Mechanisms of Arrhythmias

Ventricular Arrhythmia after Acute Myocardial Infarction: ‘The Perfect Storm’

Justine Bhar-Amato, William Davies and Sharad Agarwal

Papworth Hospital NHS Foundation Trust, Papworth Everard, Cambridge, United Kingdom

Abstract
Ventricular tachyarrhythmias (VAs) commonly occur early in ischaemia, and remain a common cause of sudden death in acute MI. The
thrombolysis and primary percutaneous coronary intervention era has resulted in the modification of the natural history of an infarct and
subsequent VA. Presence of VA could independently influence mortality in patients recovering from MI. Appropriate risk assessment and
subsequent treatment is warranted in these patients. The prevention and treatment of haemodynamically significant VA in the post-infarct
period and of sudden cardiac death remote from the event remain areas of ongoing study.

Keywords
Acute myocardial infarction, ventricular arrhythmias, risk assessment, management

Disclosure: The authors have no conflicts of interest to declare.

Received: 30 July 2017 Accepted: 17 August 2017 Citation: Arrhythmia & Electrophysiology Review 2017;6(3):134–9. DOI:10.15420/aer.2017.24.1
Correspondence: Sharad Agarwal, consultant cardiologist and electrophysiologist, Papworth Hospital NHS Foundation Trust, Papworth Everard, Cambridge CB23 3RE.
E: sharad.agarwal@nhs.net

Ventricular tachyarrhythmias (VAs) most commonly occur early in
ischaemia, and patients presenting with an acute MI and ventricular
arrhythmias are a group that has a significantly increased risk of
mortality.1,2 Thrombolysis primary percutaneous coronary intervention
(PCI) and use of beta-blockers, while resulting in the modification
of the natural history of an infarct, have also reduced the incidence of
sustained ventricular tachycardia (VT) or ventricular fibrillation (VF)
occurring within 48 hours of the onset of an acute coronary syndrome
(ACS), over the past decades.3 The prevention and treatment of
haemodynamically significant VA in the post-infarct period, and
of sudden cardiac death (SCD) remote from the event, remain areas of
ongoing study.
Prompt revascularisation and drug therapy, including anti-platelets,
statins, angiotensin converting enzyme (ACE)-inhibitors and beta-
blockers, have markedly reduced the incidence of VA.4–8 Nevertheless,
approximately 10% of post-MI survivors remain at high risk of dying in
the first months or years following hospital discharge (mortality >25%
at 2 years).9 Sudden death secondary to sustained VT or VF accounts
for about 50% of all deaths in these high-risk patients.10
There remain three vulnerable classes of patients: patients presenting
after a long period of chest pain, patients who have undergone only
partial revascularisation and those with a pre-existing arrhythmogenic
substrate.11 VA is seen more often in those with cardiogenic shock, related
to the size of the infarct. A genetic predisposition to VA in the context of
ischaemia may also exist. The finding of early repolarisation (ER) changes
being more prevalent in idiopathic VF survivors and their relatives, and
on the ECGs of patients with coronary artery disease and ST-segment
elevation MI (STEMI) who experience VA perhaps alludes to this.12,13
There is a temporal distribution to VA post-acute MI: an early, or
acute phase, of up to 48–72 hours, which is a time of very dynamic
ischaemia and reperfusion. From 72 hours to a few weeks up to a
month post event, and a more chronic phase beyond that, where
remodelling continues to occur. Premature ventricular contractions
(PVCs) are common in the early phase. The significance of these and
the occurrence of non-sustained or sustained VA in terms of short-
and long-term prognosis have been debated over the years. It appears
there needs to exist a combination of biochemical, electrophysiological,
autonomic and, as yet unknown, genetic factors culminating in a
so-called ‘perfect storm’ resulting in arrhythmia in the post-MI period.
