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Archive for the ‘cardiology-Anatomy’ Category

Surprises are hall-marks of medical science . The cardiologists do  get  it ,   in enough doses   from  echo  labs  on a regular basis !   . One such thing is  the total ECG-ECHO myocardial  territorial  mismatch following  a STEMI .  Human myocardial segments are divided by cardiologists  by 17 segments by echocardiogram . Long before  echo came into vogue ,  electro-cardiologists  divided the  heart electrically into three zones to  localise MI . (Anterior , inferior and  the  poorly defined entity  lateral walls* ) .Inferior and posterior  segments are  almost used interchangeably. So , when we have 17  echo  segments to be fit into these three electrical category !   were  bound to have  some overlap . The issues of fitting in septal segments is really complex as septum  is a three dimensionally engulfs all three electrical surface of the heart .

* By the way , anatomists  never agreed about existence of walls in heart.They simply said  , heart has smooth  surfaces that blends with one another.  We cardiologist have  built imaginary walls and struggling to come out it !

We will   try to answer the question that’s been asked here .  “Inferior MI”  by ECG   . . . “Anterior MI”  by  echocardiography . How common is that ?

Possible causes for this wrong call

Technical errors  in  acquiring echo  imaging plane  or  it’s interpretation is the commonest . Many  times  ,  obliquely obtained long axis view  wrongly and strongly  suggests  a septal  MI  instead of   inferior posterior MI. This is  because  in  apical 4  chamber view  bulk of   septum  (Basal and mid third )  lies   in the  infero-posterior region .

wall motion defect

Perhaps ,  misunderstanding this  septal  geography is  the  commonest cause for  erroneously  calling inferior MI as anterior  in echocardiography . (A simple clue is the presence of MR . (It  fixes the infarct in infero-posterior zone with 90% accuracy )

Rotation  and  posture of heart

Alignment of the septum to the rest of the chambers  can influence  , how three inferior leads is going to look  at the septum (There can be  considerable errors  -Electrical myopia ? as these leads are located distantly )  . The plane of the septum is such that  in horizontal hearts  septal electrical activity  will be directed infero posteriorly inscribing a q waves in inferior leads rather than anterior leads . One can expect such ECG /Echo discrepancy in the following subset as well

  • Post CABG patients (Any pericardiotomy will make the septal motion  erratic )
  • Obese persons
  • COPD

There are three  more  situations  ,  which   mystified me   with  definite  ECG/ECHO  mismatch

  1. LVH and STEMI  is always an engima . Counter clockwise rotation when accopany  LVH  that masks anterior MI  electrically . It  however inscribes a   q wave in inferior leads.
  2.  In dominant LCX lesions  ( with at-least  one  major OM    )  and  left main bifurcation  STEMIs  ,  combination of  anterior and inferior  wall motion defects are  quiet common . When a such  a  MI evolves ( with or without  revascularization )   regeneration of R wave can be  time shifted . Septal R wave may appear  much earlier and inferior R may follow or vice versa . .Further,  anterior MI  may  evolve as  Non q MI  making it  ECG blind ,   still  echo may pick up the WMA . So there can be important  ECG-ECHO mismatch in myocardial segmental geography .
  3. Further , WMA  need not  always be an  infarct  .Any new episode of ischemia  can result in WMA . Hence a patient  with inferior Q waves  in ECG may experience anterior wall motion defect meagerly  due to fresh episode of   ischemia (This we should not attribute  to  old anterior  MI. It is also possible intra-myocardial conduction delays can elicit remote wall motion defects.

Final message

By general rule  , ECG  correlates  well  with  ECHO  for localising myocardial segments   . At times ,  it  can  really be tricky , and we  get into above situation  in echo labs.

While ,  it is common to observe  ECGs  to mimic  inferior MI  at the first look  and  subsequently echo  revealing  anterior  infarct ,  the reverse is also very much possible .

The  mechanisms are varied and technical  issues are for more frequent than true clinical discrepancy .The issue has important management implications.

