Archive for July, 2010

RHD is the scourge of mankind . While a part of the world is suffering from glamorous  lifestyle disease ,a  significant  population (The country I live – India , included)  is suffering due to  “lack of any style” in their  life !  exposed to  primitive streptococcal infections  and end up in deadly destructive heart valve disease .

While , the  privileged  cardiologists make merry in cath labs  ,  a  few toil in the deep sub Sahara forests and the tropics  of Cambodia  to bring some sense and balance  to  cardiology literature.

Mankind will benefit  much more  these committed souls* than the pseudo-research that is happening world wide !

Of course ,  we should thank the NEJM to publish  such  precious articles !

The summary of this article goes something  like this

Echocardiography ,  if used widely in general population  ( more specifically in children)  can identify rheumatic fever early with high degree of precision .With penicillin prophylaxis we can reduce the RHD burden of our planet significantly.

The message may be simple, but in the modern world  people’s suffering  is not due to lack of  sophisticated health tools , but  “lack of common sense “

This article came in 2007, unfortunately it has not  generated the  desired  impact  among the cardiac care takers  .(While  a  mediocre ,  drug eluting stent can reach 1000 cath labs in 100 countries in a matter  of weeks!)

The World health organisation (WHO) is yet to formally adopt this new  echocardiographic criteria to diagnose Rheumatic fever .We expect  the WHO , to urgently formulate new guidelines for early detection of rheumatic fever .(It is better , we stop hanging on to Jones for over  half  century !)

Will the WHO be proactive ?

If a portable echo costing few thousand dolors can save  millions of life , let the WHO the bring an ordinance to supply  (liberally ) manpower and  machines  to  all those poor countries  which lack in basic health service , but infested with  free supply of  deadly land mines , outsourced arms and ammunition !

This study was performed in  Maputo Heart Institute  Mozambique , and Cambodia .



* Three cheers to Eloi Marijon, M.D., Phalla Ou, M.D., David S. Celermaje .

Chain of Hope

Travel online to Africa : A journey into human side of cardiology  . . .

The charity  that has adapted  Maputo Heart Institute  Mozambique

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LVH is one of the commonest ECG abnormality . We know the hall mark  of LVH is increased QRS voltage .We also know , ECG is not a fool proof method to detect LVH .It has very good specificity , but little sensitivity , meaning that increase in  QRS voltage is  fairly accurate in predicting LVH  but absence of  which cannot exclude LVH.

Why Increased QRS voltage does not occur in many with LVH ?

Even though we think myocardial mass  is  the  sole determinant of QRS  voltage  , in reality  it   is determined by many other factors.

  • Distance between the ECG lead , and the myocardium is an important factor. In classical concentric LVH , the LV  cavity is not enlarged ,in fact it may shrink a little as the hypertrophy grow inwards and obliterate the LV cavity.(We do not know yet , how much of LVH grow out and how much  muscle grow in ! )
  • The blood volume within LV is a very good conductor of electricity.A good volumed LV may augment a QRS voltage.
  • This can be observed in some of the patients with DCM , where high voltage QRS  is recorded mimicking LVH.

But ,what really matters is the fine balance of blood volume and myocardial mass that determine the incidence and magnitude of LVH pattern in ECG.

QRS voltage as a tool to differentiate pathological from physiological  LVH

We know QRS current is generated from within the myocytes .If the myocytes  are  uniformly hypertrophy without altering the  basic mechanical and electrical architecture QRS complex will be amplified in a sm0oth manner and result in  classical high voltage  QRS  of LVH.

If the hypertrophy occurs in a disorganised fashion, where in myocardial fibres slips out of plane  with adjacent muscle bundles, the QRS  voltage may not increase and even be slurred or notched as we see in many cases of LVH with non specific intravascular conduction defects

The classical disarray of myocardial fibers that occur in HCM causes  pathological q waves.