Patients who develop sustained VF or VT >48 hours after their index
MI have a significantly higher rate of all-cause mortality; however, the
relationship between early (within 48 hours of the index MI) VF/VT
and mortality remains controversial. Some data have suggested that
sustained ventricular arrhythmias during the early post-MI period may
be associated with increased 30-day mortality, but without a protracted
risk over the long term.14–16
Non-sustained VT in the early-phase post-MI does not contribute to
risk assessment in this group of patients.17 The prognostic implication
of VA post PCI was studied in the Harmonizing Outcomes with
Revascularization and Stents in Acute Myocardial Infarction (HORIZONS-
AMI) Trial. In this, 5.2% patients developed VA post primary PCI with
85% of the VA happening in the first 48 hours. They reported that
sustained VT/VF after primary PCI was not significantly associated with
3-year mortality or major adverse clinical events.18
Mechanisms of Ischaemic Arrhythmogenesis:
From the Cell Upwards
Acute MI is characterised histopathologically by coagulative necrosis
of the myocardium. In a non-reperfused MI, this is seen within
30 to 40 minutes of sustained ischaemia, with the changes only visible
at the resolution electron microscopy. From 2 weeks, scar develops
from the periphery to the centre, and its formation is complete
after the second month.19 Any attempt at reperfusion potentially
alters this process.

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Thus there is a temporal distribution to the occurrence and postulated
mechanisms of ventricular arrhythmia in the post-MI period.
In animal studies, an early, potentially reversible, phase within the
first 30 minutes following epicardial coronary artery occlusion was
identified. This is followed by an irreversible phase from 90 minutes to
72 hours, during which there is rapid evolution of the characteristics
of the infarcted tissue.19 Reperfusion contributes to the profound
electrophysiological changes.
Acute ischaemia causes hypoxia, which results in an intracellular
depletion of adenosine triphosphate and the consequent accumulation
of adenosine diphosphate and the products of anaerobic glycolysis,
leading to intracellular acidosis. This drop in pH activates the Na+/H+
and Na+/Ca++ion exchange channels, with expulsion of hydrogen ions in
exchange for sodium, which passes into the cell and is then exchanged
for calcium, resulting in cell swelling and calcium overload. This is
accompanied by the build-up of extracellular potassium, cathecholamines
and lysophosphatidylcholine. This results in depolarisation of the
cell membrane and reduction of the fast inward sodium current and
increase in the late sodium current initially prolonging the action
potential duration (APD). Ultimately, abbreviation of the APD, seen during
ischaemia, results from decreased inward calcium currents (inhibited by
the acidosis) and enhanced outward ATP-sensitive potassium current
due to reduction in intracellular ATP, following hypoxia. A lower reduced
resting transmembrane potential, intracellular calcium mishandling and
reduced functional gap junctions also result. The cessation of anaerobic
glycolysis marks the next phase resulting in low glycogen and high
lactic acid intracellular content, reduction of ATP levels to below 10%,
sodium and calcium overload and further accumulation of extracellular
potassium. Spontaneous calcium oscillations trigger early and late after-
depolarisation-induced ventricular ectopics.11,19
Surviving purkinje fibres with shortened APD or reduced amplitude,
depolarised membrane potentials and reduced Vmax are thought to
be the source of automatic foci for VA. The partial and temporal
dispersal repolarisation contribute to a re-entrant mechanism
based on regions of unidirectional conduction block, fractionation
of cellular electrograms and shortened APDs.11 Tissue heterogeneity
is particularly marked in the peri-infarct or ‘border zone’ and it is here
that arrhythmogenesis is thought to arise.11,19 Of note, both human and
animal studies have shown abnormal sympathetic activity in these
border zones. These nerve terminals are more susceptible to ischaemic
damage than myocytes.20
It has been well recognised that re-entry through a stable circuit
involving the infarct scar tissue is the most-likely mechanism of
sustained monomorphic ventricular tachycardia.21 In acute myocardial
ischaemia, with no previous scar, zones of slow conduction and block
may create conditions for re-entry. These patients are likely to have large
infarct areas and a very large acute ischaemic zone may create the
conditions for a transiently stable re-entry circuit capable of sustaining
a monomorphic re-entrant tachycardia.15 Alternatively, mechanical
stretching of a failing ventricle alongside high sympathetic drive
associated with MI can result in VA because of focal triggers.22
Identifying those at Risk of Post-infarction
Ventricular Tachyarrhythmia
Various invasive and non-invasive tools have been used to identify
patients most at risk of SCD following MI. Left ventricular ejection along
with inducibility of VA during programmed electrical stimulation have
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Ventricular Arrhythmia after Acute MI
been most cited as factors identifying patients most at risk. Due to the
dynamic phase of repair and remodelling after the acute episode, the
acute assessment of these parameters may not reliably predict long-
term risk of arrhythmic death.
