Longitudinal Strain and Sudden Cardiac Death

Govindan Vijayaraghavan

doi:10.4103/jiae.jiae_23_22

REVIEW ARTICLE

Year : 2023 | Volume : 7 | Issue : 2 | Page : 147-153

Longitudinal Strain and Sudden Cardiac Death

Govindan Vijayaraghavan
Department of Cardiology, KIMSHEALTH, Thiruvananthapuram, Kerala, India

Date of Submission	03-May-2022
Date of Decision	10-Apr-2023
Date of Acceptance	11-Apr-2023
Date of Web Publication	28-Jul-2023

Correspondence Address:
Prof. Govindan Vijayaraghavan
KIMSHEALTH, Thiruvananthapuram - 695 029, Kerala
India

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jiae.jiae_23_22

Abstract

Several cardiac conditions are associated with the risk of ventricular arrhythmias (VAs) and sudden cardiac death (SCD). Identification of the individuals at increased risk of these events is essential to facilitate the appropriate measures to prevent SCD. Several clinical, electrocardiographic, and imaging markers have been used for this purpose with varying accuracy. Recently, longitudinal myocardial strain assessed using speckle-tracking echocardiography has been shown to have incremental value in the prediction of SCD risk. Strain imaging allows quantification of the abnormalities in the magnitude and timing of the segmental myocardial contraction, which is a surrogate for underlying myocardial fibrosis and myofiber disarray. Reduced segmental strain and temporal heterogeneity indicate electromechanical dispersion, which is the primary substrate for VAs and SCD. This review summarizes current evidence regarding the utility of longitudinal strain for the prediction of SCD risk.

Keywords: Global longitudinal strain, longitudinal strain, mechanical dispersion, speckle-tracking echocardiography

How to cite this article:
Vijayaraghavan G. Longitudinal Strain and Sudden Cardiac Death. J Indian Acad Echocardiogr Cardiovasc Imaging 2023;7:147-53

How to cite this URL:
Vijayaraghavan G. Longitudinal Strain and Sudden Cardiac Death. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2023 [cited 2023 Sep 27];7:147-53. Available from: https://jiaecho.org/text.asp?2023/7/2/147/382477

Introduction

Sudden cardiac death (SCD), usually due to ventricular arrhythmias (VAs), is the most devastating manifestation of any cardiac illness. Ischemic heart disease (IHD) and dilated cardiomyopathy (DCM) are the most common causes of SCD, with many other diseases contributing to it^[1] [Figure 1]. Prevention of SCD is one of the foremost goals of management of these conditions. Extensive research has been conducted to develop robust tools to predict SCD. However, the current algorithms to predict SCD risk remain imperfect.

Figure 1: Common causes of sudden cardiac death. *Cardiomyopathies include dilated cardiomyopathy, hypertrophic cardiomyopathy, and arrhythmogenic cardiomyopathy, **Inherited arrhythmia syndromes include long QT syndrome, Brugada syndrome, short QT syndrome, and catecholaminergic polymorphic ventricular tachycardia

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A number of clinical markers, electrocardiographic findings, and imaging findings have been used to predict SCD risk in different cardiac conditions. Echocardiography is a useful imaging modality for this purpose. At present, left ventricular (LV) ejection fraction (LVEF) is the most validated echocardiographic predictor of SCD risk. The current guidelines recommend implantation of an automatic implantable cardioverter-defibrillator (ICD) to prevent SCD in patients with IHD or DCM with reduced LVEF.^[2],[3] An ICD is recommended in all patients with ischemic cardiomyopathy with LVEF <35% or 30% depending on the New York Heart Association (NYHA) functional class and in nonischemic cardiomyopathy with LVEF <35% and NYHA functional class II or III.^[2],[3] For other conditions, such as hypertrophic cardiomyopathy (HCM), additional echocardiographic parameters such as maximal septal thickness, left atrial (LA) size, and LV apical aneurysm have been used to predict SCD risk.^[4],[5]

Despite the extensive literature supporting the prognostic utility of LVEF for SCD risk, it is neither sufficiently sensitive nor specific for this purpose.^[6] To overcome this limitation, several newer imaging parameters are being developed based on echocardiography, nuclear imaging, and cardiac magnetic resonance (CMR) imaging. Of these novel imaging markers, LV strain, which can be obtained using either echocardiography or CMR, has emerged as a useful tool.^[7]

Rationale for Using Left Ventricular Strain for Predicting Sudden Cardiac Death Risk

Inappropriate myocardial hypertrophy with myofiber disarray, myocardial fibrosis, and scarring are the key pathophysiological abnormalities that predispose patients with structural heart diseases to the risk of VAs and SCD [Figure 2]. These abnormalities result in asynchronous electrical activity and contraction, leading to dispersion of the regional myocardial deformation of the left ventricle. This dispersion of the electrical activity creates a substrate for tachyarrhythmias which can result in SCD.^[8]

