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Coronary artery disease is the major determinant of human  health and longevity  in this  modern era! Obstruction of a coronary artery either sudden or gradual  forms the basis of  CAD .

When a free flowing  river stumbles upon an  obstruction , it does not die , it finds it’s way to the sea. Similarly , God is kind enough to provide  alternate channels for blood flow to heart at times of crisis .Contrary to the perception , collaterals develop not only in chronic occlusions but also in acute occlusions.

A person who dies due to a primary VF few minutes after an acute occlusion is in all probability experiences his fate  ! While those who survive are protected by the immediate recruitment of collaterals and this prevents the   remote myocardium  from triggering a VF.

In chronic CAD, the collaterals are much more effective. Now we have evidence with OAT and COURAGE *trials for this. Some times , the LAD is fully supported by the RCA the flow is better than a graft.

*These trials showed us opening occluded coronary arteries routinely do not confer additional benefits.

Coronary collateral circulation is most poorly understood phenomenon in cardiology. But it comes as helping hand whenever required  only for those humans who deserve it !  God has kept the secrets of coronary  collateral circulation with himself !

A excellent article on natural by pass from circulation patient pages.

http://circ.ahajournals.org/cgi/content/full/116/11/e340

Link to related you tube video

http://www.youtube.com/watch?v=qQfUttiDgE8


Cardiac rhythm disorder remains  as a  fascinating  clinical cardiac  problem  to  the physicians for many decades. The joy of decoding cardiac arrhythmias and categorizing into supra ventricular , junctional, ventricular tachycardias is unique ,  even as  many of these patients are struggling for life !

Initially the tachycardias were labeled with reference to their origin .Later as we recognised the locating the  origin is not an easy exercise , we introduced a practical classification  : Narrow and wide qrs tachycardia  emphasizing the fact that , both SVT & VT  can be either narrow or wide !

Traditionally there is much more  confusion in labeling the  narrow qrs tachycardias than the wide  qrs tachycardia.

Is the term junctional tachycardia still relevant ?

To answer this question we need to know what exactly we mean by the term Junction.

  • Is it a particular anatomical spot  called AV node ?
  • Is it a diffuse area in the vicinity of AV node ?
  • Is the early part of the his bundle included in the junction ?
  • Or  Is it formed by  the entire rim  of both  AV groove formed by the fibroskeleton  that form a electrical  barrier between atrium and ventricle ?

Answer:

The answer to the above question is very simple “we don’t know yet !”

The nearest fact is , for the electrophysiologist,  AV junction refers to the electrical  junction box of  that connects the specialised wires coming down from the atria and from there it connects  to the specialised his purkinje fibres of the ventricle .

Is AV node  anatomically distinct structure?

No .It is not. It is a collection of different conducting cells with varying properties.The term AV node need to be abandoned by the cardiology community for the simple reason there is no such entity.

In fact the AV junctional cells are are now called as pure atrial,atrial approach CELS ,  junctional approach cells, junctional cells,transitional cells,  ventricular approach cells.These cells interdigitate with each other , and has unique cell to cell communication.The cells that are above the AV junction share atrial electrical properties while the cells that touch the his purkinje  acquire some of the properties of specialized ventricular conducting properties.

What is the function of AV junction ?

One should realize  it is the AV junction does a  a very unique job of great importance  for human   survival ! Even though SA node is the pacemaker of the heart , the AV junction does the extraordinary it receives the impulse and delays it for about 200 millisecond and then hand over it to the ventricle.

The rules that govern the  nature is so fascinating  , this delay is vital for the venous return to enter the ventricle from atrium other wise , the ventricle is under filled and cardiac output falls.The bulk of the PR interval is contributed by the AVconduction delay (also called as AH interval )

What is the clinical relevance of this new found physiology of AV junction ?

It is to be understood the electrical properties of the AV junction is determined by neural innervation the ionic currents.Much of AV junction is under the dominant control of vagal fibres, while the ventricles get more innervation from sympathetic neurones. There is considerable overlap in the AV junction area.

The classical dual nodal physiology of AVNRT is nothing but longitudinal physiological splitting of AV junction  .Strands of slow conducting cells and fast conducting cells are arranged in such a way to create a reentrant circuit.The atrial approaches in the posterior aspect contain mainly slow pathway. and anterior aspect near his contain the fast pathway.

Some times  clusters of AV junctional cells are scattered around the upper septal area giving a slow conducting properties to ventricle.These cells can be site for reentrant septal or fascicular VT.

The overlap of  these AV junctional cells explains the verapamil sensitivity of some of the VTs  arising in the vicinity.

What are the tachycardias that can be termed  as junctional tachycardias ?(JT)

By logic and realism  any tachycardia that originates in the AV junction either by reentry or ectopic activity shall be called as JT

By tradition , we have been illogical.