* Other factors that determine LVH include bundle branch conduction delay or blocks which is not discussed here.(Ex: An incomplete LBBB can amplify the qrs without any LVH )

LVH with fibrosis

Fibrosis is not a standard feature of LVH. It occurs in few who are genetically predisposed , and  mediated by heightened sensitivity to circulating growth factors.

  • Fibrosis can have wide impact on the electrical as well as mechanical function of heart.
  • Fibrotic heart has a  potential to  blunt the  high voltage  QRS complex.
  • It  may even cause  pathological q waves .It predispose to ventricular arrhythmia
  • It prevents regression of LVH , even after the loading conditions corrected.

Other conditions that  attenuate LVH features in ECG

  • Diabetic hypertensive show less ECG voltage than isolated HT .
  • CKD patients often do not show ECG features of LVH inspite of LVH

Final message

Diagnosis  of  LVH by ECG is a  simple clinical exercise , but we realise now , the underlying mechanisms are too complex .

A simple question , ie  Why  every one  with LVH  do not increase  their  QRS voltage  ?  . . . exposes  our ignorance on the subject!

But one thing is clear, physiological LVH (Meaning LVH ,  purely due to loading conditions including SHT/Aortic stenosis)  more often result in high voltage , while  in true pathological LVH(infested with fibrosis ) the  increase in voltage is not consistent .

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We have conquered  CAD with coronary  stents !  really ?  atleast , that is  what ,  many  of us  are made to  believe !

But , the fact is , modern cardiac science  with all those fancy intra coronary  devices has shifted the CAD population into  cardiac  failure population. We have extended the life of humans by at least few years and make them suffer recurrent coronary events and ultimately LV dysfunction  and cardiac failure .

We know , cardiac  failure  can not be  conquered with medicines and surgery . Cardiac  transplant  has been very successful ,  but it needs one human death to give one  life to other , and “deaths” can not be bought in stores or  donated at will !

So , the only alternative for  terminal heart failure  is total artificial   heart.(Organ farming or cloning not included ) The research is going on for the past 50 years. We are definitely on  the right track. By 2050 , my guess is  no human being  should die of heart failure .

Meanwhile , number of partial answers for  failing hearts  which are  popularly referred to  as LV assist devices are coming up.

In many cases the failing native heart supports the device  in a mutual fashion thus extending the life of the device as well .This is important because in case of total artificial heart there  is no back  up available.

These axial LV pumps just augment the overall circulation status and in the process unloads the native heart and prolongs it’s running time.

In the future one may think about  number of serial pumps in the circulatory  system rather than a single bulky artificial heart which is fraught with serious maintenance issues.

The most promising one such device is from Germany

  • A small AA battery sized tubular pump
  • Weighs 25 grams
  • Receives blood from  left atrium  pushes it into subcalvian artery
  • Can have a stroke volume of 10-15cc /beat*
  • Capacity to pump  a cardiac output of 3l/mt (This amounts to 100% augmentation in most terminal heart failure patients)
  • Can be implanted like a pacemaker

* There is little  end diastolic  residual blood in this pump .

Picutre courtesey  www.medgadget.com

Link to  http://www.circulite.net

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Life  is nothing , but the intervening time between the first heart  beat and the last heart beat of an individual  !

Human heart is not an ordinary organ.  Right from the day 22  of fetal life , when the cardiac jelly  begins to beat till  the early  new-born period ,  (In some, even longer !)  it continues to evolve.

We know  heart as a hemodynamic organ . But ,  in the fetus   it is  dynamic in  a  different sense (Embryo-dynamics) . As the mother’s  heart  takes care of the fetal circulation ,  the fetal heart concentrates  on it ‘s  own growth  .The heart learns the  lessons of life in a hard way  , it has to survive the next 70 -80 years independently .

The complexity is enormous . The cardiac muscle  comes  from  mesenchyme, the conducting system  comes from ectoderm .Systematic  events  like , looping  , partition  , regression  of the heart tube should occur at critical times .  Apart from this , the venous and arterial  connections ( Aorta IVC,SVC)  develop concomitantly and has to fuse with respective  chambers without any error.

