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Archive for July, 2012

LAD is  graded into three types according to

Type 1  :  Falls short  of Apex

Type 2 :   Reach up to the LV apex

Type 3 : Wraps around LV apex and travels some distance in the posterior Inter-ventricular groove.

Clinical  Importance of Wrap around LAD

As the name implies , LAD   should descend only in anterior aspect  in about 15 %  population it can take a posterior descending course as well .

When LAD  wants to conquer more areas of heart is it a clinical advantage  ?

When LAD wraps around the LV apex,  anterior MI due to LAD occlusions can show changes in inferior leads. (Antero Inferior MI )

In ideal anatomic /Physiologic conditions  LAD  should nearly  meet the  PDA   to prevent any water shed  area.

There is usually a trade off between the  terminal LAD and  length of PDA ( whether it arises from LCX or RCA.)

There is some evidence to  suggest the site of ventricular rupture in anterior MI is related to the gap  in the LAD/PDA drainage zones.

Patients with Type  1 LAD  are at risk of   LV apical  ischemia if the  dominant LCX /RCA is  not supportive .

Final message

A long LAD is definitely a  hemo-dynamic  advantage   in physiology ,   Of course  it goes  without saying    . . .   when  it’s   likely  to get  obstructed it is always better to have a Type 1 !

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The other day a patient developed acute left main occlusion within 20 minutes of a  what looked like a successful PCI. When the angiogram was analysed  there was a distinct possibility of left main dissection.

The common causes  for left main injury during PCI include

  1. The guide catheter can it self  injure the tender left main ostium  by  size mis-match
  2. The frequent adjustment of  guiding catheter to get a co -axial alignment caries a definite risk
  3. The guide catheter slipping and subsequent repositioning  with the guide wire precariously snaring the left main ostia is the single important cause for left main injury.

How to prevent left main injury ?

  • Optimal guide catheter size and shape is vital.
  • Smaller the size it is better .(6 F is ideal for most )
  • As for as possible minimal handling of guide catheter is adviced . (Hands always  on guiding catheter  approach  is to be discouraged )
  • Deeper  engagement of guide catheter  as far as  possible  without hemo-dynamic compromise.This will ensure  not only better support for guide wire and balloon ,  low chances for guide wire to injure the left main ostia
  • Tapering guiding catheters with  soft ends are ideal. ( Which are available I think !)
  • Finally  and most importantly keep  the PCI procedure as short as possible ,  come out quickly  . After all ,  we  play  the   dangerous    coronary  game  right  in the mouth of the mysterious   coronary  cave  ( of Alibaba ! ) called Left main !

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Identifying the P wave is the key to decode  any  narrow QRS  tachycardia . Though the  the relationship to  p and  qrs is vita ,  many times it is  not  easy to  relate them.More easily one  may  get  a  clue to the mechanism by analysing   P wave timing .This is the basis of calling narrow qrs tachycardia as short RP and long RP.

Wonder   . . .  why  the  relation “P to R” became  “R to P” here !

Since  in the   common narrow qrs tachycardias  AVNRT/AVRT  ,  atria  activates  the atria  in a  retrograde manner , we look  for the relationship of qrs complex on subsequent P wave . Hence the interval between R to P become the focus.

In other words RP interval indicates retrograde  conduction property of AV tissue .

If it is slow the P wave will be well separated from QRS .

If it is fast it will be close to QRS complex .

If it is ultra fast as in some AVNRT ,it can fall within the qrs complex and completely invisible .

(The so called  r’ prime in classical AVNRT is nothing but a distorted p wave on the terminal qrs complex.)

Based on  RP interval  the following classification is used (List is incomplete)

Short RP Tachycardia

  • AVNRT (Slow-Fast )
  • AVRT

Long  RP tachycardia

  • Atypical AVNRT(Fast -slow)
  • Atrial tachycardia*
  • Sinus tachycardia*
  • SA nodal re-entry*
  • Some forms of AVRT

* Please note ,  here the P wave is not determined by the preceding qrs unlike other tachycardia in the list.

