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It is a well known anatomical fact  the grooves in the heart

  • Right and left  Atrio ventricular grooves.
  • Anterior  and posterior  inter-ventricular   grooves.

sincerely carry the  main stem of right and left coronary artery . It can be compared to a train running   with dedication   on its track .

Image source : AJR June 2007 vol. 188 no. 6 1665-1674

But God has not  enforced  strict rules   especially in human biology . The coronary arteries in few individuals   wander away  from the grooves.

This is very common  for Left circumflex  , followed by  RCA.  It is  relatively  for LAD to jump out of  its groove.(Except in rare Dual LAD system)

Here is a right coronary artery which enjoys its journey outside the right AV groove for   a good distance , only  rejoin the  groove at the crux.

Importance of  “Non- Grooval” coronary artery

It is true large diagonals and OMs ,ramus do   run without any  special tracks  .  But ,  it becomes ab  entirely different issue  when  the main stem of RCA,LCX or LAD itself   derail from its groove. There is no  fixing agents or vascular sheaths  that keep the coronary arteries within the groove. Surgeons  tell us circumflex is  often absent in its groove.

Note the stress and strain on the mid RCA : What will happen if that segemnt requires a stent ?

Hemodynamic implication of such free flowing non grooval coronary arteries is not been studied much .It is also observed  these   coronary  arteries   show  a  tortuous  course.This is  important   for  the  interventionist  as stenting  these segments is fraught with excess mobility and  tortuosity induced crimping .

Final message

The prevalence  of such drifting coronary arteries from its  groove  can be much more prevalent than we would  believe . The anatomical and physiological , surgical  issues need to be explored.

We know the atrial pressure  wave forms vary between right and left  atrium .In the right atrium “a” waves are  prominent and taller than “v” waves, while the reverse is true in left atrium .

Typical filling pattern of Right side chambers .Note The tall A waves . Source : http://www.ncbi.nlm.nih.gov/books/NBK2213/

Note the left atrial a waves are diminutive and v waves are tall .The dark black  wave is pulmonary venous waves. Source :http://heart.bmj.com/content/89/2/231.full

The  reasons for  tall  left atrial v waves are

  1. V waves are passive atrial  filling waves and  are timed  during ventricular systole .Left atrium is relatively  thick *,stiff , less compliant chamber .( Compliance : Rate of raise of pressure per unit change in volume .)
  2. Apart from relative thinness,* right atrial volume is more , hence  it can  accommodate more volume without raising its pressure .
  3. The left atrium is decompressed by  relatively stiff  pulmonary veins  with a mean pressure of 8 mmhg ,  can not adequately  dampen the   refluxing tides of  v waves , while the low pressure vena cava  of RA  dampen the right atrial v waves with ease  .
  4. Further ,the adjoining  systemic  left ventricle  ,  adds up to the stiffness of  left atrial   filling .

(*Thickness of RA -2mm,  LA -3mm )

Related article .

What is left atrial pressure volume Loop ?

http://www.wellsphere.com/heart-health-article/left-atrial-pressure-volume-loop/1208152

It is a combination of biochemical and  pulmonary receptor mediated dyspnea.

1. Hypoxia gets accentuated on exertion and it stimulates  chemoreceptors  located  in brainstem  as well as  aortic arch and its branches.

2. Equally important is the ventilation /perfusion mismatch that occur during exertion as the pulmonary blood flow significantly drops while the lung will continue with normal ventilation .This  increases the  Vp/Vq   (> 1) and  worsen the hypoxia  and   can independently trigger the sensation of dyspnea due to stretching of airway mechanoreceptors..

(It is  prudent to recall ,the later mechanism (Vp/Vq mismatch ) is  explicitly involved in  isolated  valvular pulmonary stenosis .Here , there is no admixture  mediated hypoxia , still the patient experience significant dyspnea  due  to meager  reduction  in pulmonary blood flow.)