It is a wonderful biological marvel  happening inside every fetus without the help of any architect  !

The changes do not stop at birth. It continues , well  after delivery . One  hole gets closed(PFO), one conduit disappears (PDA) .One chamber regress (RV) . We, expect all these things to happen in a  meticulous and  sequential  way.

Yes , it happens in most. But , in many with altered bio – genetic forces  things   fail to unfold  in  the programmed way.    It is not at all a surprise ,  to find some common aberration .

So , when some body is born  with a congenital heart defect , don’t blame  it on God .He does his job , in billions and billions of heart in the right manner .

It is our ancestral gene  code that gets awry in a few  !

In Hindu  philosophy  the  defects  we inherit  are the wages we pay for our ancestral misdeeds  .

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Coronary stent implantation , which   was once  considered  , a state of the art procedure is now   practiced even  in,  remote towns and small nursing homes all over the world.

While , it is a blessing to  have such a technology disseminate all over , we have also  witnessed problems due to indiscriminate work ethics inside human coronary arteries. One of the deadly complication  is coronary artery perforation.( It is not a surprise to experience this complication , especially  when inexperienced, cardiologists  try to manoeuvre fancy hardwares  into the coronary artery for the first time !)

Ellis , fore- saw this yeas ago !

He classified coronary artery perforation into three types.

For type 3 perforation , the   only emergency intervention is deploying a stent graft .

A  covered stent with    Polytetra fluro ethylene   (PTFE)( Jostent ) is often used .

Final message

  • Anticipate this complication  , especially when negotiating CTOs and fragile venous grafts , or  while dealing  any complex lesion.
  • Every cathlab should have a crash cart ready with anti perforation kit .( A large bore needle to tap tamponade is much more important than a PTFE stent graft !)
  • Referring for an emergency surgery is one option , but it is often too late !


Link to jomed

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How  central cyanosis occurs  in primary pulmonary hypertension ?

While , peripheal cyanosis*  is easily explained in PPH ,the mechanism of central cyanosis is not straight forward.

The following explanations are offered

  1. PFO**  getting  opened due to high mean RA pressure
  2. Pulmonary arterio venous channels.(Neogeneis or dormant channels activated )
  3. Altered QP/QS .This effectively means lung shunts some blood without oxygenation(A right to left to shunt within lungs )
  4. Associated lung pathology -like pneumonia resulting in pathological right to left shunt across the alveolar circulation.

* Peripheral cyanosis can occur in PPH with cardiac failure

**PFOs are often anatomically patent in 20 % of normal population , which gets functionally patent  when exposed to high RA pressure

Cyanosis -A brief  description .

Cyanosis occurs when the arterial saturation goes below 85 % . Cyanosis  manifests in two ways . Central and peripheral.The term peripheral  does not  denote  peripheral parts of the body  rather it is  peripheral  circulation.(Capillary) The mechanism of peripheral cyanosis is somewhat  different from central cyanosis . It is generally due to sluggish circulation ,  more  oxygen extraction and resultant bluish discoloration .

Peripheral cyanosis is seen in finger tips, lips etc . Peripheral cyanosis can not occur in warm areas of the body for the  simple reason warmth  causes vasodilatation , better tissue perfusion  which prevents stagnation of  deoxygenated blood.

Central oxygenation defect alone can not result in  classical central cyanosis .

For central cyanosis  to occur ,  there need to be mixing of  deoxygented and oxygenated blood somewhere in the  circulation.(Right to left shunt in the heart or lungs )

Since it is a defect in central  oxygenation it  manifests  in both warm mucous membranes as well as cold extremities.

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Infective endocarditis continues to be a challenge for the cardiac physicians.

While we have innovated too much( More than what is required !)  in the interventional arena little is progressed in the last few decades on  this vital  area  of  “Infections of heart”.

