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What are the determinants of qrs width in ventricular tacycardia ?

Posted in Uncategorized, tagged on November 13, 2009| Leave a Comment »

Every one knows VT  presents as a wide qrs tachycardia  .Few of us ,   know VT can be narrow or even a normal qrs complex . But .none of us know what is the exact reason , why the width of  qrs complex  in VT swings from narrow  to wide.

Factors determining qrs width in VT.

  • Origin of VT :Septal, freewall , apex etc
  • Epicardial exit points make it wider
  • Rate dependent Intraventricular conduction (VT with aberrancy a possibility ?)
  • Drugged VT(Cumulative dose of amiodarone widens the  VT  )
  • Associated LV dysfunction/Myopathy
  • Electrolytic milieu (K + etc )
  • Preexisting bundle branch blocks (Surprisingly common and still more a surprise some BBB  may convert  a VT from wide qrs to narrow qrs ) 

* Another unique , but common observation is  variation in qrs width between different leads.This again points to different exit points and tachycardia circuits traversing and looping around the epicardium to endocardium at different depths  from the chest wall leads.

The commonest explanation of VT being narrow is it’s origin near the septum and travel down the fairly physiological his purkinje tracts and resultant uniform depolarisation.While myocardial,free wall apical VT are bizarre and wide. We now know , many factors come into play in determining the  qrs width.In fact , we are only beginning to understand the complex conduction pattern of VT.

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How will you differentiate a wenkebach’s Mobitz type 1 AV block from type 2 second degree AV block if the conduction ratio is 2: 1 ?

Posted in Uncategorized, tagged on November 11, 2009| Leave a Comment »

It is the classical description of wenkebach AV block type 1 there is progressive prolongation of PR interval followed by a blocked p wave and hence a dropped qrs complex. The usual conduction ratio for wenkebach AV block is 3:2 or 4:3 .

It is well known wenkebach AV block is usually a benign form of AV conduction defect and it recovers spontaneously without any pacemaker support.The block is at the level of AV node and since the his purkinje conduction is intact and the prognosis is good. In type 2 AV block the disease is often(Not exclusively ) located in the infra hisian area .This makes this type of block very unstable and these patients have a high risk for going in for complete heart block and often require pacemaker implantation. The reason for the poor outcome in type 2 AV block is now more attributable to the more extensive myocardial damage these patients suffer than the location of the block itself .

So it is important for the physician to differentiate the two entities .

It is a simple task in most situations , but when the condition ratio is 2:1 one can imagine the difficulties as none of the classical criteria of wenkebach’s AV block are applicable .When alternate qrs complex is missing there is no question of progressive PR prolongation .

How common is 2:1 AV wenkebach ?

It is considered rare , but may not be recognised in surface ECG so real prevalence is under reported.

What are points to differentiate the two ?

  • The qrs width : A normal qrs width suggests wenkebach .A widened qrs indicate the block is infra hisian.
  • The conducted basic PR interval is usually normal in ttype 2 AV block. In wenkebach the PR interval is usually prolonged.(Not always though! )
  • Response to atropine *:Wenkebach tend to accelerate while type 2 AVblock tend to worsen.
  • Response to excercise :Wenkebach conduction ratio improves , type 2 does  not, some times worsens
  • Response to carotid massage: Wenkebach AV block worsens ,Non Wenkebach improves

*The principle behind the varying response is due to the fact that AV node is under the influence of vagal fibres than the his purkinje system.

**It should be noted the atropine effect on AV conduction  is a complex one .Atropine by it’s direct vagolytic action improves AV conduction , while it’s effect on sinus node accelerates the heart rate and make the AV node more prone for physiological AV delay (Decremental conduction: Increased refractionary period at fast hear rates) .This effect is in exact opposite of it,s direct action on AV node.So the net effect will be the balance between these two.Hence atropine effect on heart can be quite variable in both physiological pathological situations.

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Is aberrancy same as functional bundle branch block ?

