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Posts Tagged ‘RCA’

This is an  RCA of   a  patient who had chronic stable angina  , class 2  with moderate anti anginal medication.

What shall we do ?

  1. The RCA needs  multiple stenting
  2. Multiple plain balloon angioplasty
  3. CABG to PDA
  4. No intervention ?
  5. It depends upon status of LAD  and LCX

The correct response would be 5

Without knowing  the status LAD and LCX . . .  RCA should not be touched . Further,  the concept of tackling  the  coronary artery  by itself  is   fundamentally wrong !  We are supposed to tackle patient’s symptom ,   reduce future risk of  events and   not merely  their coronary artey !

His LAD and LCX was near normal. In the weekly  cath   meet   PCI to mid RCA  covering  the critical segment was  strongly debated but  lost a close race .

The final decision was to allow the patient to continue   intensified   medical management (Statin 80mg /Metoprolol 100mg ) . He is comfortable with that .

Medical management  in a tight  single vessel disease  can never be digested by  any   Interventional cardiologist  whatever   may be  the guidelines !

Final  message

Do not decide PCI on the basis of   how ugly a coronary artery looks , rather spend some time on true  symptomatology ,  optimise baseline therapy  and re assess risk profile

One learned dictum is ,  do not  meddle a RCA ,  however severe the lesion may be   if  LAD and LCX are fine.*

*This  rule is not applicable in ACS

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Sinus node which orchestrtes the rhythm of life  gets it’s blood supply by a small blood vessel arising from either RCA or LCX. (55 :45%) . The  course of sinus node  branch  is highly variable .

There are three distinct pattern observed.

  1. Posterior encircling  of  SVC .(50%)*
  2. Anterior  encircling  of  SVC(40%)
  3. Form a  “garland like ” anastomosis  on either side of SVC (10%)

* Some refer to as clockwise and counterclockwise course.

SA node is a spindle shaped structure with a length up to 20mm . Extending from cranial to caudal aspect.The pecularity of the blood supply to SA nodal artery is  , it enters the SA node either in it’s superior aspect or inferior aspect never  in  the mid part. There can be water shed area in the either ends depeding upon the entry.This can have  electrophysiological and  pathological significance .

The other consistent feature is that ,  the major trunk of SA node artery courses through the central core of SA node.In fact , many times pathologists recognise ther SA node ,  with the help of   this arterial course.

Is there a collateral blood supply to SA node ?

It is not common  . Rarely  atrial branches of LCX /RCA  can have extensive anastomosis with SA nodal branches .The hemodynamic significance  of which is  not known. 

Ischemic SA nodal disease has become an important entity . As the cardiologists are preoccupied with opening  occluded coronary arteries  in cath labs , it  is not  surprising to note, there is little  ongoing  research  in the anatomy and physiology of SA nodal  blood supply.

We have to go back in time to get some great articles on the  subject

At this point of time ,  we should realise  the 1ooth anniversary of  SA nodediscovery passed of silently  .  Kieth and Flack  found the SA node with bare eyes  in the year 1907 , when none of the present-day investigations  including ECG and X RAY were  not even conceptualised !

With  tributes to those humble pathologists like  M.J Davies, R.H .Anderson, T.N. James,M. Lev ,J.L.Titus  who   followed   the foot steps  of  Kieth and Flack ,

Here is a  link to one of the great articles on the blood supply to SA node

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC514694/pdf/brheartj00203-0035.pdf

Related point : How do you  recognise  the  SA nodal artery in coronary angiogram ?

During RCA angiogram it is many times confusing  to identify the SA nodal branch . In RAO and LAO views the plane of exit  of SA nodal branch from RCA  will be determined by the  course  it is going to take .(Anterior vs posterior encircling pattern). The conal branch  which is often the first branch of RCA  ,  also behaves aberrantly  many  times. So, we can’t have a rule of thumb in identifying SA nodal branch .

When SA node branch originates from LCX it has to take a long route but once it reaches the SVC/RA junction it takes  one of the above described course. It is not clear whether LCX  fully understands it’s responsibility  , when RCA ignores it 45 % of times .  There is reason to suspect the commitment and dedication of LCX  because it rarely supply  the SA node by a   seperate branch.  It is often the left atrial CX  that comes to the rescue  and give a twig to the  SA node .

Considering the complexity of SA nodal blood supply  , one can understand  why some develop premature sinus node failure. One can never determine with evidence , how much of SA node destruction is due to ischemia and how much is due to age related degeneration and fibrosis.

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Persistent ST elevation is the  general technical term for  failed thrombolysis.Regression of 50%  of admission ST elevation is the required criteria for susccesful thrombolysis .

Thrmobolysis fails in about 40-50% .

Main determinant is the timing of thrombolysis – not the thrombolytic agent ! do not get carried away with all those curent hoopla  about Tenecteplase stuff

If we take 100 patients with persistent ST elavation 90-95 will be in anterior LAD territory .

