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Mr Seldinger you made the difference . . . to all of us !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged , , , , , on March 26, 2011| Leave a Comment »

Interventional  cardiologists should revere  few  names for ever  . . .

They are

  1. Werner Forssman
  2. Masan Sones
  3. Andreas  Gruentzig
  4. Sven-Ivar   Seldinger

Sweden's Pride and cardiologist's ultimate Hero !

The  other men  in the  above  list  gave us insight  to enter the heart and do cardiac catheterization  and selective  angiograms

Ironically ,   the  man who  provided an easy access* to cardiovascular  system  from the  periphery is less often  remembered.  Still , it is because of him millions of procedure  are done every  year .

Every cardiologist should  read the life history of this great man.

*Previously all interventions are done in laborious  arterial or venous cut down

How the invention came about ?

“It is a  sudden attack of common sense”   That  is how seldinger described in his own words

Why not a Nobel prize for  Seldinger’s  sense which was so  uncommon to others  ?

If common sense has to be rewarded Nobel price ,  Seldinger’s    would probably will rank   first  among  all !

Reference

  1. http://ww.ajronline.org/cgi/reprint/142/1/8
  2. http://www.ajronline.org/cgi/reprint/142/1/8.pdf

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Metabolic Imaging of atheroscerosis

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, cardiology innovation, cardiology journals, Uncategorized, tagged , , , , , on March 23, 2011| Leave a Comment »

Non invasive imaging of inflamed macrophages  within athersclerosis

The medical  imaging science is  reaching new heights. With most of the  research so far within the anatomical arena we are moving into the  physiologic  and metabolic  imaging. Identifying vulnerable  plaques  within the coronary  artery is a separate field. Most of them are catheter based and invasive investigations.

We  have ben  searching for an  ideal PET scan based metabolic imaging of atherosclerosis. Macrophages are the key elements in an inflamed plaque.

Image Source : Circulation. 2008;117:379-387 .Note the Acttive Macrophages in the Aortic arch area and Coronary ostia

Can we take a photograph of these  inflamed zones   within  the  atherosclerotic plaque  ?

  • It seems we are approaching  that possibility. Every time we screen a person for CAD we can risk stratify on the basis of  percentage inflammation of their coronary artery or aorta .
  • This will complement the CT  or conventional angiogram .
  • If this technology is perfected it can be useful in the evaluation of response to medical interventions .
  • It  could also tel us  the  significance of  raised CRP /cytokines in other wise asymptomatic individuals

PET scan with newer tracers are constantly evolving . One such tracer is  based on copper molecule   64cu-TNP.

Reference

http://jnm.snmjournals.org/cgi/reprint/45/11/1898.pdf

 

 

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How can Troponin get elevated in Pericarditis ?

Posted in pericardial disease, Uncategorized, tagged , , , , , , , on March 19, 2011| Leave a Comment »

Heart has three layers

  • Epicardium
  • Myocardium
  • Endocardium

    • Epicardium is same as visceral pericardium . If pericardial inflammation dissusely occurs ,  it is bound to injure  the epicardium and subepicardium .

    Does  the  troponins  located deep inside the  myocardium  ?

No .It  can  even be present just few microns below the visceral pericardium  . Hence  severe forms of pericarditis can elevate the troponin levels without any issues .

Is troponin  release related to ST elevation ?

 Ideally  most forms of  pericarditis can be termed as epicarditis. The mechanism of ST elvation in pericarditis is actually a sign of  epicardial injury.In fact ,  there is no easy way to  differentiate  a  slice of epicardial infarct from an   inflammatory pericarditis accurately .

Is there any form of pericarditis which invlove only parietal pericardium ?

We do not know as yet ,  about  existance of such  an entity. It is distinctly possible. However , if present it is unlikely to result in significant  ST elevation in ECG.

In pericarditis ,  troponin release is due to inflammation  or necrosis  ?

Both are possible .Even transient wall motion defects are reported in isolated pericarditis.

What is myopericarditis ?

It is  a general term used  to indicate the above situation . In practical terms Pericarditis + Troponin positivity can be termed as myopericardits. It is well known pericardits can extend to endo- myocardium but it is rare other way  around( ie endocarditis extending to pericardium )

What is pancarditis ?

It is the carditis  involving all three layers of heart ,Cassically occura in rheumatic fever. Fulminant carditis is known to raise the troponin to significant levels.

Does troponin elevation  in pericarditis  occur in all  ?

We are yet to collect adequate data about this .  Diffuse , extensive pericarditis ,gross ST elevation ,  and associated pericardial effusion  correlate with troponin.

Crazy questions in pericardiology

What is the pericardial blood supply ? Is there  an entity called ischemic pericarditis ?

