CA is characterised by regional variations in LS from base to apex. A relative 'apical sparing' pattern of LS is an easily recognisable, accurate and reproducible method of differentiating CA from other causes of LV hypertrophy.

Strain-based imaging techniques (and specifically speckle-tracking echocardiography) have been shown to have clinical utility in a variety of settings. This technique is being embraced and increasingly adopted in many echocardiography laboratories worldwide. This review appraised speckle-tracking echocardiography in a clinical context by providing a critical evaluation of the prognostic and diagnostic insights that this technology can provide. In particular, we discuss the use of speckle-tracking strain in selected areas, such as undifferentiated left ventricular hypertrophy, cardio-oncology, aortic stenosis, and ischemic heart disease. The potential utility of regional and chamber strains (namely segmental left ventricular strain, left atrial strain, and right ventricular strain) are also discussed. Future directions for this technology are explored. Before its clinical application, it is particularly important that physicians be cognizant of the technical challenges and inherent limitations of strain data, which are also addressed here.

Ischemia caused by coronary artery disease and myocardial infarction leads to aberrant ventricular remodeling and cardiac fibrosis. This occurs partly through accumulation of gene expression changes in resident fibroblasts, resulting in an overactive fibrotic phenotype. Long-term adaptation to a hypoxic insult is likely to require significant modification of chromatin structure in order to maintain the fibrotic phenotype. Epigenetic changes may play an important role in modulating hypoxia-induced fibrosis within the heart. Therefore, the aim of the study was to investigate the potential pro-fibrotic impact of hypoxia on cardiac fibroblasts and determine whether alterations in DNA methylation could play a role in this process. This study found that within human cardiac tissue, the degree of hypoxia was associated with increased expression of collagen 1 and alpha-smooth muscle actin (ASMA). In addition, human cardiac fibroblast cells exposed to prolonged 1% hypoxia resulted in a pro-fibrotic state. These hypoxia-induced pro-fibrotic changes were associated with global DNA hypermethylation and increased expression of the DNA methyltransferase (DNMT) enzymes DNMT1 and DNMT3B. Expression of these methylating enzymes was shown to be regulated by hypoxia-inducible factor (HIF)-1α. Using siRNA to block DNMT3B expression significantly reduced collagen 1 and ASMA expression. In addition, application of the DNMT inhibitor 5-aza-2'-deoxycytidine suppressed the pro-fibrotic effects of TGFβ. Epigenetic modifications and changes in the epigenetic machinery identified in cardiac fibroblasts during prolonged hypoxia may contribute to the pro-fibrotic nature of the ischemic milieu. Targeting up-regulated expression of DNMTs in ischemic heart disease may prove to be a valuable therapeutic approach.

AimsHypertension is one of the main drivers of the heart failure (HF) epidemic. The aims of this study were to profile fibro-inflammatory biomarkers across stages of the hypertensive heart disease (HHD) spectrum and to examine whether particular biochemical profiles in asymptomatic patients identify a higher risk of evolution to HF. Methods and resultsThis was a cross-sectional observational study involving a population of 275 stable hypertensive patients divided into two different cohorts: Group 1, asymptomatic hypertension (AH) (n ¼ 94); Group 2, HF with preserved ejection fraction (n ¼ 181). Asymptomatic hypertension patients were further subdivided according to left atrial volume index ≥34 mL/ m 2 (n ¼ 30) and ,34 mL/m 2 (n ¼ 64). Study assays involved inflammatory markers [interleukin 6 (IL6), interleukin 8 (IL8), monocyte chemoattractant protein 1 (MCP1), and tumour necrosis factor a], collagen 1 and 3 metabolic markers [carboxy-terminal propeptide of collagen 1, amino-terminal propeptide of collagen 1, amino-terminal propeptide of collagen 3 (PIIINP), and carboxy-terminal telopeptide of collagen 1 (CITP)], extra-cellular matrix turnover markers [matrix metalloproteinase 2 (MMP2), matrix metalloproteinase 9 (MMP9), and tissue inhibitor of metalloproteinase 1 (TIMP1)], and the brain natriuretic peptide. Data were adjusted for age, sex, systolic blood pressure, and creatinine. Heart failure with preserved ejection fraction was associated with an increased inflammatory signal (IL6, IL8, and MCP1), an increased fibrotic signal (PIIINP and CITP), and an increased matrix turnover signal (MMP2 and MMP9). Alterations in MMP and TIMP enzymes were found to be significant indicators of greater degrees of asymptomatic left ventricular diastolic dysfunction. ConclusionThese data define varying fibro-inflammatory profiles throughout different stages of HHD. In particular, the observations on MMP9 and TIMP1 raise the possibility of earlier detection of those at risk of evolution to HF which may help focus effective preventative strategies.--

Background Treatment-related cardiac death is the primary non-cancer cause of mortality in adult survivors of childhood malignancies. Early detection of cardiac dysfunction using modern echocardiographic techniques may identify a high risk subset of survivors for early intervention. Objective To determine the prevalence of cardiac dysfunction in adult survivors of childhood malignancies using state of the art echocardiographic evaluation of cardiac function including strain imaging Methods Echocardiographic assessment included three dimensional (3D) left ventricular ejection fraction (LVEF), global longitudinal and circumferential myocardial strain and diastolic function, graded per American Society of Echocardiography (ASE) guidelines on 1,820 adult (median age 31 [range 18-65] years) survivors of childhood cancer (median time from diagnosis 23 years [range10-48] years) exposed to either anthracycline chemotherapy (N=1,050), chest-directed radiotherapy (RT, N=306), or both therapies (N=464). Results Only 5.8% of survivors had an abnormal 3D LVEF (<50%). However, 32.1% of survivors with a normal 3D LVEF had evidence for cardiac dysfunction by either global longitudinal strain (28.0%), ASE graded diastolic assessment (8.7%), or both. Abnormal global longitudinal strain was associated with chest-directed RT (1-19.9 Gy, Rate Ratio (RR) 1.38, 95% Confidence Interval (CI) 1.14-1.66; 20-29.9 Gy, RR 1.65, 95% CI 1.31-2.08; >30 Gy, RR 2.39, 95% CI 1.79-3.18) and anthracycline dose >300 mg/m2 (RR 1.72, 95% CI 1.31-2.26). Survivors with metabolic syndrome were twice as likely to have abnormal global longitudinal strain (Rate Ratio [RR] 1.94, 95% CI 1.66-2.28) as well as abnormal diastolic function (RR 1.68, 95% CI 1.39-2.03), but not abnormal 3D LVEF (RR 1.07, 95% CI 0.74-1.53). Conclusions and Relevance Abnormal global longitudinal strain and abnormal diastolic function are more prevalent than reduced 3D LVEF and are associated with treatment exposure. They may identify a subset of survivors at higher risk for poor clinical cardiac outcome who may benefit from early medical intervention.