Of course ,  coronary angiogram will pin point the   anatomy , still  it also has  strong limitations in localizing myocardial segments (to which it supplies ) especially with multi-vessel  CAD and  collateral dependent circulation .

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Most  cardiologists  are familiar with  “Circulation” . We know  it  is a top  cardiology  journal with highest impact factor.  Few of us are  aware  of  a journal called  “Circulation  research” ( I wonder  why it is named  like that ,  as if  the regular   circulation journal  does  not carry research stuff  !)

It is one of the  path breaking   journals that regularly  churn out state  of  the art , often  mind  boggling research stuff.  Once in while we should get a feel of  basic science  research  as it  happens.

How else we are going to know an  atrial cell is to be bio engineered  shortly to behave like a  SA node  in patients with sinus node dysfunction. (Biological pacing )

This team from academic  medical  centre Amsterdam   should be credited   for  publishing   this gem of  an  article   from  a  study  involving the  measly mice !

It  deals elaborately  about the embryonic basis of AV nodal  disorders  . Specifically it  explains  the genesis of  WPW syndrome and how AV rings get muscularised  .

(It  is  due to   error in  bio-genetic forces ,which  affect the    incorporation  of AV nodal tissue  in the  fibrous  skeleton .This   results  in ectopic  junctional  tissues appear   any where along  the AV ring . This is the basis of  accessory AV pathway and   clinical  re-excitation.)

Final message

Once in a while  we should develop the habit of reading  tough  journals  like circulation research . After all ,   if a cardiologist  is not reading   these stuff who else  . . . will  ?

Reference

http://circres.ahajournals.org/content/107/6/728.full.pdf+html

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The other day when  I was  observing  my colleague   puncturing  the inter atrial septum  with heavy bore needle  during a PTMC  procedure  the patient   was  comfortably watching and   enjoying   the procedure .

Even as  multiple wires  criss-crossed  the left atrium  and  the  balloon  hitting  the mitral valve repeatedly   there was  absolutely no pain.

Next day ,   in an another  patient  when IAS was punctured  it got stained  along with pericardium  ,  the patient had   severe  back pain and procedure was  to be  stalled temporarily  .

What  is the lesson learnt  ?

The pericardium and the epicardium (same as visceral pericardium )  has rich  pain  fibers. The above  patient  who had  stain  of epicardium had severe pain .

The former patient who had a perfect IAS puncture did not develop pain while the  later  who  had an  epicardial track   experienced pain.

The same analogy can be seen in patients  with myocardial rupture .While  sever chest pain is a rule  with a free wall tear , it is very rare for  patients with ventricular septal  rupture  to complain  sever pain as  IVS   rupture do not cleave the epicardial layers  .It is also uncommon for papillary muscle or chodal rupture to generate  significant pain .

What is the difference between  epicardium and endocardium in terms of pain fiber  innervation ?

Sub- endocardium has less  dense nerve supply than sub-epicardium. This is one more reason why isolated sub-endocardial  stress  less commonly result   angina ( Eg Hypertension and sub endocardial strain  often silent  ) while  even minimal irritation or insult of sub-epicardium induce severe  pain.

Further , cardiac  pain receptors   respond differently to type of stimuli  .The density of these receptors also  vary depending on planes of myocardial  tissue  .

What are  triggers for cardiac pain ?

Any of the following can trigger cardiac pain.The pain receptors in heart are not well developed as that of somatic system.

It is not clear whether the layers of heart has specialized receptors for various sensations.

  • Stretch*
  • Prick
  • Guide wire poke ,
  • Needle prick
  • Temperature .
  • Infection ,
  • Inflammation of  myocardium , pericardium*
  • Pressure injections
  • Cardiac ischemia*

These  three factors   are responsible for bulk of the cardiac pain . Please note needle prick on the heart is least painful !

How does ischemia   generate pain ?

