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Archive for the ‘cardiology- coronary care’ Category

Traditionally we believed VT can originate only  from the ventricular myocardial cells . Then we realised many of the VTs shared the characteristics of SVT. When these were analysed , it was found VTs , after all ,   do not have   a big deal of   difference wth SVT s ! especially when it arises from the high septum .Contary to the conventional teaching  the AV node is not a anatomically distinct and discrete  structure  .Instead it is made up of  thousands of specialised cells located in AV junctional area .These cells ramify both superiorly and inferiorly like an octopus . Hence  , it does not require great academics to understand AV Nodal properties extend downward into the IVS for some distance . In some individuals   clusters of cells with  slow conducting  property (Which is a hall mark of AV nodal tissue )  may invade deep into the IVS .The interface of  these slow conducting tissue with that of  fast septal purkinje fibres , make it a  perfect platform for  the potential slow-fast reentry within IVS. This forms the basis of fascicular  VT.

Clinical features

  • Since it shares the  properties of SVT , the natural history is also relatively beningn
  • Occurs in young
  • Hemodynamically stable ( More physiological conduction : Superi inferior Like SVT)
  • Narrow qrs (Narrow because the VTdoes not travel by cell to cell instead  run through the normal conduting system for most part in the circuit)
  • Verapamil sensitive .(Mimic AV nodal Tach)
  • Degeneration into VF is  rare  and hence  SCD is not a big  issue
  • Tachycardic myopathy can occur.

fascicular vt ventricular tachycardia  ecg  svt avnrt avrt wpw

Note:

Fascicular tachycardia is also known in several names.

It forms the bulk of the causes for  idiopathic left ventricular VTs .Other being LVOT VT.

Described first by Cohen in 1974 , followed by Zipes , when they noticed  it was possible to reproduce atrial induction of VT.

Belhassen in 1984 found the verapamil sensitivity of this VT

Other synonyms some times used are

  • Septal VT
  • Narrrow qrs VT

Download high resolution table

Fascicular tachycardia

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  1. Do 64slice MDCT  in all patients who has  a coronary event and follow it up with catheter based CAG.
  2. Use liberally the new biochemical marker ,  serum  B-naturetic peptide (BNP) to diagnose cardiac failure in lieu of basal auscultation.
  3. Advice  cardiac resynchronisation therapy in all patients  who are in class 4 cardiac failure with a wide qrs complex .
  4. As it is may be considered a  crime to administer empirical  heparin, do ventilation perfusion scan in all cases with suspected pulmonary embolism.
  5. Do serial CPK MB and troponin levels in all patients with well  established  STEMI .
  6. Open up all occluded coronary arteries irrespective  of symptoms and muscle viability.
  7. Consider  ablation of pulmonary veins as an  initial strategy in  patients with recurrent idiopathic AF. If it is not feasible  atleast occlude their left atrial appendage with watch man  device.
  8. Never tell  your patients   the  truths  about the  diet , exercise &  lifestyle modification (That can  cure most of the early hypertension) . Instead encourage the  use of  newest ARBs  or even  try direct renin antoagonists   to treat all those patients in  stage 1 hypertension.
  9. Avoid regular heparin in acute coronary syndromes   as  it  is a disgrace to use it  in today’s world. Replace all prescription of heparin with  enoxaparine  or  still better ,  fondaparinux  whenever  possible.
  10. Finally never discharge  a  heftily  insured patient   until  he completes all the  cardiology investigations  that are available in your hospital  .

Coming soon :  10 more ways to  increase cost of cardiology care . . .beyond common man’s reach

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Conduction disturbance is a fairly common occurrence following  MI. Inferior STEMI is especially prone for AV blocks. This is because  the  blood supply to AV nodal  tissues and the inferoposterior surface of the heart  share the same arterial territory . AV node gets it supply  90% of time by right coronary artery(RCA )  and 10% by  LCX. Very rarely from both .

The common bradyarrhytmias that we encounter in inferior MI are

Sinus bradycardia

Sinus pauses ,SA blocks

AV blocks

Functional

Vagotonic

Organic

Ischemic

Necrotic

ECG types

1  degree AV block

2 degree  AV block – Type 1 Wenke bach

Complete heart blcok

Mechanisms

The inferior aspect of the heart has rich innervation of vagal nerve terminals (While the  sympathetic adrenergic system is concentrated in the anterior surface) . The moment infero posterior MI occur it stimualtes the vagus and a prompt bradycardic response occur .Many times the classical hypotension /bradycardia reaction is simply a reflection of heightened vagal tone.