It is estimated that around 15–20% of all AMI patients will have LVEF ≤35%
at the time of revascularisation for AMI.23 However, recovery of reduced
LVEF after AMI with or without immediate PCI is often unpredictable. In
a study by Solomon et al., 3 months after AMI, 22% of all patients with
abnormal LV function at the time of AMI recovered to normal LV function.24
Assessment of LVEF to risk stratify and subsequent implantation of
ICD early (within 40 days) post-MI has not been shown to be of
prognostic benefit.25,26
Left Ventricular Ejection Fraction
The incidence of VA is directly proportional to the size of an infarct
and inversely related to the LVEF. Late presenters, and in those whom
there is failure to achieve adequate patency of the culprit artery, are
the most at risk. In addition, over a third of patients with STEMI, and the
majority of those with STEMI complicated by cardiogenic shock, have
significant bystander coronary disease, and appear to be at increased
risk of VA,11 presenting a valid argument for early full revascularisation.
Transthoracic echocardiography is used routinely to assess the extent
of infarct and to risk stratify patients on the basis of LVEF. When
quantifying LVEF alone, there is greater operator variability in echo
compared with MRI. Irrespective of the mode of LVEF determination,
there are limitations in its use in identifying those at risk of VA and SCD.
The multicenter automatic defibrillator implantation trial (MADIT)
identified a mortality benefit from ICD in 5.6% of patients with a post-
infarct LVEF of 30% or lower over 27 months from the index event.27
The sudden cardiac death in heart failure trial (SCD-HeFT) identified a
mortality benefit of 7.3% over 60 months in those with an LVEF of 35%
or less.28 Apart from being quite modest numbers, most patients who
suffer a cardiac arrest post-MI have an LVEF higher than 35%.29 When
looking at VA and SCD risk in the longer term it is worth noting that less
than 20% of ICD recipients in the above-mentioned studies received
appropriate ICD therapies in their respective follow-up periods.27
Additionally in the setting of chronic coronary artery disease, an
analysis of the multicenter unsustained tachycardia trial (MUSTT) study
would seem to advise caution in attributing risk based on LVEF alone.
Those who experienced non-sustained ventricular tachycardia (NSVT),
a condition of recruitment into the study, and an LVEF of anywhere
between 30% and 40%, demonstrated higher risk of arrhythmic death
or cardiac arrest compared with LVEF of or less than 30% when other
factors were taken into account.30 The variables having the greatest
prognostic impact in multivariable analysis were functional class,
history of heart failure, NSVT not related to bypass surgery, EF, age, LV
conduction abnormalities, inducible sustained ventricular tachycardia,
enrolment as an inpatient and AF. Non-invasive assessments of
scar burden, ventricular conduction and repolarisation, as well as
autonomic tone, have been explored in risk prediction. Cardiac
magnetic resonance is far superior at characterising infarcted tissue
and assessing scar burden compared with other imaging modalities.
Increased tissue heterogeneity31 and a larger peri-infarct or ‘border
zone’ has been found to correlate with increased mortality risk and
MRI is better able to assess these.32 Large-scale data assessing how
primary prevention ICD therapy could be guided by MRI beyond LVEF
assessment is lacking. A study of 48 patients with known coronary
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artery disease referred for PES did find that infarct surface area and
mass measured by cardiac MRI more accurately identified patients with
a substrate for monomorphic VT, compared with LVEF.33 The majority of
patients were studied beyond a month post-MI. DETERMINE-ICD is a
current large, randomised trial looking into prophylactic ICD therapy
in post-MI in patients with an LVEF greater than 35% and extensive
scarring assessed by MRI.
