Archive for March, 2011

Atherosclerosis  probably ranks first among all  human diseases that cause maximum suffering  to  mankind.Since it is a disorder of blood vessel  it has an easy  access to every  vital organ  in our body to inflict the damages . Histo pathologically , atherosclerosis is an all in one disorder where inflammatory , degenerative and lipid injury  collectively  contribute to the disease progression. Diabetes and hypertension play a vital amplification role.

Atherosclerosis begins very early in life as fatty streaks in every individual and takes different avatars ( or remain indolent)   depending upon the risk factors and life style.

How to estimate plaque burden ?

It has  always been a difficult task to estimate the  atherosclerotic  plaque burden inside the  coronary  arteries.The fundamental flaw for many years is ,  we always thought  if there is a plaque it must  encroach  into the lumen.

Coronary angiogram  , has become the  default investigation  in clinical cardiology . Since it   can  visualize  only the coronary lumen ,  this  flaw  got further  curious  with skewed  interpretation as well.

When things were as it is . . .  Glagov suggested , what  could  possibly be   the  most important  concept in the interpretation of coronary  angiogram .

The concept  suggested  the  atherosclerotic  process  could  actually spread  within the  vessel wall  in a predictable manner .

What determines a plaque to either grow into the lumen or grow away from the lumen?

If we could decode the mechanism of direction of plaque growth we will probably conquer the atherosclerosis  at least by mechanical means . The implications are too many.

A stented coronary artery may be re-engineered to grow the atherosclerosis  towards  the adventia .This could grossly reduce  the incidence of restenosis.

Further , in post Glagov days we realised  mechanical factors like plaque stiffness, eccentricity , plaque mass effect, drifting , lipid core density, medial lysis , elasticity of elastic lamina all could determine the   plaque  movement.

Why compensatory lumen enlargement does not occur in some lesions ?

We do not know the exact reasons . We may call it a fate . . . shall we ?

Curious blessing  : Atherosclerosis  for  some unknown  reason  blesses a  few with coronary artery  dilatation rather than narrowing .

This is called coronary  ectasia . Medial necrosis , weakness of internal elastic lamina or  destruction paves way for plaque shift towards the adventia . It is estimated , if the medial necrosis occurs in at least  50 %  of  circumference of vessel wall   it will  result in ectasia .And  paradoxically if  the media  shows resistance   the plaque grows into the vessel wall.

Endoleak  and Glagovian phenomenon.

Endo leak is the Achilles heel of   endovascular intervention . In fact , many would  consider  it as  a dignified terminology  for graft failure . Endo Leak   occurs when  the artery outgrows the stent  graft and bllood starts  collecting  in the graft vessel -wall interface . When the  scaffold is  placed  within the lumen ,  one may wonder how it is going to prevent  the  artery  dilatation . (Which is basic defect in any aneurysm}In fact , the aneurysm does continue to grow  along with   centrifugal  atherosclerotic  forces ,  possibly by  Glagovian phenomenon .

This makes it obvious  endo- leak is a distinct threat in every vascular  intervention.

Final  message

Most cardiologists  think their ultimate  job  in this world is to  deploy  a stent deep inside a LAD  or RCA.  While a few others indulge in more exotic  adventure of  crushing a plaque ,  trap the debris and  catch it with a  with  a basket .

There  are bigger and bigger   blind areas  in the vessel wall ,  infiltrated with  deadly atherosclerosis which is conveniently ignored  .If only we realize   this fact  , we  can move forward in our war against coronary atherosclerosis.

Of course the good old   medical  interventions  . . .  exactly try  to address  these issues . Let us  think  straight , and  not succumb to glamor  in cardiology !


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Coronary artery stenting  , many consider  as the 2nd revolution in cardiology after   the invention of  cardiac catheterisation .  Millions of angioplasties  take  place  world wide every year .  Suddenly it would appear that medical therapy  was forcibly  thrown  out into the  bin .This in spite of  the fact there is no  major difference in ultimate CAD outcome in the long term between PCI and medical  therapy in chronic CAD.

