Archive for December, 2009

This is a real life experience of  a patient who underwent a electrophysiology study and   ablation   procedure for atrial fibrillation  .The blog describes  how the procedure became a nightmare .Written in a  most  readable fashion .  Interventional cardiologists need  not get hurt by this  narration  instead  they should  do a  reality check on the dangers  of  the some  of the  complex  procedures !

Adventures in Cardiology

Click over the  image to  read the real  time experience of   Pulmonary vein  ablation

Image courtesy Mayo clinic

The message from the above story  :

  • Atrial fibrillation is  one of the  relatively  benign  cardiac arrhythmia , that  can be treated  with   simple and effective  drugs . Now we have strong evidence to say rate control is equally , if not more effective than the rhythm control  modalities .
  • The RF  ablation  , which aims at rhythm control  is a too complex a procedure with  lots of expertise  technology  .
  • This should be  reserved  as a last resort  in an occasional patient who had exhausted all other  options .
  • Patients should  realise ,  the consent forms they sign  before any new and innovative  procedure is always  incomplete and  he may be the first person to experience  a new complication  hitherto unreported .
  • A cath lab is run by a team ,  you can’t  expect  the chief doctor to be on your  side always.   Many of the procedures  are  done by either experienced or inexperienced  fellows . That’s  only the  way medicine  can be practiced !
  • So beware all patients , many times, modern medicine is nothing but  experiments on live humans  !

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Pessimism, from the Latin pessimus (worst), is a state of mind which negatively colors the perception of life, especially with regard to future events.

Understanding pessimism is not that simple  . Some people argue  optimism   represents a strong mind while  a pessimism  is the domain of the weak . But it is not necessarily true.  Both pessimist and optimist are unreal , and playing the dangerous game of predicting the future. So realism is the answer .

In this era of information highways , commercial exploitation of science ,  our thought process is grossly determined by our perception of events.We hardly have an intention or time to analyse our thought process.

  • An optimist  ( Rather , unregulated optimist ! ) is a person who welcomes  any growth good or bad.*
  • A pessimist  is  a  person who welcomes only good growth.*

So how to identify good growth ? That is the million dollar question!

  • Many of the  optimists may not  bother about the final outcome of a treatment *
  • A pessimist bothers only about that .
  • An optimist  rarely asks questions, blindly accepts every thing !
  • A pessimist never believes any thing !

Actually the fundamental principle of scientific medicine lies in proving the null hypothesis null and void.Any treatment is useless until proved other wise .  So pessimist can be argued to follow true science , while  many of  the hardcore  optimists are blind believers ..

*It may be  a harsh   way of  interpreting an optimist  but  uncontrolled optimism  has played havoc in our  patients like many of the failed treatments (Some of them released prematurely into patient domain   has  killed many lives  . Power of positive thinking should be within the  realms of scientific feasibility !

So in  our  journey   to  conquer human health ,   we   may  proceed with  an optimistic mind and  a pessimistic eyes !

This understanding is all the more important in this era of contaminated science .It is a well known fact ,  now last 50 years of  planet earth has inflicted the maximum damage  to ourselves  than our ancestors did in 5000 years. That’s why we are compelled to meet at Copenhagen .(We never learn from our mistakes, that’s a different story !) .

There is definite and urgent  need for world summit  on  cleansing the medical science from  the clutches  of commerce  and ignorance . A medical green house effect, with dangerous holes in health care  is imposing on us (Another pessimistic thought . . . of course in the interest of human kind !)

World health organization ,  a sleeping giant has to be awakened on this issue

Final message:

Mankind has evolved over many millenniums ,  probably with a sole  purpose of living ,  that is reproduction and propagation of our genre without harming the environment and other species.

Unrestricted  and unregulated growth of any kind is dangerous we call it as malignancy in pathology .In science , we tend to call it a” great future ”

Our  sixth sense*  has  outgrown  miserably  out of  reality  , as have we decided to take on the nature and GOD .Now , many developing country men do not believe in death .They are fighting a losing battle against the God. And they suffer with escalating health costs of keeping the elderly ,  alive who are  knocking at the doors of heaven or hell . The same countries,  which deny funds for curable illnesses of the poor is a different story altogether !