Consequence of vagal tone on SA nodal and AV nodal conduction

As expected, vagal stimulation can result in a spectrum of arrhythmias from the  simple bradycardia to complete SA block  to  AV block. Extreme bradycardia , may release the junctional pace maker and result in junctional rhythm with a rate of around 40-50. There can be a functional AV dissociation between SA node and AV node. Careful ECG analysis is required here ,  as it can mimic organic AV block.The simple way to differentiate between organic AV block from simple AV dissociation is to look at the p waves.In AV dissociation both atrial rate and ventricular rate are nearly equal or VR  is slightly more than AR .In CHB atrial rate  exceeds ventricular  rate.

SA and AV block occur due to various mechanisms in inferior  MI

  • High vagal tone
  • Ischemia of SA/AV node
  • Necrosis of AV node
  • Drug effects -Like morphine
  • Reperfusion bradycardia*

Ischemic AV nodal arrhythmias are  some times very difficult to differentiate from vagotonia especially if occur within 24h.

Irreversible AV nodal block due to necrosis is rare.But if occur , usually  associated with extensive inferior mI/RVMI/ .AV block  that  persist beyond 48-72hours should raise the suspicion of damage to AV node.( As vagal tone is very unlikely;y to last beyond 48h)

* Some time a an episode of sudden severe  bradycardia  can be manifestation of RCA reperfusion.Flushing of SA nodal or AV nodal branch of RCA might trigger this. This has a potential  to  bring the heart to asystole.The resultant extreme bradycardia often triggers VT/VF .The reported high incidence of primary VF in infero posterior MI is attributed to this sudden RCA perfusion.

Medical management for CHB

Brady arrhythmia’s due to high vagal tone are generally benign .No specific intervention is required.Atropine will be suffice in most situations.Some times isoprenaline may be required. Aminophyline , now Ivabradine may have a role. Atropine not only corrects the HR it raises the BP also as  it counters  both cardioinhibitory and  vasodepressive  limbs of vagal stimulus mediated by  acetyl choline .

Pacing for Bradycardias in inferior MI.

  • Generally not necessary for sinus bradycardia.
  • Few with CHB require it
  • Persistent hypotension and RVMI  needs it often.(Dual chamber temporary pacing preferred as AV synchrony is vital here.)

Weaning of temporary pacing in inferior MI.

This could be a tricky issue. It can be weaned off in less than a week.A practical way is to use temporary pacing  only in back up mode at a heart rate of few beats less than the patients rhythm.Pacing for long hours  at high rates may delay the resumption of patients own rhythm and may result in false diagnosis of irreversible CHB and a subsequent PPM

How many will require permanent pacing following infero posterior MI ?

Only a fraction of patients with CHB require long term pacing . There are some centres tend to overuse PPM in this situation. Wait and watch policy may be the best.A unnecessary lead  within a  infarcted ventricle  has a potential to create problems .There have been  occasions a stable RV MI has been destabilised due to RV pacing lead triggered recurrent VF.

Tachycardias in inferior MI

It is relatively uncommon.Atrial involvement is more common with infero posterior MI and hence a greater incidence of atrial fibrillation .

RV MI can induce ventricular tachycardia arising  from the RV myocardium

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cardiologist Is he a person who puts  a   metal coil  coated with a synthetic fungus   in  a   incidentally  detected  block  inside a  small coronary artery and sends the bill to the Insurance company ?

Is he a person in a  cosmopolitan  hospital  who opens up a    chronically   closed  coronary artery , in an asymptomatic patient  and  live telecasts  his achievement trans continentally ?

Is he a person who   checks in by  the early morning flight and  puts multiple wires in  an  aged   patient   with  class 3 heart failure and  make  him walk  20 meters extra at a cost of  1000$ / Meter ?

Is he a person living in   Wall   street  ,   who   looks  for variety of holes In  the heart and trying to occlude  it  with   exotic   devicespci ptca stent

Is he the unknown   physician   who Intervenes in the natural history of Rheumatic heart disease   and arrests   immune mediated   valve damage by giving the  monthly injections  penicillin in remote parts of our country ?

