Archive for October, 2015

This year’s Noble prize for economics was conferred  for Dr Angus Deaton  from Princeton,  for an unique revelation, that measurement errors in economic indices such as estimation of poverty and nutrition levels in society  is real and huge .

The crux of argument (My version )  could be , data collection errors , planning with that contaminated data , sets in a chain reaction , that sustain a flawed intellect in young researchers , which  ultimately leads to human beings becoming  victim to their own  data . While Deaton addressed this in economic issues,  one can guess how critical these errors could be , when  one deals with a  continuously variable  biological parameters .

Every day , medical professionals are confronted with  diverging data measured with dubious methods. Measuring health as quantifiable semi mathematical parameter itself is intrinsically flawed , unfortunately this is the only way we can do it as of now.

If  logical extrapolation is the accepted norm and poverty is the most prolific disease  of humanity  (coded in ICD by WHO) its obvious Deaton’s work will have tremendous impact on medical science than any  other field .

As a cardiologist ,I struggle to understand for the past 30 years  , why we need to work towards a goals of  reducing few mmhg of blood pressure  (or few mg of LDL ) in elderly population knowing fully well the evidence for which is  soft with questionable end points. It  appears some times comical , when healthy people who are not taking these medicines in poor countries  are labelled as medically deprived ! by certain non Governmental agencies.

Final message

With existence of people like Deaton , there seems to be light at the end of tunnel , (Hope we don’t create new tunnels) It is heartening , we are witnessing major innovations in the assessment of health outcome,efficiency and impact in recent rimes.. Let us hope some common sense would be infused over the complicated number science !


Here is an awesome piece of writing  by Reetika Khera an associate of Angus Deaton at  Princeton .(Reproduced with the courtesy of Of “The  Hindu ”  -From the open page,   on the significance  of  Nobel Economics this year 2015)

Angus Deaton, the winner of this year’s Nobel in economics, has contributed immensely to the understanding of poverty, prices, nutrition and well-being in India. His work has been guided by the belief that economic progress must lead to better lives for everyone.

Much of the work by Angus Deaton, the winner of this year’s Nobel Memorial Prize in Economic Sciences, has been focussed on measurement issues. He has questioned the quality of data collected in large surveys and suggested ways of improving the surveys. He has also thought very hard about how these data could or could not be used, how to reduce measurement errors, and what inferences one can, or cannot, draw from data that might suffer from measurement errors.

Boring as that may sound, it has ensured that economists pay attention to detail, and do the hard work that empirical analysis demands. Good data is fundamental to good economics.

One example of this is from India. His contribution to the understanding of price indices and relatedly, poverty estimation, has been very important. He has highlighted the problems with the computation of price indices in India and how these affect poverty estimation. His proposal to use prices implicit in the data collected by the National Sample Survey Office was implemented by the Suresh Tendulkar committee some years ago.

His book on these issues, The Analysis of Household Surveys, published in 1997, remains the best to learn about data issues. Along with poverty estimation, he has applied his deep understanding of several disciplines (ranging from biology to philosophy) to work on mortality, health, nutrition and well-being. In his latest book, The Great Escape: Health, Wealth and the Origins of Wellbeing Inequality, he generously acknowledges Amartya Sen’s influence on this aspect of work.

India-focussed work on poverty

Much of this body of work on nutrition in India (and elsewhere) has come since the 2000s. A large part of it is India-focussed, much of it co-authored with Jean Drèze. In 1999-2000, there was a lot of interest in the poverty estimates as these were the first post-liberalisation estimates. Supporters of liberalisation were keen to show that poverty had declined, and that its rate of decline had accelerated since liberalisation. Those against it were unwilling to accept this.

A change in the methodology for data collection between 1993-94 and 1999-2000 made a straightforward comparison between the two point estimates impossible. Deaton’s work (with Drèze) on comparable estimates disappointed both camps. They found that while the official claim that poverty had declined in the post-liberalisation period was true, the claim that there had been an acceleration in the rate of decline was not.