Globally , deaths continue to occur in prime ages due to rampant infections of the heart valves.

Prevention of IE was recently deglamorised by diluting the criteria for prophylaxis by ACC/AHA (Cost issues ,  overwhelming science ? )

So, what is left in the war against IE ?

Early diagnosis and recognition

How to diagnose it early ?

Suspicion is the key  . . .

When to suspect ?

Suspect in all with fever and h/o heart disease . So far  no case of afebrile IE reported !

Get rid of the common myths

  • You don’t require vegetations to diagnose IE
  • Blood culture need not be positive
  • Fever can be low grade
  • Rarely severe fatigue is the only sign

This effectively means , one can diagnose IE without a major criteria of Dukes.

One can diagnose IE with 5 minor criterias

If you wait for a major criteria to develop to start treatment , it could be a  costly miss .

So have a open mind, suspect IE, treat early.

Do not unduly worry about , overuse of antibiotics in case of  false diagnose of IE.This  attempt is worth in weight  of gold !

Million ton of antibitics are used indiscrininately in this world by all walks of physcinas for simple cold and surgeions  non existing peripopertaive infections .

While , the global medical community has  accepted this concept with total submission (Intentional harm condoned !) , it is funny to ask for 100% appropriateness in the therapy for a  deadly infection of heart.

It is absolute necessity  to  inject an  anticipatory antibiotic in all cases of suspected IE with high risk valve lesions. (Of course ,  it need to be a reasonably appropriate antibiotic with microbiologists consultation to avoid interference in the subsequent culture evaluation !)

Minor only infective endocarditis.

Please note IE can be diagnosed with the following 5 minor criteria

  1. Predisposing lesion
  2. Fever >38c
  3. Immunological / Vascular lesion
  4. Culture eqivocal
  5. No clear cut vegetation , but high suggestion of vegetaion, New valve regurgitation

A related article in this blog

Vegetation negative infective endocarditis .

Final message

Never hesitate to start empirical antibiotic therapy in suspected high risk IE

Let us err . . . for the patient’s sake  !

Fever + New murmur*= IE until proven otherwise (Oxford handbook of  clinical medicine  P 136 7th Edition )

*It can be read as , presumably new murmur to increase the sensitivity.

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Patent foramen ovale is probably  the commonest  congenital heart defect.  (Bicuspid aortic valve will run close to it ! )

Note : PFOs  cannot be  called as a  true disease , since it is a  benign anatomical defect with little or no hemodynamic impact.

Consider  this scenario . . .

The incidence  of PFO could be as high as 20% of adult population. It means nearly 100 crore people of this planet  will suffer from this entity !

When does it become significant ?

Paradoxical embolism : In young persons with cerbro vascular accident , PFO s are more commonly observed , implicating some form form of venous to arterial embolus .

In some persons it is believed , it can shunt few CC of blood from right atrium to left atrium at times of right atrial hemodynamic stress. Like severe physical  straining  (valsalva like )

In seriously ill ventilated patients  PFOs can worsen the  hypoxia especially with  PAPP  mode .

When does it become a life saving savior ?

  • In patients with DTGV and intact IAS  even a a small PFO can sustain a life  till , emergency surgery or intervention is done .
  • In patients  with severe  pulmonary hypertension the PFO may act like a safety valve, opening at a critical moment and decompress the  right atrium and which  indirectly relieves  the RV wall stress as well .

Fancy relationships

Now , it is  considered PFO  is related to migraine by some means ! ( What means !)  The belief has strong evidence base that has lead  the aggressive  interventional cardiologists to  find a new hole to close  . This indication ,  if  approved will have a perennial supply of patients  as there are 100 crores of them .

How will you differentiate a PFO from a small ASD ?

Size alone can be a useful pointer in differentiating a ASD from PFO.

A PFO can  measure  between  2 to 10mm  ( most measuring between 4-6mm diameter)

Size matters !  The upper limit of PFO is the lower limit of ASD .