Programmed Electrical Stimulation
Current data only support the use of PES in post-MI patients with
LVEF of 40% or less. The timing of programmed electrical stimulation
(PES) is an area of debate. In MADIT I, patients with inducible VA and
LVEF of 35% or less late post-MI were found to derive most mortality
benefit from an ICD.34 The same finding in beta-blocker Strategy plus
Implantable Cardioverter Defibrillator (BEST+ICD) less than a month
post-MI suggested that inducibility early after the event may do the
same but was really unable to predict benefit.35 The Cardiac Arrhythmias
and Risk Stratification After Acute Myocardial Infarction (CARISMA)
trial, however, found that inducible VT at 6 weeks post-MI was a strong
predictor of future arrhythmic events.36 Beyond the fact that differences
in stimulation protocol is one factor that can account for the variation in
study findings, PES is still marred by low sensitivity demonstrated in part
by the fact that more than a quarter of patients with an LVEF of 35% or
less and a negative study went on to have serious events.37
Other Risk Assessment Modalities
None of the non-invasive assessments of ventricular conduction
and repolarisation or autonomic tone have yet been individually
found to be of use in accurately predicting risk of VA or to guide ICD
therapy.29 Measures of ventricular conduction include QRS duration,
signal-averaged ECG and Wedensky modulation (the identification
of local perturbations within the QRS following delivery of a sub-
threshold impulse during the ventricular refractory period). Measures
of ventricular repolarisation include QT variability and dispersion,
T loop morphology variations, T wave variance, the QT/RR slope and
T wave alternans. Measures of autonomic tone include assessment of
linear and non-linear heart rate variability (HRV), baroreflex sensitivity,
heart rate turbulence and deceleration capacity. Risk Estimation
following Infarction Non-invasive Estimation (REFINE)-ICD has been
designed to evaluate prophylactic ICD therapy in post-MI patients with
LVEF of 36% to 49% and abnormal Holter T wave alternans and heart
rate turbulence.29
An increased incidence of ER on the ECG in the form of a slurring or
notching in the terminal portion of the QRS complex in the inferior
and/or lateral leads has been found in patients with coronary artery
disease. Patel et al. compared 50 individuals with VA within the first 72
hours post-STEMI and 50 individuals without VA. Arrhythmias included
sustained VT, non-sustained VT and VF. When looking at ECGs recorded
1 year prior to the MI, they found a higher prevalence of ER among
those with VA, even after adjusting for creatine kinase (CK)-MB levels
and LVEF.38 Another group reported a higher prevalence of ER in over
400 SCD victims ascribed to acute coronary syndrome following post-
mortem.39 This was in addition to the findings that more victims were
male smokers with a lower BMI, higher heart rate, with prolonged QRS
durations and a lower prevalence of history of cardiovascular disease.
Early repolarisation syndrome (ERS) may be a marker of vulnerable
substrate. The same finding of increased incidence of ER in idiopathic
VF survivors40,41 and their relatives42 would suggest that there exists a
phenotype with a predisposition to VA in the context of ACS.
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Therapeutic Options
The incidence of sustained VT and VF occurring within 48 hours of the
onset of an ACS seems to have decreased over the past decade, likely
due to the widespread availability of revascularisation therapy, limiting
the size of infarction and to an increased use of beta-blockers.43
Anti-arrhythmic Drugs
Robust evidence for anti-arrhythmic drug (AAD) use in the early
dynamic phase of ischaemia and reperfusion within the first 48–72
hours post-MI is lacking in comparison to use in the chronic phase.
Despite the availability of early revascularisation and beta-blocker use,
6% of patients in this early phase are still affected by sustained VA.44
While the immediate treatment for VA with haemodynamic collapse
remains direct current cardioversion, recurrent sustained VA in the
absence of need for further revascularisation and normal electrolytes
usually calls for some form of drug therapy. AADs are not without their
side effects in addition to their effects on transmembrane voltage and
heart rate, all of which can further exacerbate instability.
Beta-blockers have been effectively used in patients with acute
coronary events, reducing major cardiac events including SCD.45
In a meta-analysis by Huang et al., use of beta-blockers was
associated with reduction of all-cause death in patients with acute
MI undergoing PCI. The benefit was restricted to those with reduced
EF, low use of other secondary prevention drugs or with none STEMI.
The association between the use of beta-blockers and improved
survival rate was significant only in <1-year follow-up duration. They
concluded there was a lack of evidence to support routine use of
beta-blockers in all patients with AMI who underwent PCI.46 In the
carvedilol post-infarct survival control in left ventricular dysfunction
study (CAPRICORN) trial, Carvedilol was shown to have significant
anti-arrhythmic effect after AMI. It suppressed both atrial and
ventricular arrhythmias in these patients.47
There have been conflicting reports concerning the class Ib drug
lidocaine of either a significant trend towards a lower risk of death
in the early period post-MI,48,49 and less VA and a survival benefit
post-cardiac arrest when used prophylactically to a neutral effect on
overall mortality or a trend towards excess mortality.49,50 Prophylactic
lidocaine use has largely been discouraged although it remains a
potential intravenous treatment of recurrent sustained VA post-MI. The
class Ic drugs like flecainide and propafenone cause significant slowing
of conduction, which may exacerbate VA in the post-MI setting and
should not be used.50
Amiodarone remains the most commonly used AAD post-MI and
is particularly useful in the presence of severe structural disease.
