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Qing Zhu,1 Cuiting Zhao,1 Yonghuai Wang,1 Xinxin Li,1 Yixue Xue,2– 4 Chunyan Ma1 1Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, People’s Republic of China; 2Department of Neurobiology, School of Life Sciences, China Medical University, Shenyang, People’s Republic of China; 3Key Laboratory of Cell Biology, Ministry of Public Health of China, China Medical University, Shenyang, People’s Republic of China; 4Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical University, Shenyang, People’s Republic of ChinaCorrespondence: Chunyan MaDepartment of Cardiovascular Ultrasound, The First Hospital of China Medical University, No. 155 Nanjingbei Street, Shenyang, Liaoning, 110001, People’s Republic of ChinaTel +86 2483282129Email cmu1h_mcy@126.comBackground: Coronary slow flow (CSF) is an angiographic phenomenon characterized by delayed coronary opacification with normal or near-normal epicardial coronary arteries. The pathogenesis of CSF is closely related to inflammatory response. Accumulating evidence shows that long non-coding RNAs (lncRNAs) play an important role in cardiovascular disease. However, the mechanism underlying the influence of the lncRNA nuclear enriched abundant transcripts 1 (NEAT1) on CSF is still unknown.Patients and Methods: Forty CSF patients and forty control subjects were included in the study and underwent coronary angiography, Seattle angina questionnaire (SAQ) and echocardiography. The plasma levels of the inflammatory factors soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) were determined by ELISA. The expression levels of NEAT1, miR-148b-3p and ICAM-1 in cells were measured by qRT-PCR or Western blotting. Cell proliferation was measured by 5‐Ethynyl‐2ʹ‐deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assay. Cell apoptosis was detected by apoptosis assay. The relationship between NEAT1 and miR-148b-3p was verified by luciferase reporter gene assay, RNA immunoprecipitation (RIP) assay and avidin-biotin pull-down assay. The relationship between ICAM-1 and miR-148b-3p was verified by luciferase reporter gene assay and avidin-biotin pull-down assay.Results: This study showed that plasma sICAM-1, miR-148b-3p, and NEAT1 as independent predictors of a CSF diagnosis. Furthermore, plasma NEAT1 level showed superior diagnostic ability for CSF compared with sICAM-1 and miR-148b-3p. It was also shown that high expression of NEAT1 in oxygen-glucose deprivation (OGD)-treated human umbilical vein endothelial cells (HUVECs) functions as a competing endogenous RNA (ceRNA). By specifically binding miR-148b-3p, it weakened the negative regulatory effects of miR-148b-3p on the ICAM-1 target gene leading to upregulated expression of ICAM-1. This interaction was also shown to inhibit HUVEC proliferation and enhance apoptosis.Conclusion: This study demonstrated for the first time the important mechanism of action of the NEAT1/miR-148b-3p/ICAM-1 axis in the progression of CSF disease, and indicated the potential of NEAT1, miR-148b-3p, and ICAM-1 as a new target for the diagnosis and treatment of CSF.Keywords: coronary slow flow, ncRNA, inflammation, biomarkers, cell biology

PURPOSE The echocardiographic measurement of left ventricular (LV) ejection fraction (EF) is dependent on professional experience and adequate visualization. Tissue motion of mitral annular displacement (TMAD) can be easily assessed using speckle-tracking echocardiography (STE), even in patients with poor acoustic windows. Therefore, this study aimed to assess whether left ventricular ejection fraction (LVEF) can be estimated using STE-derived TMAD when LVEF is not available. METHODS Four-hundred fifty-six outpatients were enrolled after excluding the patients whose LVEF measurements remained challenging or TMAD value could be confounded. An optimized regression model for LVEF-TMAD was developed in the derivation set (n = 287), and its reliability was verified in the validation set (n = 123) and regional wall motion abnormalities (RWMA) set (n = 46). RESULTS In the derivation set, the power models had the highest F-value. Therefore, the power equations were chosen to estimate LVEF by TMAD in the validation set. There was a near-zero bias and a narrow range between the observed and estimated LVEF. The highest intra-class correlation coefficient was found between the observed and the estimated LVEF by normalized TMAD at the midpoint of mitral annular (nTMADmid). Moreover, there were no significant differences between the observed and the estimated LVEF in the RWMA set. CONCLUSION The LVEF can be estimated with STE-derived TMAD, even for patients with RWMA, and nTMADmid may be the optimal parameter.

Background Shear wave elastography (SWE) directly quantifies the local arterial wall stiffness by calculating the elastic modulus. However, whether carotid wall elastic modulus can predict obstructive coronary artery disease (CAD) is not well known. We aimed to investigate the value of carotid wall elastic modulus measured using SWE in identifying obstructive CAD. Materials and methods We prospectively enrolled 61 patients without carotid plaque referred for clinically indicated coronary angiography. Twenty-seven (44.3%) patients were diagnosed with obstructive CAD (≥50% coronary stenosis). The elastic modulus of common carotid artery was quantified using SWE. Ankle--brachial index (ABI) and echocardiographic global cardiac calcium score (GCCS) were measured. Results Patients with obstructive CAD had significantly higher elastic modulus than those without obstructive CAD. The maximum elastic modulus (EMmax) was independently associated with obstructive CAD after adjusting for the Framingham risk score, ABI, and GCCS. EMmax had the highest area under the curve (AUC) to identify obstructive CAD (AUC 0.70; P = 0.003). In the nested models, the model based on the Framingham risk score and ABI (χ2 = 3.74) improved by adding GCCS (χ2 = 9.95) and further improved by adding EMmax (χ2 = 15.86). Adding EMmax to the combined ABI and GCCS model increased integrated discrimination index from 0.10 to 0.19. Conclusion Carotid wall elastic modulus measured using SWE is a useful predictor of obstructive CAD in patients without carotid plaque. We demonstrated the incremental and independent value of carotid wall elastic modulus in identifying obstructive CAD compared with clinical risk factors and other imaging predictors, including ABI and GCCS. Video abstract Please see the video, in Supplemental Digital Content 1, http://links.lww.com/HJH/B551 for more insights from the authors.