This is a stunning a cardiology secret no book of cardiology address . . . Implication of which could be very significant . Primary PCI  will always struggle to  prove it’s superiority over thrombolysis  in the right coronary artery .(Note LCX STEMI is different , infact it is more tricky than even even LAD .This issue will be addressed seperately in my blog.)

Read the following link  for  answer to the title question .

How common is persistent ST elevation in inferior leads following STEMI ? https://drsvenkatesan.wordpress.com/2008/09/22/why-thrombolysis-rarely-fails-in-right-coronary-artery/

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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

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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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NSTEMI  constitutes a  very heterogeneous population .The cardiac   risk   can vary  between very low to very high .  In contrast ,  STEMI patients  carry  a high risk for  electro mechanical complication including   sudden death .They all need immediate treatment  either with  thrombolysis or PCI to open up the blood vessel  and salvage the myocardium.

The above concept , may  be true in   many situations  ,  but what we fail to recognize   is  that ,   STEMI   also  is  a heterogeneous clinico pathological  with varying risks and outcome !

Let us see briefly ,  why this  is very important  in the management of STEMI

Management of STEMI  has undergone great  change  over the past 50 years and  it is the standing example of evidence based coronary care in the modern era ! The mortality  ,  in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15%  in 1960 /70s . Early use of heparin , aspirin   further improved the outcome .The inhospital mortality  was greatly  reduced to a level of  7-8% in the thrombolytic  era. And ,  then  came the interventional approach, namely primary PCI ,  which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence   for the   superiority  of PCI  , it is only a fraction of  STEMI patients get  primary PCI   even in some  of the  well equipped centers ( Could be as low as  15 %)

Why ? this paradox

Primary PCI   has   struggled  to establish itself  as a global  therapeutic concept  for STEMI ,   even after   20 years of it’s introduction (PAMI trial)  .  If we  attribute ,  lack of   infrastructure  , expertise are  responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world ,   reluctant to do primary PCI  for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI  patients !

All STEMI’s are not  same , so all does not require same treatment !

Common sense and logic would   tell us any medical condition should be risk stratified before applying the management protocol. This will enable  us to avoid applying “high risk  – high benefit”  treatments in low risk patients . It is a great surprise,  the cardiology community has extensively researched to risk stratify NSTEMI/UA   ,  it has  rarely  considered risk stratification of STEMI before  starting the treatment.

In this context , it should  be emphasized  most of the clinical trails on   primary PCI  do not address  the clinical  relevance and the  differential outcomes   in various  subsets of  STEMI .

Consider the following two cases.

Two young men with STEMI  , both present within  3  hours   after  onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL   ,  Low blood pressure , with severe  chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal  or no  discomfort .

In the above example,   a  small inferior  MI by a distal RCA occlusion  ,  and a proximal LAD lesion jeopardising entire anterior wall , both  are  categorized as STEMI !

Do you want to advocate same treatment  for both ?  or Will you  risk stratify the STEMI and treat individually ?  (As we do in NSTEMI !)

Current guidelines , would  suggest PCI for both situations. But , logistic ,  and real world experience would clearly favor thrombolysis for the second patient .

Does that mean,  the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a  random basis  by  not so well experienced cath lab team.

(Note : Streptokinase  or TPA does not  vary it’s action ,  whether given by  an ambulance drive or a staff nurse or even a  cardiologist !  .In contrast ,  the infrastructure and expertise have the  greatest impact on the success and failure  of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc)  need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

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Can we advice CABG for single vessel disease  ?

Yes, CABG  may be indicated  in

  • Critical , proximal , complex  LAD disease   with or without  ostium involvement.
  • Many of the bifurcation lesions with large and significant  side branch
  • Small caliber LAD with diffuse disease .

When these occur  in diabetic  subjects , the  indication for CABG is more certain .

* Present generation cardiologists  would feel  every  lesion  is  stentable and should not be referred to the surgeon .But it should be emphasized here,   technical feasibility alone  ,  does not  imply  PCI is superior and ideal in all coronary interventions.

Can we do a CABG  in  single vessel disease  with  normal  LAD ?

CABG is  very rarely  indicated   for isolated RCA or LCX disease. It should be consciously avoided in this patient population.

This is because the at risk myocardium  supplied by these vessels are far less than that of LAD. PCI  is  preferred    in these vessels .(Ofcourse , after considering medical management  ) .

CABG is  ,  too traumatic a  surgery , to  offer  in this  low  risk  coronary  lesions.

Exceptions

CABG  can still be done in following situations  for non LAD single vessel disease.

  • Left dominant circulation  with  complex lesions in LCX /OMs.
  • It is common to see diffuse , long segment  and severe disease of RCA with normal LAD /LCX system .PCI is not feasible in this subset.
  • Failed PCI
  • Recurrent instent restenosis.
  • Bail out CABG after a acute complication during PCI

One should remember ,  inability to do a PCI  does not  mean ,  the patient  should   land in surgeon’s table .We should recall , from our memory medical management is an effective and established form of treatment in single vessel disease ( Mainly for non LAD , and some cases of LAD also !)


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