However, it does take time to reach therapeutic levels. Its use following
out-of-hospital cardiac arrest in patients with shock refractory VF was
associated with a survival benefit in comparison with lidocaine.51 In
patients who survived more than 3 hours after MI, use of amiodarone
was associated with increased short- (30 days) and long-term
(6 months) mortality compared with lidocaine for use in the ACS
setting.49 No added survival benefit has been shown with amiodarone
use over and above concomitant beta-blocker therapy post-MI52 and its
significant side-effect profile has been shown to increase mortality in
the longer term. There are no data to support the use of dronaderone
in the post-MI period. Other class III drugs, such as dofetilide, prolong
cardiac repolarisation and do suppress VA,51–53 but there are no data
showing added beneficial effects of their use. All class III drugs prolong
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the QT interval thus risking polymorphic VT, though the incidence of
polymorphic VT is low with amiodarone.54
Ranolazine is a relatively new entry into the arena. The metabolic
efficiency with ranolazine for less ischemia in non−ST-elevation acute
coronary syndromes (MERLIN)-TIMI 36 trial did not show a significant
difference in the combined primary endpoint of cardiovascular death,
MI or recurrent ischaemia but it did significantly reduce the incidence
of non-sustained VT when compared with placebo.55 More investigation
is needed, including how it stacks up against current drug therapy.
Similarly, eplerenone 25 mg/day, in addition to conventional therapy,
significantly reduced all-cause mortality 30 days after randomisation
in patients with an LVEF ≤40% and signs of heart failure. There was a
37% relative risk reduction of SCD in patients receiving epleronone.56
When considering drug therapy, the use of deep sedation must not be
forgotten. In addition to the necessary use if a conscious patient is to
undergo direct current cardioversion, a reduction of the sympathetic
drive associated with post-MI VA afforded by it makes it a viable
therapeutic option.
Overdrive Pacing
If the above measures fail to suppress VA in the early post-MI period,
temporary overdrive pacing may be used. An automatic focus may be
captured and suppressed, or exit block achieved by making surrounding
myocardium refractory. Alterations of conduction and refractoriness
due to pacing may terminate a tachycardia caused by a re-entrant
mechanism. This measure can be used in refractory VA to reduce the
need for recurrent cardioversion while waiting for drug therapy to take
effect, or prior to further revascularisation or catheter ablation.
Radiofrequency Ablation
Catheter ablation for VA in the acute phase is not commonly
performed. The acute success rate is in the region of 70% and carries
with it a peri-procedural mortality of 3% in unstable patients, and a
long-term mortality of 18% due to decompensated heart failure.57,58
Ablation is primarily subendocardial and in the border zone. The
targets are the re-entrant circuits in the heterogenous myocardium
and the after-depolarisations and automatic foci arising from purkinje
fibres. Activation mapping can be performed in the presence of
frequent PVCs. Pace mapping can be performed against prior recorded
PVCs if they are less frequent. Endpoints include suppression of the
triggering PVC and loss of the purkinje potential. On the occasions
that PVCs are not present, routine induction manoeuvres including
PES or drug provocation can be non-specific in the acute period
is often unsuccessful and can be non-specific. In these situations,
substrate ablation guided by voltage mapping can be undertaken.59
This cohort of patient is often haemodynamically unstable and the
complexity of the procedure means it is best undertaken in high-
volume centres by experienced electrophysiologists, with the use
of 3D electroanatomical mapping systems and, one would argue,
advanced supportive care including the ability to provide mechanical
circulatory support if needed.
Mechanical Circulatory Support
VA is common in MI complicated by cardiogenic shock and is associated
with high short-term mortality. Sustained VT occurs in 17–21% and
VF is seen slightly more often (24–29%) in selected patients with
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cardiogenic shock and acute MI, undergoing thrombolysis or primary
PCI.60 Revascularisation improves survival. The use of inotropes can
exacerbate VA and the amount needed can potentially be reduced
if used in conjunction with mechanical support. Beyond supporting
revascularisation procedures, mechanical support may help maintain
cardiac output adequate for tissue perfusion in the post-MI period.
The most widely used form is the intra-aortic balloon pump (IABP).
This counter-pulsation device primarily reduces afterload, augments
diastolic coronary perfusion and contributes towards the cardiac
output. It is unable to provide support in VF, whereas other forms
of mechanical support can. Use of the Impella assist device in
this cohort of patients was associated with reduction of tissue
hypoxia, haemodynamic stabilisation and improvement of neurological
outcome.61,62 Veno-arterial extracorporeal membrane oxygenation
(VA–ECMO)-assisted PCI was shown to improve survival in patients
with cardiogenic shock and refractory VT/VF compared with IABP.61–63
These forms of support can act as bridges to recovery or eventual
heart transplantation.