Background Accurate assessment of left ventricular (LV) systolic function is important after coronary artery bypass grafting (CABG). LV ejection fraction (LVEF) is conventionally used to evaluate LV systolic function; deformation parameters can be used to detect subtle LV systolic dysfunction. It is unclear whether an incised pericardium without sutures during CABG could affect LV morphology and function. We investigated the effect of pericardial incision on LV morphology and systolic function during CABG. Methods Intraoperative transesophageal echocardiography was performed in 27 patients during elective off-pump beating heart CABG 5 min before and after pericardial incision. LV longitudinal and mid-cavity transversal diameters, sphericity index, volumes, and LVEF were measured. LV global longitudinal strain (GLS), global circumferential strain (GCS), global radial strain (GRS), and twist obtained by two-dimensional speckle tracking echocardiography were measured simultaneously. Results LV mid-cavity transversal diameter increased, while the LV sphericity index decreased (P P Conclusions Pericardial incision immediately transformed LV morphology from an ellipsoid to sphere, with decreased longitudinal and circumferential strain and twist, and increased radial strain, while LVEF remained unchanged. This should be considered when evaluating LV systolic function in patients after CABG.

Pulse wave velocity (PWV) measured by ultrafast ultrasound imaging can early evaluate arteriosclerosis. The study aimed to establish normal reference range for ufPWV in healthy adults and explore its influencing factors, and evaluate the ufPWV changes on coronary slow flow (CSF). ufPWV at the beginning and end of systole (ufPWV-BS and ufPWV-ES, respectively) was measured in healthy adults (201 cases). CSF was diagnosed based on thrombolysis in myocardial infarction (TIMI) frame count during coronary angiography. ufPWV-BS and ufPWV-ES were compared between CSF (50 cases) and control groups (50 healthy age-, body mass index-, and blood pressure-matched adults). In healthy adults, average ufPWV-BS and ufPWV-ES was 5.36 ± 1.27 m/s and 6.99 ± 1.93 m/s, respectively. ufPWV-BS and ufPWV-ES positively correlated with age, body mass index, and blood pressure. ufPWV-BS and ufPWV-ES in the CSF group were higher than in the control group (ufPWV-BS, 6.05 ± 1.07 vs. 5.26 ± 0.89 m/s, P

Objective: This study was conducted in order to determine the reference values for right ventricular (RV) volumes and ejection fraction (EF) using three-dimensional echocardiography (3DE) and to identify sources of variance through a systematic review and meta-analysis.Methods: This systematic review was preregistered with the International Prospective Register of Systematic Reviews (https://www.crd.york.ac.uk/PROSPERO/) (CRD42020211002). Relevant studies were identified by searches of the PubMed, Embase, and Cochrane Library databases through October 12, 2020. Pooled reference values were calculated using the random-effects model weighted by inverse variance. Meta-regression analysis and Egger's test were used to determine the source of heterogeneity. A subgroup analysis was performed to evaluate the reference values across different conditions.Results: The search identified 25 studies of 2,165 subjects. The mean reference values were as follows: RV end-diastolic volume, 100.71 ml [95% confidence interval (CI), 90.92–110.51 ml); RV end-systolic volume, 44.19 ml (95% CI, 39.05–49.33 ml); RV end-diastolic volume indexed, 57.01 ml/m2 (95% CI, 51.93–62.08 ml/m2); RV end-systolic volume indexed, 25.41 ml/m2 (95% CI, 22.58–28.24 ml/m2); and RVEF, 56.20% (95% CI, 54.59–57.82%). The sex- and age-specific reference values were assessed according to the studies reporting the values of different sexes and age distributions, respectively. In addition, the vendor- and software-specific reference values were analyzed. The meta-regression analysis revealed that sex, frame rate, pulmonary artery systolic pressure, and software packages were associated with variations in RV volumes (P < 0.05). Inter-vendor and inter-software discrepancies may explain the variability of RVEF.Conclusions: The reference values for RV volumes and RVEF using 3DE were assessed. The confounders that impacted the variability in RV volumes or RVEF contained the sex, frame rate, pulmonary artery systolic pressure, inter-vendor discrepancies, and inter-software discrepancies.

The purpose was to evaluate left ventricular (LV) systolic function in patients with coronary slow flow (CSF), and compared the incremental values of 3-dimensional (3D) speckle-tracking echocardiography (STE). Seventy-three patients with CSF and 60 control subjects were enrolled. CSF was diagnosed during coronary angiography. Two-dimensional (2D) and 3D global strain were measured using STE. Sex, mitral E, 2D GLS, and all 3D strain parameters were independent predictors of CSF. Combination of sex, mitral E, and 3D GTS had the highest area under the curve (AUC) for identifying CSF (AUC, 0.81; P < 0.001). Integrated discrimination index (IDI) improved adding 3D GTS to the combined sex and mitral E model (IDI = 0.12, P = 0.01) or 2D GLS model (IDI = 0.14, P < 0.001). LV systolic function was impaired in CSF patients. 3D GTS had an independent and incremental value for predicting CSF compared with 2D echocardiography.