Posted in Uncategorized, tagged on November 8, 2009| Leave a Comment »

Is aberrancy  same as functional bundle branch block ? Some electrophysiological entities are used too liberally  without much meaning . The terms  functional bundle branch block or rate dependant bundle branch block  is actually used  interchangably with aberrant conduction .It should be noted aberrant conduction can occur at extremes of heart rate .Even though tachycardia is expected to produce aberrant conduction extreme bradycardia as it can also  make the  cardiac  conduction turbulent  . Why aberrant conduction happens ? The his purkinje system expects some discipline and order from the SA node. Abnormal  fluctuations in sinus  heart rate  keeps  the downstream  cardiac conduction system guessing and confused. The antegrade  impulse penetrate to various levels and get struck with different refractory periods. In this scenario  , if  suddenly the basal heart rate swings further  to different rates ,   the new  incoming impulse  finds , the preceding impulse has produced a functional block /barrier at the his purkinje level  . (Note it should be called functional delay in conduction  rather than a block as every impulse gets conducted ultimately with a widened qrs complex ).

  • This type of  conduction velocity mismatch between atrium and ventricle occurs in many of the SVTs and also in AF.
  • It is found , aberrancy occur more commonly in the right bundle.
  • It is usual for the aberrancy to disappear after the rate correction . Some times there could be a temporal delay . The conduction system might have gone for prolonged stunning . Some times this is referred to as ” memory blocks”
  • Underlying heart disease, ischemia , degenerative heart disease  may amplify this aberrancy or  convert this transient aberrancy into a permanent block .
  • It is also possible  even a ventricular tacycardia might conduct with aberrancy ,  widening the already wide qrs tachycardia .(Refer this blog 🙂

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Forgotten concepts in cardiology : Over drive pacing

Posted in Cardiology-Arrhythmias, Uncategorized, tagged , , , , , , , , , , , , , , on November 7, 2009| Leave a Comment »

It is one of the greatest innovation in medicine  . . . that is . . . electric current being  used as  a  drug to  treat disorders of heart . Of course ,  it is not a surprising finding  when we know heart is an  electro mechanical organ ,  and electricity can be used  to treat various disorders of heart by delivering it  in an optimal dosage and site.

Devices  that help administer  electric  current in cardiac disease.

  1. External  cardiovertor and defibrillator
  2. Implanted defibrillator
  3. Anti bradycardia  pacemaker
  4. Anti tachycardia pacing
  5. Cardiac  resynchronisation device

What  is  the  difference  between cardioversion and  pacing ?

Cardioversion  is reverting  a tachycardia with  a electric shock that is delivered diffusely throughout the heart This  electrical wavelets traverse the  focus of tachycardia  and the adjoining myocardium  which is called critical electrical mass (Usually reentrant) .This depolarises the cells responsible for tachycardia and extinguishes the abnormal electrical activity.

Defibrillation is same as cardiversion except that it is a high energy shock  and delivered without synchrony with qrs complex . In VF, we defibrillate in all others  we cardiovert .

What are the disadvantages of cardioversion ?

Eventhough it is a very successful modality for treating cardiac arrhythmias it also has some issues.

  • Cardioversion is not infallible. It rarely works in tachycardia due to enhanced automaticity (Multifocal atrial tacycardia , Automatic junctional tacycardia , Digoxin induced tacycardia it may even be dangerous !)
  • Many times multiple shocks are required and may result in myocardial damage, stunning , and elevated cardiac enzymes.
  • In susceptible patients, especially in elderly it may depress the natural pacemaker ie the sinus node and dangerous  bradycardia

over drive pacing paired pacing anti tachycardia

What is difference between cardioversion   applied externally on the chest wall and intracardiac cardiversion as in Implantable cardiovertor defibrillator(ICDS) ?

The underlying principle is same except that the energy required is a fraction of that applied in the chest wall . The average energy required is up to 20 joules . while it requires up to 300 joules

What is anti tachycardia pacing ?   Why this concept came into vogue ?

When it became clear , cardioversion may not work in all forms of tachycardia and risks of multiple shocks  on the myocardium  not be taken lightly , experts in those times (1970s)   thought  a pace maker lead in a optimal site can do the job of cardiovertor. .