Figure 2: Pathogenic mechanisms of sudden cardiac death in various cardiac disorders. In most of the cases, myocardial fibrosis and myocyte disarray are responsible for ventricular arrhythmia and sudden death. However, in case of channelopathies, there is no structural abnormality of the myocardium. HCM: Hypertrophic cardiomyopathy

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Myocardial strain imaging provides us with the ability to image the deformation of each of the 16 LV myocardial segments. When all the segments shorten synchronously to peak at the aortic valve closure or end-systole and the percentage of shortening is similar, there is synchronous electromechanical activity of the left ventricle with optimal LV function [Figure 2]. The lack of this synchronicity indicates vulnerability to VAs and SCD [Figure 3]. Myocardial strain imaging permits quantification of both the magnitude and the timing of the segmental contraction.

Figure 3: Left ventricular longitudinal strain curves in a normal heart. There is synchronous peaking of all the myocardial segments at end-systole. The global longitudinal strain is above 20% (i.e., less negative than 20%)

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Although LV strain can be measured using either echocardiography or CMR, the former offers a much simpler and preferred option. Speckle-tracking echocardiography (STE) is the technique used for measuring myocardial strain by echocardiography. STE is a non-Doppler-based and angle-independent technique that utilizes grayscale images for the measurement of myocardial strain.^[9] Using STE, different components of LV myocardial deformation, such as longitudinal strain, circumferential strain, radial strain, rotation, and twist, can be measured. The technique can also be extended to other cardiac chambers for measuring the deformation of those chambers.

Among various strain measurements for the left ventricle, longitudinal strain is the most robust. It represents the shortening or lengthening of the LV myocardium in the long axis. The magnitude of reduction in systolic length is expressed as a percentage of diastolic length, and hence, longitudinal strain is expressed as a negative value. A longitudinal strain value of −16% or more is considered normal in healthy adults.^[10] The magnitude and timing of longitudinal deformation of each of the LV myocardial segments can be derived individually and depicted in the form of color-coded curves or parametric displays. In addition, the peak strain of all the LV segments can also be displayed as a bull's eye plot for a quick overview of the LV contractile pattern. The average of the peak systolic longitudinal strain of all the LV segments is known as global longitudinal strain (GLS), which is the most validated and the most used strain measurement for clinical purposes.^[11]

Case Vignettes

Patient 1

A 36-year-old male presented with NYHA class II dyspnea and palpitations. After clinical assessment and echocardiography, a diagnosis of HCM was made. [Figure 4] shows LV strain in this patient. His average longitudinal strain was reduced (−13.9%), but the segmental strain pattern was much more striking. Although the longitudinal strain peaked at end-systole in most of the segments, the values differed from basal to mid and apical segments. The variation in strain from the base to the apex can be easily appreciated from the bull's eye plot, which shows the dispersion of strain with respect to severity. Peak systolic strain over the interventricular septum and basal anterior wall was reduced and the reduction in strain was inversely proportional to the thickness of the myocardium. The thickest part of the LV myocardium, as seen in the two-dimensional and M-mode images [Figure 4], showed the lowest systolic strain, indicating that these segments had the lowest contribution to LV ejection. This disparity arises due to muscle fiber disarray and fibrosis and may form a nidus for VAs and SCD. The massive myocardial hypertrophy in HCM is accompanied by increasing myofiber disarray and fibrosis with scarring and consequent reduction in strain values as well as altered timing of peak contraction.^[12] Earlier workers had pointed out that a wall thickness of more than 30 mm was a warning sign for SCD.^[12] Our patient had a wall thickness of 35 mm in the anterior septum. For comparison, [Figure 5] shows longitudinal strain curves from a patient with apical HCM. Unlike our patient, in this example, there is a reduction in the strain at the LV apex, which is again consistent with the site of maximum LV hypertrophy.

Figure 4: Left ventricular longitudinal strain curves in a patient with previous myocardial infarction. There is marked temporal heterogeneity of the segmental strain (the arrows point to the peaks of the different segmental strain curves)

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Figure 5: Left ventricular longitudinal strain in a patient with hypertrophic cardiomyopathy. Maximally hypertrophied septum (a and b, yellow arrows) have the least strain (c and d, yellow arrows). Note the inferior-posterior region with normal thickness has normal strain values (a, c and d, green arrows)