The COURAGE trial which gave a renewed lease of life to medical therapy , was  severely criticized by the interventionists. 5 years after the COURAGE  the inappropriate stent usage continues unabated.

The term inappropriate usage ,  some how undermines the seriousness of the issue.  Few realise  the fact , inappropriate usage  actually amounts to  mal-practice or  an act of  medical  negligence (Guideline  violation)   which deserve  a strong  condemnation .

The general media is just been exposed to the tip of the Iceberg  (Not even the tip !) At least in USA and other developed countries  they  have systematic data  about  the usage of stents. In a country like India  . . .less said is better. There are many  like  Dr Mark  Midei  camouflaged  in every country.

More pro active Media is required like the ones below.

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Human atria is a rough terrain infested with peaks and  troughs like the  Himalayan range . The two atria together has a minimum of ten entry or exit points . Cardiac arrhythmias are   something similar to the  uneven  earth plates  triggering an  earth quake.  Like the earth surface there are  areas in the atria  with high seismic activity !

It is now discovered there are nine vulnerable points in human atria that can initiate focal electrical activity at times of hemodynamic/ischemic/metabolic stress .

The common causes for Focal /Ectopic atrial tachycardia are

  • Hypoxic AT -COPD ( Probably the most common cause .If persistent it will degenerate to MAT- AF )
  • Structural atrial disease
  • Hypertensive heart
  • CAD
  • Valvular heart disease
  • Drug induced

Note ,  all these  vulnerable points are located either in the  junction of  an anastomosis  with a venous structure or valve or septum.

Further, these sites are often the  embryological fusion points making it still more vulnerable due to tissue defects.

Why free wall of atrium  is  a less common  focus ?

They are relatively smooth, lack ridges and joints. Unless the walls of atria are diseased  focal tachycardias are less common from these sites .

Other forms of Focal atrial tachycardias

Indian perspective  and Rheumatic atrial tachycardia.

In developing  countries  focal atrial tachycardia in rheumatic heart  differ very much from the tachycardia described above. In fact many of the rheumatic atria present straight away  to atrial flutter or fibrillation.

Pulmonary vein focus should rarely be considered in atrial tachycardia that occur in RHD.

Post operative tachycardias

Surgical scars can result in what  is called  Incisional tachycardia.(Especially after complex atrial  surgeries like Sennings, Glean/TCPC  etc )

Multi focal atrial tachycardia .

This is nothing but a focal tachycardia which tend to fire from different angles towards different targets  often lead to a chaotic atrial rhythm .  Digoxin and DC shock paradoxically aggravate this arrhytmia.

Atrial epicardium/pericardium interface as a focus

When pericarditis is the predisposing  event  then it can emanate from anywhere from  epicardial surface .

Since left atrium is only  partially covered by pericardium it is not logical to assume pericarditis related AT arise from RA epicardium.

Atrial tachycardias in congenital heart disease.

Complex atrial anomalies, SVC type ASDs, PAPVCs can  give raise to abnormal  electrical focus


An excellent original work from  Royal Melbourne Hospital, Melbourne  Australia.

A must read  . . . http://content.onlinejacc.org/cgi/reprint/48/5/1010.pdf


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Is there a ECG marker for recent syncope ?

Yes . This was classically described many  decades ago. Following a Stokes -Adam attack  when the patient recovers from the loss of consciousness a peculiar ECG pattern was observed.

A typical ECG from our CCU

The mechanism is not clear.It can be due to

1. Repolarisation abnormalities due to ischemia.

2.Acute adenergic surge triggered  due to  transient   cessation of circulation* .

3.CNS  injury  and extreme  vagal with drawl


* Thought to be the major mechanism

Out come

The ECG is more dramatic .The physician is usually more tense than the patient !

It  is often  benign .Prompt pace maker implantation is required.