Pacing rapidly  in the tachycardia zone  provide us an opportunity  to  enter  the  tachycardia circuit , interfering , interrupting  and blocking the reentrant circuit  (We call it entrainment)  . If it is an automatic tachycardia pacing in close vicinity of the tachycardia   focus result in a  electrical  line of  barrier  which acts as an  exit  block ( Like the lakshman  reka !  in Ramayana )

The term ATP is used as a  general term as anti tachycardia pacing .Over drive pacing  can be used synonymously.

What is the  main advantage of ATP ?

  • Less injury as it avoids recurrent shocks  .
  • Can be administered as many time as  required .
  • Some tachycardias specifically respond to ATP only (Read below)

How to perform overdrive pacing ?

Can we use the external transcutaneous pacemaker paddles for overdrive  pacing ?

Yes we can, it may be termed a  non invasive external overdrive pacing .This  mode is not popular among cardiologists  not because it is ineffective  , rather we have not fully realised it’s  potential .

Different types of  overdrive pacing

What is coupled pacing ?

It is a type of overdrive pacing where   patient’s own spontaneous  rhythm   is used trigger a  pacemaker stimulus    and  hence only alternate beats or pacing beats which is coupled with the pateint,s own rhythm it is called coupled pacing . This  is different from from paired pacing  in that only single pacemaker stimulus per cycle .

What is paired pacing ?

Two pacing stimulus are given.The first impulse is maintained constant and the second impulse is done with varying coupling interval to scan the entire cardiac cycle .It is expected at some point of paired pacing the second impulse would  block the reentrant circuit.

What is random paired pacing ?

The atrium is   delivered a   pair of random stimulus ( . . Like a bite of snake !) is  delivered into the atria .This can revert many of the reentrant atrial and ventricular  re entrant tachycardia.

What is the  unique value of  sinus paired  pacing ?

In patients  with persistent sinus tachycardia,  especially  in patients with  high MVo2 situations or dysfunctional ventricle we have no option to control the heart rate without depressing myocardial contraictility . Most of the negative chronotropic drugs have negative inotropic action also.  In these situations pairing a pacemaker stimulus with a sinus impulse can produce a compenstatry pause  and result  in reduction in net heart rate as well  as increased  contractility due to post extrasystolic potentiation.

How does a  catheter whip inside the atria   terminate many of the procedure related  tachycardias in cath lab ?

It is a common maneuver  in cath lab ,  to  forcibly whip the   catheter for   terminating  many of the transient procedure related  SVTs and outflow tract VTs . The arrhythmias get terminated  either due to catheter hit induced mechano  electrical  cardioversion   (5 joules ?) or  the atrial subendocardial stretch due to the  whip lash .

What are the tachycardias that may  respond to overdrive pacing ?

It is logical to expect any of the reentrant tachycardia  might respond to ATP. The  exact success rate can  not be established  since this modality  is not applied  in vast majority of  patients . Only if a patient  is not responding to drugs or multiple DC shocks ATP is thought off . Of course ATP can not  considered  a first option   unless othe  patient is  on a temporary pacer.

What is the caution for using ATP ? Why  atrial overdrive pacing   is preferred over  ventricular  overdrive pacing ?

Pacing a ventricle rapidly carries a risk of inducing ventricular fibrillation . So whenever  possible ATP  should be administered  through  an  atrial lead. This may not be possible always as in the presence of AV block a VT  can not be captured  by atrial pacing  .

It is also  a fact  many times   when the    ventricular overdrive pacing  fails to revert a VT , an  atrial overdrive pacing has been successful . This is due to the  more uniform    depolarization  wave fronts , that reach the ventricle and reset the VT .

Currently ATP is useful in

  • Recurrent atrial tachycardia
  • Refractory ventricular tachycardia especially with enhanced automaticity (Early ischemic VT )
  • Digoxin induced tachycardias
  • Some cases of Tachy brady syndrome

 

 

In some of the modern pacemakers and  in all ICDs ATP is a an important programmable parameter .In fact, using this mode liberally would conserve battery life .Many times a simple hemodynamically stable VTs are shocked by ICDs  instead an ATP will  do the job . It is a well recognised fact that   ATP is underutilsed in ICDs .This issue needs to be addressed.