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Patient 2

[Figure 6] shows the LV strain images from a 57-year-old patient who had presented with NYHA functional class III dyspnea for 2 years following an episode of viral infection. He had been diagnosed as a case of DCM and was on guideline-directed heart failure therapy. He had now presented with ventricular tachycardia. His LV GLS was low and measured only −5.6%. [Figure 6]a shows segmental strain in the bull's eye format. All the myocardial segments had markedly reduced peak strain values (in the range of −1%–−12% instead of the normal strain of −16%–−30%). [Figure 6]b shows the strain curves from the three apical views, namely the apical long-axis, four-chamber, and the two-chamber views. It can be easily appreciated that not only there is a marked reduction of segmental strain but some of the curves also do not peak at the end-systole. This means that there is a dispersion of strain curves in terms of both magnitude and timing. The dispersion of longitudinal strain severity seen in the bull's eye display correlated with the scar tissue identified on CMR imaging. The ventricular tachyarrhythmia in this patient was likely triggered by the electromechanical dispersion resulting from myocardial fibrosis secondary to previous myocarditis.

Figure 6: Left ventricular longitudinal strain in a 35-year-old athlete with apical hypertrophic cardiomyopathy showing reduction of strain values in the apical segments. Two apical segments (magenta and green) can be seen lengthening during systole as the strain curves go above the baseline and the bull's eye plot shows blue color in the corresponding segments

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Patient 3

[Figure 7] is from a patient who had developed heart failure following an anterior wall myocardial infarction (MI) and was on guideline-directed heart failure therapy. He had now presented with paroxysmal palpitations. His 24-h ambulatory electrocardiographic monitoring showed paroxysmal nonsustained ventricular tachycardia. Strain curves from the three apical views show a bizarre pattern. Three apical segments and some adjoining mid segments show markedly reduced systolic strain, whereas two segments show paradoxical systolic lengthening (double-headed arrow). There are also segments with postsystolic shortening (vertical arrows). Overall, there is considerable heterogeneity in both the magnitude and the timing of the segmental strain curves. This is a common occurrence in post-MI patients with LV scarring and is associated with the risk of VAs and SCD.^[8],[13] This heterogeneity occurs as a consequence of the healing process after infarction which invariably causes myocardial fibrosis resulting in electromechanical dispersion [Figure 8].

Figure 7: Strain imaging in a patient with postmyocarditis dilated cardiomyopathy. Note the decreased strain in all the left ventricular myocardial segments, with some of the curves peaking in mid-systole. (a) Bull's eye plot, (b) Segmental strain curves

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Figure 8: Left ventricular longitudinal strain images from a patient with anterior wall myocardial strain. Note the dispersion of strain curves in relation to the timing of peak strain, postsystolic strain (yellow arrows), and paradoxical stretch represented by positive strain in two segments (green arrows)

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Evidence Base

Ischemic left ventricular systolic dysfunction

Haugaa et al. were the first to demonstrate the prognostic value of LV mechanical dispersion (MD) assessed using STE for predicting VA risk.^[8] They included 85 post-MI patients undergoing ICD implantation for primary or secondary prevention of SCD. MD was calculated as the standard deviation of time-to-maximum shortening of all the LV myocardial segments in a 16-segment model. Over a mean follow-up period of 2.3 years, 38 patients developed one or more VA requiring appropriate ICD therapy. There was no difference in the LVEF between patients with or without VAs, but MD was significantly prolonged in those who had VAs (85 ± 29 ms vs. 56 ± 13 ms, P < 0.001). MD was found to be a powerful, independent predictor of VAs requiring ICD therapy, with each 10-ms increment in the MD associated with a 25% increase in the risk of VAs.^[8]

In a subsequent much larger study of 569 patients with an MI at least 40 days ago, Haugaa et al. once again showed the predictive value of MD for VAs and SCD risk.^[13] The patients with VAs (defined as sustained ventricular tachycardia or SCD during the follow-up) had significantly lower LVEF and GLS and higher MD as compared to those who did not have VA. MD was an independent predictor of VAs. Both MD and GLS, but not LVEF, predicted arrhythmic events in patients with preserved LVEF. In another even larger study, Ersbøll et al. included 988 acute MI patients and followed them up for 29.7 months.^[14] Both GLS and MD were independent predictors of SCD/VA risk. GLS also significantly improved SCD risk stratification compared to conventional markers. However, MD did not have incremental value over GLS.

Several other studies have demonstrated the utility of GLS and MD in prediction of SCD/VA risk in post-MI patients.^{[15],[16],[17],[18]} Recently, a meta-analysis was published of 12 studies that evaluated the role of MD in the prediction of VAs.^[19] These studies included patients with both ischemic and nonischemic LV systolic dysfunction. LV MD was significantly greater among patients with VAs than those without VAs. LV MD was a stronger predictor of VA risk than GLS or LVEF.

