09-04-2014, 02:16 PM
Post-Infarction Sustained Monomorphic Ventricular Tachycardia
Classification of Ventricular Tachycardia
Ventricular tachycardia (VT) is defined as a tachycardia (rate >100
beats/min) with three or more consecutive beats that originates
below the bifurcation of the His bundle (HB), in the specialized
conduction system, the ventricular muscle, or in a combination of
both tissues, independent of atrial or atrioventricular nodal (AVN)
conduction.
CLASSIFICATION ACCORDING TO TACHYCARDIA
DURATION
Sustained VT lasts for more than 30 seconds or requires termina-
tion (e.g., cardioversion) in less than 30 seconds because of hemo-
dynamic compromise, whereas nonsustained VT is a tachycardia
at more than 100 beats/min lasting for three or more complexes
but for less than 30 seconds.3 However, during electrophysiological
(EP) testing, nonsustained VT is defined as more than five or six
complexes of non–bundle branch reentrant (BBR) VT, regardless of
morphology. BBR complexes are frequent (50%) in normal individ-
uals in response to a ventricular extrastimulation (VES) and have
no relevance to clinical nonsustained VT. Repetitive polymorphic
responses are also common (up to 50%), especially in response to
multiple (three or more) VESs with very short coupling intervals
(less than 180 milliseconds). The clinical significance of induced
polymorphic nonsustained VT is questionable.3 Incessant VT is a
continuous sustained VT that recurs promptly over several hours
despite repeated interventions (e.g., electrical cardioversion) for
termination.4 Less commonly, incessant VT manifests as repeated
bursts of VT that spontaneously terminate for a few intervening
sinus beats, followed by the next tachycardia burst.
CLASSIFICATION ACCORDING TO QRS
MORPHOLOGY IN V1
VT with a left bundle branch block (LBBB)-like pattern has a pre-
dominantly negative QRS polarity in lead V1 (QS, rS, qrS), whereas
VT with a right bundle branch block (RBBB)-like pattern has a pre-
dominantly positive QRS polarity in lead V1 (rsR′, qR, RR, R, RS).
However, the VT may not show features characteristic of the same
bundle branch block (BBB)-like morphology in other leads
Mechanism of Post-Infarction
Ventricular Tachycardia
The majority of sustained monomorphic VTs (SMVTs) are caused by
reentry involving a region of ventricular scar. The scar is most com-
monly caused by an old myocardial infarction (MI), but right ventric-
ular (RV) dysplasia, sarcoidosis, Chagas disease, other nonischemic
cardiomyopathies, surgical ventricular incisions for repair of tetral-
ogy of Fallot, other congenital heart diseases, or ventricular volume
reduction surgery (Batista procedure) can also cause scar-related
reentry. Dense fibrotic scar creates areas of anatomical conduction
block, and fibrosis between surviving myocyte bundles decreases
cell-cell coupling and distorts the path of propagation, causing areas
of slow conduction and block, which promotes reentry. In post-MI
VT, a variety of different circuit configurations are possible. Gener-
ally, the reentrant circuit arises in areas of fibrosis interspersed with
bundles of viable myocytes, producing a zigzag course of activa-
tion of and transverse conduction along a pathway lengthened by
branching and merging bundles of surviving myocytes, leading to
inhomogeneous anisotropy (see Fig. 3-18).
PREABLATION EVALUATION
Patients with post-MI VT should be evaluated for comorbidities that
can alter the approach to mapping and ablation. Treatment of con-
gestive heart failure and myocardial ischemia should be optimized.
Coronary revascularization should be considered in patients with
reversible ischemia, because substantial ischemic burden can
often be aggravated by the potential induction of prolonged peri-
ods of tachycardia or hemodynamically unstable arrhythmias dur-
ing the ablation procedure. In patients with frequent or incessant
VT, however, catheter ablation may be required on an urgent basis
before the assessment for coronary artery disease in order to gain
prompt control of the ventricular arrhythmia.
LEFT VENTRICULAR EJECTION FRACTION
Multiple studies evaluating survival of patients with prior MI estab-
lished a clear relationship between reduced LVEF and increased
mortality. LVEF behaves as a continuous variable, with gradually
increasing mortality risk until the LVEF declines to 40% and then
markedly increasing risk for values less than 40%. Nevertheless,
the exact mechanisms involved in the strong correlation between
decreased LV systolic function and increased incidence of SCD
are not clearly defined.14
Although low LVEF identifies one patient population at relatively
increased risk for SCD, there are clear limitations to LVEF as the
ideal risk-stratification test for deciding whether to implant an ICD
for primary prevention of SCD. LV systolic dysfunction lacks speci-
ficity. There is no evidence of any direct mechanistic link between
low LVEF and mechanisms responsible for ventricular tachyarrhyth-
mias and no study has demonstrated that reduced LVEF is specifi-
cally related to SCD. In fact, in studies that enrolled all patients after
MI, patients with LVEF less than 30% to 35% account for no more
than 50% of sudden cardiac arrest victims.