Final message

Pacemakers are not only meant to treat bradycardias but also tachycardia. Even though it is a well-known fact for over 3 decades, for some reason this simple and effective concept is not getting the  attention of the current generation cardiologists which it definitely deserves!

Reference

  1. Overdrive Pacing for Ventricular Tachyarrhythmias: A Reassessment    P. R. KOWEY andT. R. ENGEL
    ANN INTERN MED November 1, 1983 99:651-656
  2. Pacing Techniques in the Treatment of Tachycardias  I. WIENER  ANN INTERN MED August 1, 1980 93:326-329
  3. Treatment of Recurrent Symptomatic Ventricular Tachycardia R. A. WINKLE, E. L. ALDERMAN, J. W. FITZGERALD, and D. C. HARRISON ANN INTERN MED July 1, 1976 85:1-7
  4. Treatment of Tachyarrhythmias by Pacing J. E. Batchelder andD. P. Zipes

 

Over-drive pacing : A practical approach

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The impact factor of diabetes , hypertension , smoking and dyslipidemia on human vasculature : Aren’t they different ?

Posted in Uncategorized, tagged , , , , , , , , , , , , , , , , , , , , , , on November 5, 2009| Leave a Comment »

This was written originally in 2009 early days of this blog. Now, re-posting it in 2021  , wonder any one has new data on this! 

We know diabetes, smoking, hyperlidemia, hypertension are major risk factors for progressive vascular disease. They damage the vascular endothelium either directly or indirectly , by aggravating the atheroscelortic process .  Diabetes apart from affecting the medium sized arteries , also affect the microvasculature.  Smoking  has a direct effect on endothelial function .It depletes vascular nitric oxide. High levels of circulating lipids injures the sub endothelial structures and invades the media by entering macrophages .So , all these 4 risk factors either operate independently or interact with each other and result in progressive vascular    disease.

While we  believe , these risk factors do not have any bias in attacking the human vascular  tree, in the real world it is observed they have their own  behavior pattern and  have unique predilection and a deadly alliance .

For example , in  chronic smokers TAO is the commonest manifestation , thrombo angitis is far too less common to occur in the coronary arteries.

Similarly  hypertension  per se  rarely results in an acute coronary syndrome while it is  the  single  important  cause for cerebro vascular  disease. Diabetes especially in women has very strong predilection for CAD , while diabetic per se is a lesser risk for stroke. Hyperlipedimia may be the one which has fairly even risk throughout the vasculature. Similarly there is  a difference in renal and   carotid arterial involvement with reference to  the conventional  risk factors .

SHT diabetes dyslipidemia coroanry risk factor

Why this apparent difference ?

We are unlikely  to get an answer to this question in the near future .  Left to the youngsters  . . . of tomorrow !

* Note of  clarification

The source for the above chart is collected from various studies and also a huge observational data from our hospital. There could be some geographical variation , a given individual may respond differently to these risk factor depending upon his genetic predisposition and susceptibility . So the above data can be applied to general population and not to a individual.

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How common is ischemic SVT ?

Posted in Uncategorized, tagged , , , , , , , , , , on November 4, 2009| Leave a Comment »

Ischemic ventricular tachycardia is a  too well recognised clinical  entity  . But , ischemia triggered atrial arrhythmias are less often encountered .

Does that mean , atria are relatively protected from the effects of ischemia ?

Not really  . . .  It  is possible  it may not be  that rare ,  as we think .

And then ,  the semantics play  a major  role !

Atrial fibrillation  is the commonest supra ventricular  arrhythmia  in human ,  we also know CAD is the leading cause of the AF apart from HT & Cardiomyopathy . So technically , ischemic SVT  is  more common than Ischemic VT ,but we do not call it so !

If we analyse the triggers for AF it is more often hypoxia  (than ischemia )  . . .yes there is huge difference between the two .In the ventricles it is more often ischemia that  trigger a VT.

Atrium is very sensitive to systemic  oxygen saturations especially in elderly and COPD patients. This is the reason we get many of the complex atrial arrhythmias in hypoxic situations ( Ectopic atrial, Multi focal atrial , etc) .These arrhythmias are difficult to control unless oxygen saturation is corrected. While  many of AF episodes are transient and disappear after correction of hypoxia.