Aims: Sweroside, a secoiridoid glucoside extracted from Swertia pseudochinensis Hara, is reported to possess antioxidant and anti-inflammatory activities. However, whether sweroside has a protective effect on myocardial ischemia–reperfusion (IR) injury is yet to be elucidated. The present study aimed to confirm the cardioprotective effect of sweroside and to identify its underlying mechanism.Methods and Results: H9c2 cells were pretreated with sweroside and then underwent hypoxia–reoxygenation. Cell Counting Kit-8, creatine kinase-myocardial band (CK-MB) and lactate dehydrogenase (LDH) assays were conducted to detect cell viability and myocardial injury, respectively. The Langendorff method was used to induce myocardial IR injury ex vivo. Triphenyltetrazolium chloride staining was performed to detect myocardial infarct size, while protein expression was analyzed using western blotting. Overall, the results indicated that sweroside pretreatment dose-dependently led to a significant enhancement in cell viability, a decrease in release of CK-MB and LDH, a reduction in infarct size, and an improvement in cardiac function. Additionally, sweroside pretreatment caused a marked suppression of oxidative stress, as evidenced by the fact that sweroside decreased the accumulation of reactive oxygen species and malondialdehyde, while enhancing the activities of superoxide dismutase and glutathione peroxidase. Moreover, sweroside was found to notably repress pyroptosis, as sweroside blocked pore formation in the cell membrane, inhibited caspase-1 and interleukin (IL)-1β activity, and decreased the expression levels of NLR family pyrin domain containing 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD, cleaved caspase-1, and IL-1β. Mechanistically, it was found that sweroside inhibited Kelch-like ECH-associated protein 1 (Keap1) and induced nuclear factor E2-associated factor 2 (Nrf2) nuclear translocation. Furthermore, the inhibition of oxidative stress and pyroptosis by sweroside could be abrogated via the inhibition of Nrf2 expression, which suggested that the protective effect induced by sweroside was Nrf2-dependent.Conclusions: The present study demonstrated that sweroside pretreatment could protect against myocardial IR injury by inhibiting of oxidative stress and NLRP3 inflammasome-mediated pyroptosis partially via modulation of the Keap1/Nrf2 axis.

Background: To evaluate the clinical efficacy of serum high-mobility group box-1 (HMGB1) released from the left atrium to predict atrial fibrillation (AF) recurrence in paroxysmal AF (pAF) patients after catheter ablation (CA) at 1-year follow-up.Methods: We included 72 pAF patients who underwent CA. To determine the expression levels of HMGB1, left atrial blood samples were collected from the patients prior to CA and after the procedure through the transseptal sheath placed into the left atrium. Patients were followed-up for AF recurrence after 1 year of CA.Results: A total of 19 (26%) patients of the 72 experienced AF recurrence. No significant differences were noted in the clinical baseline data between the AF recurrence and AF nonrecurrence groups. The level of postoperative HMGB1 (HMGB1post) was higher in the AF recurrence group than in the AF nonrecurrence group (298.51µg/L vs. 278.17 µg/L; P = 0.03). However, no differences were noted in the levels of other biomarkers such as preoperative high-sensitivity C-reactive protein (hs-CRPpre), postoperative hs-CRP (hs-CRPpost), and preoperative HMGB1 (HMGB1pre) between the two groups. Multiple logistic regression analysis revealed that a higher level of serum HMGB1post from the left atrium (HMGB1post: ≥279.35 µg/L) was an independent predictor of AF recurrence (odds ratio [OR]: 5.29 [1.17–23.92], P = 0.04). Receiver operating characteristic (ROC) analysis revealed that HMGB1post had a moderate predictive power for AF recurrence (area under the curve [AUC]: 0.68; sensitivity: 72%; specificity: 68%). The 1-year AF-free survival was significantly lower in patients with a high serum HMGB1post level than in those with a low HMGB1post level (hazard ratio [HR]: 3.81 [1.49–9.75], P = 0.005). Conclusion: In pAF patients who underwent CA, the level of HMGB1 from the left atrium immediately after CA was associated with AF recurrence and demonstrated a moderate predictive power. Thus, we offer a potential predictor to identify pAF patients at high risk of AF recurrence.

Background Left atrial (LA) volume (LAV) is one of the recommended key variables for evaluating left ventricular (LV) diastolic function. However, only LA anteroposterior diameter (LAAP) is available in numerous large-scale existing databases. Therefore, this study aimed to validate whether LV diastolic function could be evaluated with estimated LAV from LAAP. Methods A total of 552 inpatients with sinus rhythm were consecutively enrolled. LAV was measured by biplane Simpson’s disk summation method. LV diastolic function was evaluated according to the 2016 proposed recommendations. Best-fitting regression models of LAAP index (LAAPI)–LAV index (LAVI) were developed and equations with the highest F-value were chosen in the first 276 subjects (derivation set), and concordance for evaluating LV diastolic function between using estimated and observed LAVI was verified in the remaining 276 subjects (validation set). Results In the derivation set, the linear model has the highest F-value in all subjects and in the subjects with normal or depressed LV ejection fraction. In the validation set, using the linear equation (LAVI = 2.05 × LAAPI − 13.86), the higher area under curve and narrower range of difference were shown between estimated LAVI and observed LAVI, respectively. Further, concordance for diagnosis (overall proportion of agreement, 88.4%; κ = 0.79) and grading (overall proportion of agreement, 84.8%; κ = 0.74) of LV diastolic dysfunction was substantial between using estimated and observed LAVI. Conclusions LV diastolic function can be evaluated with estimated LAVI from LAAPI, which might provide a surrogate method when the direct measurement of LAV is not available.