3. Further ,  there are some morphological changes that occur in pulmonary vasculature in patients with TOF.This is due to chronic hypoxia as well as  “chronic low flow” mediated vascular reactivity. Micro vascular dysfunction in the alveolar capillary bed  is  possible in TOF. There  is  some evidence to suggest pulmonary gaseous exchange is impaired when compared to normal lungs.This can also contribute to the dyspnea in TOF.

Reference

The following article excellently describes the pulmonary dysfunction  that occurs in patients with TOF .It is prudent to note  ,the abnormal  lung function fails to get corrected even after total surgical correction in many.

http://onlinelibrary.wiley.com/doi/10.1002/ppul.1950160106/abstract

During   primary PCI , the weakest link  for a  cardiologist  is  , he is never sure whether  the  metal jacket  has covered the entire  disease segment with optimal apposition .  (Geographical miss is another issue !)

This is because  , even though the inflation pressure is  uniform  within the balloon ,  the required  apposition pressure is not the same .This is obvious as the lesion surface has a varying consistency and uneven surfaces . It is a  huge guess to quantitate the relative  contribution of thrombus and plaque  within  the 100 % occlusion  that has resulted in the STEMI. Hence  some areas may get over apposed and others lesser apposed. Further , the stent -vessel wall interface  in all likely hood enclose a   layer  of clot .This is almost certain  during complex primary PCI. One can imagine the sequel if this thrombus layer dissolves later ! (Edentulous stent )

It is surprising , why cardiologists has  so far not  thought  of a  self expanding stent  which  can snugly appose the vessel wall in this setting  . The   radial strength   from the  stored potential energy can be used up future use. This is most important  in first few days following STEMI  , when the coronary arterial lumen can vary depending  upon the

  • Vasomotor  tone .
  • presence of thrombus
  • Plaque   ploughing /milking  effect
  • Vascular remodeling

Cardiologists  deploy a stent  based on the morphology  on day zero of STEMI  .This may be  totally irrelevant  , since after a  few days    the lesion may change its morphology ,  thrombus may migrate , vascular  dimension may change. In such a  situation*  , a self expanding stent can tackle these issues very effectively by constantly adjusting  and fine tuning the luminal  diameter and  the apposition pressure . It  does not give any chance  for  thrombus to form  between the vessel wall and stent .

Here is a study that gives fresh insights regarding the role of self expanding stents during STEMI .

Note the “Auto adjusting”  of stent diameter  in the first few days after  the stent deployment, depending upon the luminal needs !

Animation

http://www.stentys.com/file_bdd/annexes/1284135580_video_stentys_en.swf

* Logically  during  primary PCI for  STEMI  ,  POBA and thrombus suction  may be the best option in many as all stent related complication is instantly eliminated .But it is a battered concept ,  most of the current day cardiologists would feel guilty to come out of  the cath lab  without a stent  in  primary PCI scenario  !

Final message

Self  expanding stents during primary PCI :  Is it a  perfect solution  for optimal stent apposition  ?

It seems so  . . . but  the track record of current cardiology devices never fulfilled the initial promises !

Off label prescription 

  1. Is a great scientific concept
  2. Is a deceit camouflaged  with a pseudo scientific fabric.
  3. Can be encouraged in very selective patient  population and diseases by experienced  cardiologists , as  it may be really useful when no other options are available.
  4. Is diagonally opposite  to evidence based medicine , should be banned in toto !

Answer:

4 is the correct answer .occasionally 3 can be true

Some of the examples of off label indication

  • Statins for Aortic stenosis
  • VSD device for RSOV closure
  • Ivabradine for cardiac failure

By the way how does an off label become on label?

It is not the ” God ” who  gives the label to them

There are few “Demi Gods” sitting aside  in the regulatory corridors of  New york and  Geneva who decide the fate of these drugs and devices . Ultimately the integrity of these organizations that will either protect or injure our patients !

Final message

Medical science grows my mistakes  . . . hence  we should be encouraged to do more of that  . . . so that we can grow !

Primary PCI (pPCI) is probably*  the   best modality in the management of STEMI .