If the ventricle also  responds with fibrillation  at times of systemic  hypoxia ,  one can  imagine the disastrous consequence ! God is kind enough , systemic hypoxia per se  rarely trigger a VF ,  though  it can maintain a VT which was initiated by some other mechanism.

So what are the causes of  narrow qrs tachycardia in the coronary setting

Apart from AF ,  Ischemic SVT  can occur in the following situations

  • STEMI -RVMI
  • Atrial infarction -Focal AT -Atrial flutter /AF
  • Post Pericarditis
  • Refractory , ischemic JT (Junctional tacycardia ) in elderly , perioperative , hypoxic patients

*Atrial arrhythmias are very rare during unstable angina for some unknown reasons . Atrial scar induced ischemic focal AT is underdiagnosed.

** Never  diagnose AVNRT /AVRT in a patient   who has an ACS. It is likely you will be 99.9% wrong.

*** Preexcited AVRTS are very rare in elderly CAD patients even in those with a history of SVT  .This is because as the age advances the accessory pathways undergo degeneration either by ischemia or  the wear and tear  and get self ablated .

Many times the associated , HT and diabetes may contribute to the arrhythmia.

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What is the difference between isoelectric P waves and absent p waves ?

Posted in Cardiology-Arrhythmias, Uncategorized, tagged , , , , , on November 4, 2009| 1 Comment »

P waves represent atrial depolarisation. The p wave height  and width depends not only the size of the RA and LA but also the site of  origin of atrial  impulse .A normal SA nodal origin of P wave produce the normal shaped p waves.

We know  ectopic  p waves can have a wide variation of morphology.(Fully inverted, partially inverted, slurred, bi phasic, notched, rounded , deformed, etc. The morphology is dictated by the direction of p wave vector and thus it is quite variable in different leads. Further  it is also determined by the inter atrial and intra atrial conduction.So in summary , an ectopic p wave can have any morphology we can think off !

What is isoelctric P waves

It is rather a surprise we have not thought about so long,   like a low voltage QRS ,  a  p wave can also be very low amplitude and it may be entirely isoelectric , which could actually mean the p waves are as good as absent.This can happen in all leads or in few leads. .Atria gets electrically activated but fails to inscribe a p wave .This is termed as isoelectric p waves

The importance of isoelectric p waves

It  can  happen , both  in sinus rhythm  and in ectopic atrial rhythm . Absent p waves should be differentiated form isoelectric p waves. It is typically described in focal atrial rhythm arising from the right side  of  the  inter atrial septal near the   perinodal  tissue.The atrial tachycardias arising from this site are classically have isoelectric p waves in most of the leads especially  V1 .

Other causes of absent p waves

  • Atrial fibrillation

The classical example .in fact here p waves are replaced by fine or coarse fibillatory waves

  • Sinus arrest  plus Junctional rhythm with retrograde VA block

Not all junctional rhythm result in absent p waves .Many record inverted retrograde p if there is VA                            conduction.

  • Sino ventricular conduction .P waves appears  absent in surface ECG. It occurs in hyperkalemia /renal failure is due to high levels of pottassium   which suppress the atrial activity sort of atrial electrical paralysis but still impulse originates in SA node traverses  the inter atrial pathway and reach ventricles.typically P waves are absent or can be termed isolectric.
  • Atrial  stunning following cardioversion

Long standing atrial tacycardias may fail to resume it’s mechanical (or even electrical ) activity after  cardiversion  .If it is electrical stunning the p waves do not immediately appear  but occurs later .In fact this could be termed as failed cardioversion.

* Note  p waves are failed to identified in many of the VTs AVNRTs

Final message

Absent p waves ,  isoelectric p waves , hidden p waves, merged p waves , low voltage p waves , unrecorded p waves,  selective absence of p waves in some leads all can happen in clinical cardiology practice.

One should realise the importance  differentiating   absence of   p waves in the given strip of ECG from failure of p waves to  get recorded by the  ECG machine .This has diagnostic significance.

