Archive for the ‘echocardiography’ Category

Why should mitral  annulus gets calcified ? .  Degenerative  calcification can be benign in  elderly .  If it occurs prematurely (say < 55 years )   there is enough reasons to worry .  This may represent a systemic vascular inflammation and  is considered a surrogate marker for athero- vascular -sclerosis .  A study from Cidar Sinai  , Los angels  has well documented the link way back in 2003  !

mitral annular calcification mac cad link

This is a  large study involving  17 735 patients (who were investigated for symptoms of CAD )   were screened.

The incidence  of MAC was high (As expected !)

  • 35% > 65 years
  • 5 %  < 65 years
Angiography  revealed more surprises .
  • The incidence of angiographic  CAD among those who had MAC and no MAC   was  88% v68% respectively ,( p = 0.0004),
  • Left main coronary artery disease  was (14% 4%, p = 0.009)
  • Triple vessel disease  was (54% v33%, p = 0.002).
mitral annular calcification  www_drsvenkatesan_co_in

Image source  S.Atar ,  Heart 2003 : 89, 161-164

This study concluded ,  CAD is more aggressive in patients with MAC. It can  also be  an independent  predictor of  high risk CAD .
Further Implications  of MAC
  1. MAC is more common in women, especially diabetics .
  2. Degenerative Mitral regurgitation  is common ,rarely  mitral stenosis
  3. Recurrent VPDs and even  trouble some mitral annular VT is possible
  4. Extensive calcific lesions in coronary  artery is also reported with MAC.
Link between Stroke and MAC .
This was well proven by this paper  published in  NEJM in 1992.

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lsvc persisitence lsvc left superior vena cava

While 2D echo visualizes the LSVC , it is the color Doppler flow (in blue ) that confirms the flow going away from transducer towards coronary sinus .Please note , if the LSVC shows red flow it indicates the left vertical vein and the flow is from below up .This is supra cardiac TAPVC . It makes immense embryological sense to understand LSVC and and left vertical vein are both same entities only the connections are different .

Click over  for a high resolution Image

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VPDs are such a common cardiac arrhythmia . We also know most are benign .Still modern science demands to rule out structural heart disease in any patient with multiple VPDs.

When ventricles get irritated it reacts with VPDs . ( The irritants  can be anatomical , physiological or primary electrical)

Echo can detect only anatomical irritants .We are recognising  more such focus for VPDs . Hence idiopathic VPDs  may simply reflect our ignorance !  A focused  echocardiogram is  required .

The following conditions are often observed in patients  with recurrent VPDs

  1. Posterior Mitral annular calcification (Especially in women ) –Annular VPDs
  2. Aortic valve degeneration /Bicuspid aortic valve with calcification – Cuspal VPDs
  3. Mitral valve prolapse in young -Stretch induced  Pap muscle VPDs
  4. Minimal  pericardial effusions with adherent epicarditis
  5. LV false tendons-Stretch VPDs
  6. RVOT lipid focus -Subclinical ARVD
  7. LVH and Hypertension –Fibrotic VPDs    
  8. Asymmetric septal hypertrophy
  9. Scars in MI/ DCMs
  10. infiltrations in RCMs (Any Interstitial heart disease )

(Conditions 7 and 8 are  common disorders myocardium  just included to  complete the list )

**Please note ,above mentioned entites are anatomical irritants .There is a whole lot of physiological  irritants

that can induce VPDs .  ( Hypoxia, Excess catecholamines ,  K + fluxes ,  acidotic milieu etc ) .

*** Another group is primary electrical diseases inherited channel disease can induce VPDs

Also read

A crash course on ventricular ectopics


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Anterior  mitral leaflet (AML)  is an  unique structure  in the heart .It is the fastest moving structure inside the heart . It is the first structure visualised by echocardiogram by  Elder and Hertz in early 1950s .

While AML is known for vigorous motion , the PML motion is subdued . By tradition AML shows a  motion which resembles alphabet M .

But AML is not be taken lightly .  It can change it’s  motion  not only  in pathological states but also in health . One such  pattern is trifid   motion of AML . Following is a Echo Image in  a  perfectly  normal Individual .

mitral valve motion trifid m pattern  in m mode echocardiography

mitral valve motion in m mode echocardiography trifid

Possible mechanisms underlying Trifid motion of AML

  •    The plane of  M-mode cut  will change the  mitral valve motion .(May  be this is most common ).M-mode at tip of mitral valve may be trifid  ,however a little beyond may record a  bifid-M pattern .
  • Redundant  mitral valve
  • Mid diastolic AML drag
  • Signs of elevated   LVEDP
  • Finally ,  it could be a   sign of  mitral valve  fatigue after excrcise  . Some of these persons   revert back to M pattern after a brief period of  Trifid motion following exercise .

Does trifid AML motion  result in Tri-phasic doppler  flow as well ?

Mitral valve filling is classical E and A .

This usually correspond to M pattern of anatomical  AML motion .

Do the anatomy goes hand in hand with physiology ? Will the mid diastolic  AML  drag result in augmented flow ?

We are looking  at this phenomenon .

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We always look at the thickness of  Inter ventricular septum for LVH . The Normal IVS thickness is up to 11 mm in diastole .  LVH is definite if IVS measure > 11 mm .It is  certain if it is > 12mm . But , we need to realise LVH by definition is not simply wall thickness .