( *Probably because ,    we  know “Time” ( fate !) is  still the  most crucial determinate of ultimate outcome of STEMI )

Any experienced interventional  cardiologist will be aware of the surprises  and difficulties  they encounter during primary PCI.

The pPCI  is all about  opening up the IRA rapidly and  wheel  out  the patient  from cath lab at the earliest.

But ,  ironically , an often  under- reported   issue  is the difficulty in  identifying IRA itself  !

One may wonder  , how this can happen ?

Following difficulties  can occur  in identifying IRA during  primary PCI*

(* There are some  hyper-talented  cardiologists who would never consider IRA recognition as an issue  .This article is not meant for them.)

The problems can range anything between the following   queries

  • Where is the IRA?
  • Is that the IRA?
  • No IRA ?
  • Multiple IRAs !

Angiographic encounters during  pPCI  and  IRA  trouble shooting .

  • When there is diffuse multivessel disease.
  • Thrombus vs  eccentric plaque  both  showing  intra luminal filling defect .
  • Thrombus spill over to adjacent branch or A mid LAD lesion with  stagnating thrombus extending to LCX ostium  mimicking two IRA
  • A bifurcation lesion with both LAD and LCX  ostial occlusion.
  • Multiple active looking  plaques with thrombus
  • STEMI in patients with preexisting CAD . Is it a CTO ?  ATO ? (Acute total occlusion ) A  CTO  ,which is  fed by collaterals from contralateral artery  ,  if this feeding vessel is  occluded even  partially ,  STEMI will occur in CTO territory . Here  , for rapid salvage you need to open the vessel that feeds the CTO territory.
  • Post CABG and post PCI form a special subset . Some times it is very difficult or even impossible   to label a graft as an IRA

Finally and most importantly  , when  there is no visible lesion in any of the coronary arteries   and look  near normal  !   Is that  no IRA  ?  or Wrong diagnosis of STEMI ?  Every one blinks  in cath lab . The consultant  howls the fellow to verify the ECG . Finally it may  well turn out to be an early  repolarisation  syndrome . These are wages we  often pay for the modernity !

How to approach  the situation when one is confused with  identifying the IRA ?

The good old ECG will come to  our  rescue sometimes. Realise in a multivessel CAD  , ECG is also vested with errors.

Echocardiography  rarely  gives a convincing answer to localise IRA. (Segmental overlap , preserved sub epicardial  contraction , residual ischemia all tend to confound )

Most confusions occur between LAD and  diagonal /LCX as there can be a huge overlap in the ECG territory  anterolateral segments

In a infero posterior STEMI, if  you have both  RCA  / LCX lesion and you wonder which  is the IRA  it is easy to solve by looking for RV involvement. (LCX lesions however dominant they are  . 99/100 times can not infarct the RV significantly  !)

If the lesion  is in PDA  the  issue is made simple.

Doing a primary PCI  blindly without knowing the IRA

This is  modern-day cardiology  at its scientific  low ! . Cardiologists  indulge in such  things much more commonly than one would imagine.

Probably  they would reason ,  it is safe to stent every vessel that is potentiality  an  IRA  , rather than  missing it. Though the concept of  multivessel stenting in STEMI   may help   patients with complicated MI ,  like pump failure ,  it generally increases   risk of primary PCI outcome in otherwise stable STEMI. Primary PCI procedure must be as short as possible. The other option is to do plain balloon angioplasty in less deserving vessels.

Important considerations  in the setting of complex multivessel CAD  during pPCI .

  1. Fall back on medical therapy
  2. Staged PCI
  3. Deferred or Immediate CABG
  4. Hybrid procedures like PCI  with CABG

Final message

IRA identification can  indeed be a difficult task  during primary PCI.  Sound knowledge and experience about coronary anatomy and its draining territories especially  in  the setting  of  multivessel  CAD  is essential to avoid errors.

Do you fear to deploy DES during primary PCI ?

