In recent years, myocardial strain has emerged as a very useful and reliable tool for function analysis, not only of the left ventricle (LV) but also of right ventricle and atrial function. It can detect subclinical myocardial disease, when LV ejection fraction is still in the normal range, and for that reason it is particularly useful for LV function assessment. However, some limitations still exist for strain because it is also load dependent.1–4 In fact, strain can be reduced in response to increased afterload, leading to misinterpretations of the true contractile function.2,4

Myocardial work (MW) can be assessed invasively from LV pressure – volume loops. Pressure-strain loops can be used for the same purpose. However, this analysis has been not implemented in clinical practice due to its invasive nature. In recent years, non-invasive techniques have been developed to obtain LV pressure-strain loops. This tool is presently included in new echocardiographic software, and it is easy to perform in clinical practice.5 It has the advantage of being less load dependent and it can be used as an additional tool in strain analysis when assessing LV function. It considers both deformation and afterload. The combination of LV strain data and non-invasively estimated pressure curves allows estimation of MW by the area within the pressure-strain loop. It has been previously shown that all these parameters have excellent correlation both for intra- and inter-observer variability.6

This non-invasive method has been used in research in several areas, such as acute coronary syndromes, hypertension, dilated cardiomyopathy, and response to cardiac resynchronization therapy or to new drugs.2,6–10 It was our objective to assess LV function in adult patients with repaired aortic coarctation (rACo), a condition associated with long-standing increased afterload.

We included a total of 42 patients, with a mean age of 37±10 years (24 to 66 years), 38% males. Mean age for intervention was 12±10 years (0-45 years), mostly with surgery, and only four patients (9.5%) were treated percutaneously, with aortic stent implantation. Percutaneous re-intervention was necessary in six patients (14.3%) with a median time of 18 years between interventions, due to residual significant aortic gradient at the site of coarctation. In our population, 52.4% had hypertension, and were on specific medication and 64.3% had bicuspid aortic valve with mild disease. Table 1 shows baseline and main echocardiographic characteristics of the patients with rACo. In 18% of the patients, the ascending thoracic aorta showed mild dilation.

Myocardial deformation assessment with strain using 2D speckle tracking echocardiography has brought about major advancs in LV quantification beyond the traditional ejection fraction. However, strain imaging is relatively load dependent, with an inverse relationship between strain and afterload, and it can affect diagnostic accuracy in myocardial function evaluation.1–6 After several years of research, Russell et al. developed a non-invasive tool to estimate LV pressure during a cardiac cycle and used LV pressure-strain loops to assess MW, showing a strong correlation with invasive measurements.5 Since then, MW has been associated with improvements in the identification of cardiac resynchronization therapy responders7,8 and coronary occlusion in patients with acute coronary syndrome.2 Myocardial work considers both load and deformation and it can offer incremental value in myocardial functional assessment, particularly in the presence of changes in afterload that could lead to misleading results by strain analysis. Increases in afterload can negatively impact on myocardial strain.2 Previous papers showed good repeatability and reproducibility of myocardial work indices obtained by echocardiography.5,6,15,16,19

Aortic coarctation is a condition characterized by chronic increased afterload. Even after repair, some patients have some residual gradient in the descending thoracic aorta, remaining hypertensive and for that reason LV changes can occur. Our patients had been previously exposed to chronic increased afterload, some of them for a long time due to correction at a mean age of 12 years, and some are still on chronic overload despite repair and this might cause some chronic damage in the LV. In fact, 52% were hypertensive patients (on medication), and in general, blood pressure control was adequate in most of the patients at the time of examination, albeit higher compared to the reference population, particularly SBP. However, despite a normal mean SBP, it ranged from 97 to 152 mmHg, and there was also a mild increase in the descending aortic peak gradient, ranging from 3 to 43 mmHg. For that reason, some patients still have a significant and persistent increase in afterload.

