The document discusses approaches to treating different types of ventricular arrhythmias that can occur after a myocardial infarction, including conservative management of premature ventricular contractions, use of antiarrhythmic drugs like lidocaine and amiodarone for ventricular fibrillation and tachycardia, and recognizing reperfusion arrhythmias that may not require treatment. It also provides recommendations for evaluating patients at higher risk of arrhythmias and managing electrical storm through correcting underlying issues, antiarrhythmic drugs, and device programming.

1. How to approach my patient with ventricular arrhythmia
post myocardial infarction?
Samir Morcos Rafla, FACC, FESC, FHRS
Emeritus professor of cardiology
Alexandria University
smrafla@yahoo.com
01001495577

2. Ventricular Arrhythmias Post MI
Ventricular Premature Beats (PVCs)
Commonly seen in patients with acute MI .
Usually pursue a conservative approach and do not
routinely need antiarrhythmic drugs but instead
determine whether recurrent ischemia or
electrolyte/metabolic disturbances are present

3. • Ventricular Arrhythmias Post MI
• Ventricular Fibrillation
• Ventricular fibrillation occurring in association with marked
LV failure or cardiogenic shock entails a poor prognosis,
with an in-hospital mortality rate of 40-60%
• Tx : defibrillator
• Management : lidocaine, amiodarone,

4. Ventricular Arrhythmias Post MI
Accelerated Idioventricular Rhythm
Defined as a ventricular rhythm with a rate of 60- 125
beats/min . Frequently called “slow v. tach”
Seen in up to 20% of patients with AMI . Occurs
frequently during the first 2 days . Probably results from
enhanced automaticity of the Purkinje fibers .
Often observed shortly after successful reperfusion

5. • Reperfusion arrhythmia: most reperfusion arrhythmias occurring
after brief durations of ischemia (<30 min) . Reperfusion results in a
rise in intracellular Ca2+, normalization of extracellular K+
concentration and recovery of the action potential duration.
• However, these changes occur in an inhomogeneous manner, This
leads to dispersion of refractoriness, which forms the substrate for re-
entry .
• Re-entry is however not the only mechanism responsible for
reperfusion arrhythmia, and triggered arrhythmia resulting from early
and delayed after depolarizations also play a major role,

6. Ventricular tachyarrhythmia in the first minutes after
successful reperfusion therapy can be transient without need
for treatment, known as reperfusion arrhythmias.
– If frequent premature ventricular complexes and non-
sustained ventricular tachycardia continue despite successful
reperfusion therapy under sufficient beta-blocker therapy,
they should only be treated if hemodynamically important.
This treatment should follow the same principles as the
treatment of sustained VA.

7. Ventricular Arrhythmias Post MI
Ventricular Tachycardia
When continuous ECG recordings during the first 12 hours
of AMI are analyzed, nonsustained paroxysms of VT may be
seen in up to 67% of patients
Hypokalemia and hypomagnesemia may increase the risk of
developing VT
Treatment may include: lidocaine, procainamide,
amiodarone

8. The incidence of sustained VT and VF occurring within 48 h
of the onset of an ACS seems to have decreased over the
past decades.
This is most likely due to the widespread availability of
revascularization therapy, limiting the size of infarction and
to an increased use of beta-blockers.
EuroIntervention. 2015 Jan;10(9):1095-108.

9. The role of AAD therapy for the treatment of sustained VT/VF
in ACS has been strongly debated and questioned.
Almost all AADs act either in a voltage or rate-dependent
manner, and some drugs have both characteristics.
Thus, AAD action may be significantly altered in
ischaemic/reperfused myocardium as compared with non-
affected myocardium.
This may result in significant electrophysiological heterogeneity
and gradients in conduction and refractoriness.

10. Occurrence of
arrhythmias in
STEMI patients
during and
immediately after
primary PCI

12. ARRHYTHMOGENIC SUBSTRATE
• Pre-existing reduced LV function and myocardial scars are at
risk for sustained VA.
• Patients with increased sympathetic activity, or with extreme
cardiogenic shock, are at increased risk of sustained VA .
• Sustained VA in the setting of an ACS is also dependent on an
individual genetic predisposition to such events. This is most
obvious in patients with inherited cardiomyopathies that
confer electrical instability.

13. Recommendations for evaluation of patients with acute
coronary syndrome at risk for ventricular tachyarrhythmia
– late from the onset of the symptoms,
– incomplete revascularization,
– presence of substrate prior to the event,
– or those patients with complications, should be considered
at increased risk for arrhythmia development during initial
evaluation.

14. In the context of ACS, amiodarone therapy – compared with
lidocaine –
has shown an increased short- and long-term mortality.
On the other hand, in the setting of out-of-hospital cardiac arrest,
amiodarone was associated with better survival to admission rate
as compared with lidocaine in patients with refractory VF.
- Amiodarone should be considered for the suppression (I.V. or
oral) and prevention (oral) of recurrent arrhythmias along with
beta-blockers.

15. Flecainide, propafenone, exert their antiarrhythmic potential by
significant slowing of conduction. In the setting of ACS, these
effects may result in aggravation rather than termination of
VT/VF. Thus, these drugs should not be used in ACS.
All class III AADs increase the QT interval with a risk for torsade
de pointes tachycardias.
Only few data exist on the use of dronedarone for the
treatment of VA

16. • Ranolazine is a piperazine derivative with a chemical structure
similar to that of lidocaine. The MERLIN-TIMI 36 study :
there was no significant difference in the combined primary
end- point of cardiovascular death, MI, or recurrent ischaemia,
but the incidence of non-sustained VT was significantly
reduced by ranolazine compared with placebo.

17. Recommendations for antiarrhythmic therapy in patients with
acute coronary syndrome and ventricular tachyarrhythmia
For patients with acute coronary syndrome (ACS) without
ventricular arrhythmias, prophylactic antiarrhythmic drug
treatment should not be administered.
Early treatment with beta- blockers, balancing electrolytes, and
sedation to reduce sympathetic drive and/or overdrive
stimulation, repetitive electrical cardioversion/defibrillation
should be considered first.

18. – If antiarrhythmic drug therapy is necessary on top of these
measures, administration of intravenous amiodarone is
reasonable, followed by intravenous lidocaine, if necessary
(Figure ).
– When experience is available, early catheter ablation should
be considered when other treatments fail (see below)

19. • Revascularization:
• Revascularization has a key role to play both in the prevention
of ventricular arrhythmias and in the management of recurrent
arrhythmias.
• The benefits of primary PCI (PPCI) in patients presenting with
ST elevation myocardial infarction are well established.

24. Recommendations for management of electrical storm and
inappropriate shocks in patients with acute coronary syndrome
– Initial management of patients with electrical storm requires
identifying and correcting underlying ischaemia.
– Amiodarone, beta-blockers and electrolyte correction as needed
form the cornerstone of antiarrhythmic therapy.
– Patients who have implantable cardioverter-defibrillator may require
device reprogramming.
– A focal rescue ablation approach targeting the trigger for ventricular
fibrillation early after acute myocardial infarction seems promising.

26. Samir Rafla, FESC, FACC, FHRS
Prof. of Cardiology, Cardiology
Department, Alexandria University
smrafla@yahoo.com
01001495577
Dr. Samir Rafla Lectures
YouTube channel- Samir Rafla