  1. No. Not at all !
  2. May be  “Yes”
  3. Yes, definitely
  4. It depends upon which drug it Elutes !

Answers  that might  decode  the  cardiologist  mind. ( Excuse me  if it errs !)

If the answer is 1 ,  You are the most optimistic cardiologist  and scientifically  updated ,   data driven  cardiologist , and with little concern for the patient welfare.

If the answer is 2 , Your are a cautious cardiologist may be . . . may be . . .  an   ideal one . The chances of you , using a  DES is  still low in  STEMI.

If the answer is 3 , You are a pessimist and  with   anti technology thoughts but still you  have more concern  for  your patients!

If your answer is 4 ,  You are undecided  and probably  ignorant as well . Most likely   you would not use it  for some reason  .You need to read more  on the topic .

By the way , my answer is  response three.

Read further ,  the EXAMINATION trial just released in ESC 2011 Paris .

Left ventricular hypertrophy (LVH) is the most common structural abnormality of the heart. Hypertension and LVH are close associates . Still ,not every one with HT develop LVH .  So,  there  obviously  is a missing link . Similarly , diabetes  in the company of   hypertension  love to  target the  heart muscle with more vigour .  The  incidence of LVH  can be near  100%  when DM  join hands with HT.

So, what is the secret ?

Sustained elevation of afterload  due to high BP   inflate the myocyte ,  result  in myocyte hypertrophy , which is more of a physiological response.  The diabetes mellitus  adds some spice to the hypertensive LVH.

Diabetes causes glycation of  myocyte cell membrane  proteins . This  opens the  flood gates  and  the  cell permeability barrier vanishes. Hence there is exudate collect in the  cardiac interstitium. This is  equivalent to diabetic microangiopathy seen in retina and  kidneys.

There is  well established link between diabetic LVH and microalbuminuria  , suggesting  a  protein  leak  equivalent  in   heart  (Myocardial proteinuria)  . The only difference  here  , is the  protein leaks into the interstitium   instead of  renal  tubules  .  As we know interstitial leak is a  powerful  stimulant for   fibrotic reaction and  new cell growth. Fibroblasts in combination with extracellular matrix  and macropahges form  a rigid  and timid myocardium . If the patient is also a dyslipidemic(  which is usually the case !)  the leaked LDL , TGL adds to the chaos .

Pathological  effects of  diabetic LVH

  • Increased LV mass
  • Early LA enlargement
  • Early diastolic dysfunction
  • Prevent regression of LVH  even after good BP control

Can  diabetes per se cause LVH without Hypertension ?

Yes .this is also possible , but it  is less recognised.Diabetic LVH  can be a part of generalised organomegaly seen.(Right from the days of fetus diabetes has a  tendency to increase solid  viscera  size –  Large babies in  diabetic mothers , diabetic kidneys rarely shrink !)

Other factors that are related to LVH in diabetes include

  • Female Gender
  • Insulin resistance
  • The lipid connection – Hypertriglyceridmia is linked to LVH

Can tight blood sugar control reverse diabetic LVH ?

We hope so . It may not happen in real life .it depends upon the extent of interstitial invasion of abnormally glycated proteins.

Can echocardiography identify diabetic LVH from hemodynamic LVH of SHT ?

The diabetic LVH is fundamentally different in that ,  the classical septal hypertrophy is uncommon, instead the overall LV mass is increased .This is logical,  as septal LVH is more often reflect hemodynamic stress .

Diabetes  infested myocardium   bright echoes arise  from within . This is due to reflection from  interstitial  proteins.

The newer modalities of echocardiography  like integrated back scattering  analysis can characterise  tissues.

Tissue doppler  myocardial spectral analysis  can identify LVH contributed by DM..

Final  message.