Is he the person   who   Intervenes to prevent young   persons   from  smoking and help maintain  their  coronary endothelium  enriched with nitric oxide  & arrest  the coronary epidemic ?

cardiologist 2

Is he the small town doctor  who  Intervenes  to treat a breathless cardiac failure patient  with  digoxin and frusemide  and  dramatically alleviate the  symptoms and  prolong the  life of our poor country men?

Is she the village health nurse from an inaccessible health  centre  located in a  hilly terrain ,  Intervening  successfully, by   pulling out  live babies  from  severely anemic pregnant  mothers with failing hearts ?

pci ptca cardiologist coronary angiograms

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Fundamental principle  of  human biological system is to live in harmony with nature and environment.Each cell  has a unique reaction  when it comes into contact with  external  material. This reaction can be acute or chronic  ,   local or systemic. The most severe form of allergy is called anaphylaxis  that can result in instantaneous loss of life. There  is a whole gamut of disorders  that  resulted  in a  separate  speciality called allergic medicine .

Further ,the transplantation  science have   taught us  an  organ or cell can be rejected at any point of time after implantation (Hyperacute -chronic) .With advancement of science we have started implanting a variety of devices  with complex metallurgy ,inside human body, metal clips, prosthesis, valves, wires, etc .How the body handles them .The consequences can be a mild reaction to major ones occasionally.

Consider ,a local allergy due to a orthopedic prosthesis  in one of the leg bones  is far less serious than a metal within a coronary artery  irritating the intima .

Remember hypersensitivity reactions can be severe . This lady reacted  like this to a sandal slipper -A  fiery red  infiltration

contact dermatits stent allergy pci coronary

Imagine  if a stented coronary artery react like this what would be the possible consequence ?

In susceptible  individuals  , can a metal cause

  • Intimal hyperemia
  • Intimal induration
  • Intimo-medial edema  following stent deployment

pci stent coronary angiogram thrombosis des

Why drug eluting stents are more prone for hypersensitivity ?

The answer is simple , while metal allergy is a comparatively rare phenomenon, the drugs we  coat and the polymers used are  many fold likely to result in hypersensitivity reaction.

While  the world is worried  more  about penicillin , sulpha allergy which occurs in 1 in 100000 ,  we tend to ignore the metal and drug  reactions within  the tender coronary arteries.

stent des rejection virmani  pci

What is  the clinical expression of  stent hypersensitivity ?

It is  often a coronary event in the acute phase and restenosis in chronic phase.

How much of acute stent thrombosis is related to stent allergy mediated reaction ?

The exact incidence  will  never be known. It could be high. Whenever a sudden unexpected early stent occlusion can be a suspect .

Is stent allergy a local reaction or systemic reaction ?

It is most often local .The drugs the stent elute can elicit a systemic reaction occasionally.

So what can be done to prevent this complication ?

Drug companies in it’s  package regularly  include the warning  message ! What does it imply to have a caution  on the covers ? .This warning simply represent about our ignorance in this issue. We presume it is a minor problem.

pci stent thrombosis stent allergy metal

Questions unanswered

  1. How does a cardiac patient knows whether he is hypersensitive to stainless steel or nickel ?
  2. Is it practical to have a stent allergic test in every patient before PCI ?
  3. Is routine administration of corticosteroids for few days after PCI an answer ?

Reference

R.Virmani , circulation 2004

http://circ.ahajournals.org/cgi/content/full/109/6/701?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=stent+%27allergy%22+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

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Myocardial infarction (STEMI)  occurs in two distinct arterial  territories .The anterior LAD circulation and postero- inferior RCA/LCX circulation.The incidence is equally shared.

There has been some  learned and unlearned perceptions about Inferior MI.

Inferior MI is less dangerous than anterior MI.  True or false ?

Answer: Essentially true in most situations.

Reasons.

Inferior wall of the heart (strictly speaking there is no walls for heart , only surfaces , which blends with adjacent areas)  inferior wall  is formed by diaphragmatic surface and posterior surface.Inferior MI can occur by either RCA or LCX obstruction.The outcome of inferior MI is determined by mainly by  the extent  of   LV myocardial   damage it inflicts.To  quantitate this  we need to know , how much of LV is supplied by RCA , or LCX or combination of both ? This depend on the coronary dominance .It is estimated , the bulk of the LV is supplied ( up to 75%  ) by LCA. This becomes further high in left dominant circulations . In fact , it is believed LV can never get involved in non dominant RCA occlusions. This has brought in a new terminology  called “Small inferior MI”.Inferior STEMI due to PDA  occlusion or in a co -dominant circulation is not yet studied

Apart from the above  anatomical considerations the following clinical observations  have  been made regarding inferior MI.