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Does the esophageal spasm get relieved by sublingual nitroglycerine ?

Posted in Uncategorized, tagged on November 2, 2009| Leave a Comment »

Esophagus and the heart are closely related structures. Both can generate chest pain that can mimic each other. The squeezing substernal pain  is very characteristic of esophageal spasm  .The smooth muscle of esophagus can exactly mimic a vascular smooth  muscle  .The relief of chest pain following nitrates  though very classical of angina it can very well alleviate the pain of esophagal spasm also. This has important clinical implication

Also read

Cross talk between heart and esophagus

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What is being rescued in rescue angioplasty ?

Posted in Uncategorized on October 18, 2009| Leave a Comment »

Rescue angioplasty as a concept in PCI is advocated for the past  two decades. Rescue angioplasty  continues to enjoy the  controversy over the years. A procedure which fails to shrug off the controversy for so long   inspite of multiple studies ,  would indicate there is something seriously wrong in the  procedure  or in the conceptualization.

The fundamental question   that  is often  and not answered properly is :

What is being rescued in R angioplasty ?

Is it the

  • Patient’s life ?
  • Myocardium  ?
  • Rescues ischemic myocytes
  • Infarct related  artery ?

*Or it simply rescues physician  from the legal issue arising out of  labeling his patient as  failed thrombolysis

The term rescue generally implies  tackling an  impending crisis .The threat is either  to the patient’s life or to the myocardium or both.

In STEMI when the initial reperfusion strategy fails (Usually thrombolysis)  R -angioplasty is considered. Here the aim is  to  rapidly  rescue  and salvage  myocardium . The problem  here is   , contrary to our expectation   the population of failed thrombolysis is not a homogenous one .In one end of the spectrum ,  is a patient with  persistent ST elevation ,   totally comfortable and pain free and  hemodynamically stable.The other end is , deteriorating blood pressure , tachycardia , progressive angina and impending cardiogenic shock. Considering the above situations it is very simple to guess who will  require the rescue  and  who will benefit more. In fact,  R -angioplasty  in   patients with  asymptomatic  failed thrombolysis  without ongoing  ischemia defies logic and conveys no meaning !  .This is especially true if the patient has crossed 12 hours of time since the first symptom.

In deteriorating patients R- PCI has a role where one can potentially  arrest the progression of cardiogenic shock  or even reverse it.

A third  group  among failed thrombolysis have  predominate  angina  with  hemodynamic stabilty. This group will benefit from R angioplasty  irrespective of time window , as the pain is often due to a critical non IRA lesion .Technically again we can’t call this PCI as rescue as nothing is done to salvage the myocardium . (Of course one wish to call it so ,  as the  patient is rescued from angina !)

A tricky issue is to know where does the pain come from in a post MI patient ?

It should be realised a post MI patient can have variety of source of chest pain. There has been instances where a persistent  pericardial pain has resulted in emergency  R-PCI !

The critical question that  has not  been  answered by cardiologists is

How long a STEMI pain last and when does post infarct angina begin in a  susceptible patient .

 

In other words how do differentiate present(Index event)  infarct angina from post infarct angina ?

Studies on pain signal transmission (medullated type c)  would suggest a dull aching retrosternal pain may occur in a substantial number of  patients  following STEMI .These pain signals come from  necrosed cells and not from  ischemic cells. This pain ceases after complete  ischemic destruction of nerve endings . The threshold , duration and central perception of this pain is highly variable.

One can imagine the importance of the above issue ,  as   there is a potential  to  misdiagnose recurrent post MI angina   for the relatively benign infarct related pain. Though experience have suggested a 12 hour cut off to define post MI angina ,  it is too empirical .

Final message

  • Rescue angioplasty remain as  disputed entity in vast majority of  post MI population .
  • It is most useful when  it is done in  impending cardiogenic shock .Note the word. Impending  . . . not established cardiogenic shock. (After prompt recognition of failed thrombolyis ,  within  overall time window < 6h*  ideally ,  but may be done  to up to 12h) There is no role for routine rescue in all failed thrombolysis patients , for the simple reason there may not be any clinical or  live myocardial  targets for rescue.