With high blood pressure and afterload, there is a reduction in stroke volume, compensated by a shift in the LV pump function to work at a higher energy level, allowing for GLS and ejection fraction to be preserved, and this can be reflected by higher GWI.20,21 However, chronically increased afterload eventually leads to increased LV stiffness and concentric remodeling and eventually LV failure.20,21 In previous studies conducted in hypertensive patients, grade 1 hypertension is associated with an increase in both constructive and wasted work, with preserved MW efficiency and increase in GWI.6 In grade 2-3 hypertension, the increase in constructive and wasted work is more significant, in a proportional way, enabling preservation of GWE and a further increase in GWI.6 Wasted MW increase can be related to the increase myocardium wall stress against high afterload.6 In fact, myocardial hypertrophy caused by chronic increased afterload is a compensation mechanism for increased wall stress and increases significantly GWI.6 When dysfunction appears, with LV dilation and elevation of end-systolic wall stress, wasted work is further increased, now with a reduction in constructive work, leading to a reduction in both GWE and GWI.6

Based on previous observations, we would expect our group of patients to show the same pattern of increased GCW, GWW and GWI with preserved GWE as in hypertensive patients. However, we found lower GCW and GWI, without the expected and proportional increase in GWW but still with preserved efficiency. Global work index and GCW are being recognized as indices of myocardial performance, as an expression of positive LV work, hence contractility. Based on this assumption, the sample studied, despite normal LV systolic function (as assessed by ejection fraction and GLS), already had changes compatible with impaired myocardial performance, but mechanical efficiency remained preserved, as assessed by GWE. Our sample also had an increased LV mass and E/e’ ratio suggesting compensating changes due to this chronically increased afterload. Our findings are consistent with a possible cardiomyopathic process, not reproducing what could have been expected from a chronic afterload increase model without overt dysfunction by classic evaluation. Previous studies have reported that structurally normal hearts, even in the presence of cardiovascular risk factors, retain their mechanical efficiency, better inferred by preserved GWE, as we found in our work.22 However, in our study, despite GWE preservation, GWI and GCW were abnormally low, and this can be an indicator of a transitional stage to overt systolic dysfunction.

Previously published papers on reference values for MW indices showed some divergent data regarding gender comparisons.15,19 Galli obtained significantly lower GWI and GCW in men, with similar GWW and GWE.19 Those results were explained by the authors by the fact that both GLS and E wave velocity, that were correlated with GWI and GCW, were significantly lower in men than in women. However, Manganaro obtained higher GWW, similar GCW, lower GWE and a trend to lower GWI in men.15 These GWW higher values were thought to be related to the effect of blood pressure, which was higher in male, but multivariate analysis did not confirm the effect of blood pressure on GWW. In fact, multivariable analysis has consistently shown in all studies, including ours, an absence of effect based on age or gender in MW parameters and a strong correlation of GWI and GCW with SBP and correlation of LV GLS with all MW parameters. But despite the absence of correlation between blood pressure and GWW, Chan showed that in hypertensive patients, there is an expected increase in GWW and for that reason, we would assume some possible influence of blood pressure.6 To further increase the discrepancy in results from different studies, in our sample we found that GWW was higher in females and the other MW parameters were identical. The main differences between genders were lower LV mass index, higher E wave velocity and a trend to higher E/E’ ratio in females. But these differences were also observed in Galli and Manganaro studies. Also, GLS (the only independent predictor of GWW) was identical between genders. However, if we compare mean SBP between genders in our sample and in the reference group, we found that the group with the highest SBP is the female group with rACo, suggesting again a possible relationship between blood pressure and this increase in GWW. This question remains unanswered and additional studies with larger samples are needed.

The introduction of non-invasive MW estimation by speckle tracking echocardiography, a method validated against invasive measurements, has brought a new promise in the clinical evaluation of myocardial performance in previous studies, particularly because it can unmask myocardial at risk of future failure in face of normal deformation indices and impaired MW parameters.

In patients with rACo, we found a lower GCW and GWI, suggesting some degree of LV dysfunction, despite normal ejection fraction and GLS, confirming the usefulness of myocardial work compared with standard techniques. Systolic blood pressure is an independent predictor of GWI and GCW and GLS the other independent predictor of all MW parameters. For that reason, strict control of blood pressure is essential in these patients.

We can postulate that MW analysis may offer additional information about cardiac performance at a very early stage of the disease. However, the prognostic role of this promising tool requires additional longitudinal research. MW impairment can forecast or anticipate overt dysfunction, particularly in the context of increased afterload, and research with serial assessments of patients at risk of developing systolic dysfunction is warranted.

Ana Teresa Timoteo - concept and design, data collection, data interpretation, statistical analysis, drafting of the manuscript, critical revision, and approval of the article.

Luisa Moura Branco - data collection, critical revision, and approval of the article.

Ana Galrinho - data collection, critical revision, and approval of the article.

Pedro Rio - data collection, critical revision, and approval of the article.

Lidia Sousa - data interpretation, critical revision, and approval of the article.

Rui Cruz Ferreira - data interpretation, critical revision, and approval of the article.

The authors have no conflicts of interest to declare.