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Ventricular tachycardia as a group , constitute a major  group of cardiac arrhythmias. Most of the VTs are managed  by cardioversion  followed by medical management.  Few require , implantable defibrillator when there is severe LV dysfucntion .(ICD) Localising the origin of  VT and subsequent , ablation is the treatment of choice in some of the  patients  with VT.

Traditionally VT was thought to arise fro the endocardial aspects of myocardium. Now  we realise many times VT originate from the epicardial aspects of  ventricle.

Epicardial VT : Defintion

Epicardial ventricular tachycardia (VT) is defined as VT in which the critical sites of the reentrant circuit (or the ‘sites of origin’) are located exclusively in the subepicardial tissue, as shown by entrainment manoeuvres or VT that is terminated within 10 s with standard radiofrequency (RF) pulses, or both.  E. SOSA,M. SCANAVACCA et  all  http://www.springerlink.com/content/w608142674154tp5/ 

 

 How to recognise epicardial origin of VT by surface ECG ?

  • Terminal S wave in V2 and q in lead 1 strongly suggest VT of sub epicardial origin.
  • Pseudodelta wave 
  • Intrinsicoid deflection time of  85 ms
  • RS complex duration of  >120msec

Suggest   epicardial origin of the VTs.

Important Links

http://www.circ.ahajournals.org/cgi/content/full/113/13/1659 

Berruezo      criteria ,http://circ.ahajournals.org/cgi/content/full/109/15/1842  ( Must  read)

http://cogprints.org/4222/2/tada.pdf

 

What is the clincal significance of epicardial VT ?

Endo cardial ablation  not likely to be successful

Trans pericardial approach may be needed.

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Ventricular  tachycardia (VT)  is one  of  the   dangerous form of  cardiac arrhythmias.

When it occurs , it may present  in  many ways

  • Cardiac arrest with immediate degeneration into ventricular fibrillation. 
  • Pulseless VT in a  conscious patient but in  in shock.
  • With pulse, relatively stable , not much fall in blood pressure.
  • Incidentally detected.*(Rare)

This , gives us  an idea  that VT  as an electrical abnormality has wide clinical presentations , life threatening  at one end and,  patient walking into the hospital with minimal palpitation on the other hand !

The management issues

  • In patients with hemodynamic instability , decision making is easy as there is only option of DC shock.
  • In patients with stable VT, it is natural for the physicians to get tentative or even confused.This is because , dangers of shocking a stable patient has to be weighed against the currently available excellent antiarrhytmic drugs( Amiodarone, Ibutilide etc) .

 

The major issue here is  in  ruling out underlying structural heart disease.

Never shock a stable VT, without knowing the myocardial and valvular function.There has been many occasions underlying  severe LV dysfunction is missed   and they may go for asystole.

VT in the setting of cardiomyopathy, Post MI(Scar mediated) are often refractory even to DC shocks.It is the drugs that will  ultimately control the arrhythmia.DC shock is just used to terminate the VT.

VT  structurally normal heart , especially arising the outflow tracts of LV or RV  behave very differently (Fortunately they are more benign)

  • Have less hemodynamic  impact as it involves the outflow tract and  not over the  the pumping  zone of LV as in conventional ischemic myocardial VT .
  • They  respond to calcium blockers  verapamil to be precise (As they share properties of SVTs)
  • Sensitivity to verapamil by no way convey a meaning of Amiodarone resistance.Out flow tract VTs will also respond to Amiodarone many times.
  • Degeneration into VF is rare.

 

Also  read  Therapeutic issues in stable ventricular tachycardia

Presented and published in Indian heart journal

vtvt-therapeutic-issues1

Click  on link download PPT ventricular tachycardia

 

Related topics

Why some ventricular tachycardias are resistant , even to multiple DC shocks ?

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                                       Aortic dissection is a complex cardiac problem and a  killer disease .Even though it is a fancier to make a  diagnosis  of aortic dissection in any intractable chest (or back )pain   the  most common error  committed by physicians is failure to recognise it  .

Is it possible to diagnose or atleast suspect aortic dissection  by a rapid screening biochemical test ?

Yes,  it seems so

  1. D Dimer , a product released consequent to  intravascular thrombosis is elevated  by >500ng in most of the patients with dissection.
  2. Aortic smooth muscle heavy chain estimation is the other option.

aortic-dissection-d-dimer

Read this original article by Patrick Ohlmaan

Click on the link

http://www.medscape.com/viewarticle/530783_print   Courtesy Medscape

 What happens once a diagnosis of aortic dissection is made ?