In 2009, Deaton and Drèze published a paper in the Economic and Political Weekly (EPW) on the nutrition situation in India which once again provoked economists on both sides of the ideological spectrum. On the one hand it led to a debate, in the same journal, with Utsa Patnaik — widely considered to be on the Left — who felt that the decline in calorie consumption was a symptom of rising poverty. They, however, pointed out that calorie intake was declining even at given levels of real per-capita expenditure, especially among the better-off households, and discussed other possible reasons for this pattern.

On the other hand, in 2013, Arvind Panagariya challenged a long-held understanding among economists and nutritionists about anthropometric outcomes. The argument was not so much about whether height is a good indicator of nutrition, human development and well-being. Panagariya’s thesis was that Indians are short, not because they are undernourished but because they are “genetically programmed to be so”. Deaton and his co-authors pointed out in their response, again in the EPW, that “all of his arguments about the role of genetics is residual: if we cannot think of anything else [we assume that] it must be genetics.”

These two debates are illustrative of Deaton’s careful analysis and unwavering honesty, his ability to separate his social commitments from what his meticulous data work suggests. Indeed, at a press conference at Princeton University just after the prize was announced, he said that sometimes his work leads him to “very uncomfortable” places.

Questioning the dominant trend

Another important part of his contribution has been to question dominant fashions in development economics. When “instrumental variables” were a popular tool to establish causality, he wrote “students no longer look for a thesis topic, but for an instrument”.

More recently, a new technique “randomised control trials” (RCTs) has taken development economics by storm. For some, RCTs are seen as the only form of evidence, disregarding not only other forms of quantitative evidence but also other forms of qualitative evidence. Deaton has been among the few voices to question our over-reliance on RCT experiments while that acknowledging it as a valid body of evidence.

“I argue that experiments have no special ability to produce more credible knowledge than other methods, and that actual experiments are frequently subject to practical problems that undermine any claims to statistical or epistemic superiority,” he said.

The “randomistas”, a term used by The Economist, have been influential in several states in India. The Government of Tamil Nadu has signed a Memorandum of Understanding (MoU) “to institutionalise an evidence-based approach to policymaking”. Some experiments have led to greater hardship for the poor — for example, delays in wage payments to National Rural Employment Guarantee Scheme (NREGS) workers — without any accountability for these adverse outcomes.

For Deaton, the problem is not with RCTs per se — some of his current work is on how to use RCTs — but rather with the view that it is the only form of evidence that matters or that it should be the only driver of policy decisions. He has his differences with arguments like that advocated by Abhijit Banerjee when he said that “the World Bank should cease to fund any activity, including presumably macro policy advice, that has not been previously subject to evaluation by an appropriate RCT.”

Advocate for a greater state role

Apart from claims of statistical or epistemic superiority, Deaton has questioned the divorce between policymaking and public discussion. His contribution has not only been as a rigorous economist, but equally as a public intellectual. He is a firm supporter of government action for social policy. Without being blind to the problems of governments in poorer countries, he forcefully argues for their greater accountability.

“The absence of state capacity — that is, of the services and protections that people in rich countries take for granted — is one of the major causes of poverty and deprivation around the world. Without effective states working with active and involved citizens, there is little chance for the growth that is needed to abolish global poverty,” he argued.

On the consequences of inequality, while some inequality can be a good thing, Deaton has argued that too much could potentially have negative consequences for us all.

He noted that:

“The very wealthy have little need for state-provided education or health care… They have even less reason to support health insurance for everyone, or to worry about the low quality of public schools that plagues much of the country…To worry about these consequences of extreme inequality has nothing to do with being envious of the rich and everything to do with the fear that rapidly growing top incomes are a threat to the well-being of everyone else.”

These messages are important because public debate in the past few years in India have tended to belittle various forms of public support through terms like ‘doles’, ‘freebies’, and ‘handouts’. Repetition succeeded in creating an impression — unsubstantiated by facts — that India has gone overboard in its social spending. We have witnessed strong rhetoric on evidence-based policymaking, combined with a resolute disregard for inconvenient facts. We need to engage with Deaton’s contributions very carefully.

(Reetika Khera teaches at IIT Delhi. She did her post-doctoral research at Princeton University under Angus Deaton.)

