The etiology of sudden cardiac death is multifactorial. Several risk factors have been identified, such as decreased LVEF, history of coronary artery disease, cigarette smoking, hypertension, obesity, male sex, heart failure, ventricular arrhythmias, increased ventricular ectopy, diminished heart rate variability, baroreflex sensitivity, and heart rate profile during exercise [5]. Randomized clinical trials indicate that 84 % of sudden deaths are due to ventricular tachyarrhythmias, while bradyarrhythmias were responsible for 16 % of sudden cardiac deaths. VF was the most common ventricular tachyarrhythmia, usually secondary to VT, whereas the rest of the arrhythmias were caused by torsade de pointes [6]. The best method to prevent sudden cardiac death in high-risk patients is ICD. ICD reduces mortality in patients selected for primary prevention of SCD on the basis of reduced LVEF. ICD can prevent sudden cardiac death caused by bradyarrhythmias, torsade de pointes associated with congenital long-QT syndrome (LQTS), and pause-dependent VT [7]. An impaired EF (< 35 %) is the main indication for cardioverter–defibrillator implantation in patients after myocardial infarction. Hypertrophic obstructive cardiomyopathy, long QT and Brugada syndromes, and idiopathic VF are additional indications. Although LVEF is still regarded as a good predictor of ventricular arrhythmias [8, 9], it has several limitations in terms of predicting sudden cardiac death. In the Oregon Sudden Unexpected Death Study, only 30 % of sudden cardiac death cases met the criteria; 65 % of patients, who had LV function measured before sudden cardiac death, did not have severe LV dysfunction [10]. Other clinical studies indicated that 52 % patients with sudden cardiac death had some decrease in LV systolic function, while 30 % had severely decreased LV systolic function. Therefore, based on current LVEF guidelines for sudden cardiac death prevention, only 30 % would have qualified as candidates for a prophylactic ICD. Patients who had sudden cardiac death and normal LVEF were more often female, younger, more likely to have a seizure disorder, and more likely to be taking antiepileptics compared with patients with decreased LVEF [11‐16].

A variety of mechanisms in heart failure can lead to sudden cardiac death such as remodeling of the myocardium, altered neurohumoral signaling, slowed conduction, impaired repolarization, poor coupling of myocardium, and delayed-paced ventricular activation. These factors make the myocardium susceptible to arrhythmia triggers [17]. The presence of scar tissue in the myocardium after myocardial infarction causes electrical heterogeneity, changes in expression of ion channels, delayed electrical conduction, a dispersed recovery of excitability, and dispersed electrical repolarization. Electrophysiological testing could be an objective screening tool; however, it is invasive, expensive, and impractical. Therefore, there is a need for a sensitive tool for evaluating the risk of sudden cardiac death.

Electrical dispersion results in altered myocardial function. Regional and global myocardial function and timing can be evaluated by tissue Doppler imaging of strain [18]. Mechanical dispersion, which can be defined as heterogeneous contraction assessed by myocardial strain, is useful for the noninvasive measurement of LV function and the timing of myocardial contraction, and it may be a good predictor of arrhythmic episodes. Clinical trials indicated mechanical dispersion to be a good tool for predicting VT/VF in patients with long QT syndrome [19]. Moreover, mechanical dispersion by myocardial strain is related to episodes of ventricular arrhythmia in patients with ARVC.

The concept of using ultrasound-based mechanical dyssynchrony as a marker of sudden cardiac death was introduced for the first time by Norwegian researchers [20]. The results of our study confirmed to some extent their findings that greater mechanical dispersion occurs in patients with documented severe ventricular arrhythmias. Mechanical dispersion may become an important parameter for evaluating the risk of sudden cardiac death and the necessity for cardioverter–defibrillator implantation. Segmental contractility disorders are the result of electrical abnormalities that appear in the place of postinfarction scars. The asynchronous work of all segments causes hemodynamic cardiac inefficiency, and therefor there is a need for ICD therapy. Measurement of mechanical dispersion might help to better select patients who will be at risk of severe ventricular arrhythmia and sudden cardiac death. This parameter may be useful in clinical work for selecting patients who are in need of better care so as to avoid sudden cardiac death.