Background The accurate measurement of left ventricular (LV) ejection fraction (EF) is highly dependent on professional experience and adequate visualization. The tissue motion of mitral annular displacement (TMAD) can be easily and quickly assessed using speckle tracking echocardiography (STE) for evaluating the LV systolic function, even in patients with poor acoustic windows. Therefore, this study aimed to validate whether LVEF can be estimated using the STE-derived TMAD when LVEF is not available. Methods Four-hundred fifty-six outpatients were consecutively enrolled in this study. An optimized regression model for LVEF-TMAD was developed in the derivation set (n=287), and its reliability was verified in the validation set (n=123) and regional wall motion abnormalities (RWMA) set (n=46). Results In the derivation set, the power models had the highest F-value, and the power equations were chosen to estimate LVEF according to TMAD in the validation set. Near-zero bias and a narrow range of differences were observed between the observed and estimated LVEF. The highest intra-class correlation coefficient was observed between the observed LVEF and estimated LVEF according to the normalized TMAD at the midpoint of mitral annular (nTMADmid). Moreover, there were no significant differences between the observed and estimated LVEF in the RWMA set. Conclusion The LVEF can be estimated with the STE-derived TMAD using a power equation, even for patients with RWMA, and the nTMADmid may be the optimal parameter. The proposed method may provide a clinically acceptable alternative for evaluating LV systolic function when the direct measurement of LVEF is not available.

Background Ultrafast ultrasound imaging has been demonstrated to be an effective method to evaluate carotid stiffness through carotid pulse wave velocity (PWV) with high reproducibility, but lack of reference values has precluded its widespread use in clinical practice. This study aimed to establish reference values of PWV for ultrafast ultrasound imaging in a prospective, multicenter, population-based cohort study and to investigate the main determinants of carotid PWV. Methods A total of 1,544 healthy Han Chinese volunteers (581 [38%] men; age, 18–95 years) were enrolled from 32 collaborating laboratories in China. The participants were categorized by age, blood pressure (BP), and body mass index (BMI). The basic clinical parameters and the carotid PWV at the beginning of systole (BS) and end of systole (ES) were measured via ultrafast ultrasound imaging techniques. Results The PWV at both BS and ES was significantly higher in the left carotid artery than in the right carotid artery. The PWV at BS was significantly higher in men than in women; however, no significant difference was noted in the PWV at ES between men and women. Multiple linear regression analyses revealed that age, BP, and BMI were independently correlated with the PWV at both BS and ES. The PWV at BS and ES progressively increased with increase in age, BP, and BMI. Further, the age- and sex-specific reference values of carotid PWV for ultrafast ultrasound imaging were established. Conclusions Reference values of carotid PWV for ultrafast ultrasound imaging, stratified by sex and age, were determined for the first time. Age, BP, and BMI were the dominant determinants of carotid PWV for ultrafast ultrasound imaging, which should be considered in clinical practice for assessing arterial stiffness.

Barlow's disease is a complicated form of degenerative mitral valve (MV) disease. Infective endocarditis (IE) often occurs on the basis of primary heart diseases and may be combined with valve perforations. Cleft-like indentations (CLIs) were suggested by Ring et al. in 2013. They are located at the inter-scallop position and involve at least one-half of the valve. Herein, we report a case of Barlow's disease combined with IE and CLIs, which was confirmed intra-operatively and by histopathological examination. The CLIs were misdiagnosed by two-dimensional transthoracic echocardiography as perforations, but rightly interpreted by preoperative three-dimensional echocardiography. The possibility of CLIs should be considered in the evaluation of mitral regurgitation caused by myxomatous MV diseases.

Bicuspid aortic valve (BAV) is a common congenital cardiac malformation, frequently combined with ascending aorta dilation. However, isolated abnormalities of the aortic arch are less frequent in BAV patients. Here, we present a rare case of BAV combined with right-sided aortic arch aneurysm, aberrant left subclavian artery, and Kommerell's diverticulum, diagnosed by echocardiography and computed tomography angiography. The patient was followed-up regularly because of the life-threatening risks of aortic arch aneurysms.

Aims: Mechanical dyssynchrony has been reported in heart failure with preserved ejection fraction (HFpEF), with a majority of patients having a narrow QRS complex; however, whether any benefit is observed with restoration of dyssynchrony remains unclear. We sought to assess left ventricular (LV) dyssynchrony and function in HFpEF and elucidate the underlying mechanisms that may account for HFpEF. Methods: Seventy-eighty patients with a narrow QRS complex including 47 with HFpEF, 31 with heart failure with reduced ejection fraction (HFrEF) patients, and 29 with asymptomatic left ventricular diastolic dysfunction (LVDD) were recruited. Forty-five normal subjects acted as controls. Systolic LV longitudinal strain (LS), systolic longitudinal strain rate (LSrS), early diastolic longitudinal strain rate (LSrE), and late diastolic longitudinal strain rate (LSrA) were measured using speckle tracking echocardiography. LV diastolic and systolic dyssynchrony (Te-SD and Ts-SD) were calculated. Results: Te-SD and Ts-SD were prolonged in HFpEF and HFrEF patients than in the control group (p

A leftward motion of the ventricular septum prior to ejection, known as the septal flash (SF), is frequently observed in patients with left bundle-branch block (LBBB). We investigated whether the abnormal motion of the ventricular septum affects right ventricle (RV) contractile performance in LBBB patients with preserved left ventricular ejection fraction (LVEF). Forty-four patients with complete LBBB were selected using standard 12-lead electrocardiograms (ECGs), with 30 healthy individuals serving as controls. According to the presence of SF, patients with LBBB were allocated to two subgroups: those with SF (LBBB-SF, n = 24) and those without SF (LBBB-NSF, n = 20). RV longitudinal strain (LS) decreased in LBBB patients with preserved LVEF compared to control subjects (p = 0.002). And RV LS decreased significantly in LBBB-SF patients compared to NSF-LBBB patients (p = 0.04). RV LS correlated negatively with involved septal myocardial segments of SF (r = −0.36, p = 0.02), but did not correlate with the magnitude of SF. RV contractile performance deceased in LBBB patients with preserved LVEF. SF, particularly the extent of this phenomenon, may further affect RV contractile performance.