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Hot debate in STEMI

Acute total obstruction (ATO) of coronary artery is an emergency .Opening it  by pharmacological or catheter is the  standard ( logical ) protocol.However, time plays a crucial role in this coronary re-perfusion game.It can either be a sure shot of success or end up in total spoilsport. One more issue as important as time is from the overflowing scientific data  fired  by different regulators  in conflicting directions  (Also called knowledge) .

What to do with STEMI coming late ?

  • ATO with cardiogenic shock is an  absolute emergency at any time.
  • Symptomatic ATO  other than CS beyond 24 hrs still  considered  emergency for most.(Symptom should be true angina )
  • Hemodynamic instability is misunderstood term . Stabilizing it medically is not forbidden.

Asymptomatic stable ATO  beyond  24-72 hours can be  semi emergency, true emergency or as cool  as a cucumber depending upon the cardiologist’s wisdom , experience or inexperience  and the  Institutional Integrity !

*Please be reminded ,LV dysfunction is not an absolute indication for urgent intervention unless it is due to ischemic dysfunction attributable  to a critical non IRA lesion

When does a ATO become safe CTO ?

1 month , 3 months, 6 months ?

Why we are  not defining a sub-acute ATO ? or CTO in transition   ?

Is living peacefully with sub acute ATO or CTO a coronary crime ?

We don’t require a debate , whether these  questions are worth answering  or not !

Final message

Though cardiac professional  are committed  to open up occluded arteries to save  lives , reality is repeatedly teaching different stories ! The greatest danger of keeping an artery open( In disputed indications ) is the newly conferred risk of sudden closure and the attendant  unpredictable aftermath !

Or should we conclude : Living with CTO is ok , but don’t intentionally create one by denying PCI in late  post STEMI ATOs


Arguing closed artery is better than an open artery is straw man argument and inability to interpret positive things in science.  However it may still be right  when science suffers  from hostile incursions from non academic forces.

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Car tyres warrant  replacement  every  20,000 km or so .Its batteries do require periodic attention. Human heart , which runs non stop from womb to tomb . . . deserves how much ? Unfortunately no one (What about your cardiologist?) can  provide  a flawless lifetime maintenance contract to this restless bio-mechanical pump ! Fortunately still, God has  created this wonder organ ,that can with stand the stress of life for nearly 10 decades . . . if we live a proper life !

However ,there are many areas in heart that are prone for mechanical stress even if it’s structurally normal .These are  the zones where the relatively fixed parts  rub against the dynamic zones .The joint between inflows ,outflows to the respective ventricle are at risk . Aortic root, along with the leaflets and annulus  formed by the fibrous skeleton is delicately close to the critical part of the conduction system namely the branching portion of AV node and His Purkinje.The process of degeneration is linked to age, valvular abnormality and genetic and  systemic metabolic profile also seem to matter in few .(Hypercalcemia and cardiac calcification ?)

Importance of the interface between Aortic valve and  AV conduction system in the current Era 

Degenerative aortic valve disease along with  the adjacent conduction system  of elderly is going to be a key cardiovascular disease in the future as the population is aging .We have made a big step forward in tackling this with innovative percutaneous aortic valve implantation  (TAVI) . However ,the artificial valve  is positioned vulnerablely  close to conduction system and incidence of complete heart block either during implantation or follow up is  high and a permanent pacemaker seems to be an integral part of this procedure for many.

aortic valve his bundle complete heart block 003

Heart seen from behind , Mitral annulus to left and tricuspid valve ring to the right .

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A  classification of  Polymorphic VT .

It can be classified according the etiology,  morphology  or hemodynamic stability . However , for some reason classifying  PVT with reference to the preceding QT interval and  the manner in which  tachycardia twists its axis along the qrs axis has been the most popular theme . ( Obviously ,the classification  process should  evolve further , and management strategies should be linked with it )

classification of polymorphic vt, torsades de pointes , long qt syndrome

Read a related article :Different Avatars of polymorphic VT

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Mitral regurgitation is expected to occur only in systole during  left ventricular contraction. In rare pathological states , if   LV pressure exceeds the mean LA pressure at any point in diastole , small  puffs of regurgitation into LA can occur.The genesis of this MR and its  hemodynamic  significance has generated much interest .


