Pathophysiology of dispersed ventricular contraction
The prediction of sudden cardiac arrest from ventricular arrhythmias remains challenging. Ventricular arrhythmias can occur from all major myocardial diseases and are the most common cause of sudden cardiac death. Malignant arrhythmias are most frequently due to coronary artery disease but can also originate from nonischemic cardiomyopathies. Patients who are at risk of suffering from ventricular arrhythmias can receive medical treatment to lower their risk and most often receive an implantable cardioverter defibrillator (ICD).
The most common diagnostic echocardiographic tool to predict patient risk has traditionally been left ventricular ejection fraction (LVEF). Although the LVEF has been used as a criterion for ICD placement, it has limited abilities in predicting arrhythmic risk. In contrast to the normal left ventricles, in which all segments contract synchronously ( Fig. 5.1 ), pathologic ventricles show temporal dispersion of contraction ( Fig. 5.2 ). Mechanical dispersion has been proposed to be a more accurate measure for risk prediction and the pathophysiology, and its assessment and potential use in risk prediction will be presented in this chapter.
Ischemic cardiomyopathy
There is general agreement that conduction abnormalities and dispersion of action potential duration are required for the occurrence of malignant ventricular arrhythmias. The presence of myocardial scar is regarded as important for the electrical mechanisms and substrate leading to lethal reentrant ventricular arrhythmias. , Scar tissue causes areas of slow conduction that generate dispersion of cardiac action potentials. Electrical dispersion of repolarization does exist in normal myocardium—there are differences in action potential duration from the endocardium to the epicardium, and from the LV apex to LV base. This electrical heterogeneity and dispersion increase in ischemic myocardium and have been shown to be arrhythmogenic. , These mechanisms have been linked to myocardial tissue heterogeneity present after myocardial infarction (MI), and presence of infarcted tissue or scar forms the substrate for malignant reentrant arrhythmias. , More extensive tissue heterogeneity correlates with increased ventricular irritability by programmed electrical stimulation. The magnitude of myocardial scar can be assessed by cardiac magnetic resonance (CMR) imaging and has been correlated with the risk of arrhythmias in patients after myocardial infarction.
The heterogeneous contraction patterns will cause delays in the LV maximum shortening that can also occur during early diastole and after mitral valve opening. These patterns may be detected by careful assessment of LV function. Speckle-tracking echocardiography has been repeatedly demonstrated to be an accurate and sensitive means of assessing LV function and is well suited to explore a heterogeneous contraction pattern. , Mechanical dispersion is defined as the standard deviation of time from the onset of the Q/R wave on the electrocardiogram (ECG) to peak negative strain in 16 LV segments. Mechanical dispersion has been introduced as a measure of heterogeneous ventricular contraction patterns, and its ability to predict ventricular arrhythmias has been demonstrated in numerous studies ( Fig. 5.3 ).
Nonischemic cardiomyopathies
The electrically dispersed patterns in nonischemic cardiomyopathies originate from mechanisms other than those described in ischemic cardiomyopathy. However, clear similarities in the mechanisms leading to the heterogeneous ventricular contraction patterns of ischemic cardiomyopathy may exist in patients with nonischemic cardiomyopathy. Fibrotic tissue, scar, and tissue heterogeneity provide a substrate for ventricular arrhythmias similar to ischemic cardiomyopathies. Myocardial scar will ultimately lead to a heterogeneous contraction pattern, which can be reflected by mechanical dispersion assessed by speckle-tracking strain echocardiography.
Assessment of dispersed contraction pattern
Mechanical dispersion in ischemic and nonischemic cardiomyopathies
The assessment of electrical dispersion can be performed by invasive methods, but noninvasive methods for assessing electrical dispersion have been challenging and the accuracy in predicting lethal arrhythmias has been very limited.
Heterogeneous patterns of contraction can easily be assessed by speckle-tracking echocardiography. In contrast to global longitudinal strain (GLS), which is a measure of the maximum amplitudes of myocardial contraction, mechanical dispersion has been related to electrical dispersion, which is the arrhythmic substrate. , Different myocardial diseases can result in a delayed contraction with different regional timings of maximal shortening. This heterogeneous pattern of contraction has been named mechanical dispersion and has been linked to increased arrhythmic risk after myocardial infarction, in different cardiomyopathies and channelopathies. , , , As opposed to the contraction pattern in left bundle branch block (LBBB), mechanical dispersion by speckle-tracking echocardiography is thought to reflect conduction abnormalities not discovered by the ECG.
The echocardiographic assessment is performed from ordinary gray scale loops from the three apical four-chamber views. The first step is to assess LV GLS and then assess the timing from the start of the Q/R wave on ECG to maximum shortening in each of the 16 segmental strain curves. Most vendors have included semiautomated software for a faster calculation of mechanical dispersion.