The Implantable Cardioverter-Defibrillator
Current guidance advocates ICD implantation from 40 days post-MI
in patients with an LVEF of 35% or less in New York Heart Association
(NYHA) class 1, 2 or 3. The Defibrillator in Acute Myocardial Infarction
Trial (DINAMIT) and the Immediate Risk Stratification Improves
Survival (IRIS) showed that there was no survival benefit in
implantation under 40 days from the event.25,26 In the DINAMIT trial,
ICD implantation within 6–40 days of an acute MI (average time from
MI to randomisation of 18 days) was compared with conventional
medical therapy. This was a primary prevention study and excluded
people who had VA post-48 hours after MI. The DINAMIT study
included a measurement of HRV, with an EF of <35% as study inclusion
criteria. The study demonstrated a reduction in the arrhythmic death,
which was largely balanced by an increase in the non-arrhythmic
cardiac death in the ICD arm when compared with the control group,
but there was no reduction in the total mortality.
Similarly, the IRIS trial enrolled patients, 5–31 days after MI. The
inclusion criteria included a reduced LVEF (≤40%) and a heart rate of 90
or more. This was also a primary prevention study and failed to show
any benefit of prophylactic ICD in this group of patients, though the
rate of arhhythmic deaths was lower in patients with ICD.
Though both the trials showed no significant benefit of ICD in this group
of patients, they did not include people who had VA after 48 hours of
the myocardial event and such patients need to be studied further.
Risk stratification tools are required to assess these people who may
be at a higher risk of VA. In the absence of robust risk stratification
tools, wearable defibrillators may have a role in the prevention of SCD,
particularly in patients with depressed LV function, but such a strategy
will need to be evaluated in further randomised studies.
The risk of VA and consequent ICD therapy appears to reduce with
increasing time from the infarct and the majority of patients fitted with
a primary prevention ICD (and without further ischaemia) do not have
sustained VA, implying that there might be other factors at play beyond
LV function and stable scar.64
An ICD prevents sudden death from VA but does not prevent VA itself.
It certainly does not prevent death from progressive pump failure
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and may in fact just allow for change in the mode of death. Both
appropriate and inappropriate shocks have been associated with
increased mortality, whereas ATP-treated arrhythmias were not. The
psychological impact of ICD therapy must not be underestimated.
More aggressive ATP, extended detection and redetection algorithms,
onset and stability criteria and morphology discrimination can help
reduce the frequency of inappropriate shocks.65
Further ischaemia or infarction may precipitate an electrical storm
in patients who already have an ICD. In such situations, treatment
should be as for someone without an ICD but an added consideration
may be to reprogramme the device to deal with increased frequency
or altered characteristics of arrhythmia and perhaps even switching
device therapies off in the short term in a well-monitored environment
to prevent excessive or inappropriate ATP and/or shocks.
Future Directions
A greater understanding of the cellular and electrophysiological
mechanisms of arrhythmia in the context of acute ischaemia
is needed. It is clear that risk stratification based on LVEF and
PES alone is inadequate and more robust investigations used in
combination are likely to be required. Current therapy is limited to
drugs with significant side effects and catheter ablation techniques.
The concept of a genetic predisposition and therapies targeted at
autonomic modulation are fascinating and warrant further research.
Timely and thorough revascularisation appears to be a strategy to
prevent death due to VA but it cannot be achieved in all patients
presenting post-infarct.
Perhaps the future for some does lie in molecular and stem cell therapy,
with the potential to regenerate lost or damaged myocardium.66 Stem
cell therapy has been used to treat heart failure. In early trials in an
animal model (rat), and subsequently in humans, stem cell therapy was
shown to increase propensity to ventricular arrhythmias (ventricular
ectopics and non-sustained VA), perhaps due to lack of effective
integration to the connexin network.67,68
Though further studies using stem cell therapies in the animal model
and subsequently in the humans have been reported to either reduce
propensity for cardiac arrhythmias or show no change in incidence
of sustained ventricular arrhythmias, further studies are required.69,70
Ventricular arrhythmias in patients with acute coronary syndrome
could influence the immediate and long-term mortality in these
patients. Appropriate risk assessment is needed to identify patients
at risk of further risk of VA and sudden cardiac death, and research is
needed in this field. n

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