  1. Aortic regurgitation -Severe . (Occurs mainly in acute AR or chronic AR with decompensated LV )
  2. AV blocks (especially complete AV block )
  3. Any cardiomyopathy with severely elevated LV diastolic pressures


No single mechanism is  responsible.

  • Common hemodynamic denominator  is transient cross over of LV pressure over and above LA pressure curve .
  • This tends to happen often soon after the atria contracts  specifically so , if the atrial contraction is not followed by a QRS complex as in heart block .
  • The fact that its reported even in the presence of atrial fibrillation (As in some cardiomyopathy ) atrial mechanism is not exclusive.
  • In Aortic regurgitation the mechanism is  different (More of  volume dependent ,  Read below )

diastolic mitral regurgitation animationTiming of  diastolic MR

It occurs in later part of diastole as it takes a time lapse for raising LV diastolic pressure  to cross the LAP and generate a reversed ventricular gradient.

Will there be a clinical evidence for this MR ?

Its silent in most cases .Some patients with complete heart block may  generate  mid diastolic murmur . (Rytand AHJ 1946) .Retrospectively this could be due to diastolic MR

Is there a link between Austin flint murmur and diastolic MR ?

Many researchers believe the generation of diastolic murmur in severe AR is attributable to premature closure of mitral valve and the poorly compliant LV  is not able to accommodate the leaking blood and it tends to regurgitate into  LA  through partially closed mitral valve in diastole (Ochaya  S,  Am Heart J. 74 1967:161-169)

Echo features

  • Doppler flow signal in mitral inflow is diagnostic
  • Color M-mode is ideal to map  diastolic MR.

Cath correlation

Wong has demonstrated this phenomenon by direct hemodynamic  recording in 4 patients

Further research

While the field of diastology is growing , still we are not clear how significant this MR in clinical diastolic dysfunction and acute LV failure that results in flash  edema.


5.Diastolic atrioventricular valve closure and regurgitation following atrial contraction: their relation to timing of atrial contraction.Okamoto M1, Tsubokura T, Kajiyama GClin Cardiol. 1989 Mar;12(3):149-53.
7. An auricular diastolic murmur with heart block in elderly patients.Rytand  DA; Am Heart J. 32 1946:578-598.
8. Late diastolic mitral regurgitation secondary to aortic regurgitation its relationship to the Austin-Flint murmur.ochaya  S, Igarashi  M, Schaffer  AB; Am Heart J. 74 1967:161-169

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Failure of  enocardardial  cushions  to separate and reach the  predesignated destination  ie  right and left AV valve is the basic embryological feature in AV canal defect .This brings whole AV ring  down and stretches the distance between  the semi-lunar valve (especially aortic)  with that of LV , thus elongating  the LVOT into a classical  goose neck deformity.The defect  has a profound  impact on how the AV node and its branches penetrate the ill-formed AV junctional tissue and fan out into the ventricle. There are  four basic issues  that are responsible for the various conduction defects in AV canal defect.

  1. Postero- inferior  displacement of the A-V node is the key abnormality .
  2. Hence  AV node penetrates the ventricle at the level of crux which is abnormal .This results in short his bundle  (AV node short of compressed with His  early direct origin of the left bundle branching)
  3.  Left bundle branching system by itself is also abnormal  with hypoplasia   left anterior bundle branches.
  4.  Right bundle branch is relatively long and elongated

Physiological effects

  1. Prolonged PR interval (50%)
  2. QRS  axis shift can be extreme right or left , but superior direction is a rule .Typically its around -180 . Left axis deviation is distinct in downs syndrome (Counter-clock wise rotation q in lead 1 and  AVL ) .It should be learnt , the ECG features (due to  anatomical defects in AV conduction system  ) can be be  easily modified by the hemodynamic stress of  ventricles  due to associated conditions and classical pattern may non exist )
  3. Surprisingly high grade AV blocks are rare (“viz a viz” LTGV )


Short HV interval is documented  in AV canal defects inspite of prolonged PR due to small his bundle length.

membranous ventricular septum 2

conduction system in av canal defect vsd

A large Inlet VSD , simply takes over the place meant for the conducting system and its pushed down and out


Robert Feldt from Mayo clinic did excellent work about this issue and published in Circulation, Volume XLII, September 1970

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Oh , it’s a well recannalised IRA  and its flowing TIMI 3  as well.  Now, what shall we do sir” ?, An apparently worried senior resident queried after a second look at the images from a 8 hour old STMEI .Why you sound unhappy  man ?  As if recanalisation is an untoward event” ! I teased my resident !
and went on to ask . . .

