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Posts Tagged ‘naspe’

Acute coronary syndrome is the commonest cardiac emergency. STEMI and NSTEMI are the two clinical limbs of ACS. Generally they have distinct clinical, ECG, angiographic features.(Ofcourse,  with some degree of overlap) . It is  a  mystery , both clinical presentations differ so much inspite of the common denominator  , namely ,  an injured plaque with add on thrombus  within the coronary artery.

The mystery is since  decoded , the primary difference between these two entities is STEMI the occlusion occurs sudden and complete and in NSTEMI it occurs slow and incomplete

In STEMI ,  most of the clinical features and , need for emergent treatment , response to thrombolysis /PCI are dictated by the time dependent risk to myocardial loss .

Cardiac arrhythmias in ACS

It is a  much published  factoid   for  many decades  only one third of STEMI patients  reach the hospital alive ! The reason being , STEMI  is very much prone for primary VF.

Contrary  to this ,  almost all patients with NSTEMI reach the hospital alive ! How ?

Both are ACS, if ischemia is a powerful trigger for dangerous ventricular  arrhythmia’s ,  NSTEMI should also behave  similarly .

So what protects against arrhythmias in NSTEMI ?

  • We realise ,  by observational experience (Not EBM !)  It is the suddenness and totality of ischemia that trigger dangerous form of arrhythmia  .
  • Further, a balanced  ischemia in two contralateral segments (or global  ischemia) some how protects against development of ventricular  fibrillation .This may be due to preservation  of  electrical homogeneity  , and the spherical VT spiral waves are not sustainable.
  • In contrast , STEMI has a sudden  focal , ischemic  zone that initiates the VT and    ischemia free  contralateral segment  welcoming  and sustaining the  reentrant wavelet.
  • The observation of primarily single vessel disese in STEMI and multivessel disease in NSTEMI also give credence to this concept.
  • Further , ischemic preconditioning can exert an important anti arrhythmic  effect in NSTEMI as  patients with unstable angina have   slow, repetitive episodes of ischemia prior to the index event .
  • Post MI scar mediated VT/VF is independent of degree of overall ischemia
  • It is also established ,  a sub group of  STEMI pateints  who  had  preinfarction angina(  ie . a brief  period of UA/NSTEMI) have very low risk of SCD  supporting the concept of sensitising the myocardium against ventricular arrhythmias.

Final message

Even though , there is a convincing concept  of   ischemia induced  cardiac arrhythmia in literature , in real patients it is very difficult to link the two.

UA/NSTEMI is the most common  acute ischemic event but the incidence of VT/VF here,  is far less than one would expect.

In ACS , focal , total  ischemia is more likely to precipitate a VT/VF than multifocal and global ischemia.

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Ventricular tachycardia as a group , constitute a major  group of cardiac arrhythmias. Most of the VTs are managed  by cardioversion  followed by medical management.  Few require , implantable defibrillator when there is severe LV dysfucntion .(ICD) Localising the origin of  VT and subsequent , ablation is the treatment of choice in some of the  patients  with VT.

Traditionally VT was thought to arise fro the endocardial aspects of myocardium. Now  we realise many times VT originate from the epicardial aspects of  ventricle.

Epicardial VT : Defintion

Epicardial ventricular tachycardia (VT) is defined as VT in which the critical sites of the reentrant circuit (or the ‘sites of origin’) are located exclusively in the subepicardial tissue, as shown by entrainment manoeuvres or VT that is terminated within 10 s with standard radiofrequency (RF) pulses, or both.  E. SOSA,M. SCANAVACCA et  all  http://www.springerlink.com/content/w608142674154tp5/ 

 

 How to recognise epicardial origin of VT by surface ECG ?

  • Terminal S wave in V2 and q in lead 1 strongly suggest VT of sub epicardial origin.
  • Pseudodelta wave 
  • Intrinsicoid deflection time of  85 ms
  • RS complex duration of  >120msec

Suggest   epicardial origin of the VTs.

Important Links

http://www.circ.ahajournals.org/cgi/content/full/113/13/1659 

Berruezo      criteria ,http://circ.ahajournals.org/cgi/content/full/109/15/1842  ( Must  read)

http://cogprints.org/4222/2/tada.pdf

 

What is the clincal significance of epicardial VT ?

Endo cardial ablation  not likely to be successful

Trans pericardial approach may be needed.

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                                         Ventricular  tachycardia is considered as a dangerous electrical rhythm abnormality .It can immediately degenrate into ventricular fibrillation and result in SCD in many.Ironically, it is also a fact , a patient with VT can  present silently  without any symptom  .Some VTs are slow and recurrent without much affecting The hemodyanmics.