Background Coronary slow flow phenomenon (CSFP) involves the delayed opacification of the coronary distal vessel, in the absence of an obstructive lesion in the epicardial coronary artery during angiography. Since the link between left atrial (LA) function and decreased left ventricular function is still unclear, we evaluated LA function using real-time three-dimensional echocardiography (RT3DE) in patients with CSFP, and subsequently determined the incremental value of RT3DE. Methods This study enrolled 60 patients with CSFP and 45 control subjects. CSFP was diagnosed based on thrombolysis in myocardial infarction frame count (TFC). The LA phasic volume and function was evaluated by both two-dimensional echocardiography (2DE) and RT3DE. Results The LA maximal volume (Volmax), pre-systolic volume (Volp), and minimal volume (Volmin) increased, but LA total and active ejection fraction decreased in patients with CSFP. Based on our results, Volmax, Volp, Volmin, and LA total and active ejection fraction correlated with TFC, and with the number of arteries involved. The LA total ejection fraction by RT3DE was the only independent predictor for CSFP (odds ratio, 0.64 [95% confidence interval, 0.49–0.83]; P = 0.001). Also, the LA total ejection fraction by RT3DE demonstrated good predictive power for CSFP, with a cut-off value of 54.15% (area under curve, 0.85; sensitivity, 84%; specificity, 83%). Conclusions The LA reservoir and contractile function decreased in the patients with CSFP and correlated with coronary flow rate and with the number of arteries involved. The LA total ejection fraction by RT3DE can independently predict CSFP, and RT3DE demonstrated incremental value for evaluating LA phasic function in the patients with CSFP compared to 2DE.

Background Coronary slow flow phenomenon (CSFP) is an angiographic entity characterized by delayed coronary opacification in absence of evident obstructive lesion in the epicardial coronary artery. However, whether patients with CSFP exhibit differing responses to exercise is still not known. This study aimed to evaluate results of exercise stress electrocardiography (ExECG) and left ventricular (LV) function during exercise, and study the value of ExECG for stratification of exercise capacity and LV function in patients with CSFP. Methods Thirty patients with CSFP and 24 controls were enrolled in the study. Diagnosis of CSFP was made by Thrombolysis in Myocardial Infarction frame count. ExECG and LV function measured by echocardiography at rest, during exercise and recovery phase were evaluated. Results Negative ExECG was found in 24 (80%) patients with CSFP. At rest, LV global longitudinal strain (GLS) decreased and mitral average E/e’ increased in patients with CSFP compared with controls; however, there were no differences in these parameters between CSFP patients with negative ExECG and patients with positive ExECG. During exercise, CSFP patients with negative ExECG and controls had significantly increased LV GLS and decreased mitral average E/e’, but CSFP patients with positive ExECG had significantly decreased LV GLS and increased mitral average E/e’. Conclusions About 80% patients with CSFP exhibited negative ExECG. CSFP patients with negative ExECG exhibited improved LV function but CSFP patients with positive ExECG exhibited impaired LV function during exercise. ExECG may aid in the stratification of exercise capacity and LV function in patients with CSFP.

Slow coronary flow (SCF) is an angiographic entity characterized by delayed coronary opacification without an evident obstructive lesion in the epicardial coronary artery. However, patients with SCF have decreased left ventricular (LV) global longitudinal strain (GLS). SCF is associated with inflammation, and soluble endothelial protein C receptor (sEPCR) is a potential biomarker of inflammation. Therefore, under evaluation herein, was the relationship between SCF and sEPCR and the predictive value of sEPCR and LV GLS for SCF was investigated.Twenty-eight patients with SCF and 34 controls were enrolled. SCF was diagnosed by the thrombolysis in myocardial infarction frame count (TFC). The plasma level of sEPCR was quantified using enzyme-linked immunosorbent assay. LV GLS was measured by two-dimensional speckle-tracking echocardiography.Plasma sEPCR was significantly higher in patients with SCF than in controls and was positively correlated with the mean TFC (r = 0.67, p0.001) and number of involved vessels (r = 0.61, p0.001). LV GLS was decreased in patients with SCF compared to that in controls. sEPCR level (OR = 3.14, 95% CI 1.55-6.36, p = 0.001) and LV GLS (OR = 1.44, 95% CI 1.02-2.04, p = 0.04) were independent predictors of SCF. sEPCR predicted SCF (area under curve [AUC]: 0.83); however, sEPCR9.63 ng/mL combined with LV GLS-14.36% demonstrated better predictive power (AUC: 0.89; sensitivity: 75%; specificity: 91%).Patients with SCF have increased plasma sEPCR and decreased LV GLS. sEPCR may be a useful potential biomarker for SCF, and sEPCR combined with LV GLS can better predict SCF.