AVNRT is never referred to as JT  in spite of the fact that,   it is initiated by a pathological reentry right  in the middle of AV junctional tissue.

So currently we are authorised to call only few arrhythmias as true junctional tachycardia  .

  • Non paroxysmal junctional tachycardia( NPJT)
  • Incessant junctional tachycardia
  • Permanent  junctional reciprocating  tachycardia(PJRT)
  • Accelerated junctional  rhythm

NPJT

This occurs in following situations

  • Digoxin toxicity(Classical description)
  • Post operative hearts
  • Occasionally during acute MIR
  • It may be observed during AV nodal ablation in EP LAB

NPJT is an automatic tachycardia .arising focally from AV junctional tissue . Ideal terminology should be focal junctional tachycardia(FJT) .The rate is between 70 -140. Accelerated junctional rhythm can be termed as a benign form of JT.DC shock has no role.

Incessant junctional  tachycardia

This was first described in infants .Thought to be congenital in origin.Now adult forms also recognised.Very malignant arrhythmiaRate is between 150-300. AV dissociation is the norm.May mimic atypical atrial flutter or ectopic atrial tachycardia .High risk for tachycardic cardiomyopathy. Amiodarone may be effective.Surprisingly ,verapamil may worsen it .There is a overlap between adult postoperative NPJT and Incessant JT.DC shock is not effective may worsen . RF ablation rarely effective.

Permanent form of junctional tachycardia

It is not clear what the  term permanent denotes ! May be because   these tachycardias occur with fixed anatomical substrates.In fact this can be called as a type of AVRT. But the difference is the retrograde ventricular circuit does not travel in any free wall but within the septal his bundle   . PJRT,  infact  may be labeled as AHRT -Atrio hisian  recipocrating tacycardia

It is a reciprocating tachycardia with antegrade condction through AV node and retrograde through a slow conducting accessory pathway in posteroseptal location.

The rate is between 90-150. Mimics long RP tachycardia like AT or fast slow AVNRT.Some believe , In fact a fast slow AVNRT can be  nothing but a variant of PJRT.

DC shock may be effective only to recur again.RF ablation is very effective .

Final  message

Junctional tachycardias are a unique group of narrow qrs  tachycardias  with differet mechanisms.It is diagnosed in specific clinical settings. They are generally difficult to treat,as the mechanism is often ectopic in nature (Except PJRT).Accelerated junctional rhythm can be termed as a benign form of JT. AVNRT need not be confused with JT , even though it may considered as a junctional reentrant tachycardia.

 

Reference

Rosen Circulation 1973

Role of d dimer in acute aortic syndromes

D -Dimer is a marker of  intravascular fibrinolysis .It is a degradation product of fibrinogen. A level more than 500ng/ml is significant.In acute aortic dissection this level is reported to be more than 2000ng/ml.

The beauty of this molecule is it is elevated in three important chest pain emergencies.

  • Acute myocardial infarction
  • Pulmonary embolism
  • And now aortic dissection.

The issue is not simple , as we know any intravascular coagulation and lysis can elevate this molecule.In patients with chronic CAD as like a chronic thrombotic lesions within the coronary arteries can also elevate d dimer.

Similarly , in portal, cortical, deep venous thrombosis all result in elevated D dimer.

So , such a non specific test  , how can be  useful in the diagnosis of aortic dissection ?

Yes, you are right ,

D Dimer helps us  not in diagnosing aortic dissection but  helps us in ruling out a possible dissection

D-Dimer levels <500 has a negative predictive value of 98% .

What is the bio- chemical  dynamics of  D dimer in dissection ?

D dimer in aortic dissection is mainly secreted within the false lumen. For d dimer to secrete into  systemic circulation  the clotted area should be exposed to a adequately flushed systemic blood at a good perfusion pressure.The contact area between the clot and fresh blood  is of critical importance.

d dimer aortic dissection false lumen

So ,  even though it has been reported d dimer has near 100% negative predictive value . . . is there a chance a dissections might occur with normal  d dimer levels ?

Yes, very well possible with due credits to published data

  • A dissection without thrombus(Rare . . . but still possible !)
  • A clot confined to false lumen with entry or exit points sealed.
  • A dissection without a exit point.
  • Intramural hematoma with no communication with aorta

Infrequently asked questions

  1. Time window ? Dimers are mainly useful in  patients who report before 24h after the onset of chestpain.
  2. How long it takes for the dimers to  get excreted ?
  3. Can coronary dissections in STEMI elevate dimer ?

Final message

D dimer is  mainly useful in  “not making a diagnosing” aortic dissection.

If  dimer levels are strongly  positive and  clinically the patient  has  has no evidence for acute MI or acute pulmonary embolism  and continues to have chest/back/atypically located pain  suspect aortic dissection , and order for further imaging like TEE,MRI, MDCT etc.

