Layer-specific strain in acute coronary syndrome: back to the future!

This editorial refers to ‘Association between layer-specific global longitudinal strain and adverse outcomes following acute coronary syndrome’, by K.G. Skaarup et al., pp. 1334–1342. Coronary artery disease, and more specifically acute coronary syndrome (ACS) are major contributors to morbidity and mortality in developed countries. Although ACS has greatly benefited from major improvements in terms of detection and therapy with the development of early revascularization, patients are still facing morbidity and mortality of long-term complications such as heart failure. Thus, the new challenge is to identify ACS patients at risk in order to optimize their management. Early assessment of the transmural extent of necrosis after acute myocardial infarction has become crucial, because large infarct transmurality is associated with a great number of complications, such as left ventricular thrombus, arrhythmias, and death. Indeed during a prolonged coronary artery occlusion, irreversible injury of the ischaemic myocardium and thus myocardial necrosis progresses from endocardium towards epicardium as a ‘wave-front phenomenon’ and ultimately becomes nearly transmural.1 While experimental and clinical studies have demonstrated that early reperfusion of the ischaemic myocardium can salvage jeopardized tissue, anatomic-pathological studies revealed the great heterogeneity of the reperfused myocardium that contains a variable amount of necrosis surrounded by a viable but transiently stunned epicardium. This structural and functional heterogeneity complicates interpretation of wall motion abnormalities by conventional echocardiography. Therefore, such a myocardial heterogeneity needs to be taken into account in analysis of functional recovery in patients with coronary artery disease. In addition, conventional methods use endocardial motion to assess regional myocardial function, which may overestimate the extent of irreversible myocardial injury because of the impossibility of distinguishing viable but severely stunned or hibernating from necrotic myocardium. Myocardial strain is a sensitive and quantitative marker of myocardial deformation that may diagnose ischaemia by showing reduction in peak systolic strain and displaying systolic lengthening and post-systolic shortening which are characteristic features of ischaemic dysfunction.2 In addition, global longitudinal strain (GLS) is also a strong clinical predictor of morbidity and mortality associated with myocardial dysfunction. However, current assessment of global myocardial strain does not provide information on the non-uniformity of myocardial contractile performance across the different layers of the left ventricular wall. Indeed experimental studies using sonomicrometry have demonstrated that myocardial fibre thickening varies across the different layers of myocardial walls and is more pronounced in endocardium than in epicardium.3 This transmural heterogeneity in myocardial contraction is associated with non-homogeneous transmural myocardial blood flow, metabolism, and relaxation dynamics. In the normal myocardium, contraction is greater in the subendocardial layer, as is wall stress, accounting for the higher subendocardial energy requirements. As a consequence, ischaemia becomes more severe and myocardial cells undergo necrosis first in the subendocardium. Therefore, this transmural inhomogeneity is important to take into account in the setting of ischaemic cardiomyopathy to differentiate the various patterns of contractile abnormalities that may occur during acute ischaemia, hibernation, or stunning3,4 and thus to improve prognosis assessment after ACS. New developments in speckle tracking echocardiography allow layer‐specific measurement of strain with the ability to differentiate epicardial from endocardial deformation. While conventional myocardial strain measurements are reliable to detect myocardial ischaemia, layer‐specific strain has been shown to be a sensitive marker of infarct transmurality as compared with cardiac magnetic resonance.5 Together with the findings in chronic ischaemia, layer‐specific strain is also useful in studying the effects of acute ischaemia, where layer‐specific differences may be present as ischaemia progresses from the endocardium to the epicardium. The objective of the present study by Skaarup et al.,6 was to investigate the association between layer-specific GLS and the risk of developing heart failure and cardiovascular death in a population of 465 ACS patients. Interestingly they confirmed that all three layer-specific GLS measurements are superior to conventional systolic and diastolic echographic parameters to predict heart failure and cardiac death. In addition, they demonstrated that the epicardial layer GLS was the only independent variable predicting cardiac death alone. Such an observation is coherent with animal studies and confirms that the more the ischaemic lesion extends from the endocardium to the epicardium, more severe is the myocardial damage, and higher is the risk of late adverse outcome. In addition to the presence of extensive necrosis in both myocardial layers, we may also speculate from experimental studies that the decrease in epicardial layer GLS may be related to a too limited rim of epicardial viable tissue which is tethered to the underlying necrotic endocardium, which further impairs epicardial contraction. Additional data on myocardial blood flow would have been of interest to investigate the potential role of no reflow in the different myocardial layers. This study underlines the important information carried out by a comprehensive evaluation of regional myocardial function using strain imaging which provides interesting insights in the complex pathophysiology of ACS, and highlights the importance of assessing the extension of ischaemic myocardial injury in order to better identify the risk of late adverse outcomes. Conflict of interest: none declared.