What we mean by recannalised  IRA ? (Recan-IRA)

  • It is akin to natural or pharmacological angioplasty (or combination of the two )
  • It can be complete or incomplete from the IRA perspective.
  • It can either result in partial or fully salvaged myocardium.
  • It should be understood even a 30% recanlisation can result in TIMI 3 flow and result in near complete salvage
  • Even a 90% recannalisation may not accrue the same benefit if it has happened late. So its all in timing
  • Spontaneous recannalisation can some times even be  superior  to thrombus aspiration . However , some degree of residual thrombus would be present in most
  • Residual plaque burden is also an important factor that will decide the extent of angiographic recannalisation.
  • Some times the recannalisation  will make the vessel near normal with only luminal  irregularity
  • IVUS/OCT may provide accurate assessment of Recan-IRA , it’s is not logistically acceptable in STEMI setting.
  • After listening to my briefing on recannalised IRA , the fellow looked more confused than before. He bothered to ask again , what am I supposed to do once a well recannlised IRA is detected ?  Should I intervene or not ?

The term recanlised IRA generally convey a hemodynamic  meaning for a successful  early (natural plus or minus pharmacological ) reperfusion .If every parameter is fine , and the lesion is not significantly obstructing better to pause any further procedure ,  as consequences of deploying  stent in a well recannalised segment is not yet clear with a stro ng trend towards harm .The decision is to be taken on individual basis with reference to  symptoms, stability ,  residual ischemia and quantum of incomplete salvage and lesion morphology .

If you believe ,a spontaneously recannalised  IRA has provided a TIMI 3 flow , it is equivalent to well done job of natural thrombus aspiration by  a hidden hand and catheter . Consciously respect that .Most cardiologists would have  realised atleaset once ,  that any aggression on a God handled IRA can be counterproductive !

Is there a non academic angle to this issue ?

Undoubtedly yes , strangely  inspite of a positive phenomenon for the patient , recannalised IRA leads to a difficult debate  in cath lab .Suddenly , the  entire collective scientific wisdom of the cardiologist is put into a stress test. There is direct fight between reality , expectations .True patient benefits , obligations to hospitals , the parasitic  relations with device industry , do have a big say !

Final message

Practicing cardiology is simple , but when scientific and non scientific realities of life are in direct confrontation with patient welfare it becomes a huge struggle and only a determined few can win over this infinite fight against conscience !

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Dengue is a global infectious disease caused by Flavivirus  (RNA) transmitted by day biting mosquitoes Ades aegypti .It is primarily a tropical or sub tropical disease , India is marked  among the epicentre . 75% of dengue infections  are asymptomatic. Among  the remaining 25 % only 5 % develop severe dengue and a fraction of them go for a dreaded  circulatory and bleeding complication leading to a likely fatality.Severe hypotension is the hall-mark in dengue shock .

The mechanism of shock

The sine-qua non of dengue shock is the  capillary leak syndrome .This is due to some unknown vascular toxins acting in micro circulatory network making it exude fluid .This is something similar to septic shock where mal-distriubution of fluids in the extravascular  or third  spaces occur . This is also referred to as  re-distributive or vasodilatory shock due to lack of effective circulatory volume. Significant serous cavity effusions  (Both pleural effusion and ascites )  contribute to the shock syndrome .  Meanwhile there can be accompanying  fluid loss due to vomiting as well  .Adding further complexity ,direct cardiac involvement in few in the form of myocarditis can cause lung congestion and confusing the true mechanism of shock .This has important  hemodynamic implication as overzealous fluid therapy without recognising a possible myocarditis can be counter productive.Few sick patients will drag the lung into the vicious cycle ending up with ARDS , refractory hypoxia and worsening shock.

