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True patients* present with symptoms , please , don’t ever think all your patients  bring their coronary artery for general servicing !

Ofcourse , we are the service provider to our patients . Though  heart is a mechanical pump it can never be considered equivalent to automobile engine .

For a Heart service station equipped with 24/7 lab,  the benefits may be  more if you treat the angiogram rather than the  patient.

Let us not misunderstand the word service , please show restraint, your patients will thank you forever.

* Silent significant CAD are indeed a problem in minority that requires selective wisdom.However, we can’t be aggressive hunters for CAD in population, as there is huge cost for human hunting !

Reference

Recent article which debates the issue of PCI in CTO
http://circ.ahajournals.org/content/135/15/1382?etoc=#sec-1

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Coronary artery lumen has unique character . Its well-known  LAD diameter is not constant , it tapers in its distal course.(Unlike RCA which is more tubular ) It is estimated LAD looses 15 % of its diameter for every 30mm length.Fortunately LCX has no such long course to make tapering a visible threat. (Though it may still be an Issue !)

Is there a hemodyanmic purpose for this tapering in LAD ?

Should be, God never designs anatomy without a physiological purpose.We have to find it  out.(Can it be meant for  flow acceleration as the flow is entriely diastolic in LAD while in RCA its both in systole and diastole ?_

What is the relationship between tapering angle and final distal diameter?

Schematic of an artery with a tapered angle of 0:16 .Ref XIANG SHEN Journal of Mechanics in Medicine and Biology Vol. 16, No. 8 (2016)

So, if you have a long lesion in proximal LAD and planning to stent with a 40 mm or long  stent the distal end is hyperinflated by atleast 1.5mm, if we use a non tapered stent. Though , gain of extra  diameter  in distal segments might appear attractive, this may not work to our advantage , since it defies and distorts  the natural hemodynamic flow pattern. Further , when you have tapering vessel, proximal optimisation becomes more important.

How about a tapering coronary stent ?

It should be a welcome addition to our already overflowing coronary hardware in fixing long lesions . Its still a surprise why only very few are making this type of stent.

Meril has developed a  tapered stent up to 60 mm long  (Biomime morph).It should be useful in specific lesions sub types.Its worthwhile to note  tapering stents are used more often in carotid artery .

Advantages of long tapering stent over two stents of different sizes.

  • It avoid the vulnerable overlapping zone with double metallic load.
  • Possibly cause less restenosis
  • Low risk for stent fracture
  • It reduces procedure time and of course the cost of stent by 50 %

Why the concept of Tapered stent is not that popular ?

I can only guess, probably lack of free availability and  to a certian extent ignorance as well !  However ,current status about tapering stents is expected to evolve, though many cardiologist still  feel it’s not clinicaly important issue to use a tubular stent in tapering vessel.

Alternative  interventions in tapered vessel.

  • Wall stent and other self expendable stents
  • Tapered balloon Angioplasty (Laird Am Journal of card 1996)

Experts  in this modality are  welcome to share their experience.

Reference 

1.Zubaid MC, Buller C, Mancini GB. “Normal angiographic tapering of the coronary arteries”. Can J Cardiol 2002; 18: 973-980

2.Timmins LH, Meyer CA, Moreno MR, Moore JE Jr. “Mechanical modeling of stents deployed in tapered arteries”. Ann Biomed Eng 2008; 36: 2042-2050

3.Javier SP, Mintz GS, Popma JJ, Pichard AD, Kent KM, Satler LF, Leon MB. “Intravascular ultrasound assessment of the magnitude and mechanism of coronary artery and lumen tapering”. Am J Cardiol 1995; 75: 177-180

4.Laird JR, Popma JJ, Knopf WD, Yakubov S, Satler L, White H, Bergelson B, Hennecken J, Lewis S, Parks JM, Holmes DR. “Angiographic and procedural outcome after coronary angioplasty in high-risk subsets using a decremental diameter (tapered) balloon catheter. Tapered Balloon Registry Investigators”. Am J Cardiol 1996; 77: 561-568