It is not a great achievement to make a diagnosis of aortic dissection.It is only, a  beginning of a long  and often   tedious decision making process . A real tough task , on hand for the cardiothoracic  surgeons. It is a team work , needs the interaction of cardiologists, radiologists and cardiac surgeons to bring an optimal outcome.

The major issues are

  1. Never try to  manage this problem in a small hospital or facility. Always send the patient to a teaching hospital ( of course , not all teaching hospital can  tackle  this   either , so enquire about their expertise ! )
  2. No credits for making a simple diagnosis of dissection.One has to exactly locate the entry point and exit points if any.
  3. Aortic root and arch  involvement  is of major importance in determining the modality of therapy.
  4. Debaky classification is not  of academic interest ! it has a purpose . Generally type A dissection(Proximal ) require emergency surgery
  5. Differentiating true lumen from false lumen is of critical importance , it needs a meticulous transesophageal echocardiogram.( Some times one may , never  be  sure which is true and which is false lumen  , funnily .in descending aortic  dissection it may never matter for the patient !) Self healing of many dissections with thrombus is possible. 
  6. Controlling hypertension with powerful parentral antihypertenive drugs (Labetalol . . . ideally )  is vital.
  7. Side branch  involvement (spiral dissections) especially arch vessels and renal arteries  make this entity much more complex
  8. Isolated distal dissections and some low risk proximal dissections  can indeed  be managed conservatively(Also called non surgical ! ) Some cardiologists or even institutions  hesitate to  put a aortic dissection with medical management .They feel it is inferior form of treatment . . . but realise , it is not  necessarily so !)

 

What is the other bichemical marker for disscetion ?

The aortic smooth Muscle Myosin Heavy Chain was proposed as a useful marker for diagnoisng dissection.

Diagnostic Implications of Elevated Levels of Smooth-Muscle Myosin Heavy-Chain Protein in Acute Aortic Dissection: The Smooth Muscle Myosin Heavy Chain Study  Toru Suzuki, MD; Hirohisa Katoh, PhD; Yasuhiro Tsuchio, MD;  Annals of internal medicine 3 October 2000 | Volume 133 Issue 7 | Pages 537-541

 The abstract from annlas of internal medicine follows Readers from India can get the full text article free

  1. http://www.annals.org/cgi/content/abstract/133/7/537 
  2. http://www.annals.org/cgi/content/full/133/7/537
  

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                                                    Drugs are poisons , whenever it is administered without valid purpose. it can enter human body  in many ways (Oral, intravenous, percutaneous etc ) And now we have another route namely intracoronary !

                                                   In quest for prevention of restenosis, many of the anti cancer drugs are now delivered directly inside the coronary arteries .These drugs are secreted  like a sustained release  tablet from the drug coated stents.These drugs are expected to prevent restenosis within the stented segment.But, after years of  intense debate and research  , we realised that ,  drugs  eluted from the stent  could damage the distal coronary vascular bed and coronary microcirculation.( And thus came the epidemic of acute stent thrombosis ! )

                                                The tender and sensitive coronary microvasculature  is constantly exposed to  these  powerful anticancer and immmunosuppresive  drugs .It is a great surprise , no body thought of  this dangerous drug -coronary artery interaction ! It required the genius of Renu virmani and others to point out this.

But still , the cardiology community by and large , fails to consider  this an important issue.This is proven by the fact, usage of DES is  still increasing  and used mainly as an off label indication.

Read this land mark article from circulation

picture1

http://circ.ahajournals.org/cgi/content/full/115/8/1051?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&author1=renu+virmani&andorexacttitle=and&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=1/1/2007&tdate=12/31/2007&resourcetype=HWCIT

 

Questions that need to be answered

  • What is the long term effects of drugging a coronary artery ?
  • Is no reflow or slow flow  more common after DES , because of the adverse drug reaction in the distal vascular bed ?
  • If a patient  with  DES  undergoes a CABG later what  would be  the impact of the  drug on the graft ? Will the functional vasodilatation   affected ?

Final message

                                  A drug , to get a legal clearance it has to undergo  hundreds of rigorous tests . Finally it is cleared for that  specific indication for which it is tested  .Just because a drug is cleared for one purpose ( Paclitaxel for malignancy ) it does not mean it is safe to use for any other  purpose for which it is deemed to be useful . Exactly the  opposite is happening   in the  the field of interventional cardiology . No body wondered to think what would be the effect of these drugs on the normal coronary endothelial cells and vasculature.Is it not a crime ,  without analysing this particular issue  , dozens of drug eluting stents have been released in the market . And now,  sounds of crying  foul is heard world wide !