Practical experience suggest any defect  above 7mm should alert  us about the possibility of true ASD.

Other useful clues

  • PFO are always restrictive  (Use pulse doppler probe right across the PFO /ASD in subcostal view .If you pick up a gradient > 4mmhg (velocity 1 m /sec) PFO is confirmed.
  • Most ASDs do not show any significant  gradient
  • Right ventricle and right atrium should be normal in PFO  (Unless due to some other cause )
  • Doppler flow across  pulmonary valve can be very useful . If it exceeds 1.5m/sec , left to right  shunting is likely to be significant and PFO is unlikely.

Is there an entity called restrictive ostium secundum ASD ?

If so ,  how will you  differentiate it from PFO ?

Yes , we have ,especially in  cyanotic heart disease

Like TGA , Ebstien etc .

Isolated restrictive secundum ASD is extremely rare .

* There is no way to differentiate a restrictive ASD from a similar sized PFO .

What is the role of TEE in diagnosing PFO

It has a major  role in delineating the IAS anatomy .

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Coarctation of aorta  continues to be an  important  acyanotic heart disease  . Now , early recognition  and intervention  is possible with the availability of sophisticated imaging and interventional modalities.

Our understanding of this  entity , even though appears complete  . . . it  is not ,   especially the complexities of the collateral  circulation and the associated malformation.Even in this 21 st century , unexpected circulatory  compromise are reported in the postoperative phase from various vascular  beds (Spinal, mesentric, limbs etc)

It is also  surprising to note ,  much innocuous entities like  ASDs ,VSDs  have  popular  anatomical and functional classification.It is a  rare excercise ,  for cardiology fellows  to classify co-arctation of aorta .This ,  in spite of the fact,  we have a  meticulous classification suggested by Amato , way back in 1991  published in Annals of thoracic surgery .

Let us  be  aware of this  . . .  Click  the link below for Amato’s classification

Amato’s  surgical classification of  coarctation of aorta

Type 1  Primary Aortic Coarctation

Type 2 Coarctation with Isthmus  hypoplasia

Type 3 Coarctation with Tubular hypoplasia of distal arch

3A- With VSD

3B-With complex LV outflow lesions

* Ideally  we need to include BCAV and status of ductus , suitability of aortic stenting in the classification.

Other old classifications

Bonnet’s classification 

Infantile :which later became known as pre-ductal, and adult which later became known as post-ductal . These became obsolete , as we came to know all coarctation or juxta-ductal .(Very difficult to separate into pre or post ductal coarctation  by simply  looking at it  , without knowing the hemodynamics )

Conte et all      **  Backer

1.Isolated coarctation  2.Co- arctation with  VSD 3.Co arctation with complex heart anomalies.



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Aortic hypoplasia is a common observation in many congenital heart diseases  especially  acyanotic CHD. It is  important  to know the adequacy of systemic blood flow , in left-sided embryonic flow  defects like , co- arctation of aorta, interrupted aortic arch, shone’s complex etc .

The hypoplasia is thought to be due to two mechnaisms

1. Low flow state in utero( fetal heart) and the  resultant hypoplasia.

2.Ductal tissue migration into adjacent arch  which leads to  friendly arch  contraction !  when the  PDA gets closed

in the immediate new born period .

When do you suspect aortic hypoplasia ?

There is no strict definition available.But the Becker’s  data base provides a working rule.

Hypoplasia is diagnosed when ,

  • Isthmus is , < 40 % of  diameter of ascending aorta
  • Proximal  transverse arch  is ,  < 60 %  diameter of ascending aorta
  • Distal transverse aortic arch is , < 50%  of diameter of ascending aorta

Why ascending aorta is taken as reference ?

It is least likely to affected by the shrinking ductal tissue . Descending aorta can be a reference but it is at a  remote location and difficult to image .


Becker’s  CHD nomenclature and data base project . Annals of thoracic surgery  2000

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