5. YONG-QUAN DENG, ZHONG-MIN XIE and SONG  ASSESSMENT OF CORONARY STENT DEPLOYMENT IN TAPERED ARTERIES: IMPACT OF ARTERIAL TAPERING XIANG SHEN*, Journal of Mechanics in Medicine and Biology Vol. 16, No. 8 (2016) 1640015 

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Knowledge can be a dangerous asset sometimes . A modern day cardiologist reassured a patient  who had an unusual dyspnea after a muti-vessel stenting for a not so complex lesions following an anterior MI.The doctor  was not mystified when the patient uttered this complaint. In fact he was so cool , reassured the patient since he was taking  Ticagrelor ,and it’s well recognised to cause dyspnea in some patients.

Few days later patient  called  again and informed that the  dyspnea is getting more intense  and ultimately he was rushed to hospital only to diagnose  subacute stent occlusion and a fresh ACS.

What do you learn from this story ?

Caution , extreme caution is required when dealing with symptoms following PCI and especially dyspnea.

A brief review about  Ticagrelor dyspnea conundrum

  • Ticagrelor  ,a reversible P2Y12 blocker  has a peculiar side effect of dyspnea (Which happens to be a cardinal symptom of heart disease as well )
  • Its reported by up to 30 % of patients who receive it.
  • It can be either exertional  or even at rest.
  • It seems to be dose dependent
  • Onset within 24 hrs , upto 1 week.
  • Pulmonary function not affected.
  • Cardiac function thought to be unaffected.(No correlation with LVEDP though)

Mechanism of dyspnea with Ticagrelor (Presumed)

  • Its direct cortical effect due  sensory neurone  P2Y12 blockadae.
  • Due to Adenosine

Remedy 

  • Reassurance(Possible in few , but risky unless absolutely confident)
  • Encourage Tea intake (Theophylline might nullify if its Adenoisine induced .
  • Discontinuation is  the specific option (up to 10%)

Final message.

Dyspnea is a  unique side effect of Ticagrelor. Unexplained dyspnea is a delicately dangerous symptom in a post MI patient as it may directly imply a silent ischemia induced LV contractile dysfunction and acute raise in LVEDP.

Don’t ever take it easy and attribute all episodes of  dyspnea to Tiacagrelor .If you are really not convinced consider switching the patient to a different anti-platelet drug. Its simply not worth for both patient and physician to spend anxious moments.

Reference 

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We know,  classical Atrial flutter (Also referred to as typical /Common AF) records  saw toothed F waves  due to continuous atrial electrical activity across a macro- reentrant circuit within right atrium.

Though this  saw tooth pattern is easily recognised , it’s often difficult to say  whether the saw is facing upwards or downwards ?

ie  Is the flutter waves are inverted or upright ?

The general rule is the shallow stroke (one with a lesser slope) is to be termed  as antegrade  / initial deflection that will determine the direction of flutter waves.

mechanism-of-inverted-flutter-waves-in-atrial-flutter-saw-tooth

This is because , the forward limb traverses the slow path  of the circuit namely the cavo-tricuspid Isthmus, it then ascends up in the inter atrial septum (There by inscribing inverted F  waves  in leads  2,3,aVF .The return circuit  is relatively fast,  crossing the antero -lateral   free wall  right atrium and hence the later half saw tooth has a  sharp deflection )

In Reverse typical flutter  the flutter waves are upright (with a shallow slope ) in inferior leads but still uses the cavo- tricuspid Isthmus

* Note: In lead the polarity of F waves in V1 it will be opposite of that of inferior leads.

mechanism-of-flutter-wave-upright-or-inverted

Why should we bother about direction of flutter waves  ?

