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Abstract Background In ventricular tachycardia the heart rate is significantly increased. The main cause is an underlying heart disease (previous myocardial infarction or cardiomyopathy). Dysionia (hypokalemia and hypomagnesemia), acidemia, hypoxia, side effects of drugs contribute; Long QT syndrome is associated with torsade de pointes. Idiopathic ventricular tachycardia is not linked to a heart disease that can be diagnosed with currently available tests. A protection mechanism that the heart applies in the presence of ventricular tachycardia has been discovered: a sort of self–defibrillation. Clinical Case A forty–year–old smoker comes to the emergency room suffering from heart palpitations, dizziness and syncope. Physical examination: hypotension and asthenia. ECG: sinus rhythm with single and paired ventricular extrasystoles, monomorphic. Blood tests normal. Echocardiogram: mitral prolapse. Admitted to Internal Medicine, the patient presents a brief loss of consciousness; ECG: non–sustained ventricular tachycardia treated effectively with beta–blockers and amiodarone. Transferred to Cardiology: negative instrumental investigations for structural heart disease; on the Holter ECG, runs of non–sustained ventricular tachycardia. Discharged with beta–blockers. Asymptomatic at follow–up. Conclusions By studying the electrical dynamics underlying ventricular tachycardia, it was found that in the presence of rapid cardiac rhythms, complex electrical oscillations are established which lead to a sort of "self–defibrillation" of the heart. The electrical signals that precede the spontaneous termination of a ventricular tachycardia are characterized by an oscillatory dynamic of impulses with different durations from one beat to the next called alternans; when alternans increase, there is a greater susceptibility on the part of the heart to self–termination of the arrhythmic event, highlighting its cardio–protective effect as a defense mechanism triggered by the heart to resynchronize. It is therefore possible to develop new drugs and devices that exploit as a mechanism of action the increase in alternans during arrhythmic events and therefore the cardioprotective mechanism of the heart itself. A possible future clinical application could be the design of a low–energy implantable cardiac defibrillator, compared to current ones whose effectiveness is limited by the painful electric shocks that characterize them.
Luca et al. (Mon,) studied this question.