  • When thrombolysis was introduced , many studies  suggested the the ST elevation in inferior  leads toched the isolectric levels  in most situations even without thrombolysis.Technically, this implies spontaneous , successful thrombolysis are more common in RCA. Among the thrombolysed ,persistent ST elvation is a rare phenomenon.
  • The well known difference in the conduction defect between anterior and inferior MI  is an important contibutor for better outcome in the later.(AV blocks in inferior MI , are often transient, non progressive, supra hisian location rarely require permanent pacemakers)
  • During acute phase cardiogenic shock occurs in a minority (That too , only if RV shock is included )
  • Even in the follow up the ejection fraction in inferior MI is  almost always above  40%. In many EF is not affected at all.
  • Progressive adverse remodelling of LV is rare

When can Inferior MI be dangerous ?

Anatomical factors

Inspite of the  above  factors  inferior MI can not be taken lightly . Especially when it  extend into posterior, lateral , (Rarely anterior) segments.

While  posterior extension  is often  tolerated , lateral extension is very poorly tolerated .This is probably explained as  the extension involves the vital free wall of LV and the laplace forces could precipitate LVF. Free wall rupture is also common in this situation.

Posterior extension , predominantly involves the surface of RV which is less important hemodynamically. Of course incidence of MR  due to it’s effect on posterior mitral leaflet can be trouble some.

inferior MI ECG

High risk clinical catagories.

Out of hospital STEMI  are at  equal  risk irrespective of the territories involved  .This is because,  primary VF does not differentiate , whether  ischemia comes from RCA or LAD .

  1. In elderly , dibetics and co existing medical condtions  the the established  benign   character  of  inferior MI disappear, as  any  muscle loss  in LV has equally adverse outcome.
  2. Even though  inferior MIs are immune  to cardiogenic shock  , a equally worrisome  prolonged hypotension due to high vagal tone, bradycardia, plus or minus RVMI can create trouble. Fortunately , they respond better to  treatment. Except a few with extensive transmural RVMI outcome is good.
  3. Presence of  mechanical complications of  ventricular septal rupture , ischemic MR can bring  the mortality on par with large anterior MI.

How different is the clinical outcome of infero-posterior  MI with reference  to the  site of  coronary arterial  obstruction   ?

The sequence of  outcome  From  best to worse  : Non dominant RCA* → Dominant RCA but distal to RV branch → LCX dominant with large OMs

* It is believed   an  acute proximal  obstruction of a  non dominant RCA may not be mechanically significant, but can be electrically significant as it retains the risk of primary VF and SA nodal ischemia. The ECG changes  can be very minimal or  some times simple bradycardia is the only clue. One should be able to recognise this entity (Non dominant  RCA STEMI)  as the outcome is  excellent and these patients  would never require procedure like primary  PCI

** A inferior MI due to a dominant LCX and a large OMs have comparable outcome as that of extensive anterior MI. The ECG will reveal ST elevation in both inferior and lateral leads.

***In patients with prior CAD  and collateral dependent  multivessel disease  the  inferior anterior sub classification does not make much sense as  entire coronary circulation can be mutually interdependent.

Final message

Inferior STEMI  generally lacks the vigor  to cause extensive damage to myocardium in most situations .Further they respond better to treatment. Risk stratification of STEMI based on the location of MI has not been popular among mainstream cardiologists. This issue needs some introspection as  the costly and complex treatment modalities like primary PCI  is unwarranted in most of the low risk inferior MIs.

Related posts in my blog:

1.Why thrombolysis is more effective in RCA?

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Total coronary artery occlusion is a common finding in CAD  especially in chronic stable angina. Normal coronary blood flow is 5 % of cardiac output  that amounts to 250-300ml/mt.At an average  heart rate of  70/mt  , each  beat  injects  about 5cc blood into the coronary circulation.This is shared between two coronary arteries.  This means , only few CC (2-3cc) of blood enters  each coronary artery with each cardiac cycle .

When one of coronary artery is totally occluded what happens to the coronary

blood flow ?

