Is circumferential strain in the back pocket of the longitudinal strain or not?

This editorial refers to ‘Link between myocardial deformation phenotyping using longitudinal and circumferential strain, and risk of incident heart failure and cardiovascular death’, by K.G. Skaarup et al., https://doi:10.1093/ehjci/jead075. Some data demonstrate that subtle impairments of systolic function are independently associated with incident heart failure (HF).1 Over the past decade, we have been focusing on showing the value of global longitudinal strain (GLS) in different clinical settings2 with the goal of demonstrating the complementary role of GLS to left ventricular ejection fraction (LVEF). Therefore, it is important to be convinced about the reproducibility of GLS. Also, it is, and it remains, important to ensure that the measurements can be made widely available and remain independent from the echo vendors.3 GLS is getting more and more accepted by each passing day. There is still room for improvement, and automation of the measurements will help.4 Accumulating evidence is justifying the use of GLS in clinical practice day by day. Nevertheless, GLS is not perfect: We have no real demonstration that we could use GLS as a key parameter for decision-making about patient management because of the lack of randomized controlled data exploring the clinical value of GLS in different clinical scenarios.5 Also, longitudinal strain represents only a single component of myocardial deformation. It has already been reported that the functional anatomy of the myocardium resides on a complex interaction between differently oriented myofibres. Circumferential fibres are predominant and have been demonstrated to interplay with the other components of heart deformation.6 When longitudinal deformation is affected, circumferential fibres can, up to a certain point, compensate.7,8 Myocardial fibre orientation is complex and must be put forward to decipher the adaptation mechanisms. Right-handed endocardial helical fibres and left-handed epicardial helical fibres that are generating opposing vectors of contraction with the dominance of the epicardial forces because of the larger radius of curvature provide a perfect mechanism for compensation. When endocardial fibres are affected, by means of the unopposed epicardial helical fibre contraction, left ventricular (LV) twist tends to increase and compensate the loss of endocardial function. This contributes partially to circumferential strain because of the helical orientation of the fibres. Also, circumferential fibres are relatively spared early during an insult to blood flow because of their deeper location within the wall. The consequence of these architectural configurations is nicely reflected in the clinical study by Skaarup et al.,9 showing an early increase in circumferential strain followed by a late decrease during LV dysfunction associated with the reduction in ejection fraction. A more complete computation of the circumferential strain could include apical and basal short-axis levels, in addition to the mid-LV level, because a healthy heart is supposed to demonstrate an apicobasal gradient of contraction. This sequence might also be affected during the adaptation and compensation period. In addition, the timing of deformation counts in the sum force generation for an efficient pumping function of the LV that is altered with disease states due to interstitial fibrosis, unequal regional pressure load, or electrical alterations. Echocardiographic acquisition should be optimally performed in parasternal short axis. Skaarup et al.9 have reported that parasternal short-axis view at the most basal level where the medial and lateral papillary muscles appeared to connect to the LV wall as a landmark to identify the mid-ventricular level and acquire appropriate images (Table 1). In the upcoming future, the 3D volumic acquition will become the method of choice for measuring circumferential strain. For now, using 2D images, the methodology proposed by Skaarupe et al should be applied rigourously.6 Optimizing the LV function assessment Optimizing the LV function assessment Investigating the interplay between the LV endomyocardial right-handed orientated fibres and the epimyocardial left-handed orientated fibres in early LV dysfunction, as assessed by circumferential strain, GLS, and LVEF is relevant. Compensation of a decrease in longitudinal function can lead to an increase in circumferential function.8 According to Skaarup et al.,9 a normal LVEF and higher GCS were associated with an increased risk of HF or cardiovascular death, while the opposite was observed in patients with abnormal LVEF. A U-shaped relationship between circumferential strain and HF and cardiovascular death was observed. This finding is relevant. However, it needs prospective confirmative studies, and if these are done, it might have a real impact on our practice. LVEF impacts on this relationship between strain and outcome. But circumferential strain remained an independent prognosticator of HF and cardiovascular death after extensive multivariable adjustments. Recently, the same team demonstrated that sacubitril/valsartan improves global circumferential strain but not longitudinal strain when compared with valsartan alone during a 36-week period in heart failure with preserved ejection fraction (HFpEF) patients (PARAMOUNT Phase II study).5 This is a confirmation that the findings of Skaarup et al.9 are of great value. What our community should really have in mind is that LV deformation is altered despite preserved LVEF in conditions predisposing to HF including diabetes, hypertension, stable angina, obesity, and renal dysfunction. These early signs of impaired LV are characterized by reduced GLS and good circumferential deformations. This myocardial deformation pattern may be a natural cause of the anatomical distribution of myocardial fibre orientation throughout the LV with longitudinal fibres formed in a left-handed helix in the sub-epicardium and a right-handed helix in the sub-endocardium and the cardiac mid-wall consisting of circumferential fibres.10 In conditions leading to mainly sub-endocardial impairment, GLS will be impaired, circumferential strain might be relatively preserved or augmented, and LVEF preserved. This pattern is probably something to look for in many patients at risk for HF, such as patients being studied in the cardio-oncology field and diabetic or hypertensive patients. If confirmed, the results obtained from Skaarup et al.9 might add another parameter to diagnose and monitor HFpEF. Congratulations are due to the authors, and let us have an eye open on the circumferential part of LV systolic function! None declared. Data sharing is not applicable to this article as no new data were created or analyzed in this study.