The ischemia of myocytes secrete

Bio chemical

Substance P ,  prostaglandins, serotonin, adenosine, bradykinin,   and other mediators are involved

Neural

Carried by  myelinated A-d and unmyelinated C fibers run in the cardiac sympathetic nerves . It is understood ,both the fibers  respond to mechanical stretch while Type C fibers also carry chemo signals from bio chemical mediators as well .

Vagus  nerve has a major role in carrying  afferent signals of pain . It is  well known ,   if pain stimuli  is substantial the vaso vagal reflex is activated and bradycardia  and hypotension  occurs.

How is infarct pain different from Ischemic pain ?

Necrosis of nerve terminal will result in more intense pain and lasts longer .

Clinical examples for stretch induced cardiac pain

  • Acute RV/LV dilatation of any cause
  • Pulmonary artery/Aortic dilatation
  • Pericardial stretch could contribute more in generating this   pain
  • Mitral valve prolapse (Stretches  LV free wall )

Interventional  cardiologist should thank god for not innervating  the heart extensively . This  only allows  us to  spend  hours  together  inside the patients heart , other wise one would require a general anesthesia for doing a PCI

Does pericardium  suffer from  ischemia or necrosis ?

Pericardium is not an  avascular  structure . Pericardium gets its blood supply from twigs  of LIMA and phrenic arteries.So there  must be some impact of ischemia on pericardium . Since pericardium has  rich nerve supply there  is every reason to suspect existence of ischemic  pericardial  pain as well .

But  pericardial pain induced by   mechanical stretch  and inflammation is much more common  .While acute pericardial stretch is painful chronic stretch as in slowly accumulating    pericardial effusion is  a painless event !

Pain relief  after CABG

One of the reasons for angina relief  post CABG is attributed to the interruption to  pericardial nerve supply.

Reference

This 1957 article from circulation still  rules cardiac pain literature . http://circ.ahajournals.org/content/16/4/644.full.pdf+html

http://www.annualreviews.org/doi/full/10.1146/annurev.physiol.61.1.143

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Proximal LAD lesions require  specific and early Intervention.Hence we need to know what exactly  we mean by proximal LAD disease.Unfortunately , it means different things to different cardiologists .There is no dispute regarding the  origin of  LAD since it begins with bifurcation point  .The problem comes with  this question !

Up to what distance LAD can be termed as proximal ?

  1. Bifurcation  to   “First   diagonal” of  any size
  2. Bifurcation  to   “First Major diagonal”
  3. Bifurcation to     “First septal”  of any size
  4. Bifurcation to    “First  major septal”
  5. Bifurcation  to   “Any major  first branch ” (Either septal or diagonal )

Answer : I think  4 is the correct answer . But many believe  5 can be correct as well !

Why  there is  confusion in the  definition of proximal LAD ?

This is because the first branch of LAD itself is not a  constant one  . It can either be a septal  or  uncommonly  a diagonal.

It should be noted , the septal and  the diagonal  branches  neither respect   seniority  nor follow a  hierarchy .The first diagonal may be diminutive while the   second or third diagonal may be major one  and vice versa .Further  ,  there can be a trade of  in length and caliber of   septal and diagonal branches  .This  phenomenon is also  common between  diagonals  and   OMs  . All these confound the picture .

Cardiologists even though they are  primarily physicians they are  pro-anatomy  like surgeons when it comes to coronary interventions .

                                  In the strict sense ,  we  need to differentiate a  lesion  from being   physiologically proximal  or anatomically proximal  !

Is there a proximal LAD equivalent ?

There are three  situations  this can occur .

  • Some times a lesion  by  definition may not fit in  as proximal  LAD  but physiologically  few major diagonals  will arise after the lesion.
  • Other situation is , LAD lesion may be  mid or distal but  a major first  diagonal may be diseased  , making it  equivalent  to proximal LAD in terms of physiology.
  • A mid LAD  with a large OM lesion which is running in the D1  territory

Final message

It is ironical  millions of cardiology interventions happen  for proximal  LAD lesions  every year without  even  proper understanding of what we mean by  it ! Youngsters are argued to ponder  over this issue whenever  they indulge in  such cases for revascularisation!