Let us thank  , the so called negative forces in cardiology  for making this an  issue . In science ,  the watch dogs should bark  at  times of danger not wag the tail !

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 Selected on the basis of ,  impact  on survival , relief of  human suffering index and also innovation

10.Percuateneous interventions

9.  Electrocardiography

8 . Hemodynamics of cardiovascular system

7.Fruesemide

6.Thrombolysis

5.Pacemakers

4.Defibrillation

3.Heparin

2.Prosthetic valves

1.Coronary care units

 

Waiting list

Concept of vascular biology

Statins

RF ablation

Nitric oxide

Total Artifitial heart

Echocardiography

 

Ten least important concepts and  inventions in cardiology

Selected based on duplication of research, futile scientific concepts and   of course impact on survival

10.Low molecular weight heparins

9.Cardiac resynchronisation

8.Rotablator

7.Multi  chamber pacing

6.Newer ARBs

5.C reactive protein

4.Three dimensional echocardiography

3.

Comments welcome  and please contibute

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A poorly deployed drug eluting stent is far inferior to a properly deployed bare metal stents

  • Doing a plain old balloon  angioplasty ( POBA)  is not a scientific crime , millions of coronary lesion just  need that! ( Click here -Why POBA is important ? )
  • PCI is most effective during an ACS than a chronic coronary syndrome
  • Primary PCI is a race against time and muscle , not a race against money ! Don’t do it  for a  evolved   MI
  • Recognise , from the patient point of view  the term no reflow is  generally  synonymous with   failed primary PCI( It is semantics !)
  • Side branch  can be more important than main branches , so don’t sacrifice it often
  • Attempting a trifurcation  angioplasty is generally not in  the interest of the patient but  to show interventional expertise
  • Make sure surgical back up means, a table is reserved with a surgeon fully informed and ready

When in  doubt , it is always  better to err on a longer stent than a shorter one

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The irony of medicine is unlimited !  100 years of active clinical  research   failed  to find a specific cure for the rhino virus mediated common cold.In fact  US Govt stopped funding for this .

While ,   complete cure is possible  for many of the cancers, especially hematological ones !

Message 

In medicine there are thousands  of disorder  which have no cure ! 

Cancers ,  constitute  only a  fraction of  them !

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sinus-node

 

Sinus node  as the pacemaker , orchestrates the rhythm of life . It has  to fire for the entire life time of  a person.It  can not afford to take any rest ! But it can pause a little bit , of course that pause  could  be less  than 15% of it’s basic sinus length. This variation of sinus  cycle length is called sinus arrhythmia.This is physiological. When it exceeds 15 % of the previous sinus cycle it is referred to as sinus pause.

 Have a look at this ECG

sinus-pause-2

 

What follows a long pause ?

By strict terms  of definition a sinus   pause should be followed by  a delayed , next sinus  beat only. A  sinus pause  , many times  is followed  by   JPD – Junctional escape beat.This situation should be ideally  referred to sinus arrest as the sinus node is taking too much of rest and it is not able to wake up from the slumber and it needs assistance form the junctional pace maker.

So even though sinus pause and sinus arrest is used many times interchangeably, it should be avoided. 

What are the electrophysiological mechanisms of sinus pause ?

  • Simple sinus bradycardia . The commonest  mechanism is  the  increased vagal tone. This occurs more often in young athletes. Eventhough increased vagal tone  conveys   a innocuous meaning , at times  this can also be symptomatic  and require intervention.
  • Sinus node exit block.
  • First degree, second degree, complete SA block can occur as in AV node.

First degree SA block can not be diagnosed by surface ECG. Third degree SA block is same as sinus arrest and subsidiary pacemaker will function in these patients.  Second degree SA block is usually diagnosed when the sinus pause is in the multiples of resting sinus cycles. If the pauses are not in exact multiples  sinus arrest is diagnosed. All these arrhythmia’s are collectively called sinus node dysfunction(SND)

How do you manage these patients?

Sinus node disorders can occur in number of systemic diseases*. It  needs to be  ruled out.

  • Infiltrating diseases like amyloidosis, hypothyroid states can result in SND.
  • Drug induced SND like beta blocker and calcium blockers are fairly common and should be excluded
  • Some congenital heart disease (SVC ASD) can involve sinus node.
  • Ischemic SA node disease is rare but can occur  following  infero posterior  myocardial infarction
  • Sinus node disorders are  very often related to degenerative atrial diseases associated with HT, cardiomyopathy etc

*The list is not exhaustive

A very important association is noted  with atrial fibrillation as  a part of tachy brady syndrome .The link between SND and AF  is obvious as   atrial pathology is the common denominator in both ! This will be discussed later.