A.Total coronary blood flow  can be be  maintained   normal  at rest  as it  forms  only about 5% of cardiac output  (or it is only  slightly reduced )

B. It is believed , the unobstructed coronary artery  could receive the blood meant for the contralateral coronary artery. This  possibly explains the increased coronary artery diameter in the non obstructed artery.

C. It’s nature’s wish ,  that the  contralateral  coronary artery  shall share  50% of  it’s  blood through  collaterals if available.

D.If collaterals are not formed it , the unobstructed coronary  artery  may be over perfused with double the amount  of blood flow.

E. Some times , the collaterals steal  much more than what  the  obstructed coronary artery  deserves and make the feeding coronary artery ischemic. This is many times observed in  total RCA occlusion with well formed  collaterals  from LAD/LCX.

F.The collateral flow  in CTO also depend on whether flow is directed from LAD system to RCA or from RCA -LAD system. The LAD is better placed to assist RCA than vice versa.This is for two reasons.1.LAD blood flow is higher than RCA so it can share it.2.The driving pressure is more  from LAD -RCA , as RCA can receive  blood flow even during diastole .

F.During exertion , the coronary hemodynamics become further complex.The collateral’s are traditionally thought to be less than adequate during times of exercise.But it is more of a perception than solid scientific data.This rule  may be applicable in only certain group of patients. We know CTO patients with very good exercise tolerance who have documented collateral’s.

G.Collaterals can be either  visible or invisible by CAG. The strength of collateral circulation is not in it’s visibility but it’s capacity to dilate and  respond to neuro humoral mediators at times of  demand.  Currently  , there is lot to be desired  regarding  our knowledge about  the physiology  of visible collaterals , no need to  mention about invisible collaterals !

Final message

The above statements  are based  on logics and observations .

Is it not a  irony  in cardiac literature ,  where  thousands of articles  are coming out every month  to tackle  totally occluded coronary artery(CTOs) ,  there is  very little data   regarding the coronary hemodynamics in chronic total occlusion .   How  does a patient with CTO can manage a active life with only one functioning  coronary artery ?

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Ventricular remodeling  follows large myocardial infarction .This term denotes to  change in size , shape  and function  of the ventricle   due to altered  myocyte geometry .It is now believed  , this  process begins to occur very early  following a STEMI.(less than 24hours)

lv-remodeling

In which MI remodeling is more common ?

Any MI of large size , especially  anterior  and lateral MI.  Inferior and posterior MI are less affected by adverse remodeling.The incidence is up to 20% of all myocardial infarction ,  if left untreated. Ventricular aneurysm formation and dyskinetic segments can be termed as the worst form of remodeling. The old terminologies of infarct extension and expansion could by synonymous with ventrilar   remodeling .(Note : Every patient with STEMI undergoes some form of physiological remodeling that should not be confused with progressive pathological remodeling , we are discussing  here ! )

What is the clinical impact of remodeling ? How to prevent it ?

Progressive cardiac failure and a  poor outcome .  It may provoke ventricular arrhythmias. ACE inhibitors (CONSENSUS study 1992 )  has since revolutionized  the pharmacological  prevention of adverse remodeling.

How to recognise left ventricular remodeling ?

Many methods are available .

  • 2 D Echocardiography
  • Tissue doppler
  • LV angiogram
  • MRI

These imaging methods diagnose remodeling  only after it manifest* .We know remodeling is a cellular and molecular process .The earliest trigger for remodeling is the mechanical stretch and wall stress on the ventricles.Large areas of necrosed myocardium and  the adjacent normal myocardium sets a perfect stage for eccentric pulling of myocardial segments and unregulated slippage of myocytes.

* Diagnosing fully established  ventricular remodeling  serves ,  no great   purpose as it is very difficult to reverse it by pharmacological methods.it requires complex surgery.

What is the effect of mechanical stretch on cellular function ?

It is well known  myocyte granules secrete Type B  -Naturetic peptide  in response to stretch. It could be a very early sign of adverse remodeling. So monitoring of  BNP may give us an opportunity to intensively treat those patients who are likely to land in progressive cardiac failure.

A baseline level of NT-proBNP >120 pmol/L identified patients  prone for adverse remodeling .Serial measurements showed further increase. It is possible to identify adverse remodeling of LV by documenting fresh elevation of BNP following MI .

Reference :

1 )Nilsson JC, Groenning BA, Nielsen G, et al. Left ventricular remodeling in the first year after acute myocardial infarction and the predictive value of N-terminal pro brain natriuretic peptide. Am Heart J 2002;143:696-702.