It is increased LV  mass .

LV mass can increase without wall thickening . This is  referred to eccentric LVH . For example in chronic  volume overload  states  (or even DCMs )  LV mass may increase without septal thickneing .

Final message

LVH is possible without IVS thickening .

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If only  . . . we get  an  image like this , echo can help rule out most  left main disease with conviction .

Have a close look  at it ! One can get a good image of  coronary ostia in short axis view . But , here it is well visualized  in long axis .

left main

I tried to put color flow within left  main .

left  main color flow

What about pulsed  Doppler across left main ?

After all it needs 2mm sample volume and this left main was near 4.5mm . So keep trying !

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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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Here is a patient with class 3  dyspnea  who was referred  for echocardiography

X ray chest showing cardiomegaly

         Moderate TR due to dilatation of tricuspid annulus.This patient had dilatation of all 4 chambers of the heart.LV EF was 24 %

Right ventricular dysfunction is major determinant of  clinical outcome in patients with dilated cardiomyopathy. The  myocardium of the  entire heart is now known to be a single sheet of muscle rolled into different chambers . So any primary disease of myocardium will involve the entire musculature . This is the reason  , all the  4 chambers of heart goes for dilatation in  primary cardiomyopathy . Of course there can be minor variations  due to differential hemodynamic impact.

But it is certain ,  RV  function will definitely be compromised  In  most patients  with  Idiopathic DCM (Less common in Ischemic DCM ) Rapid assessment of RV function is difficult  . Of course We have some clues .

2 d Features

  • Simple dilatation  of RV is suffice to say it is struggling with the  loading conditions
  • Septal bowing
  • Tricuspid annular dilatation
  • RV ejection fraction (Continues to be complex for routine usage )

TR jet

  • Dp/Dt
  • Morphology may be useful (Mainly for TR severity )

Tissue doppler

  • RV strain rate Imaging etc.

And  now  , we have observed a new echocardiographic  sign   ie  TR jet alternans  in patient with  DCM .

Note the changing TR velocity implying severe RV contractile dysfunction.

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A young man with   VT  (LBBB morphology ) and  apparently normal heart by   echocardiogram  is  a  real  diagnostic challenge .
Here is a comparison  of  the two  closely mimicking  entities. RVOT VT and ARVD .
Please note -Micro reentry and triggered activity  are very closely related cellular evens. For all clinical reasons there is generally no purpose in differentiating the two.

*Please note -Micro reentry and triggered activity  mimic each other at the cellular level . For all clinical reasons there is generally no purpose in differentiating the two.

*RVOT- Right ventricular outflow tract. ARVD/ARVC -Arrhythmogenic  right ventricular dysplasia /cardiomyopathy

(Caution : RVOT vs ARVD  -In  the traditional medical teaching system , we are often taught to differentiate  two closely related  entities.Our brain also loves to look things in either black or white . Realise , medical science always brings  surprises . There can be significant overlaps between the very entities we want to differentiate.Bear that in mind)


1. Hoffmayer KS, Machado ON, Marcus GM, Electrocardiographic comparison of ventricular arrhythmias in patients with arrhythmogenic right ventricular cardiomyopathy and right ventricular outflow tract tachycardia. J Am Coll Cardiol. 2011 Aug 16;58(8):831-8.

2 .Ainsworth CD, Skanes AC, Klein GJ Differentiating arrhythmogenic right ventricular cardiomyopathy from right ventricular outflow tract ventricular tachycardia using multilead QRS duration and axis. Heart Rhythm. 2006 Apr;3(4):416-23.

T wave inversion in V1 TO V3 for diagnosing  RVOT VT .

3.Daniel P. Morin,  Andreas C. Mauer, Kathleen Gear, Usefulness of Precordial T-Wave Inversion to Distinguish Arrhythmogenic Right Ventricular Cardiomyopathy from Idiopathic Ventricular Tachycardia Arising from the Right Ventricular Outflow Tract .Am J Cardiol. 2010 June 15; 105(12): 1821–1824

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Under physiological condition ,  pre-load , after load , and cardiac  contractility should be a sequentially matching parameters . After load mismatch is an important concept , where myocardial contractility is temporarily  depressed due to  lack of adequate pre-load for a given level of after load .

This is also  referred to as descending limb LV function paradox .

The three  common clinical situation  AL mismatch  occurs

  1. Critical Aortic stenosis              (High aortic after load )
  2. Acute Hypertension                   (High after Load -Normal and  low pre-load)
  3. Severe diastolic dysfunction  (Pre-load is high -After load is normal )

If it happens acutely the myocardium becomes dyfunctional  due to  mechanical non ischemic stunning .Once the after load comes down the contractility improves .

What  is the chronic adoptive response to after load mismatch ?

LVH is the major  chronic adoptive response to AL mismatch.

LVH reduces the wall stress which will reduce the after load  indirectly .

So LVH neutralises the   high  after load .Laplace law at work . (Wall stress is equal to  2 times the radius divided by thickness of the wall )

Here  is the Link to the great lecture by John Ross Jr  in LA Jolla , California in one of the annual scientific session of AHA   more than 25 years ago . http://www.ncbi.nlm.nih.gov/pubmed/966366 .The concept is alive and kicking even today .I am sorry to  note   this  important physiological concept   never received the attention it deserves .  I would vouch , it  can be as   important as Frank starling  principle .

Reference :



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