Nonischemic dilated cardiomyopathy

A number of studies have reported the value of MD in predicting SCD/VA risk among patients with nonischemic DCM. Haugaa et al. studied 94 patients with nonischemic DCM. The patients with arrhythmic events had lower LVEF and GLS and a higher MD. MD predicted arrhythmic events independent of LVEF.^[20] Similar findings have been reported in many other studies.^{[17],[18],[21]}

Hypertrophic cardiomyopathy

SCD is the most feared complication of HCM. Several criteria have been developed to predict the risk of SCD and guide prophylactic ICD implantation in patients with HCM.^[4],[5] These criteria include clinical risk markers (unexplained syncope and family history of SCD), echocardiographic findings (maximum LV wall thickness, LV systolic dysfunction, and LV apical aneurysm), or evidence of VAs on Holter monitoring. Risk scores have been developed that integrate these criteria and predict SCD risk. However, further refinement is needed to enhance the predictive accuracy of these algorithms. Late gadolinium enhancement (LGE) on CMR has emerged as the most promising imaging marker for this purpose,^{[22],[23],[24],[25]} but STE-based strain imaging has also shown potential.

Myocyte disarray and myocardial fibrosis are the hallmark of HCM and provide the substrate for VAs. Strain imaging can detect these structural abnormalities. Several studies have shown that HCM patients have much lower GLS than healthy controls;^[26],[27] segmental longitudinal strain is significantly reduced in the most hypertrophied segments;^{[26],[28],[29]} and the reduction in longitudinal strain correlates with the extent of myocardial fibrosis detected using CMR.^{[27],[28],[29]} Layer-specific strain abnormalities have also been reported in HCM.^[30] These strain abnormalities occur despite preserved LVEF. Based on these findings, strain imaging has been used for predicting SCD risk in HCM.

In a large study involving 427 patients with HCM, GLS and LA volume index (LAVI) were found to be independently associated with the primary endpoint, which was a composite of all-cause mortality, heart transplantation, SCD, and appropriate ICD therapy. There was 99% event-free survival at 6 years among patients with preserved GLS (<−15%) and LAVI (<34 ml/m²) but only 63% in those with abnormal GLS and LAVI.^[31]

In another study which included 150 HCM patients and 50 healthy individuals, GLS was significantly lower and MD significantly greater among those with HCM. These abnormalities were even more pronounced in patients who had had VAs. MD correlated with the extent of myocardial fibrosis as depicted by LGE on CMR and was an independent predictor of VAs.^[27] A few other studies have also shown GLS and MD to predict VAs in HCM.^[32],[33]

Vergé et al. studied 217 patients with HCM and evaluated the diagnostic and prognostic value of longitudinal strain reduction in the hypertrophied segments. It was found that the mean longitudinal strain of the hypertrophied segments correlated with the LV outflow gradient and LAVI and was a predictor of SCD and appropriate ICD shocks.^[29]

Other conditions

Arrhythmogenic cardiomyopathy (AC) is a disease characterized by the replacement of myocardium with fibrofatty tissue in the right ventricle, left ventricle, or both. The patients may present with VAs, heart failure, or a combination of the two. Conventionally, regional wall motion abnormalities, aneurysm formation, ventricular dilatation, and dysfunction have been the main echocardiographic findings used for the diagnosis and risk stratification of AC.^[34] However, recent studies have shown that STE may also have a role to play, especially for the prediction of SCD risk. It has been demonstrated that in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), right ventricular (RV) longitudinal strain predicts SCD or ventricular tachycardia.^[35] A cutoff value of − 17.3% had the optimum predictive accuracy. RV MD has also been shown to be an independent predictor of VAs in ARVC.^[36]

Channelopathies such as long QT syndrome, Brugada syndrome, short QT syndrome, and catecholaminergic polymorphic ventricular tachycardia are the other common causes of VAs and SCD. They result from genetic alterations in ion channels or associated proteins and are characterized by malignant arrhythmias in structurally normal hearts. The changes in action potential, synchronization, and propagation of electrical impulses predispose to potentially malignant arrhythmias. However, since these electrical abnormalities do not have any associated mechanical abnormalities in the myocardium, strain imaging has no role in the prediction of SCD risk in these conditions.

Conclusions

Several cardiac conditions are associated with the risk of VAs and SCD. Identification of the individuals at increased risk of these events is essential to guide prophylactic ICD implantation to avoid the tragic loss of life. Several clinical, electrocardiographic, and imaging markers have been used for this purpose with varying accuracy. Recently, longitudinal myocardial strain assessed using STE has been shown to have incremental value in the prediction of SCD risk. Strain imaging allows quantification of the abnormalities in the magnitude and timing of the segmental myocardial contraction, which is a surrogate for underlying myocardial fibrosis and myofiber disarray. Reduced segmental strain and temporal heterogeneity indicate electromechanical dispersion which is the primary substrate for VAs and SCD.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

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