Archive for September, 2011

The prosthetic cardiac valve which saved so many lives  in the later half of 20th century is no more. A valve which is not only  known for its excellent durability  but also  devoid  of sudden  mechanical  occlusion , unfairly  lost its place  by the rival  mechanical  bileaft valves. (Supposedly superior hemodynamics !)

Here is a nice video  from Indian surgeon  which  describes the hardware of  Starr Edwards valve .

Please read a related article from my site

Who killed Starr Edwards valve ?

Read Full Post »

Heart is a dynamic organ . It can alter  its force of contraction with every beat  according to the needs.Generally it responds to  length  of  previous  diastole.This is famously called frank starling law , ie the force of contraction is directly proportional to the end diastolic fiber length. So changing diastolic  duration as in atria fibrillation classically result in varying amplitude of LV contraction and pulse volume.

However , the commonest cause for  pulsus alternans  is  due to  severe left ventricular systolic dysfunction .There has  always been a suspicion about the existance of  beat to beat variation in  diastolic function as  well.  We have recently observed a  new* explanation for pulsus alternans .We know AV inflow is subjected to respiratory swings . Non  respiratory swings in mitral and tricuspid valves are rarely described. This pattern is now increasingly recognised.

These  non respiratory swings in the mitral inflow doppler pattern  is seen in  some of the  patients with hypertension and LVH.This  probably confirms the existence of  beat to beat variability of diastolic function . This phenomenon is relatively a new observation . Such pattern are common in patients who have had a recent hypertensive failure .


Here is a doppler of mitral inflow recorded from a patient with hypertension with LVH .

This is the doppler mitral inflow profile of a patient with Hypertension, LVH and class 2 dyspnea .Note the non respiratory swings in both "e" and "a" velocity

It is proposed  to  define  a new class of diastolic dysfunction that can be referred to as diastolic  mitral inflow  alternans .This phenomenon probably indicates a more severe grade of diastolic dysfunction.At the molecular level this is related to  undulating flux  in the calcium uptake from cytoplasm into SERCA .There is one more possible explanation for diastolic alternans  -Left atrial  dysfunction .

Occasionally one can visualise  a chaotic pattern of  diastolic filling waves  (e=a e>a a> e )  Such patterns are thought  to be markers of impending acute diastolic shutdown .

Further  analysis of  this  mitral doppler inflow pattern will be reported  later.


* Though we observed this for the first time , this is not a new phenomenon .There are few reports available in the literature.



Read Full Post »

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 .

Read Full Post »

Coronary angiogram is  a videographic snap shot of  moving targets. Coronary arteries are dynamic  , tortuous  vessels of varying dimensions .Normal vessels  sometimes appear as an  illusion of lesions and tight lesions may appear innocuous at times. So the  rule is never rely on a single view before reporting.

This is an  angiogram of a patient , which  one of my fellows referred to as  “a black pearl  inside the LCX !

The same patient,s angiogram showing  origin of OM1

Final message

Beware of radiological artifacts in various angiograms. It can lead to erroneous interpretation and interventions !

Read Full Post »

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.

Read Full Post »

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 ?


Read Full Post »

Ventricular tachycardia can be classified in a variety of ways. Monomorphic VT  and polymorphic VT  is one such classification based on VT morphology.Polymorphic VT  generally conveys a meaning of origin from multiple focus .But in reality  bulk of the polymorphic VT originate from a single focus .

How does a single focus have a multiple QRS  morphologies ?

This is possible because ,  even though VT arises from a single focus , the route it takes to exit  from the myocardium is different and hence they inscribe different QRS morphology for each  beat. It is also possible ,  as the conduction time varies with each  exit route  the VT  becomes  irregular. This  phenomenon   is called  polymorphic VT.

It is assumed the VT focus  is often located in the sub endocardium and breakthrough occur in the epicardial side as  we record  the activity  in the surface ECG. Electrophysiology of VT is not that simple ,  focus  of VT can be anywhere ,  the focus can be single or multiple and exit pathways  can also be multiple it and  it may even exit into endocardial cavity . Please note , even  a single  electrically abnormal cell  shall  act as a  focus . To confuse us further ,  some of  VTs  may not exit at all , extinguishes before reaching the surface.

It is  a  difficult  job to fix  a given  polymorphic VT  to arise   from a single focus or from multiple focus  .  Multifocal VT  can be  diagnosed  with  confidence only  after a through electro physiological  study.Clinically few clues are there. Electrolytic disorders and ischemia  are usually  multifocal,  while scars VT gives single focus .Other famous  example  of polymorphic VT are Torsedes de pointes .

Polymorphic VTs are  usually hemodynamically unstable but it is not a rule. Surprisingly ,some of the polymorphic  VTs are well tolerated . This is especially common in  multi focal polymorphic  VTs  which are hemodynamically and electrically  better off  . Ironically ,   presence of  multiple focus may be  a blessing  as they    compete with each other ,  in the process  pulling  down the other focus from triggering a VF . It  is possible  one focus acts like a natural anti tachycardia pacing for a  VT from another focus.

Ventricular fibrillation can be termed as an extreme form of irregular polymorphic VT as the wavefront breaks into innumerable fragments  each exiting the myocardium at will in a random fashion bringing ventricles to a standstill.

Final message

The term multifocal polymorphic  VT  is generally been abandoned at the bedside  as distinguishing  it from single focal  polymorphic VT  is a difficult task*.Still  the concept of  multifocal VT  is alive and  kicking in the EP labs ,  giving sleepless nights to  our Electro-cardiologists!

*Please note , multi focal VPDs can be recognised  with ease by different coupling intervals, but  it is difficult to identify during a  run of VT .

Read Full Post »

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.


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.


Read Full Post »

Venous access for permanent pacing can be troublesome . Especially with anomalous subclavian ,  second implantation  ,obese patients with upper limb DVT . Temporary pacing through femoral vein is a well known concept.

Here is a concept of implanting the PPM  through femoral vein ,    in the upper thigh and the pacing  lead all the way reaches the right ventricle .There were few  issues which were  thought to be critical .As patients ambulate   there could be more  generator motion  than the sub pectoral location .(By the way , upper limb movement is equally common daily living is isn’t !)

Surprisingly excess  motion is  rarely an issue .  Even dual chamber  pacers were implanted  through femoral approach.Implantation  procedure  are simpler than one would have thought  and  complications are less as well .Since most of the leads are now screwing type  and  actively fixed   dis-lodgement  is never an issue.

Final message

The femoral venous access can be considered in all in whom SVC approach is difficult or not possible . 85cm lead is ideal . It is routinely available.

Always consider trans-femoral approach  whenever you encounter difficulty in subclavian .  Falling back on  epicardial  approach in such cases should be avoided at all cost. After all , epicardial approach is a major procedure.

Unfortunately,  very   few centers   practice transfemoral modality  for PPM right now . Brazil has some experience I understand.Royal Brompton  hospital ,London , Memorial  heart institute ,Long beach , California  have advocated this approach with good success.

We Indians , have a huge potential to propagate this useful concept.I wonder  why Femoral –  IVC approach  could  not be a  first choice for permanent pace maker implantation  especially in small children and adults ! The  main issue is  not technical , it is more of   perceived  fear  and reluctance to change the tradition.


The  article  by Ellsted  http://onlinelibrary.wiley.com

Read Full Post »

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 !



* 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 !

Read Full Post »

Older Posts »