*To reemphasize , even though there are  multiple components  for dengue shock , the capillary leak  is the dominant theme .

Timing of shock

The onset of shock peaks after 24-48 hours of fever .It may  even be delayed well after subsidence of fever (Deffervescence phase )

Differential effect on diastolic and systole pressure

Dengue primarily drops the systolic  pressure  due to hypovolemia .The diastolic BP may be kept artificially high due the heightened adrenergic tone .This is ironical , as even the fluid  is sequestrated into dead  space patient may appear stable but it can fall dramatically without any warning once the sympathetic reserve is exhausted .This is the hallmark of dengue circulatory  shock .

*Note : Dengue shock typically  narrows the pulse pressure, that’s responsible for the feeble thready pulse.This is in contrast to septic shock* where the PVR is low, pulse pressure is either normal or even apparently high.(* Not all situations)

Clue from hematocit regarding the status of shock

Initially the heamtocrit  tends to increase  (hemo-concentration )  as fluid extravasates . Later it strikes a balance as we attempt to replenish with fluids. During recovery as fluids reenter vascular compartment or due to sustained fluid therapy the hemo-dilution can occur and heamtocrit  may fall.

How  common is  myocarditis  in  dengue fever ?

Fortunately ,dengue fever rarely affects the heart directly  .(Of course, shock can be a killer even without involving the heart) Myocardits due to dengue virus  is randomly reported in literature (Ref 3,4). My guess is , the true incidence should be far  higher as most of the dengue cases are from countries where publications are rare ! Bed side echo will reveal a minimally dilated Left ventricle with global hypokinesia  and moderate to severe LV dysfunction. No need to prove myocarditis  by virology ,biopsy etc. ( (New onset LV dysfunction with S3 , tachycardia is suffice) .Treatment is only supportive and Inotropic  agents may be helpful. Recovery in LV function is usually complete in those who survive.

Acute pulmonary edema though expected with LV dysfunction , overzealous fluid therapy can be a trigger for this complication . Involvement  of  conduction system is  another evidence for myocardial pathology. AV block  (J Clin Diagn Res. 2015 May; 9(5)  and Atrial fibrillation have been described in association with dengue.


  • Anticipation and prevention of onset of  shock syndrome is  the key .
  • Careful monitoring of child is required.
  • Altered mentation is vital clue
  • Continuous fluid resuscitation is the only proven treatment .
  • Platelet infusion is required in clinical bleeding generally <10000)

Steroids, Immuno-suppression ,globulin have limited or no value  even in fulminant dengue fever .

Post-ample : Role of cardiologist in dengue shock .

Once , recently  I was called to see a child  with  refractory dengue shock .It turned out to be a helpless consult for the parents who had great faith in me .They believed  as a  modern day cardiologist ( circulatory specialist ?) with sophisticated devices I will be able revive the vascular system .I regretted ,there is nothing specific can be done ,the entire circulatory system is leaking and had lost its tone ,we have to wait ,watch and pray .

I realised on that day , how these tiny mosquitoes can expose us  . . . the  much hyped cardio vascular specialist’s  skills who live a celebrity life,hopping between cath labs , still unable to deliver at a critical time of need !

Reference :

1.Capillary leak syndrome in dengue fever.New Delhi: WHO Regional Office for South-East Asia and Manila: WHO Regional Office for the Western Pacific.Dec-2011


dengue myocarditis

3.Kabra SK, Juneja R, Madhulika, Myocardiald ysfunction in children with dengue haemorrhagic fever.Natl Med J India.1998Mar-Apr; 11(2): 59-61
4.Wali JP, Biswas A, Chandra S,  Cardiac involvement in Dengue Haemorrhagic Fever.Int J Cardiol.1998 Mar 13; 64(1): 31-6.

5.Horta Veloso H, Ferreira Júnior JA, . Acute atrial fibrillation during dengue hemorrhagic fever.Braz J Infect Dis.2003 Dec; 7(6): 418-22

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