What we know about LVH ,  is far less than we do not know !  , especially when  a patient has a combination of DM and HT. The interaction between them  is so intimate ,  we fail to recognise individual contribution to the process. If only we decode this  mystery , we can intervene better in the  pathological progress of  LVH.

http://care.diabetesjournals.org/content/28/9/2255.full

 Inter atrial septum(IAS)  is a delicate structure , formed by a  “curious IAS  embryological process”  , when  two septums ,  two ostiums  cross each  other .They  fold  and unfold  like  curtains  in different times ,  ultimately result in a  single membrane separating LA and RA  with a  central physiological   hollowness called foramen  ovale .

All along this process ,  blood has to shunt  from  RA to LA  untill the baby comes out ,  when the direction reverses that  result in the flap  of foramen ovale locking  against the septum secundum with raising LA pressure . So , basically the genesis of  IAS is all  about growing,   resorbing  and  sticking of two septums . This starts in utero and continues well after birth. One can imagine  complexity of  the factors that determine the thickness of IAS.

The IAS thickness varies between 2mm to 4  mm . With increasing use of trans esophageal echocardiography and also the need for cardiologists to puncture the IAS , it is becoming important to study the anatomy of IAS in detail.

A new  cause of  thickened IAS  is reported recently .

 This is refered to as Double Inter atrial septum,  fused like a sandwich  with a  potential space  in between  .

The embryological basis is not clear. (A septum primum and secundum fusion ?)

The PFO   is an  oblique orifice in many .It is some times refered to as tubular PFO . A large tubular PFO can mimic a double IAS.

An  aneurysm of IAS  may get  fused to appear like a double septum

or Is it  IAS dissection which  give an appearance like double IAS ?

Personal perspective

  • It is very difficult to embryologically  explain the concept of double IAS .  I would think  , it is  double layer  of single embryological  septum   with a  potential  space  in between .
  • It is possible an intra mural hematoma (Spontaneous or acquired ) may cleave the septal plane and mimic a double IAS   when the   thrombus gets dissolved later.

Other causes of thick IAS

Septal thickness an issue during transeptal puncture . During PTMC and left heart catheterization a thick septum may be a hurdle.

Infiltrative  myopathies especially amyloidosis is known for a very thick non -puncturable IAS  

Reference

1.http://ejechocard.oxfordjournals.org/content/9/5/707.full

2. http://www.ncbi.nlm.nih.gov/pubmed/16950474?dopt=Abstract

STEMIis numero uno of any medical emergency . The risk of death is maximum in the first  hour.

Here is a patient who presented within 30 minutes  of  chest pain.Enzyme sample was  just sent and a bed side echo  revealed a severe wall motion defect in LAD region.

What would have been  the response from a  current generation cardiologist ?

  • Alert the cath lab . Send the patient direct to cath lab .
  • This did n’t happen as we are in a underdeveloped country and the patient  is poor .
  • Should we worry about that  l ?  Not at all  . . .  He received a shot of   much ridiculed streptokinase injection which  costs 2000 Rs ( 50 dollars) in India  .

And see the result yourself !

Can you imagine this man had a major STEMI just an hour back ?

 Any intervention that is done immediately has a major impact on outcome. When the patient comes to you  early within 3o minutes and  STEMI,  or  actually a TEMI  , T wave elevation MI or Hyper acute MI .

When the patient comes to you early cardiologist should raise  to the occasion and set a new  challenge  .

What is that  challenge ?

The aim should  not to be in  salvaging  the myocardium  , rather   prevent  the  event of   ACS   and   abort the MI process itself !

How is this possible ?  Can you abort a STEMI or TEMI by primary PCI ?

Since one has  to act fast , primary PCI is a likely  loser  9/10 times in aborting a STEMI  .

The best option  is  to do an intervention which can have almost zero door to needle time* .  The good old thrombolysis  administered  at the door itself pips the pPCI  convincingly with a huge cost saving as well .

This is what  this patient received. and  see the result . His angiogram  later  showed a fully recannalised LAD .No stent  was advised .He was put on high dose  statins ,beta blocker  and antiplatelet agents.

*You  can not balloon the patient on the arrival in  door steps  !  .

Final message

Do not ridicule any modality of  therapy for being simple and cheap .  They may be most effective as well .