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Archive for November, 2009

Heart rate and human survival has an inverse relationship. This is in fact true for  all mammals.The tortoise which has a heart rate of  6/mt lives for over 200 years. The rat which has heart rate of 500 dies does not even  celebrate it’s first birth day ! Human beings with an average heart rate of 70 lives for 70 years. 

There is a belief  human heart is programmed to beat for certain trilion beats in it’s life time .It is possible ,  with evidence mounting this belief  could  indeed be true .

People with low heart rate simply outlive the ones with  fast heart rate ! Is this due to simple fact they conserve their heart rate .Each human has a reserve of few trillion heart beats for usage in his or her life time .So if this is true what does regular vigorous  exercise do to our longevity ! These are pure fantasy questions that need to be answered !

The truth may be regular excercise even though raises the heart rate to high levels it keeps our vagal tone high and maintain the basl heart rate low and there by conserving both heart rate and myocardial oxygen consumption.The other evidence for heart rate being vital in prolonging life is the proven benefits of beta blockers in patients with decompensated  heart.

Read the excellent issue dedicated to the  importance of heart rate for human survival especially in relation to cardiovascular disease .

From the  publishers of dialogues in cardiology .This knowledge sharing comes free of cost

Courtesy of  Servier

http://www.dialogues-cvm.org/pdf/19/DCVM19_05.pdf

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Atherosclerosis   remains the number one cause for all vascular disease of human beings. It probably  kills more  patients than all other causes put together .

Modern medicine has never conquered the disease. How  the vascular system ages and why some develop premature atherosclerosis remains largely speculative. While it is true , we have identified some major risk factor for development and progression of the atherosclerosis  , patients with out any of those risk factors do develop severe atherosclerosis !So researchers sought to look for some other risk factors . There lies the difficulty  and irony .

We always tend to the research with the affected population .When we know millions of people with the so called risk factors live comfortably , there lies an opportunity  to  analyse why they are protected against the onslaught of atherosclerosis .It is always convenient to blame it or bless it on the genetic predisposition .But we need to look beyond that .Of course  . every genetic expression has to  manifest phenotypically .

While the search for all those hidden secrets has to continue , we should also realize in pursuit of breakthrough we some times waste our energy in false targets  for too many decades !

The reality as on today is ,  there is no reliable  &  undisputed drug available to arrest atherosclerosis  (Some would love to call statin so . . . )

While  our basic science colleagues struggle  in molecular  factories and biological models in pursuit of answer against  atherosclerosis , our elite  cardiac physicians   carry on with the cosmetic touches over this   progressive disease  in  sophisticated cath labs.

Let us hope  man prevails over nature . . .

A cartoon , Just for laughs . . .

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Diabetes is the scourge of mankind .( Womankind too ! In fact it affect women more than men !) When we say DM  & Cardiovascular disease we mean the type 2 maturity onset DM  .Even a lay person  can  recognise  the strong  link between DM and increased cardiovascular mortality .

While logic would make the same lay person believe , that  proper  control of diabetes will eliminate  CVD risk that was acquired . Alas . . . how foolish science can be

The problem in medicine is 1 + 2 is  3  only if it’s counted antegradely   , 2 + 1 is rarely three !

Unfortunately even many of the medical professionals  do not realise this fact and keep the  logic  above reality and continue to believe in what they believe .

When we find,   a  disease process that tend to  continue even after the  offender ( Here incresed blood sugar ) is removed  then there is questionable relationship between the offender and the victim .

This is what we have learnt in over 50 years of diabetic research . Now we have so much controversy and confusion.The savior of diabetes insulin itself may be the offender (ACCORD Trial ) Or is it insulin like growth factor , or circulating peptides ( named and unnamed )

So the debate and research  goes in an unknown  and uncharted direction  . . . The drug companies periodically need some studies to bond the link between DM and CVD to keep the per capita consumption of antidiabetic drugs .

And the only fact remains  true is a good life style with physical activity  with peaceful pursuit of life  will keep the diabetes at bay . . .

So till that time we reach the reality ,  there is no other option  but to experience articles which add on to the  confusion rather than clarity .Read the latest metanalysis  about the link between DM & CVD  . . . and  I can assure you the confusion is  guaranteed

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)60697-8/abstract#

Expect soon another trial , that contradicts the above trials conclusion  .

Title talk

So now  you can answer  the title question : Why we struggle to prove the beneficial effect of strict diabetic control on cardiovascular events ?

We struggle because  , the beneficial effect is so little or  even may be non existent !

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Looks very much a infarct of  infero posterior territory is it not ?

Have a look at her 2D echo still picture . . .

Are you convinced ?

This women had normal LV systolic and diastolic function with no evidence of constriction.

The explanation for the asymptomatic pericardial thickening is due to a healed  chronic pericarditis .This sort of localised thickening in the posterior aspect is all the more likely following a loculated pericardial effusion.Tuberculosis is a very likely etiology.But this women do not have any markers for tuberculosis.Since she is symptomatic no treatment was offered.She is being followed up.

Discussion .

Q waves are not ” sacred waves” to diagnose myocardial infarction.It simply indicates the  direction of current flow is away from the  recording lead of the ECG .Any thing  electrically inert , that come in the interface between the heart and the recording electrode   can record a q waveWhat are the pathological entities that can produce q waves other than infarct ?