AIMS Left ventricular diastolic dysfunction (LVDD) is considered a key factor associated with heart failure (HF) symptoms in patients with preserved ejection fraction (HFpEF). However, LV systolic performance, including LV systolic function and synchrony, has not been well characterized in these patients. The aims of this study were to assess to investigate the underlying relationship and differences between subclinical LVDD and HFpEF. METHODS Eighty-six patients with LVDD were recruited (58 with HFpEF and 28 with subclinical LVDD). Systolic left ventricular (LV) longitudinal strain (LS), systolic longitudinal strain rate (LSrS), early diastolic longitudinal strain rate (LSrE), and late diastolic longitudinal strain rate (LSrA) were measured using speckle tracking echocardiography. LV diastolic and systolic dyssynchrony (Te-SD and Ts-SD) were calculated. Forty age- and sex-matched healthy individuals were enrolled as a control group. RESULTS LV global LS and LSrS were decreased in patients with HFpEF than in normal controls and subclinical LVDD patients (P

Background Coronary slow flow (CSF) refers to coronary arteries with no obvious stenosis but have slow coronary flow without effective treatment. The main cause of CSF is endothelial dysfunction. The long non-coding RNA (lncRNA) MALAT1 is involved in regulating endothelial dysfunction, but its role in CSF endothelial dysfunction is still unclear. Methods We included 41 CSF patients and 37 controls in the study, who all underwent coronary angiography, echocardiography, and brachial artery flow-mediated dilatation (FMD) examination. Human umbilical vein endothelial cells (HUVECs) stimulated by oxygen–glucose deprivation were used as CSF-induced HUVECs. Plasma endothelin-1 (ET-1) concentrations were determined by enzyme-linked immunosorbent assay (ELISA). The expression levels of MALAT1, miR-181b-5p, myocyte enhancer factor 2A (MEF2A), and ET-1 were measured by qRT-PCR or western blotting. Cell proliferation was determined by 5-ethynyl-2′-deoxyuridine (EdU) and Cell Counting Kit-8 (CCK-8) assays. Apoptosis was examined by flow cytometry. The relationship between miR-181b-5p and MALAT1 or MEF2A was verified by dual-luciferase reporter assay. MEF2A binding directly to the ET-1 promoter region was verified via chromatin immunoprecipitation (ChIP) assay. Results MALAT1 and ET-1 were increased, and miR-181b-5p was decreased in the peripheral blood of the CSF patients, and could be used as predictors of CSF. In the CSF-induced HUVECs, MALAT1 was highly expressed, and MALAT1 knockdown improved endothelial function. In contrast, miR-181b-5p was downregulated in the CSF-induced HUVECs, and miR-181b-5p overexpression improved endothelial function. While MEF2A was highly enriched in CSF-induced HUVECs, MEF2A knockdown reduced ET-1 and increased the endothelial function of CSF-induced HUVECs as a transcriptional regulator of ET-1. MALAT1 modulated MEF2A expression positively by sponging miR-181b-5p. Conclusions Endothelial function is reduced in CSF. MALAT1 participates in regulating CSF endothelial dysfunction through the miR-181b-5p–MEF2A–ET-1 axis, and could provide a new target for CSF treatment.

Numerical abnormalities of mitral leaflets is a special entity in congenital mitral malformations. Previously reported cases of uni-leaflet mitral valve were primarily related to absence or dysplasia of certain leaflets. We present a case here with mitral leaflets that were not divided into anterior and posterior as usual, but developed as an integral structure instead, which is different from previously documented cases of uni-leaflet mitral valves. Real time three-dimensional echocardiography (RT3DE) provides a visual presentation of the abnormal mitral structure which was confirmed by surgical operation. To the best of our knowledge, this unusual form of uni-leaflet mitral valve has not been reported yet.

Purpose Coronary slow-flow phenomenon (CSFP) is an angiographic diagnosis characterized by delayed coronary opacification in the absence of significant epicardial coronary stenosis. We previously reported impaired left ventricular (LV) function in patients with CSFP. However, the LV wall comprises three myocardial layers whose contractility can be differently affected. Therefore, we evaluated layer-specific (endocardial, mid-myocardial, and epicardial) LV myocardial contractility and assessed its relationships with the number of affected coronary arteries and their flow. Methods We studied 60 patients with CSFP and 46 controls. CSFP was diagnosed by thrombolysis in myocardial infarction frame count. Echocardiography was performed within 72 hours after the coronary angiography. LV layer-specific longitudinal strain (LS) was measured using two-dimensional speckle-tracking echocardiography. Results and Conclusions The LS of all three myocardial layers was lower in patients with CSFP than in controls. In patients with CSFP, LS of all three myocardial layers and transmural LS gradient correlated negatively with the number of affected coronary arteries and the mean thrombolysis in myocardial infarction frame count. © 2016 Wiley Periodicals, Inc. J Clin Ultrasound, 2016