Need for seperate time window for rescue angioplasty

* Even this 6 hours is emprical . We need  seperate evidence based time window exclusive for rescue angiopalsty .I would personally believe this could  be as short as 1-2 hours .

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Can medical mangement convert a patient with positive stress test into negative ?

Posted in Uncategorized on October 16, 2009| 5 Comments »

Exercise stress test is the most commonly used non invasive  diagnostic test for CAD.

It is also useful in the functional capacity evaluation.Even though medical management of CAD is a proven and accepted  method of therapy in CAD . There  is always a   perception  even   among the  cardiologists  medical management  is an inferior form of treatment.  This is primarily due to peer group  pressure rather than based on solid scientific concepts.

What is the effect of medical  management on  the common CAD parameters ?

Relief of angina  . It is a simple , and easy parameter to assess.

Functional capacity . Increased exercise capacity  is a good marker of successful medical therapy

The effect  on stress ischemia could be most objective way to assess the success of medical therapy.

But , unfortunately this does not come in the regular scheme of things  for many  cardiologists following medical  management. If we are able to document reversal of stress  test positivity it could be the ultimate marker of success in medical revascularisation. EST is an approved method of assessment of efficacy of optimal medical  management .Still ,  in day to day cardiology practice this is rarely done for the simple reason the patient often stumbles upon an  interventionist and lands up in a PCI or CABG !

Following  things can happen over EST following medical management

  • Complete correction of inducible   ischemia
  • Delayed appearance of ST depression with increased exercise capacity
  • Duration of ST depression can be reduced
  • Convert painful  ischemia into silent ischemia*
  • No response **

* Conversion of painful episodes into silent episodes may not be a real success  in physiological terms.But in patient point of view it is .It should be  recalled  even in  CABG  pain relief  is a major clinical  outcome .

** Could be termed as failure of medical management , but there  is a  group of patients who have increased exercise  capacity but still EST is positive

Real world experience of large case studies (Individual communication : Large community based stress test in over 9000 patients ( Gnanavel et all Ganesh clinic Thiruvannamalai ,India ) strongly suggest optimal medical management would indeed reverse exercise induced ST depression.

Why can’t we call medical therapy as a revascularisation procedure ?

Human mind does not accept certain things. Simply swallowing few drugs can never make us believe ( Especially the current generation cardiologists !  )  it can be  equivalent to a PCI/CABG

While , restoration of  TIMI flow ,  %  stenosis , Net luminal gain,  are the popular   scientific parameters fro effective revascularisation , the following are  the  desired outcomes  clinical well being , relief from pain, reduction of plaque volume, plaque stabilisation, maintenance of  collaterals , microvascular patency ,  reduction of recurrent events .The irony in CAD management  is  in many points clinical endpoints can be achieved without mechanical  the above  mechanical end points !( As we learn from the OAT, COURAGE trials where we learn t arterial patency is nothing to do with major  clinical end points )

While PCI and CABG inherently convey they are revascularsation procedures , realistically looking medical  therapy also does improve the vascularisation espcially where it is needed (Micro)

In the overall interest of  CAD community , and with good scientific basis ,  it is vital  to  emphazise medical management of CAD  is  also a  form revascualrisation .It is better to call OMT(Optimal medical therapy )  as medical revascularisation .This will help us  to neutralise the unfair” semantic  advantage” the PCI and CABG enjoys as   revascularisation modalities !

 

Refer: 1.AVERT study :Atorvastatin equals PCI .2.Regular excercise equivalent to PCI (esc2009)

Final message

Medical management , do reverse  the positive EST in most of the patients provided the drugs are optimally used

Stability provided by  medical management   in coronary micro and macrocircualtion is  often  significant and it can either directly  or indirectly improve coronary perfusion .  attenuate ischemia ,  improve exercise capacity and relieve symptoms. To confirm this , every patient  with medical management should periodically undergo exercise stress testing.

* One may argue , without knowing coronary anatomy  it is dangerous to  assume things and every patient with positive EST should udergo CAG. Yes ,  It may be true, ischemia due to  critical lesions in proximal locations can never be corrected with drugs

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