Most healthy individuals without any sign of myocardial disease have a homogenous contraction pattern with similar timing of maximum LV shortening in the different LV segments. A homogenous contraction pattern leads typically to a low measure of mechanical dispersion, usually <50 ms. In a healthy group of individuals ( n = 594) of 64-year-old men and women, the average mechanical dispersion was 35.7±12.7 ms. No significant difference was found for mechanical dispersion between men and women. It could also be shown that subjects with coronary artery disease, hypertension, and diabetes had mechanical dispersion values above the upper limit of normal.
Attempts to obtain excellent image quality should be made when assessing mechanical dispersion. Common pitfalls in routine echocardiographic images such as reverberations and reflections may hamper the correct assessment of mechanical dispersion.
Vendor differences may play a role in the assessment of GLS on different echocardiographic machines, but differences have been improved during recent years. Measurements of time intervals, however, have not been reported to differ significantly among the different vendors.
The feasibility of mechanical dispersion has been reported as excellent but is dependent on the assessment of myocardial strain. The reproducibility of mechanical dispersion is generally reported as very good and similar to other advanced and traditional echocardiographic assessments, with typical intraclass correlation values from 0.85 to 0.90. ,
Prognostic information from dispersed contraction patterns
Arrhythmias and mechanical dispersion
Mechanical dispersion is significantly greater in those developing an arrhythmic event during follow-up than those who do not ( Fig. 5.4 ). Figure 5.5 summarizes the prediction of malignant arrhythmias using dispersion—and this has been shown after MI in different cardiomyopathies and channelopathies. , , , The ability to predict ventricular arrhythmias in ischemic cardiomyopathies has been superior to LVEF and in particular when LVEF is >35%. , In a number of cardiac disorders, the ability of GLS to predict cardiovascular outcome has been reported to be superior to LVEF, while mechanical dispersion is better related to sudden cardiac arrest and malignant arrhythmias.
The most convincing literature on the abilities of mechanical dispersion to predict ventricular arrhythmias is in patients with ischemic cardiomyopathy. A meta-analysis showed that mechanical dispersion was significantly and independently associated with ventricular arrhythmic events. They included in their analyses >2000 patients who had suffered from MI, and >700 patients with different nonischemic cardiomyopathies. A mechanical dispersion cutoff of >60 ms was associated with ventricular arrhythmic events in the meta-analysis ( Fig. 5.6 ), while individual studies have also suggested 70 ms as a cutoff.
The most frequent cause of ventricular arrhythmias and sudden cardiac death in individuals over the age of 30 is coronary artery disease. Ejection fraction <35% is a good risk predictor of sudden cardiac arrest after MI, but most patients with prior MI who die suddenly have LVEF >30%. A large prospective study in patients after MI showed that patients suffering from arrhythmias had an average LVEF of 48±17% and that mechanical dispersion was superior to EF in predicting malignant arrhythmias. , These results have been confirmed with similar results by other studies. ,
Inherited cardiac diseases are the most frequent causes of sudden cardiac death in individuals <30 years of age. Sudden cardiac death can often be the first symptom of the disease and this challenges the way to approach patients with a known genotype but an asymptomatic phenotype, as well as in family members of those with known disease. The major challenge is therefore to correctly choose patients for an ICD implantation and the correct timing of this procedure, and new information from mechanical dispersion may play a role.
One of the most common reasons for sudden cardiac death is hypertrophic cardiomyopathy (HCM), with an annual incidence of 1% to 2%. The 2014 guidelines from the European Society of Cardiology include maximum wall thickness, left atrial size, and maximal left outflow gradient as a continuum in addition to age, family history of sudden cardiac death, nonsustained ventricular tachycardia, and unexplained syncope to calculate the 5-year risk of sudden death in HCM. Many patients fall into an intermediate group, and additional echocardiographic parameters might be useful in the decision making of further treatment. Mechanical dispersion has been demonstrated to relate to malignant ventricular arrhythmias in cardiomyopathies and to relate to fibrosis by CMR imaging in HCM patients. The predictive value of mechanical dispersion was equal to that of myocardial fibrosis by CMR imaging for the identification of high-risk HCM individuals, and it may be an important add-on to our diagnostic risk prediction tools. The cutoff value for mechanical dispersion was around 70 ms to detect arrhythmic events in HCM patients. Arrhythmogenic cardiomyopathy (or arrhythmogenic right ventricular cardiomyopathy [ARVC]) and dilated cardiomyopathies might be other potential diseases where mechanical dispersion might have an important role as a risk marker. ,
Strain patterns associated with response to cardiac resynchronization therapy
The mechanical consequences of delayed electrical activation occurring in patients with myocardial disease may be complex. Strain imaging has made a significant contribution to the understanding of the electromechanical substrate and its significance for response to cardiac resynchronization therapy (CRT) ( Table 5.1 ). The general clinical indications for CRT are for patients with symptomatic heart failure (HF), depressed LVEF, and electrical delay measured by electrocardiographic QRS widening. Currently, the class I ECG criteria for CRT are a QRS ≥150 ms and a LBBB pattern.