Final message

Do not ever underestimate the  importance of  pericardium  whenever you encounter unexplained ST elevation in ECG.

Reference

Here is an article which has   meticulously studied this issue

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How to misinterpret pericarditis in coronary care unit ?

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged , , on March 18, 2011| 1 Comment »

For  a police officer who visits a crime site  every one looks like   a culprit. For a cardiologist  sitting in coronary  care unit  all chest pain  will have to look like  an infarct  !  Then only he is a cardiologist !

A rare , but costly mistake occasionally  happens . When a  patient with severe chest pain in the  retro sternal region with ST elevation in ECG , enters the ER  there is little  reason to suspect any condition other than STEMI !

This is how medical  errors takes place

Medicine is an art , we can not take it as granted .Acute MI can present with normal ECG and a dramatic ST elevation need not be MI

Here  was  a patient who presented with this ECG and one our fellows correctly diagnosed the condition .

Most  physicians would have thromolysed this patient or  might have wheeled into cath lab.  We have such events reported from primary  PCI registry .

Key differentiating points

  • Diffuse ST elevation not confining to a arterial territory
  • Absence of reciprocal changes
  • ST  segment with concavity upwards.
  • Echocardiogram and enzymes will be useful

iFAQs  in pericarditis

What is the mechanism of ST elevation  pericarditis ?

It is actually a zone of epicardial or Sub epicardial injury.

What will be the ECG finding if STEMI is associated with fibrinous pericarditis ?

Double dose of ST elevation .Mimics  a re infarction.

What are the dangers of thrombolysing a patient with diffuse pericarditis ?

It can bleed into pericardial  space

What happens

What will be the ECG finding in localised pericarditis ?

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Is the final frontiers in lipid metabolism decoded ? The receptor X in the liver

Posted in Uncategorized, tagged , , , , , , , , on March 18, 2011| Leave a Comment »

LXR are a unique group of nuclear receptor proteins located in liver as well many body tissues where lipid metabolism is active. They are first identified in liver with apparently no ligands ,  they are  hence referred to as  X (Also called orphan receptors ) .Later  these receptors can be termed as a target receptors for cholesterol metabolites like oxysterols .

 

How this nuclear receptors modify  the subsequent events could ultimately determine the toxic effects of cholesterol in human body.

An update in NEJM appeared in 2007

The the science of lipidology  is  confronted by  with  suspicious  ,  false targets .We are  biochemically still pitch blind  beyond a point . . . after cholesterol enters  the cell .

We have been targeting cholesterol synthesis by blocking HMGCOA.

Statins though claimed to be the God sent molecule , genuine researchers would agree statins  have a   huge  limitation  and it  is a  hyped up drug in controlling atherosclerosis. In fact ,  it is  believed  (In private ) nearly 50% of people who take statin  atherosclerosis goes  unabated.

Can we modify how  LDL  cholesterol is going to be utilised inside the cell ?

LXR family of proteins along with  RXR are expected to  break  the  barrier.In knock out mice models  LXR agonists are  able to control  and prevent LDL propagation within vascular cells .

The research is ongoing. Let us believe  the right target  has been identified . Nothing is guaranteed as of now . . . but out journey should continue .

http://en.wikipedia.org/wiki/Liver_X_receptor

http://www.nejm.org/doi/pdf/10.1056/NEJMcibr075951

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The six delicate rims that hold the ASD device together !

Posted in cardiac surgery, cardiology -congenital heart disease, Cardiology -Interventional -PCI, cardiology congenital heart disese, Uncategorized, tagged , , , , , , , , , , , , , on March 14, 2011| 1 Comment »

ASD device closure as a modality is constantly improving  . . . but  the consensus is  , it is  yet to catch up with  of  good old surgical  outcome . The key to success is not only in the device but hugely dependent on the technique and pre-procedure evaluation  .In fact , the pre procedure TEE imaging technique  is as important as the procedure itself.

There are lots of discussion about this particular issue. TEE is mandatory we know  but now we realise it is  still better to have a  Real time 3dimensional  (RT3D ) TEE . Rim  size  and ASD  morphology estimation is  the primary aim.

There are  at least 6 named rims for ASD. For a circular  orifice  it  may not be logical to have a fixed number of  6  rims . Ideally the entire circumference must have a rim .( This happens in  central defects )In many,  the complex anatomy of IAS does not allow this. So we are compelled to fix the number of rims to six.

  1. Aortic (Superoanterior),
  2. Mitral (AV valve/ Inferoaterior)
  3. SVC  (Superoposterior),
  4. IVC  (Inferoposterior),
  5. Posterior ( Atrial free wall ).
  6. Coronary sinus rim

One can realise how important these rims are , as  they are the   foundation tissues on which the device is going to be seated for the rest of the patients life.

