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Posts Tagged ‘ivabradine’

Pacemaker current is   strangely  referred  by physiologists  as  funny current (I f ) . I am yet to find the exact reason .  This is the current  that  sustain  our life right from the day 22  of  embryonic life when the  cardiac jelly beats for the first time.   SA node  solemnly  follow our  entire life  before  making  a  bid-adieu !

pacemaker  potential sa node 5

 

pacemaker current if funny current poential 002

pacemaker current if funny current poential 003

What is contribution of  If  current in the overall Pace-making  activity ?
This  has not been quantified . The fact that ,  Ivabradine induced  If  current  blockade does not result in serious bradycardia indicate  , SA node has alternate reserve currents as well . ( SA node  is a such a mystery  structure , it would never be a  surprise , if we  find many more  “not so funny”  currents !)

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We now understand , heart rate reduction  could be the single most important factor  in the management of heart failure .Beta blockers have proved this time and again.We know heart rate has a linear relationship between survival .

SHIFT trial has  proven  that  Ivabradine  has a major role in the management  of chronic heart failure therapy .It is an If current blocker .  No hemodynamic  side effects was noted.

How does Ivabradine act ?

It acts on the phase 4 diastolic depolarisation in SA node by slow I f  currents.

SHIFT trial Link to lancet

SHIFT study official website

In this trial , the usage of  optimal Beta blockers  was  only in 25 %  . Patients  who received   complete beta blockade did show much benefit with Ivabradine . Further, the usage of  digoxin was only around 20% .This does not represent  the realistic  population of  cardiac  failure in many  countries  .In India , almost 70-80 % receive  it . Digoxin , the wonder drug does have an important vago mimetic action, to  reduce the heart rate .

Another  contentious issue   in SHIFT study  is , the Class 4 patients constituted <2% of the study population .It is ironical , these are the patients , one would  like to try a new rate control drugs like Ivabradine  , because we  are worried about beta blockers in this population  .A great opportunity was  lost as Ivabradine could have  been tried in this population.

We need a study  like this .

  • One to one comparison   of  beta blocker  and   Ivabradine  in cardiac failure  . Such a study will ever happen ? My guess is , it is  next to impossible !
  • Efficacy of  Ivabradine in patients with class 4  failure  , where beta blockers were contraindicated  or could not be administered.

Final message

Ivabradine , a new generation  negative chronotropic agent  is a great concept drug. But , the worthiness of this drug  is questionable , when we have  proven , well tolerated  drugs namely , the beta blockers to reduce the heart rate.. However , if the beta blockers are poorly tolerated  Ivabradine may be tried.Last , but not the least, never under-estimate the greatness of digoxin in heart failure.It is the only drug that has a positive  inotropic  properties coupled with  negative chronotropic action . Both benefits patients in CHF  . It can do wonders than any other drugs .(DIG trial was the most misunderstood by cardiologists!)

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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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