Reference

Text books differ in their definition about proximal LAD. Currently , the  SYNTAX  scoring system  has defined the coronary segments in a practical way.

http://www.syntaxscore.com/index.php?option=com_content&view=category&layout=blog&id=1&Itemid=32

Definition from SYNTAX

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Human coronary circulation stands  unique among  others as it is a   life-sustaining circulation.It is  considered   a great  medical achievement   to visualise   the right and left coronary artery  system by coronary angiogram.  Actually  what we see is   only  a  fraction   of  the surface area  of  coronary circulation . The surface area of  epicardial coronary arteries   constitutes  less than 5 % of entire coronary vascular tree .

This  is the reason  normal coronary angiogram can never mean normal  coronary circulation !

This huge gap in our perception is the single important factor  that  explains the vagaries  of modern coronary care .

This also  make any coronary  scenario  a  reality .

“A patient with normal coronary angiogram getting a myocardial infarction the next day and a severe triple vessel disease living comfortably with medical management”

So ,  it is essentially a   false  sense of  scientific accomplishment   by the  cardiac scientists  at  least in the  of coronary circulatory physiology.

There are innumerable channels of micro vessels traversing across the heart, sharing , bridging , branching, penetrating  and  perfusing the muscle mass.They can be anatomicaly patent , physiologically non patent .They can be recruited by hemodynamic stress . It is also influenzed by  favirable growth milleu and hormonal and neural stimuli.

What determines the extent of these invisible circulation ?

and

An in vitro heart with special catheters showing the true extent of coronary circulation: Courtesy http://eurheartj.oxfordjournals.org/content/28/3/278.full.pdf+html

Why many cardiologists   do not give due credit  the   coronary collateral  circulation  ?

Right from the days  of  Levine in 1970s( Who made a seminal contribution  about coronary collateral)  the  utility value of  coronary  collateral  circulation   was  never able to convince the cardiology professionals .

It has been our traditional  teaching ( without much evidence of course  !) coronary collateral circulation  is not effective to support blood flow during exercise . This fact has been  disproved  many times . Coronary collateral circulation was indeed useful in limiting damage in ACS and  relieve symptoms in stable angina.It helps  in reverse remodeling and provided electrical stabilty as well in post MI population.

Still  the concept  was  alienated  and   made   totally irrelevant  in the interventional  era  . Many   cardiologists  found well-developed collateral’s as an interference to their expertise and ego since it has a potential to alter the indication of PCI.They  continue to have  strong  scientific conviction (Pseudo ?)   that man made collaterals must always been superior to God made collaterals !

Whenever  some credible  reports emerge about  collateral circulation   being   equivalent to  revascularisation procedure , these concepts were  prematurely buried for some reason.

In the last decade there was a concern  about  performing  PCI in patients with well-developed collaterals  .The argument was , they tend to develop early stent occlusion and restenosis . It  was a genuine  query  raised by few thought leaders in the field as  collateralised vessels  suffer from  low flow states  after PCI ,   if the pre -existing collateral continue to function.

But then , few  studies countered this  , and   said PCI  is safe and  in fact may  fares well   in  patients  with  extensive collaterals .

In these  studies  interventionist’s  argument looked  amusing !  as they  seem to  define a  successful  PCI  as  not only to open the occluded vessel  but also  make sure to close  all functioning  collaterals  .(What a  a pity for our natural biological  angiogenic forces which had  worked  and  grown meticulously for months!)

Cardiac science in the current format,  makes   the future look  bleak for coronary a collateral circulation .With  early PCI  becoming a norm we will never ever allow the natural collaterals to  grow  ,  and even the  established collaterals  will have to face a stiff   fight  for survival  with  sophisticated coronary interventions .

Competing interest in the filed of  coronary collateral   research

While the basic scientists want  to  grow collaterals with angiogenesis ,  stem cells etc  interventionists   continue to  indulge in rampant angioplasties which  will suppress  collateral growth.