 

In chronic recurrent, beningn VT (Some may consider it , ” height of  absurdity ” to call a VT beningn ! but it  is a reality , the term beningn denotes –  very remote chance of converting into VF) ” Is there any other therapeutic option other than convertng into sinus rhythm. “(  Read related topics)

 

The following paper was presented in the Annual scientific sessions of  Cardiological society of India,  Kochi , seven years ago in  2002

 

VENTRICULAR RATE CONTROL  IN  VENTRICULAR TACHYCARDIA 

S.Venkatesan,,. Madras Medical College. Chennai

 

                           Mangement of  hemodynamically  stable  recurrent   ventricular tachycardia  remains a  delicate clinical problem. Reverting to  sinus rhythm  is  considered as  the only aim  of  treating  VT.While rate control is accepted as a therapeutic  option  in atrial fibrillation,  it is not  so,  for  ventricular tachycardia.In this  context  we attempted to analyse  the effect of  Amiodarone on   ventricular  rate  in stable ventricular tachycardia  which fail to convert  to sinus rhythm.

 

                            The  study cohort consisted of 49 patients with stable VT  who were admitted in the coronary care unit  of  Govt. General Hospital  between 1998 to 2002.The criteria for inclusion   were systolic BP>100mmHg and absence of  hypoperfusion of vital organs  The mean age was 52 years (range 26-68)  with a male female ratio  of 4:1.   Of the study group 36 patients  were either reverted with  IV lignocaine , Amiodarone ( 150-300mg   bolus )  or  DC  cardioversion . 13  patients  who did not respond to   either of these   were  followed up  with  Amiodaroneinfusion(1000mg)  for 24 hours.  The baseline  diagnosis were old MI (6)) DCM (3)  Arrhythmogenic RV displasia(2). Idiopathic VT was diagnosed in  2 patients.All these patients had  VT  during  most part of  the   24 hour  follow up.

                     

                         The pre Amiodarone mean  ventricular rate was  152  (124 –196).  Post amiadaorne (at 24hrs) mean ventricular rate was 128(88-142). The time taken for   50% heart  rate reduction was  6.6h (4-24h).  The average  systolic blood pressure  improved from  100   to  112mmhg . These patients were  discharged  in stable clinical status with oral Amiodarone and  were  referred for  EP study.

 

                          It is concluded that Amiodarone, apart from it’s cardioverting ability , has a distinct ventricular  rate controlling  effect  which  can be of therapeutic value in  at least certain subset of chronic recurrent VT.

Final message

 

Some of  the patients  with VT carry a very low risk of VF  and SCD .In these  patients , the only  other major  aim is to prevent tachycardiac cardiomyopathy  that can be done with drugs which  controls  the ventricular rate whenever  VT occurs !

Corrrecting the primary cause like cardiac failire , revascularisation ,detailed EP study  ,tachycardia mapping , followed by RF ablation and ICD implantation is  the state of the art approch in the management of VTs.But this small clinical observation was made to  impress rate control could also be an option  in patients  in whom these procedures are  contraindicated  or not  available . 

 

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Ventricular  tachycardia (VT)  is one  of  the   dangerous form of  cardiac arrhythmias.

When it occurs , it may present  in  many ways

  • Cardiac arrest with immediate degeneration into ventricular fibrillation. 
  • Pulseless VT in a  conscious patient but in  in shock.
  • With pulse, relatively stable , not much fall in blood pressure.
  • Incidentally detected.*(Rare)

This , gives us  an idea  that VT  as an electrical abnormality has wide clinical presentations , life threatening  at one end and,  patient walking into the hospital with minimal palpitation on the other hand !

The management issues

  • In patients with hemodynamic instability , decision making is easy as there is only option of DC shock.
  • In patients with stable VT, it is natural for the physicians to get tentative or even confused.This is because , dangers of shocking a stable patient has to be weighed against the currently available excellent antiarrhytmic drugs( Amiodarone, Ibutilide etc) .

 

The major issue here is  in  ruling out underlying structural heart disease.

Never shock a stable VT, without knowing the myocardial and valvular function.There has been many occasions underlying  severe LV dysfunction is missed   and they may go for asystole.

VT in the setting of cardiomyopathy, Post MI(Scar mediated) are often refractory even to DC shocks.It is the drugs that will  ultimately control the arrhythmia.DC shock is just used to terminate the VT.

VT  structurally normal heart , especially arising the outflow tracts of LV or RV  behave very differently (Fortunately they are more benign)

  • Have less hemodynamic  impact as it involves the outflow tract and  not over the  the pumping  zone of LV as in conventional ischemic myocardial VT .
  • They  respond to calcium blockers  verapamil to be precise (As they share properties of SVTs)
  • Sensitivity to verapamil by no way convey a meaning of Amiodarone resistance.Out flow tract VTs will also respond to Amiodarone many times.
  • Degeneration into VF is rare.

 

Also  read  Therapeutic issues in stable ventricular tachycardia

Presented and published in Indian heart journal

vtvt-therapeutic-issues1

Click  on link download PPT ventricular tachycardia

 

Related topics

Why some ventricular tachycardias are resistant , even to multiple DC shocks ?

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