When is a  pause  significant ?

Any pause that is producing significant symptoms is significant.This depends upon the overall  hemodynamic compensation of the patient.Young, and fit can even tolerate three second pause without symptoms.Underlying heart disease makes even a smaller pause symptomatic.But generally a 3  second or more  pause is almost always pathological .Pauses can be up to  5  seconds (  a 5 second pause actually means a  heart rate of 12/mt , obviously it can not go on for a minute, a patient will develop a syncope). A 3 second pause  corresponds to 20/minute.

How will you evaluate a patient with sinus pause ?

There are sophisticated electrophysiological studies (EP) available like sinus node ECG ,sinus node function studies like sinus node recovery time, activation time etc. But these are generally of  academic interest.

If a patient is symptomatic  (syncope) because of bradycardia  he requires a pacemaker and  EP study is redundant . Similarly , if  he is totally asymptomatic in spite of pauses , again  EP study is  not  indicated.

Only for patients  in the  grey zone,   further studies are indicated .This would include a extended holter, loop recorders, event monitors etc.

Another important issue to consider  is , before putting a pacemaker   patient”s   symptom  must be correlated  with their arrhythmia.

What is  the overlap  between sinus node dysfunction and neuro cardiogenic syncope ?

SND  can occur as an overlapping syndrome with neurocardiogenic syncope.(NCS ).NCS is also a very common cause of syncope .In NCS  there are two limbs .Cardio inhibitory and vasodepressive. The cardio inhibitory form can exactly mimic an SND. In a given patient  it is very difficult to pinpoint which of this limb is dominant.Head up tilt test(HUT)  might help in few.  If a patent’s symptoms are due to inappropriate vasodilatation pace maker may not reduce the symptom of dizziness or syncope.

Management

  • There is no ideal  medical therapy* available as on date
  • Withholding all drugs which might aggravate bradycardia is of paramount importance.
  • Pace maker is the specific treatment in all symptomatic patients.

*Aminophyline tablet may be useful in some patients .It acts by antagonising adnosine receptors in SA node.Other drugs which can incrase the heart rate in the short term include  Orcipranaline(Beta 2 stimulant /Alupent ) Probantheline(M 1 blocker)

The key issue is to avoid unnecessary pacemaker implants in patients who have insignificant pause.

 Which pacemaker is ideal in SND ?

pacemaker

                                                              The need for dual or single chamber pacemker will be taken by the electrophysiologist .Atrial based pacemaker (AAI)  is preferred as it gives physiological pacing .But a simple ventricle based VVI pace maker is good enough in vast majority of patients. This takes care of   future risk of AV block also. DDD pace maker is the most physiological pacemaker and it is supposed to provide better quality of life. But it has an issue of insertion and  maintenance of  two leads, multi parameters to be programmed.It should switch to appropriate modes  at different times.(Like VVI mode during atrial fibrillation etc).Trouble shooting needs expertise , while  VVI is simple,  safe , and just effective as well .(In this turbulent world, quality of life is a  too trivial an issue  to be determined by a DDD  maker)

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                                This is a  hemodynamic concept paper by Libanoff in 1968 published in circulation.This paper elegantly proved that  the rate of fall of pressure across the mitral valve will predict the mitral valve orifice.     This key paper formed the foundation on which  Liv hatle developed the echocardiographic pressure half time .This pressure half time derived mitral orifice area ( 220/PHT) is key parameter world over for assessing  severity of mitral stenosis non invasively .

Click on the link get this article .This article is available free fulltext from circualtion web site

pressure-half-time

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Why is criticism of newer scientific technologies always frowned upon or rather considered indecent ?

In science you don’t require politeness ,  we only  require correctness.This is especially true in medical sciences. But this is easier said than  practiced in the scientific community . In any scientific conferences the only a couple of minutes or few lines are allotted for the customary negative issues and  the limitations of the study.

Unscrutinised science can no longer be called as science !  it can only be termed as pseudo science!

It is believed skepticism is a powerful  dampener for the scientific growth.May be it was true in the earlier era of pre industrial world. But those days science was growing only with passion for discovery  and  an un contaminated mind.But now too many conflicts have cropped in.

 What is positive thinking ? and What is negative thinking in science ?

To be continued . . .

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