Ventricular tachycardia due to ischemic cardiomyopathy
Substantial progress in the prevention, diagnosis and treatment of coronary syndromes has led to a significant prolongation of survival after the occurrence of a myocardial infarction. Despite these advances, long-term follow-up of these patients is burdened with a significant risk of ventricular rhythm disorders and a significant increase in the incidence of sudden death. Ischemic cardiomyopathies are responsible for approximately three-quarters of documented ventricular tachycardias. Remote to an infarction, the myocardial substrate displays a number of micro- and macroscopic structural and functional alterations that may facilitate the occurrence of ventricular arrhythmias. The existence of a sequela of necrosis is associated with the presence of slow conduction zones, a prerequisite for the installation of reentry circuits and the occurrence of a monomorphic ventricular tachycardia that can appear at any time during the course of the condition, sometimes years after the constitution of an infarction.
The electrocardiogram of a ventricular tachycardia due to a sequela of infarction presents certain characteristics:
- ventricular tachycardias secondary to a reentry around a myocardial scar are generally monomorphic; it is however possible to document different morphologies in a patient for a same infarction scar (pleomorphism), with the point of emergence of the activation wave emerging from the scar able to change and alter the direction of the electrical propagation in the surrounding myocardium;
- the morphology of the QRS complexes during an episode of ventricular tachycardia is dependent on the location of the scar and the reentry circuit within this scar; analysis of the surface electrocardiogram allows guiding a possible ablation procedure even if the presence of myocardial necrosis modifies the rules of projection of the electrical activation and renders the interpretation and the attempts of localization more difficult; a right delay suggests a circuit emerging from the left ventricle; a left delay suggests a right or septal ventricular origin (possibility of left delay or right delay); a left axis beyond minus 45 degrees suggests a diaphragmatic origin, a right axis is suggestive of a high origin; a negative concordance (negative QRS complexes from V1 to V6) suggests an apical origin, a positive concordance (positive QRS complexes from V1 to V6) suggests a basal origin with possible errors in instances of significant chest deformation; in the case of left ventricular aneurysm, seemingly paradoxical electrocardiographic patterns of left delay have been highlighted; the analysis of the first part of the QRS may evoke an epicardial emergence point: presence of a pseudo-delta wave and major prolongation of the intrinsicoid deflection; determining the endocardial or epicardial origin may be determinant at the time of initiating an ablation procedure;
- ventricular tachycardias due to a myocardial infraction related scar often exhibit a relatively widened QRS (>150 ms) with a notched pattern and marked ST segment depression; the widest QRS are recorded for circuits emerging from the left ventricular lateral wall and the narrowest for those emerging from the septum; other associated factors may influence QRS duration (hypertrophic cardiomyopathy, antiarrhythmic therapy);
- the intercritical electrocardiogram is often evocative, with evidence of a sequela of necrosis compatible with the tachycardia circuit;
Various radiological techniques have allowed optimizing the management of patients with myocardial infarction. MRI represents the reference technique for analyzing the myocardial substrate, necrotic areas and border zone, for defining the transmural nature of a scar and for measuring left ventricular ejection fraction, an essential prognostic factor.
Although beta-blockers represent the reference treatment in terms of prevention of sudden death, their effectiveness remains imperfect. The value of implantable defibrillator placement has been demonstrated in large cohorts as secondary prevention in patients with an episode of ventricular rhythm disorder or recovered sudden death or as primary prevention in patients with an altered ejection fraction. Despite a demonstrated benefit in terms of survival, a defibrillator does not reduce the incidence of rhythm disorders and an ablation procedure can be proposed for the occurrence of recurrent monomorphic ventricular tachycardias resistant to medical treatment.