  • Fibrotic myocardium(DCM-Cardiomyopathy)
  • Myocardial Scars
  • Myocyte dis array(LVH, HCM)
  • Air,fluid in pericardium /pleural space
  • Pericardial thickening (As in this patient)
  • Electrical shortcircuits (WPW syndrome)
  • Rarely pure ischemia without necrosis can produce q waves (Electrically stuned myocardium)

Final message

Localised pericardial thickening is  a rare  (?unrecognised) cause for pathological q waves , that may mimic a MI.

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Ventricular tachycardia is the most common wide qrs tachycardia.It is generally taught VT is a  regular wide qrs tachycardia.It indeed appears regular most of the time but in reality it is not.

There are few  situations it shows irregularity . Of course , this irregularity may be due to the associated phenomenon ,  even as the VT focus  fire regularly. But for a physician what is manifested in the given ECG matters.

Frequent capture beats and fusion beats.

We know   AV dissociation is sine qua non of VT. Not withstanding this fact , the sinus impulses always try to enter into the ventricle and looking for the door at AV node to open.Even a fraction of a second is enough for the sinus impulse to sneak through it , the only question is the timing .It should be noted that an  intact VA conduction precludes antegrade AV conduction and fusion and capture beats are rare. So whenever the VA conduction lags behind or sluggish , more capture  beats occur.This obviously make  a VT irregular. This sort of irregular VT can occur in up to 20% .So it is indeed wrong to assume that the  presence of  irregularity one should make a diagnosis of VT.

VT induction phase cycle length fluctuations.

The other reason for VT may be irregular  during the early minutes after the onset of VT. Here the electrical circuit fluctuates till it attains a steady state.

The  VT often takes off  with a turbulent course (Bumpy myocardial boulders due to electrical reactionaries and mechanical scars ) Then the circuit optimises .This happens more so in post MI scar induced VT where the tract can be long and circuitous with considerable delay in conduction. But, once the VT reaches the cruising speed it becomes fairly regular. In ischemia mediated micro reentry or automatic focal VT cycle length variations are less common and they maintain the classic property of the VT namely the regularity.

Drugged VT: The Amiodarone effect.

The effect of class 1 a or 3 drugs on VT is a complex one.Either they revert to SR or it may reduce the VT rate, widen the qrs complex, and make it little irregular.This is especailly common after the cumulative amiodarone effect.

Polymorphic VT

The VT that has polymorphism obviously will be irregular.Torsades is the typical example.

Multifocal ventricular tachycardia(MVT)

Every one is aware of multi focal atrial tachycardia.It is surprising the MVT as an entity is rarely described in literature.Are the ventricles protected against such arrhythmia ? When multifocal VPDs occur very often why it is not transforming into MVT ? It is  possible , once a VT is  initiated it suppresses the other focus like a overdrive pacer  and extinguishes all surrounding electrical activity. But as in parasytolic tachycardia MVT can occur occasionally when  each focus is protected against the other by an entry block.

A VT may switch over from one focus to other.During the time of transition or competition between the two focus if you happen to record a ECG it can be really irregular  and chaotic !

Final message

VT is a regular wide qrs tachycardia  in majority.But this rule is applied only in monomorphic unifocal VTs. Even in monomorphic VTs there are  occasions it may show irregularity due the associated phenomenon.A grossly irregular wide qrs tachycardia always indicate a antidromic AF with accessory pathway.

* Title talks : With due respect to the  experts  ,there is no reason for getting confused .For the  practical working formula VT can be considered as regular tachycardia.

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Fetal echocardiography is an important imaging modality for screening fetuses with congenital heart disease.Not all cardiologists are familiar with this imaging . Obstetricians are also not well versed in these techniques.So, finally,  it is left to few specialised radiologists to do this job. The issue here is  they are less  in number and the need for the experise is huge.  Further , the fetal cardiac hemodynamics and anatomy  are too complex to comprehend for a non cardiologist . So it is argued every clinical cardiologist to get trained in the basics of fetal echocardiography.

There are dedicated institutes and people who do this mode of imaging.

One such place is http://www.fetal.com

See for yourself the excellent information and knowledge resource in this site.

http://www.fetal.com/FetalEcho/04%20Standard.html

Other .popular books on fetal echocardiography

Julia A Drose

Simcha yagal

Juri W. Wladimiroff, G. Pilu

Lindsey Allan

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Coronary artery disease is the major determinant of human  health and longevity  in this  modern era! Obstruction of a coronary artery either sudden or gradual  forms the basis of  CAD .

When a free flowing  river stumbles upon an  obstruction , it does not die , it finds it’s way to the sea. Similarly , God is kind enough to provide  alternate channels for blood flow to heart at times of crisis .Contrary to the perception , collaterals develop not only in chronic occlusions but also in acute occlusions.

A person who dies due to a primary VF few minutes after an acute occlusion is in all probability experiences his fate  ! While those who survive are protected by the immediate recruitment of collaterals and this prevents the   remote myocardium  from triggering a VF.

In chronic CAD, the collaterals are much more effective. Now we have evidence with OAT and COURAGE *trials for this. Some times , the LAD is fully supported by the RCA the flow is better than a graft.

*These trials showed us opening occluded coronary arteries routinely do not confer additional benefits.

Coronary collateral circulation is most poorly understood phenomenon in cardiology. But it comes as helping hand whenever required  only for those humans who deserve it !  God has kept the secrets of coronary  collateral circulation with himself !

A excellent article on natural by pass from circulation patient pages.

http://circ.ahajournals.org/cgi/content/full/116/11/e340

Link to related you tube video

http://www.youtube.com/watch?v=qQfUttiDgE8


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