is another  important caveat .This  issue  gets further complicated as we recognise “ clopidogrel  resistance” in many of this population . This , in effect  pushes these DES  patients  back into higher risk category.

So the cardiology community   cannot afford to  shy  away from answering  the following  vital questions !

How safe is DES  in the long run ? Are we really convinced ?  Is it acceptable to leave a DES patient’s life at the mercy of clopidogrel  which has it’s own idiosyncratic behavior ?



While this debate is getting hot , this new year(  2010) ,  there is  further bad news for DES .

Read this article from  European heart journal 2010

http://eurheartj.oxfordjournals.org/cgi/content/abstract/ehn553

A new complication  termed  ” Late stent malapposition” has been found  to occur  more frequently  in DES  than in other stents !

Stent malapposition could be technical in many , but when it  occurs late , it is  clearly  something to do with stent content  or it’s behavior with the vessel wall .

Some consider it as a partial  late  stent rejection due to late hypersensitivity reaction to the drug and the polymer .

Read a related blog : And now  drug abuse inside the  human  coronary artery

Final message

Drug eluting stents, ( Which  I think ,   has been  released  prematurely  into the  human domain !)  will face a strict scrutiny in the coming years and a turbulent time is expected.

Future perfect ? All the following statements can be true in isolation !

  • Even , plain balloon angioplasty (POBA) can be appropriate or  preferred over stents in many lesions.
  • Bare metal  stents are often better than DES .
  • Biodegradable  stents could prove  better than DES
  • And finally , medical management  ( if  effective and feasible  )  could be better than best stent

Reference

http://www.invasivecardiology.com/articles/Late-Acquired-Stent-Malapposition-after-Sirolimus-Eluting-Stent-Implantation-Full-title-bel

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