Palmitic acid (PA) can induce lipotoxic damage to cardiomyocytes, although its precise mechanism of action has not been completely elucidated. Growth arrest‑specific transcript 5 (GAS5) is a long noncoding RNA that serves a regulatory role in several pathological processes, including tumorigenesis, stroke, cardiac fibrosis and osteoarthritis; however, its role in PA‑induced myocardial injury remains elusive. The present study aimed to explore the role and underlying mechanism of GAS5 on PA‑induced myocardial injury. The expression of GAS5 in PA‑treated cardiomyocytes (H9c2 cells) was detected by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), and its effects on PA‑induced myocardial injury were measured by Cell Counting Kit‑8 and lactate dehydrogenase (LDH) assays. The activities of cytokines and nuclear factor (NF)‑κB were also detected by enzyme‑linked immunosorbent assay, while interactions between GAS5 and microRNA (miR)‑26a were evaluated by luciferase reporter assay and RT‑qPCR. The regulation of GAS5 on high mobility group box 1 (HMGB1) expression was detected by RT‑qPCR and western blotting. The results demonstrated that GAS5 was significantly upregulated in cardiomyocytes following treatment with PA. GAS5‑knockdown increased the viability of PA‑treated cardiomyocytes and reduced the activity of LDH, tumor necrosis factor‑α and interleukin‑1β. Furthermore, the present study identified that GAS5 specifically binds to miR‑26a, and a reciprocal negative regulation exists between the two. The present study also demonstrated that GAS5 downregulation inhibited HMGB1 expression and NF‑κB activation, while these suppressive effects were mediated by miR‑26a. In conclusion, the present study demonstrated that PA can induce GAS5 expression and that the downregulation of GAS5 alleviated PA‑induced myocardial inflammatory injury through the miR‑26a/HMGB1/NF‑κB axis. These data may provide a novel insight into the mechanism of myocardial lipotoxic injury.

Unilateral lung agenesis, a rare congenital deformity, is secondary to abnormal embryonic development, leading to a shift of the mediastinum and remaining lung. In our case reports, we describe the diagnostic courses of two pediatric patients with unilateral lung agenesis admitted to our hospital in 2014. We present and compare the findings in transthoracic echocardiography with that in CT. Echocardiography played a pivotal role in revealing pulmonary deformities and leading to the diagnosis. © 2016 Wiley Periodicals, Inc. J Clin Ultrasound 44:514-517, 2016.

// Hongyun Chen 1 , Shuang Liu 2 , Zhihong Zong 3 , Cuiting Zhao 2 , Guangyuan Li 2 , Yonghuai Wang 2 , Guoxian Qi 1 , Jun Yang 2 and Chunyan Ma 2 1 Department of Geriatric Cardiology, First Hospital of China Medical University, Shenyang, Liaoning, China 2 Department of Cardiovascular Ultrasound, First Hospital of China Medical University, Shenyang, Liaoning, China 3 China Medical University, Shenyang, Liaoning, China Correspondence to: Chunyan Ma, email: cmu1h_mcy@126.com Keywords: cardiac resynchronization therapy (CRT); SERCA2A; endo-CRT; epi-CRT; dyssynchronous heart failure Received: March 29, 2017 Accepted: December 29, 2017 Published: January 02, 2018 ABSTRACT The aims of the present study were to compare the effects of endocardial cardiac resynchronization therapy (endo-CRT) and epicardial CRT (epi-CRT) on cardiac contractile function and to delineate the underlying molecular mechanisms. Twenty-four adult mongrel canines were divided into four groups: sham-operation control group (CT, n = 6), dyssynchronous heart failure (DHF) group ( n = 6), epi-CRT group ( n = 6), and endo-CRT group ( n = 6). The global and local left ventricle (LV) systolic function, dyssynchrony and myocardium calcium handling molecular mRNA and protein levels were measured. Compared to CT group, we found the global and local LV function, dyssynchrony and SERCA2A decreased in DHF group and increased in CRT groups, particularly in endo-CRT group at LV lateral wall (pacing site). Therefore, endo-CRT appears to be an effective procedure in the treatment of DHF, which might be mediated by upregulating the mRNA and protein expression of SERCA2A in the LV at the pacing and remote site.

Loeffler endocarditis is a rare comprehensive cardiac manifestation caused by eosinophilic cell infiltrations and is present in 50%-60% of patients with hypereosinophilic syndrome (HES). Left ventricle (LV) endocardial systolic dysfunction is a major cause of morbidity and mortality in HES and Loeffler endocarditis. We present a case of Loeffler endocarditis, whose left ventricular (LV) systolic dysfunction and endocardial systolic dysfunction were first neglected by conventional transthoracic echocardiography (TTE), but were later pointed out by layer-specific longitudinal strain analysis. With timely initial therapeutic management, the patient's outcome was remarkable. Thus, we strongly recommend strain analysis as a necessary supplementary test of conventional TTE in all patients with Loeffler endocarditis.

Hypereosinophilia-associated syndrome is a rare group of systemic diseases without certain underlying causes. Hypereosinophilic syndrome (HES) and eosinophilic granulomatosis with polyangiitis (EGPA), formerly known as Churg-Strauss syndrome (CSS), are initial considerations, when underlying causes remains unexplained despite of complete evaluation of hypereosinophilia. In this study, we report two rare cases, one case of HES with Loeffler endocarditis, and the other one of EGPA with restrictive cardiomyopathy mimicking myocardial infarction, to further address differential chief cardiac manifestations between HES and EGPA. Key roles of echocardiography played in detection of cardiac involvements, diagnosis, and prognosis prediction are also highlighted.