The principle of modern medicine  would ideally  be

  • Reduce human suffering irrespective of economic status
  • Curing a illness if there is a cure
  • Prolonging life if there is useful purpose
  • Allow a good quality death if there is no cure.
  • Most importantly  , prey to god give us strength and capacity to identify which is good and which is bad for our patients  .

Read and learn for a  complete guide on optimism and pessimism

* It  is  important to recognise , the same sixth sense  has   made it possible to share our views through a great tool of  Internet  . So we should not be against the growth of science but against the misuses and wrong interpretations of it .



The traditional characters  of  a pessimist


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Here is  the link  to  one of  the best illustration for cardiac action potential  which I  have stumbled upon !

Spend some time on the following illustration  depicting  the  normal  cardiac  action potential that  explain the ionic movements . Understand why a cardiac muscle has two refractory periods , why there is a sustained dome for  myocardial action potential  and this is missing in SA and AV nodal potential ?

Click below to reach the online book

Textbook in  Medical Physiology And Pathophysiology

Essentials and clinical problems Copenhagen Medical Publisher

Note :

Red curve indicates electrical action potential .Blue depicts the mechanical contraction . Both red and blue curves together form the electromechanical systole. Realise  ,   QT interval  represents electro mechanical systole . It  includes both cardiac depolarisation and repolarisation .

There is a inherent tendency for our brains  to equate depolarisation with systole and repolarisation with diastole .It is totally a wrong perception. Please , be aware of this !

Identify the gap between the  red and blue curves that represent 50%  of ARP  .This is the time the myocytes can not be stimulated whatever be the  power of stimuli because the Na  channels are closed .

Understand ,the above action potential  represents only half of the cardiac cycle as diastole is not fully illustrated here .Recognise  the fact ,  diastole begins at the end of phase 3  and  goes into phase 4 as diastolic depolarisation  by a slow Na current.

After learning   the basics of action potential   read about the antiarrhythmic drugs . You will get to understand it better .

Learn  which drug acts on which receptors or channels and what does it do  to the various intervals  .For example ,  any drug that is prolonging an action potential  duration is fraught with risk of  ventricular arrhythmia as it is synonymous with prolonging QT interval (Eg Class 1 A /1B/Class 3) .

Sicilian gambit is the receptor & channel based classification for anti arrhythmic drugs . (Sicilian gambit 2 )

  • Understand the paradox of  QT interval getting shortens with Class 1 B (ligocaine /Mexilitine ) while 1 A  does the opposite !

Class 1   Drugs blocks sodium channels .The blockage  occurs in  a complex rate dependent fashion . It blunts the slope  the phase 0 and hence prolongs the action potential .

Class 2 . Beta blockers

Class 3 . Blocks K + Channels and hence prolongs the AP

Class 4  .Calcium blockers

Finally  don’t forget to say thanks to Copenhagen medical  publishers  for this excellent illustration .

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Modern era of cardiology aims to treat ACS  as and when it develops .That is , as soon as the vulnerable plaque ruptures or a thrombus  blocks the victim’s coronary artery.

But this can be achieved only if the patient reacts to this event.We know 20% of ACS can be totally silent. Some produce very vague symptoms especially in elderly and diabetics. ECG and enzyme changes may help us in patients who do not have clear symptoms.There are variety of markers available for STEMI & UNSTEMI.(CPK-MB, Troponin T , myoglobin etc) Now we are working at finding a marker for ischemia without necrosis. Ischemia modified albumin is one such molecule that is showing promise.

The ER department world over have vigorous screening protocols to diagnose ACS  for  the patients with chest pain. There are thousands of triaging protocol in the  emergency management of chest pain.In spite of  the highest awareness and availability of  scientific expertise , knowledge base the error rate of diagnosing  ACS  stands at an astonishing 58%.  This may seem odd , but this is what  this land mark article in NEJM tell us  (Data from Boston , Milwaukee etc).