2)http://content.nejm.org/cgi/content/full/352/7/666#R24

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The answer to this question  is not  easy  , as   one  would tend to believe . In fact this question , takes it for granted     revascularisation  will  improve the LV dysfunction in patients  with severe LV dysfunction.

The truth is , we  are not sure   about the mechanisms . How   revasculariastion  will have an effect  on  chronically dying or dead myocardium  ? (Acutely dying myocardium is a different story, where revascualrisation has a profound effect , that is called salvaging the myocardium )

This  issue is  of great clinical significance  in end stage ischemic heart disease  .A typical  myocardial segment in ischemic cardiomyopathy  has millions of  the dead cells  interwoven with dying cells  with  occasional  clusters if live cells scattered all over .Once the process of myocardial apotosis sets in ,  myocardial cell death does not result  in segmental destruction  instead  an universal cell death.(Paracrine signals of  cell death that spills over to adjacent segments  )  The current standards of revascualrisation (PCI and CABG) aims to provide blood flow  in a segmental fashion. Even if the blood flow is restored in an obstructive vessel it is not clear , how it is going to enter the chronically atrophied myocytes.

Meanwhile , many studies are available   suggesting  coronary revascularisation does indeed improve LV dysfunction. These  evidence has never been  conclusive .Real world experience would also  confirm this  simple fact , that   angina relief is definite following revascularisation but not dyspnea  relief  in patients  with LV dysfunction .

So ,  when seeking the  guidelines  for revascularisation  ( PCI or CABG )  in patients  with CAD one need to ask  this  specific  question

Does the patient has

A.Angina alone

B.Angina and dyspnea

C.Only  dyspnea

If the answer is C ,  assess the patient again , rule out systemic causes of dyspnea (Anemia, renal function etc)  rethink  or postpone  revascularisation.If primary  or secondary LV muscle dysfunction has set in revascularisation has little value.

Also read

Viable myocardium

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Coronary collateral circulation is the God’s gift to mankind.It has potential  benefits  ( and  of course real benefit !)  both during acute and chronic coronary syndrome.

Collaterals in CCS

The classical role of coronary collateral is in patients with chronic stable angina.It is quiet common to see patients with totally occluded  LAD or RCA with normal  LV function maintained  by extensive collaterals .

Collaterals during ACS.

An intact and functional  collateral circulation can prevent an NSTEMI  from converting into STEMI.In fact many of the patients with unstable angina patients carry on with viable myocardium just because thaey have good collaterals.It gives us a time window to intervene .Some times the col laterals are good enough and help us avoid a revascularisation in toto.

Collateral’s in  STEMI.

This is not well understood. Some  researchers  reported opening up of collateral channels very early after a STEMI. Logic would suggest , anatomically patent functionally closed collateral channels are  always available at time of crisis. But not every one is blessed with such rescue mechanism.

What determines  the native collateral channel development in human cor0nary circulation ?

When  the answer is unknown , it moves to  the  genetic domain also called  – God’s domain .

Our ignorance in decoding coronary collaterals is vast.

The chief cause of this ignorance is we always  tend , not believe things which we don’t see.

Coronary collaterals channels need to atleast 1mm  to be visualised by CAG.There could be a vast network of micro collaterals out there within the myocardium invisible to current imaging methods. (In fact , this has a link with outcome  of the COURAGE study )

Is coronary collaterals have all the three layers of an artery ?

Yes .But the media lacks muscle.

Is coronary collateral less prone for spasm ?

May be.

The drugs we give , Calcium blockers , betablockers, and nitrates have same  hemodyanmic effects  as in native coronary circulation ?

We don,t know as yet. Nitrates are supposed to improve collateralisation

How common is atherosclerosis to involve the coronary collaterals ?

How often is an ACS precipitated by an collateral occlusion ?

May be more common than we think.

Can we stent a  2mm wide  collateral to maintain  the patency in case of a CTO  ?

A question need to be answered by current generation interventional cardiologists.

Is coronary collateral gives protection against primary VF ?

In one sense ,  the number one killer of mankind is  in fact not STEMI but the VF that follows it .

Why only a few develop a VF following an MI ? What determines the arrhythmic response to ischemia ?

Some anecdotal observation  of     suggest a role for early coronary collateral  opening in the prevention of VF .

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