When do you call a rim is adequate sized ?

5mm is  considered suffice. But it varies depending upon the device and expertise.

Can we deploy an ASD device  in patients   with deficient rims?

Logically the answer is expected  is   “No” but  , many have liberalized the criteria now , after realizing   one may  not have 5mm rim in all six sites in a given patient. If you follow this criteria strictly   you can’t do more than few devices a year !

What is the resolution power of TEE can it miss a 3mm rim  ?

TEE has a good resolution it should pickup any thing equal to 2mm or more.

Which is most important rim and which is the least important rim ?


What are the potential complications that can arise if ASD device is deployed with a critically low rim ?

Having discussed  that every rim is equally vital  ,  we  need to answer this sort of questions  often .  I am waiting to get the  practical tips for the above issue from  my experienced colleagues .  I shall post it soon .

It is sometimes assumed Aortic rim may not be that important .Here is a   good discussion  for  ASD closure with deficient aortic rim from Saudi Arabia  . http://www.rmsolutions.net/rmfiles/SHA21/028002.pdf

Meanwhile let us learn . . .

How to perform the “all important” pre- procedure TEE ?

The following article which also  includes video clippings will be immensely useful for all those enthusiastic cardiologists.Thanks to JACC  for making this link free .

Three cheers to AMRITA team from India

http://imaging.onlinejacc.org/cgi/content-nw/full/2/10/1238/

A stylish article on the topic

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Carvajal Syndrome : A new form of Intercellular cardiomyopathy with electrical instabilty .

Posted in Uncategorized, tagged , , , , , , , on March 9, 2011| Leave a Comment »

Mystery  surrounding  the Inherited cardiomyopathies are  getting  unraveled . Now ,we have  a unique entity of cardiac muscle disease due to  Desmoplakin mutations which affects the  cardiac intercalated disks.  They are Naxos disease and Carvajal syndrome.

Source : Wikipedia

Heart has a skeleton too

We know skeletal muscles   need  a bone for its attachment   . If  we  think cardiac  muscle can work independently . . . we are mistaken !

Heart is not a simple mass of muscle.It has a fibrous skeleton around which the muscle is spun around. Myocytes  not only  need to stick with one another,  it has to  be packed over the cardiac fibrous skeleton systematically.

The cardiac  gums that do this job need to  be under strict quality control . After all ,  these muscle sticking proteins  need to be serviced constantly  throughout life span of heart. It is  simple to understand ,when there is  breakdown of this process  , protein  to protein disconnection  takes place  . It results in  cardiomyopathy.

Thus many of the  cardiomyopathies are  not  primary  disorder of cardiac  myocytes as such . They can be termed as disorder  of myocyte adhesion to cytoskelton.

These  present as cardio cutaneous syndromes .(Skin share similar adhesion molecules)

Carvajal syndrome

This is due to mutations of plakoglobin  family of protein . Involves desmoplakin ,  a defective desmosomes and disruption in myocyte adhesion  which  promote  abnormal myocardial stretch ,  dilatation  later fibrosis  and progressive cardiac failure. Non compacted LV can be a feature in carvajal syndrome. Recurrent VT/VF demands an early ICD therapy.

Natural history

  • Woolly hair at birth
  • Cutaneous changes at appear at  the age  of one year.
  • Cardiac involvement  occur in adolescence
  • Can overlap with ARVD

How  is Carvajal syndrome   different from Naxos disease.

It has

  • Predominant LV involvement.
  • Fatty infiltration uncommon

Reference

http://www.ncbi.nlm.nih.gov/pubmed/14761782

http://circ.ahajournals.org/cgi/reprint/116/20/e524.pdf

From cell biology to Inter cellular biology

For over a century biologists were concentrating  research inside the  human cells .Now we are more interested in the inter cellular planes. It  remains an ultimate mystery how the zillions of  cells are sticked together in an orderly fashion  without fighting each other with a  perfect anatomical and physiological harmony.

Understanding the molecular  basis of cell adhesion will  help us decode the pathological states   in which  inter cellular  disintegration  is the hall mark !

A review article on the topic.



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If inapproprite stenting is to be prevented . . . most cardiologists may need to be sued and banned !

Posted in Uncategorized, tagged , , on March 5, 2011| Leave a Comment »

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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What are the “Nine” vulnerable points in the atria for focal atrial tachycardias ?

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology-Arrhythmias, tagged , , , , on March 4, 2011| Leave a Comment »

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

Reference

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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Post syncope Giant T wave inversion

Posted in cardiology -ECG, Uncategorized, tagged , , , on March 3, 2011| Leave a Comment »

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

4.Hypokalemia

* 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.

Reference

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