Out of 10500 patients with suspected ACS. Only 17 % had real ACS.  55% were admitted initially as ACS  later turned out to be non cardiac .This may seem  acceptable for many  even if it is  an act of unnecessary admission and investigation. It gives us , a sense of satisfaction for not missing a diagnosis of ACS. But it has it’s own risk of complication arising out of unnecessary investigations.It is a chain reaction of  suspicion that  may end up in a coronary angiogram in many ! .It is also a well recognised fact these patients    spend  atleast an average of  2 days  to get rid of the ACS tag over their  necks .

Experience has taught us  simple presence of a human being as a patient within an  ICU ( however short the stay  may be ) can be a health hazard and risk .  This  55 % error ,  which does exactly  this to  our  patients with chest pain  who reach the ER  never bothers us  This is because  we feel credited both academically as well as financially .

In the same study 2.3 %  (About 25 patients) with true ACS  were sent home  after a missed  diagnosis . Paradoxically  this 2.3%  has worried the medical professionals too much . . . This happens  ,  even as we  do not have proper data on  how many of them had a real adverse event after a missed  ACS.

So the message here is even in best centres both missed and wrong diagnosis are  rampant. while wrong diagnosis (25 fold more here  )  is easily accepted by the medical community .We can justify  this as a screening camp for ACS  ,  akin to arresting  a group of suspected  criminals in a  preventive raid ,  later releasing for want of evidence.

In the morals of  criminal judiciary  , it is often said one can afford to  lose  a real offender from the clutches of law  , but a  innocent should  never be punished in any circumstance .

In medical parlance this  goes something like this  . . . Thousand patients shall die because of his or her illness but not even a single healthy person should die due to unnecessary treatment.

The above thoughts  were in response to  the excellent original article on missed diagnosis  of ACS from NEJM.  http://content.nejm.org/cgi/content/full/342/16/1163?ijkey=652d8337709a8bf84c813f4c9d685863ee053162

Final message : (Sorry for the  lengthy message !)

Can we afford to miss an  ACS in emergency room ?

“Definitely not” . . .but do we succeed in that ?  The answer is same “definitely not “

When we are able to accept with pride every time  we make  a  wrong diagnosis of  ACS  in perfectly normal people , It may to provocative to say  we can  also  afford  to do  the same  when we occasionally   miss a  diagnosis of ACS  as well .  Law of statistics dictates for every correct diagnosis made there is many fold number of wrong or missed diagnosis takes place. May be , reducing that is the only aim of medicine.

We need to realise  with even with a 55% of false positive initial  diagnosis  2%  real ACS  escape net !The only  fool proof method  for  not missing  ,  even a single case of ACS   is to label every patient with chest pain as ACS .

In this vexing  issue , we should realise  , in field of  medical decision  making ,  errors  due to acts of commission  ( Making an  inappropriate drug/procedure /surgery  is easily accepted by medical professionals as well as   the court of law !) . But acts of omission ,   like missing a diagnosis or failure to prescribe  a  drug or perform a procedure  is rarely accepted   and  is  considered   a great negligence and  bring intense guilty feeling among the physicians .

This  perception is definitely  not warranted in this  greatest profession  of glorious uncertainties ! Both acts of commission and omission  cause significant damage to  patients . In this modern era  ,  we have clear  statistics  that   reveal ,  acts of commission  leads far ahead over it’ s counterpart in injuring our people .

Hippocrates got it right over 2000 years  ago .  First let us do no harm  . . .

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A  good collection of resources dedicated to cardiology


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Myocardial wall motion defects are sine qua non of  coronary artery disease. This occurs as regional wall motion defects following myocardial infarction or during unstable angina.Myocardium is divided into 16 segments  for this purpose. The wall motion defect occurs in the respective segments , depending upon the compromised  coronary arterial  blood supply.

Under physiological conditions myocardial segments contract in a synchronous fashion so that the chambers have a uniform contraction and relaxation. The heart is a complex electromechanical organ. Any thing , that interferes  the sequence of  electrical conduction or mechanical  contraction or  relaxation   can result in WMD.

Apart from this , differential filling of right and left ventricle can make one ventricle bigger or smaller in relation  to other ventricle .This  makes the ventricle to  contract or relax earlier or later (ASD ).This can not produce   WMD  in the  strict sense , but since the IVS is shared between the two ventricles there can be paradoxical septal motion which mimics WMD.