It may not be important for those hifi EP guys who can ablate complex arrhythmia with intra cardiac GPS catheters and accurate electro anatomic mapping system. Still , the  surface ECG always help us understand the basic circuits of flutter.

Reference

atrail-flutter-review-best

Reverse typical flutter should not be confused with atypical flutter where typical saw tooth waves are uncommon.The later group is termed as atypical atrial flutter that arises from various other focus including left atrium.

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If you think , the  various appropriate use guidelines for cardiology practice are collection of great scientiifc truths , beware . . .many  of them hide behind semantics.  (After all , English is an unique language one can play  with it !)

Is it not funny , to note a  recommendation  that goes with a caption “may be appropriate” conveys exactly the same meaning as “may not be appropriate” as well .

Here is a rare article which tries to expose the importance of  linguistic Interventions in cath lab that can Impact the patient outcome for good or bad.

http://www.invasivecardiology.com/articles/%E2%80%9Cmay-be-appropriate%E2%80%9D-pci-ambiguities-appropriate-use-classification?inter_email=alNyWXNEY3VFR3RzZEM2b3hHRjVseDIzWjlCdkN1Snp2MDlNbnR5RkVacz0%3D

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DAPT -Dual anti-platelet therapy has become  a standard in many clinical situations of CAD.There has been significant confusion about ,Indications, best combination, duration of DAPT, withholding of DAPT, conversion to MAPT (mono) etc.The  JACC september 2016 issue  brings much needed clarity  on this issue.

Link to key summary from NEJM journal watch.

http://www.jwatch.org/na42407/2016/09/28/update-dual-antiplatelet-therapy-patients-with-coronary?

Full text guideline

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Ventricular tachycardia is a regular wide qrs tachycardia.It can be monomorphic or polymorphic.

General diagnostic  rules In VT  (Gross though, with considerable overlap)

  • Polymorphic VT is more often Ischemic , drug induced, electrolytic, and includes many inherited VTs .Most primary  ischemic VT are polymorphic.
  • Monomorphic VT occurs  more common with structurally abnormal heart.(DCM, HOCM, ARVD etc .Please note late scar induced  VT are often monomorphic , which is also being referred to as Ischemic VT in literature )

*Its important to realise any  VT will transform to polymorphic just prior to degenerating into VF.

Management Issues.

The management of VT in acute setting is same irrespective of morphology of QRS complex.Either you DC shock or administer Amiodarone, Lignocaine , and other reserve drugs.

The issue comes only in stable VTs.In stable VT or if VT recurrence it’s advisable to bother about the ethology and choose a drug.Its believed , Amiodarone is contraindicated in true polymorphic VT that was precipitated by prolonged QT interval or Brugada syndrome.

In Ischemic  VT , lignocaine may be preferable over Amiodarone as the later may prolong the QT interval and VT could recur if the index VT was triggered by ischemia induced prolonged QT and subsequently  gets worsened by the drug Amiodarone.(please note, Lignocaine has neutral or even shorten the QT)

Let me conclude with a controversial observation, many of VT storms  we are witnessing only in the era of Amiodarone.Most episodes of VT Storm are polymorphic and often precipitated after blouses of Amiodarone punctuated with DC shock. With an explicit pro arrhythmic potential of this drug, I strongly believe some of the episodes of VT Storm  is iatrogenic and it tends to disappear as the drug effect of Amiodarone weans off.

Final message

In  monomorphic VTs, drug choice and selection may not be that important , polymorphic it could make a big difference !

Always ask a query  whether the VT you are tackling  (in any setting )is likely to have precipitated by prolonged  Action potential duration (Read as QT Interval ) ? Of course  ,one  can’t get a clear answer to this in bed side .But,  if you have strong reasons to suspect , better to avoid drugs that prolong action potential duration ( Amiodarone comes top in this list, though it can terminate VT of any ethology  with any morphology because it has all 4 group action of Waghaun williams !)

Comments welcome from EP experts ,  still to understand things in perspective.

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