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Aims: Left ventricular ejection fraction is the conventional measure used to guide heart failure management, regardless of underlying etiology. Left ventricular global longitudinal strain (LV-GLS) by speckle tracking echocardiography (STE) is a more sensitive measure of intrinsic myocardial function. We aim to establish LV-GLS as a marker of replacement myocardial fibrosis on cardiovascular magnetic resonance (CMR) and validate the prognostic value of LV-GLS thresholds associated with fibrosis. Methods and results: LV-GLS thresholds of replacement fibrosis were established in the derivation cohort: 151 patients (57 ± 10 years; 58% males) with hypertension who underwent STE to measure LV-GLS and CMR. Prognostic value of the thresholds was validated in a separate outcome cohort: 261 patients with moderate-severe aortic stenosis (AS; 71 ± 12 years; 58% males; NYHA functional class I–II) and preserved LVEF ≥50%. Primary outcome was a composite of cardiovascular mortality, heart failure hospitalization, and myocardial infarction. In the derivation cohort, LV-GLS demonstrated good discrimination (c-statistics 0.74 [0.66–0.83]; P < 0.001) and calibration (Hosmer-Lemeshow χ2 = 6.37; P = 0.605) for replacement fibrosis. In the outcome cohort, 47 events occurred over 16 [3.3, 42.2] months. Patients with LV-GLS > −15.0% (corresponding to 95% specificity to rule-in myocardial fibrosis) had the worst outcomes compared to patients with LV-GLS < −21.0% (corresponding to 95% sensitivity to rule-out myocardial fibrosis) and those between −21.0 and −15.0% (log-rank P < 0.001). LV-GLS offered independent prognostic value over clinical variables, AS severity and echocardiographic LV mass and E/e′. Conclusion: LV-GLS thresholds associated with replacement myocardial fibrosis is a novel approach to risk-stratify patients with AS and preserved LVEF., Graphical Abstract Thresholds of echocardiographic left ventricular global longitudinal strain (GLS) that are associated with replacement myocardial fibrosis risk-stratify patients with aortic stenosis and preserved left ventricular ejection fraction. Some images in the figure were created with BioRender.com.

Background Left ventricular global longitudinal strain (LV-GLS) by speckle tracking echocardiography (STE) reflects intrinsic myocardial function, influenced by interstitial abnormalities. Cardiovascular magnetic resonance (CMR) detects myocardial fibrosis non-invasively, but it is limited for widespread use. We aim to establish LV-GLS as a marker of replacement myocardial fibrosis on CMR and validate the prognostic value of LV-GLS thresholds associated with fibrosis. Methods LV-GLS thresholds of replacement fibrosis were established in the derivation cohort: 151 patients (57±10 years; 58% males) with hypertension who underwent STE to measure LV-GLS and CMR for replacement myocardial fibrosis. Prognostic value of the thresholds was validated in a separate outcome cohort: 261 patients with moderate-severe aortic stenosis (AS; 71±12 years; 58% males; NYHA functional class I-II) and preserved LVEF ≥50%. Primary outcome was a composite of cardiovascular mortality, heart failure hospitalization, myocardial infarction and cerebrovascular events. Results In the derivation cohort, LV-GLS demonstrated good discrimination (c-statistics 0.74; 95% confidence interval: 0.66–0.83; P−15.0% (corresponding to 95% specificity to rule-in myocardial fibrosis) had the worst outcomes compared to patients with LV-GLS Conclusions LV-GLS thresholds associated with replacement myocardial fibrosis is a novel approach to risk-stratify patients with AS and preserved LVEF (Figure 2). Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Medical Research Council Figure 1Figure 2

ContextCoconut oil is rich in medium-chain fatty acids and has been claimed to have numerous health benefits.ObjectiveThis review aimed to examine the evidence surrounding coconut oil consumption and its impact on cardiovascular health.Data SourcesA systematic literature search of the PubMed, Embase, the Cochrane Library, and CINAHL databases, up to May 2019, was performed.Data ExtractionStudy characteristics including study design, population, intervention, comparator, outcome, and source of funding were summarized.Data AnalysisMeta-analyses included 12 studies to provide estimates of effects. Subgroup analyses were performed to account for any differences in the study-level characteristics. When compared with plant oils and animal oils, coconut oil was found to significantly increase high-density lipoprotein cholesterol (HDL-C) by 0.57 mg/dL (95%CI, 0.40–0.74 mg/dL; I2 = 6.7%) and 0.33 mg/dL (0.01–0.65 mg/dL; I2 = 0%), respectively. Coconut oil significantly raised low-density lipoprotein cholesterol (LDL-C) by 0.26 mg/dL (0.09–0.43 mg/dL; I2 = 59.7%) compared with plant oils and lowered LDL-C (−0.37 mg/dL; −0.69 to −0.05 mg/dL; I2 = 48.1%) compared with animal oils. No significant effects on triglyceride were observed. Better lipid profiles were demonstrated with the virgin form of coconut oil.ConclusionCompared with animal oils, coconut oil demonstrated a better lipid profile n comparison with plant oils, coconut oil significantly increased HDL-C and LDL-C.

Myxomatous mitral valve prolapse (MMVP) and fibroelastic deficiency (FED) are two common variants of degenerative mitral valve disease (DMVD), which is a leading cause of mitral regurgitation worldwide. While pathohistological studies have revealed differences in extracellular matrix content in MMVP and FED, the molecular mechanisms underlying these two disease entities remain to be elucidated. By using surgically removed valvular specimens from MMVP and FED patients that were categorized on the basis of echocardiographic, clinical and operative findings, a cluster of microRNAs that expressed differentially were identified. The expressions of has-miR-500, -3174, -17, -1193, -646, -1273e, -4298, -203, -505, and -939 showed significant differences between MMVP and FED after applying Bonferroni correction (p < 0.002174). The possible involvement of microRNAs in the pathogenesis of DMVD were further suggested by the presences of in silico predicted target sites on a number of genes reported to be involved in extracellular matrix homeostasis and marker genes for cellular composition of mitral valves, including decorin (DCN), aggrecan (ACAN), fibromodulin (FMOD), α actin 2 (ACTA2), extracellular matrix protein 2 (ECM2), desmin (DES), endothelial cell specific molecule 1 (ESM1), and platelet/ endothelial cell adhesion molecule 1 (PECAM1), as well as inverse correlations of selected microRNA and mRNA expression in MMVP and FED groups. Our results provide evidence that distinct molecular mechanisms underlie MMVP and FED. Moreover, the microRNAs identified may be targets for the future development of diagnostic biomarkers and therapeutics.