The other major cause for WMD in the absence of CAD is pericardial pathology .we know pericardium limits ventricular dilatation. When there is a defect in pericardium , after pericardiectomy  ( cardiac surgery patients)  part of the myocardium can bulge out  (or tend to bulge  ) .This happens  often ,  anteriorly to produce a WMD.

Similarly a pericardial pathology which constricts can cause a regional compression .This can happen in many of the adhesive pericarditis .They may resolve or end up with progressive constriction.These type of WMD is especially common in the posterior surface of the heart just near the AV groove.

Electrical disorders

  • LBBB (The classical septal wall motion defect )
  • Pacing rhythm
  • WPW syndrome
  • CRT

The much glamorous entity WPW syndromes and it’s variant can result in WMD due to pure electrical short circuiting hence altering the sequence of ventricular  contraction .In fact one can try to locate the accessory pathway origin and insertion sites depending upon the WMD .The segments abutting the insertion site , that are   innervated by  accessory pathway fibres   contracts prematurely and out of phase.

Rarely primary muscle disease like cardio myopathy can have regional WMD .This is uncommon as global hypokinesia is the hall mark . Regional variation in fibrotic processes can result in WMD.

CRT : Cardiac resynchronisation therapy is supposed to normalise  the pathological WMD sas in ischemic or non ischemic cardiomyopathies. Ironically CRT may induce new wall motion defects if lead position and stimulation protocols are not proper.

Now we have identified regional  diastolic wall motion defects as well .This is made possible by  myocardial  tissue doppler velocity profiles

*Even though it is difficult to explain , isolated electrical  de/ repolarisation defects like long QT, early repolarisation syndromes and brugada syndromes have rarely shown wall motion defects(Class 3 , type C observational evidence )

Non cardiac causes of wall motion defects

  • Abnormal heart position can result in WMD.  Ascites , High pressure pleural effusion /Pneumothorax can cause WMD of heart .
  • Post operative ventricle
  • Pregnant women may show physiological WMD due  to relative shift of  abdomen.
  • Hiatus hernia
  • Mediastinal mass

Final message

Contrary to the popular perception , wall motion defects(WMD)  are not an exclusive  property of CAD.It can occur in varied pathological states both mechanical and electrical .The implication  for not recognizing  this fact can be  enormous  .The “fancy habit”  of diagnosing acute coronary syndrome solely by means of echocardiographic  WMD (With out ECG / Enzyme changes ) is to  be strongly discouraged .


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Diastolic dysfunction is a common clinical cardiac problem which has no specific therapy.It can occur either in isolation or in combination with systolic dysfunction.The later may  be more common.

Isolated diastolic dysfunction

  • Hypertensive heart disease.
  • Aortic valvular stenosis
  • Restrictive cardiomyopathy
  • Early stages of CAD
  • Pericardial disorders
  • Idiopathic stiff ventricles

In association with systolic dysfunction

  • Dilated cardiomyopathy (20%)
  • In any form of cardiac failure some degree of diastolic dysfunction is noted .

General principles of management

Even though there is no specific drugs to tackle diastolic dysfunction the following measures may have significant impact.

  1. Correct the underlying problem.(HT/CAD etc)
  2. Reduce the basal  heart rate .At lower heart rates as diastole is prolonged , the stiff muscles has  extra time to relax and stretch itself  longer.
  3. Regular isotonic exercise  preconditions the muscle  for smooth contraction  relaxation .
  4. Optimise diuretics (Excessive diuretics has an  adverse effect on the  diastolic pressure profile across the AV valves)
  5. Avoiding positive inotropic agents like digoxin .This will not be possible in combined dysfunction.
  6. ACE inhibitors, ARBs, Aldosterone have some benefits as they could prevent tissue proliferation in the cardiac interstitium
  7. Milrinone (The non digoxin positive inotrpic)show some promise

What are the  treatments in the horizon ?

Antifibrotic drugs   ,Antiproliferative drugs

Collagen breakers ,

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