This implies we will struggle to  establish  the true  importance of  coronary collateral circulation .

Final message

Can it be an  effective form of revascularisation  ? 

My personal  inference  is   coronary collateral  circulation  “would and should”  have  a definite role  in at- least  some of the subsets  with chronic coronary  syndromes. If we think otherwise . . .    it’s against the principle of  natural biological science .

A good  collateral   system with optimal medical management  can save not only our  patient’s  lives but also  their hard earned currencies !

Reference

Here is a rare article in European heart   journal that discuses coronary collateral circulation  . Let us welcome such wonderful  reviews which keep the interest alive on the filed.

http://eurheartj.oxfordjournals.org/content/28/3/278.full.pdf+html

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Human coronary artery anatomy would  rank  top among  all human biological mysteries. The variations in their branching pattern is next only to palmar creases and cerebral gyri !

The left coronary artery can divide in to two , three  or even four branches occasionally.The trifurcation  occurs in upto 20 % of population .The ramus intermedious  can some times be a major division .Usually it supports the diagonal or OM territory.

It is very rare to see a ramus  take a long course . Here  is a patient whose LAD is small  which  falls  short of LV apex . Sensing this , the ramus travels all the way to apex and support the LAD in distress !

RAO caudal view shows the Ramus reaching all the way to LV apex! Note the diminutive LAD and absence of true OMs from LCX.

* Technically  this can  also be  referred to as a rare form of dual LAD system .

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Bicuspid aortic valve (BCAV) is  one of the common  congenital abnormality of heart . Incidence can be 1-2% of population . It can result in premature aortic degeneration with Aortic stenosis/Aortic regurgitation or both .

The normal development and arrangement of three cusps is altered ( rather interrupted )  during fetal life.

There can be two ways BCAV can occur. One is due to the   fusion* of two leaflets to covert a  tricuspid  valve into  bicuspid  ,  and the other is    two cusps develop de novo .The former has a raphe , while the later has no raphe.

The  fusion* occurs between  either

  • Right and left (R +L)
  • Right and  non coronary cusp  (R +N )
  • or Left and Non coronary cusp (L +N)

(* The fusion is embryological , not acquired )

Most often the  fusion is due to lack of division in the valve  analgen .Hence a raphe (A conjoint remnant) is noticed .

90% of BCAV has raphe  ,only 10 % lack raphe . Aortic root is also structurally abnormal in many .(Little clinical sequale though !)

Coronary artery origin anomalies  are more common with  BCAV. We also know co-arctation of aorta has a embryological link with BCAV.

The commonest type of BCAV is

The most hemodyanmic stressed BCAV is R +N type fortunately it is rare

R + N fusion is a high risk BCAV as degeneration occur fast

The least common type is

The coronary artery origin anomalies are common

BCAV in the absence of raphe is classified separately (This constitutes 10 % of all BCAV)

The nomenclature  is

  • Antero posterior (Common type ) AP
  • Lateral (L )

What is  the pathological significance of raphe ?

Many  believe presence of raphe accelerates degeneration as leaflets have  rough surfaces . Still , BCAV with raphe has less coronary anomalies and aortic root pathology .

Presence of raphe  indicate relatively  a minor embryological defect  , as the fault is in the failure to divide after the formation of analgen , while BCAV without raphe  imply  lack of development of analgen itself . This is expressed in the coronary sinus anatomy and aortic root dimension and orientation .

So currently it is  welcome  to spot  a raphe in the patient point of view  .Echo cardiogram is notoriously  unreliable to diagnose raphe. Once degeneration process sets  in ,  it is almost impossible to recognize  the  presence or absence of raphe .

* Please note ,tricsupid aortic valve with eccentric leaflet closure  shares  a close pathological relationship with BCAV. Premature degeneration ,  (AR more common than AS here ) .This entity will be discussed separately later.

 

Image courtesey

Part of the Image (The valve) is adopted from Yale university Image Bank .

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