To assess LA diastolic and systolic function and atrial dyssynchrony in patients with heart failure with preserved ejection fraction (HFpEF) and to examine whether LA dysfunction and dyssynchrony account for the patients' symptoms of HFpEF.Fifty-five patients with HFpEF, 31 asymptomatic patients with left ventricular diastolic dysfunction (LVDD) and 33 healthy individuals were enrolled in the study. The LA active ejection fraction (LAAEF) was calculated. The peak atrial longitudinal systolic strain (PALS) and peak atrial contraction strain (PACS) were measured using speckle tracking echocardiography (STE). Atrial dyssynchrony including inter-atrial dyssynchrony, LA dyssynchrony and right atrial dyssynchrony were calculated by tissue Doppler imaging (TDI).The PALS and PACS were deteriorated, whereas inter-atrial dyssynchrony was prolonged in patients with HFpEF (20.41±7.41%, 10.83±4.19%, 31±15ms, respectively) compared with the values obtained in asymptomatic LVDD patients (26.61±6.30%, 13.23±4.52%, 19±12ms, respectively) and those found in normal individuals (33.51±6.74%, 14.17±2.88%, 17±12ms, respectively) (P0.05). However, PACS and inter-atrial dyssynchrony did not reach statistical significance between asymptomatic LVDD and normal individuals (P0.05). Moreover, patients with deteriorated clinical symptoms (NYHAII) presented worse LA systolic function and prolonged dyssynchrony compared with those with NYHA=II. Inter-atrial dyssynchrony and LAAEF are independently associated with worse NYHA functional classes in patients with HFpEF.LA diastolic and systolic function were significantly impaired, and inter-atrial dyssynchrony was prolonged in patients with HFpEF. Decreased LA systolic function and prolonged inter-atrial dyssynchrony were possibly associated with deteriorated clinical symptoms.

Slow coronary flow (SCF) is characterized by delayed distal vessel opacification in the absence of significant epicardial coronary disease. Life-threatening arrhythmias and sudden cardiac death can occur; however, the pathological mechanism and influence on left ventricular function remain undetermined. We aimed to assess the risk factors and left ventricular (LV) function in SCF and evaluate the relationships between thrombolysis in myocardial infarction frame count (TFC) and the number of involved coronary arteries with LV function in patients with SCF. We included 124 patients who underwent coronary angiography because of symptoms of angina; 71 patients with angiographically proven SCF and 53 cases with normal coronary flow pattern. SCF was diagnosed as TFC >27 in at least one coronary artery. Complete blood count and biochemical parameters were compared between the two groups. Conventional echocardiography and tissue Doppler imaging were used to assess LV systolic and diastolic function. Platelet aggregation rate induced by ADP was an independent predictor of SCF and positively correlated with coronary artery mean TFC (mTFC) (r = 0.514, P < 0.001) and the number of coronary arteries with SCF (r = 0.628, P < 0.001). Early diastolic mitral inflow velocity (E) (0.66 ± 0.15 vs. 0.74 ± 0.17, P = 0.008), ratio of early to late diastolic mitral inflow velocity (E/A) (0.95 ± 0.29 vs. 1.15 ± 0.35, P = 0.002), global myocardial peak early diastolic velocity (gVe) (4.41 ± 1.25 vs. 4.96 ± 1.45, P = 0.037), and ratio of global myocardial peak early to late diastolic velocity (gVe/gVa: 1.09 ± 0.45 vs. 1.36 ± 0.58, P = 0.006) were decreased in patients with SCF compared with controls. gVe (3 vs. 0 branches, 4.08 ± 1.14 vs. 4.97 ± 1.45, respectively, P = 0.008) deteriorated significantly in patients with SCF involving three coronary arteries. mTFC negatively correlated with E and E/A (r = -0.22, P = 0.02; r = -0.20, P = 0.04, respectively). The number of coronary arteries with SCF negatively correlated with E, E/A, gVe and gVe/gVa (r = -0.23, P = 0.02; r = -0.25, P = 0.009; r = -0.25, P = 0.008; r = -0.21, P = 0.03, respectively). Platelet aggregation rate induced by ADP was an independent predictor of SCF and positively correlated with coronary artery TFC and the number of affected coronary arteries. Left ventricular global and regional diastolic function was impaired in SCF patients. Furthermore, the number of coronary arteries involved rather than coronary artery TFC determined the severity of left ventricular dysfunction in patients with SCF.

Libman-Sacks endocarditis, characterized by sterile verrucous vegetations, is a rare but typical cardiac manifestation of systemic lupus erythematosus. It primarily leads to lesions of the mitral and aortic valves, but isolated tricuspid valve involvement is exceptional. We report the case of a 40-year-old woman with large tricuspid valve vegetations, thickening, and regurgitation. Clinical findings and laboratory tests confirmed the diagnosis of systemic lupus erythematosus. The patient successfully recovered following tricuspid valve replacement. Echocardiography is the definitive imaging modality for assessing cardiac valvular involvement, choosing appropriate therapy, and evaluating the prognosis of Libman-Sacks endocarditis in systemic lupus erythematosus. © 2014 Wiley Periodicals, Inc. J Clin Ultrasound 43:265-267, 2015.

Echocardiographic detection of left ventricular (LV) diastolic function is an integral part of cardiac imaging. The recent 2016 recommendations for LV diastolic dysfunction from the American Society of Echocardiography were based on septal or lateral mitral annular early-diastolic peak velocity (e

Primary benign cardiac tumors are relatively rare, and lipomas are even less frequent. We presented a case of primary intramyocardial lipoma involving the right ventricular outflow tract diagnosed through transthoracic echocardiography and surgical pathology. The tumor was completely resected. Surprisingly, an echogenic mass similar to the one seen before the operation in terms of the echogenicity and morphological characteristics was found at the same location 1 week after the complete resection. Was it an incomplete excision or a postoperative hematoma? After regular echocardiographic follow-up, the echogenic mass disappeared. It was inferred that the echogenic mass may have been a postoperative intramyocardial hematoma.

Objective:Although the 24-h urinary sodium excretion (USE) is the golden criterion for evaluate the sodium intakes, it always seemed infeasible. Nowadays, there were three methods, Kawasaki method, INTERSALT method, and Tanaka method for estimating 24-h USE. But no evidence showed these methods woul