Active vascular events such as spasm, plaque rupture or thrombosis in the setting of acute coronary syndromes precipitate
fatal arrhythmias due to acute ischemia. Lethal ventricular tachycardia (VT) in the setting of ischemic heart disease
(IHD) results either from acute ischemia or from chronic scar. Ischemia produces several intra, and extra-cellular changes in
ionic concentration and acid-base balance. In this context, the surviving Purkinje fibers exhibit several electrophysiological
changes, namely, abbreviated action potentials of reduced amplitude, and depolarized membrane potentials, and reduced
conduction velocity. These biochemical and electrophysiological disturbances act in accordance with a number of probable
genetic predispositions.
The resultant ischemia-induced VT may be suppressed by revascularization of the occluded vessel
ameliorating the ischemic tissue. Sustained VT in the peri-infarction period may develop due to transient arrhythmogenic
phenomena in ischemic and infarcting tissue such as the following: abnormal automaticity, triggered activity, and re-entrant
circuits created by heterogeneous conduction and repolarization. Combining different diagnostic techniques, a relation between
myocardial ischemia and induction of ventricular arrhythmias can be demonstrated in patients with IHD. Coronary
revascularization must be the main goal and may constitute definitive therapy in certain patients with ischemic ventricular
arrhythmias. This pure anti-ischemic therapeutic strategy seems to be justified in certain cases of patients with preserved
left ventricular function, demonstrable reversible ischemia and non-inducible VT pre and post revascularization. In all other
instances an additional treatment with antiarrhythmic drugs and an implantable cardioverter defibrillator is paramount.
Ischemic heart disease (IHD) is the most common cause of
sudden cardiac death (SCD) resulting from fatal ventricular arrhythmias,
and some of these events occur in persons without
any history of cardiac disease. Sustained ventricular
tachycardia (VT) and, in particular, ventricular fibrillation (VF),
are the immediate causes of cardiac arrest in the majority of
the estimated 350,000 cases of SCD that occur annually in the
USA. A major cause of SCD is acute myocardial infarction
(AMI). Cardiac arrest secondary to AMI induced-VF occurs
commonly without warning. Because spontaneous conversion
of VF to non-lethal rhythms is rare, out-of hospital VF progresses
to death within minutes in more than 95% of the victims.
AMI induced-VF leads to SCD as the first manifestation of
a preexisting coronary artery disease in about 80,000 people
per year. Polymorphic VT in patients with a normal QT interval
during sinus rhythm is most frequently seen in the context
of acute ischemia. In addition, it may be also seen with
other cardiac diseases such as cardiomyopathy, heart failure,
and even in the absence of overt cardiac disease, namely, idiopathic
polymorphic VT, catecholaminergic VT.
Since the electrophysiological changes and ventricular arrhythmias
induced by ischemia could be transient and temporary
if the ischemic episode subsides, the suppression of
ventricular arrhythmias and the ischemia-induced electrophysiological
changes by coronary revascularization is the focus
of this manuscript.
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