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Aortic stenosis is the commonest valvular heart disease  in elderly. Severe aortic stenosis  requires early  aortic valve replacement . Severity of aortic stenosis is  best assessed by   echocardiogram. ( Cath studies are rarely indicated  now) Mean Doppler gradient across  the aortic valve (dPm) is the widely used  parameter to assess severity.Americans believe  in  a cut off value of  40mmhg  while  Europeans  want it  to be at  50 mmhg . Obviously, these  numbers 40/50   become  vital  as it determines the  critical decision of replacing the  aortic valve which carries up to 4-10 % mortality.

Even as we realize ,   Doppler gradients are so important , we also need to  know ,  how fragile  ( and  vulnerable  ! )  are the Doppler equations ,  especially when it is critically dependent on the angle , flow,  heart rate  , the LV  contractile  force  and associated MR etc. These errors are over and above the  the  technical simplification of Bernoulli equation  which ignores many accessories like viscous  friction ,  proximal velocity etc  .Mind you  . . .with this battered Doppler modality we make a critical operative decision !

Here comes  the ace . . . Shall we  term it as  as negligence  in clinical echocardiography ?

Apart from  the above factors  ,  a single  important  critical determinant of  pressure gradient across AV is the mean pressure in the Aorta itself .  The mean  LVOT gradient = LV cavity pressure -Systemic blood pressure.Echo derived gradient tells us only the pressure difference across the valve.It does not reveal how much is contributed by raise in LV cavity pressure and how much is contributed by the change in systemic pressure.

How many  cardiologists would  measure the simultaneous  blood pressure while recording LVOT  gradient in AS ?  ( To be precise it should be measured in the same cycle  )

If  Aortic mean pressure is high  as in systemic hypertension  LV pressure must raise considerably higher . The contractile capacity of LV is tested here. A hypertrophied LV  easily achieves this.  If the LV fails to elevate it’s intra -cavitory   pressure sufficiently high the LVOT gradient may never reach  the 40 /50 mmhg range  that is required to label  aortic stenosis as  severe.

Many hypertensive patients exactly experience  this situation . The left ventricle of  many  of the hypertensive patients  fail this stress test  and result in low gradient AS.  Note , this happens in spite of   having  normal EF.

The link between systemic hypertension and aortic stenosis is a complex one. The after load becomes double here.There is a strong vascular valvular interaction. The following effects  are seen.

The effect of SHT on AS

It is well known HT  initiates the Aortic stenotic  process by damaging the valve and  also  result in progression.

Transient elevation of systolic pressure  can result in increase aortic orifice , and a fall in gradient.

The effect of  AS on SHT

Once the AS becomes severe , the systolic blood pressure may be reduced. (This not a rule ) If the mechanism of HT is increased  vascular  tone (Which often is the case ) systolic BP will remain high .

Effect of AVR

Surprisingly ,  many times the blood pressure normalises after AVR.The mechanism is not known.

Role of Anti HT drugs.

Fixed vasodilators are thought to be contraindicated as sudden fall in systolic blood pressure against a fixed obstruction is detrimental.  ACEI may be tried cautiously.(SCOPE AS study )


The following are the excellent article on the topics .All provided free by the  “Heart” Journal




Final message

In the evaluation of  Aortic stenosis   ignorance continue to prevail over our  knowledge. The Gorlin’s  the  Hakki’s, and the Hatle’s formulas  have made the  calculation of aortic valve area  look like a   child’s  game  (Which is not !)

Referring  all patients  with a  mean gradient > 50mmhg to the surgeon for AVR (or now a  TAVI)   may be the  easiest option  for the cardiologists  (but definitely not an intelligent one ). Even  as we struggle to decode the intricacies of isolated  AS  ,  one can guess  the complexity  when SHT adds on to AS .

Understanding the hemo-dynamics in  AS in association with prevailing blood pressure is vital.  It is a more scientific way of doing  echocardiography . Every cardiologist should give their input as they encounter hypertensive patients with AS.

It  would appear  ,  an AS patient developing HT at a  later  age  and a HT patient developing AS later are two different poles in the hemodynamic spectrum.

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