* Do not forget the role of routine , simple bedside transthoracic and suprasternal echocardiogram.It can diagnose dissection correctly in good number of patients.

** Never oder for costly thoracic imaging whenever d dimer is elevated.

*** When you send the sample for dimer make sure to mention  the clinical likelyhood of dissection .If it is very high the lab has every reason to reject the sample and suggest you to go ahead with thoracic images.

This is because ,  it could be costly miss . . . if you depend on dimer to diagnose a dissection

Imagine this scenerio , while your patient has a absent left radial pulse due to dissection and you are waiting for the lab report to arrive !

Never use it for diagnosing aortic dissection.

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.

Thorax is a rigid bony box with a fixed space.The intra thoracic organs are snugly arranged within the cavity.The two lungs on either side with the heart in the middle fill the major volume of the mediastinum .In physiological conditions the volume of mediastinum remain almost constant , except for the respiratory swings.

heart lungs pulmonary function test dyspnea cardiomegaly ct ratio

It is to be noted the two major organs inside the thorax has a distinct behavioral pattern. Lung a very pressure sensitive structure tend to collapse whenever confronted with external pressure .This is evident in all cases of large pleural effusion (Note :The heart collapses only in a fraction of patients with large pericardial effusion -ie tamponade) . Similarly in any mediastinal syndromes , first the lung function is affected , logics then dictate , the low pressure venous system to get compressed resulting in SVC /IVC syndrome.Finally the right heart chambers may get interfered with .This is due the dynamic intracardiac pressures that resists any compression from exterior.

So, it is obvious , lung function is affected with raised intrathoracic volume or pressure .The increase in intrathoracic volume can be due to any thing .

cardiomegaly massive dyspnea mechanism lvedp

The volume of heart in cardiac failure can increase very significantly .For a fraction raise of CT ratio there is many fold raise in it’s volume.A CT ratio of 75% can cause a huge ” housing & accommodation ” problem for the lungs on either side . As we have discussed , the lung is passive organ has absolutely no other option but to bow down like a touch me not plant . The lung , reduces it’s ventilatory function impairing the already poor exercise capacity .The terminal respiratory units collapse significantly. This collapse is not visible in x rays as there is no intrinsic obstruction within the airways as happens in lung pathology.

The course of events in progressive cardiomegaly is often silent and heart successfully encroaches the the human breathing space until the heart failure is corrected and normal heart size is restored. Complete reversal of heart size may not be possible always !

A new unrecognized mechanism for cardiac dyspnea ?

Yes,the mechanism of cardiac dyspnea always been centered around elevated LVEDP , lung congestion etc and the resultant stimulation of lung receptors.

Now we realise a reduction in the lung ventilatory capacity may also contribute significantly in every patient with cardiac failure and cardiomegaly.

When a person with single pnemonectomy lead a comfortable life what is the big issue of heart compressing few respiratory segments of a patient ?

It is true a single normally functioning lungs is sufficient for living but what we are dealing here is patients with compromised cardiac function.Recruitment or non recruitment of even few respiratory bronchooles may have a bearing on patients symptoms and exercise capacity.

Final message

Cardiomegaly is not an inert consequence of cardiac failure. It can have important functional impact on the pulmonary ventilatory and perfusion capacity .It should be emphasised this mechanical encroachment on the lung space is over and above the hemodynamic effects on pulmonary capillary circulation .

Youngsters should recognise this fact as this offers one more explanation for cardiac dyspnea. This is not often discussed in the clinical classes.

Reference

http://10.1067/mhj.2000.110282

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.

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 🙂

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 NEJM’s breaks the  hidden truths about cardiopulmonary bypass in a beating  heart. The irony in medical science is   ,  trend setting  land mark articles usually arrive  very late . . .   to disappoint  all those  patients who  got the wrong treatment ! Off pump by pass is definitely one among them . . .

The major reason for off pump CABG’s s poor showing is

  • The surgeon’s  conflict   in defining   what is successful CABG  .The success of CABG   is   in    relief of symptoms & providing good bypass graft  with long term patency   .It is not in  less  thoracic trauma or in  a quick hospital discharge  !
  • The second major reason is denial of  the fact  that off pump CABG is indeed inferior  and hence no course correction was attempted  ! ( And  now that it   has become a hard  evidence   we expect some changes  . It  required almost 10 years for our cardiology community to  recognise this .)
  • Lesion access and  difficulty in mobilizing LIMA .Many times the the point of anastomoses is preselected by the accessibility and technical issues rather than lesion guided approach .This often happens than we imagine , and this could be a very bad advertisement for off  pump CABG

cabg on pump vs off pump beatin heart

Click on the link to NEJM abstract  ROOBY study

http://content.nejm.org/cgi/content/short/361/19/1827

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.