What is the  cut off point to call it is Short RP /Long RP ?

It is arbitrary . Following may help

If RP interval > PR interval it is long RP.

If the absolute RP interval is >  100  ms  with the heart rate of > 160 it would  generally  Indicate a long RP tachycardia .

The timing  of  retrograde P can be very complex than we believe  as the following factors heavily influence it.

  • The autonomic tone
  • Site of retrograde atrial  breakthrough point .
  • Atrial size ,
  • Atrial  refractionaries
  • Effect of drugs
  • Intact-ness of inter atrial conduction
  • Chances of the retrograde atrial activation capturing Internodal pathway

Final message

The P wave location in narrow qrs tachycardia is primarily determined by the retrograde VA  conduction and less  on the antegrade AV conduction  . Looking at the interval between R and P is a  quick way of getting the VA conduction in the bed side.

Once we get an  idea how the VA  circuit  conducts , we can narrow down the possibilities  in  Narrow qrs tachycardias !

Comming  soon

What determines the morphology of retrograde P waves in AVNRT/AVRT ?

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Rheumatic valvulits , Valvular inflammation and edema  is the traditional answer .A detailed Echocardiographic study from All India Institute of medical sciences New Delhi  ,India  which was published in circulation 1996 answers this question most authentically .

From a meticulous  Echocardiographic  study of about 70 patients  (with both first and recurrent episodes of carditis ) the following findings were observed.

After reading this article one should be able to answer variety of  questions in RHD  such as

  • How common is MVPS in RHD ?
  • How often MR dissapear with Aspirin etc ?
  • Echocardiographic correlates  for care -coombs murmur ?

Reference

http://circ.ahajournals.org/content/94/1/73/T5.expansion.html

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It is estimated multi-vessel CAD occur in about  70 % of NSTEMI/UA.In high risk NSTEMI early invasive strategy is popular (Though it is not yet  an undisputed choice !) .Tackling the culprit artery and restoring the blood flow ,   providing immediate  relief from angina is the primary aim  . Myocardial salvage is a lesser aim !

The lesion that is immediately  responsible for  angina is referred to as culprit  lesion and artery .(Ideally may  be called as Angina related artery ARA .)

If we have  multiple culprit like  lesions  it is difficult to identify the target lesion. Inexperienced cardiologists  may not consider  this as an    issue !

The following features  may be helpful

  1. The tighter the stenosis , it is  more likely to be a culprit . (Of course , blind  belief on this rule  can result in huge errors ! )
  2. Eccentric lesions
  3. Thrombotic lesions
  4. Grafts /Post PCI lesions if present carry high chances of becoming culprits.
  5. ECG characteristics may  be use full (Global ST depression can not occur with isolated  RCA/LCX NSTEMI   .It  generally indicate LAD  lesion to be  the  culprit.
  6. Deep ST depression in V1 to V3 would indicate LCX a definite culprit .(It could even be a STEMI equivalent )
  7. Echo – Angio correlation can provide a useful clue in identifying the culprit. (Example : In a patient with Multi vessel CAD  , if there is severe resting wall motion defect in Infero -Lateral segments with relative sparing of septum   LCX lesion should be the culprit .)

Exceptions

  • It is not always easy to identify the culprit artery .There can be multiple active  plaques .
  • Diffuse inflammatory vessel are reported in few with NSTEMI
  • Occasionally there can be no  culprit lesion at all (No active plaques ) ,  as the rest angina may be related to excess demand like fever or anemia with  a stable non critical plaque.

Final message

The  delicate   exercise of identifying the angina related  artery is  important  for two reasons.

  1. We can not afford to   prolong the PCI procedure in the setting of ACS  as increased procedure time is clearly related to peri- procedural events.
  2. Secondly , stenting a wrong lesion   and persistence of angina after a  PCI  will take  away  the  hard earned credentials  of  cardiologists  instantaneously !

Reference

Read a related presentation

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