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Background: Coronary slow flow (CSF) is an angiographic entity characterized by delayed coronary opacification with no evident obstructive lesion in the epicardial coronary artery. Several studies have shown that the occurrence and development of CSF may be closely related to inflammation. Soluble vascular cell adhesion molecule-1 (sVCAM-1) is a biomarker related to inflammation. The aim of this study was to evaluate the correlation between plasma soluble VCAM-1 level and CSF occurrence and thus the predictive value of VCAM-1 for CSF. Methods: Forty-six CSF patients and thirty control subjects were enrolled. Corrected thrombolysis in myocardial infarction frame count (cTFC) was used to diagnose CSF. Functional status and quality of life were determined by the Seattle Angina Questionnaire (SAQ). Echocardiography was used to evaluate the systolic and diastolic function of the left ventricle (LV) and right ventricle (RV). The plasma levels of sVCAM-1, IL-6, and TNF-α were quantified by enzyme-linked immunosorbent assay. Results: Compared with the control group, the physical limitation score by the SAQ, the LV global longitudinal strain (GLS), mitral E, and mitral E/A decreased in patients with CSF, while the plasma IL-6 and TNF-α levels increased. The plasma sVCAM-1 level in the CSF group was significantly higher than that in the control group (186.03 ± 83.21 vs. 82.43 ± 42.12 ng/mL, p < 0.001), positively correlated with mean cTFC (r = 0.57, p < 0.001), and negatively correlated with the physical limitation score (r = −0.32, p = 0.004). Logistic regression analyses confirmed that plasma sVCAM-1 level (OR = 1.07, 95%CI: 1.03–1.11) is an independent predictor of CSF, and the receiver operating characteristic curve analysis showed that plasma sVCAM-1 levels had statistical significance in predicting CSF (area under curve = 0.88, p < 0.001). When the sVCAM-1 level was higher than 111.57 ng/mL, the sensitivity for predicting CSF was 87% and the specificity was 73%. Conclusions: Plasma sVCAM-1 level can be used to predict CSF and was associated with the clinical symptoms of patients. It may serve as a potential biomarker for CSF in the future.

Coronary slow flow is taken to be indicative of delayed filling of terminal vessels of the coronary arteries in the absence of coronary stenosis, as detected using coronary angiography. Patients suffering from coronary slow flow typically experience recurrent chest pain, thereby markedly affecting their quality of life. The etiology and pathogenesis of coronary slow flow, which is gradually attracting clinical attention, have yet to be sufficiently established, although it is currently believed that they may be associated with endothelial dysfunction in the coronary arteries, inflammatory response, abnormalities in microvascular reserve function, subclinical atherosclerosis, blood cell and platelet abnormalities, and genetic factors. In this review, we provide a brief overview of recent progress in research on the pathogenesis of coronary slow flow with a view toward elucidating the possible underlying pathogenesis and identify targets and directions for the treatment of this condition.

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

Cryoballoon ablation (CBA) is recommended for patients with symptomatic drug refractory paroxysmal atrial fibrillation (pAF). However, substantial atrial fibrillation (AF) recurrence is common during follow-up. Searching for a potential biomarker representing both myocardial injury and inflammation to identify patients at high risk of AF recurrence after CBA is very meaningful for postoperative management of AF patients.To evaluate the clinical efficacy of high-mobility group box 1 (HMGB1) protein released from the left atrium to predict AF recurrence in pAF patients after CBA at 1-year follow-up.We included 72 pAF patients who underwent CBA. To determine the expression levels of HMGB1, left atrial blood samples were collected from the patients before CBA and after the procedure through the transseptal sheath. Patients were followed up for AF recurrence for 1 year.A total of 19 patients of the 72 experienced AF recurrence. The level of postoperative HMGB1 (HMGB1post) was higher in the AF recurrence group than in the AF non recurrence group (p = .03). However, no differences were noted in the levels of other biomarkers such as preoperative high-sensitivity C-reactive protein (hs-CRP), postoperativehs-CRP, and preoperative HMGB1 between the two groups. Multiple logistic regression analysis revealed that a higher level of serum HMGB1post was associated with AF recurrence (odds ratio: 5.29 [1.17-23.92], p = .04). Receiver operating characteristic analysis revealed that HMGB1post had a moderate predictive power for AF recurrence (area under the curve: 0.68; sensitivity: 72%; and specificity: 68%). The 1-year AF-free survival was significantly lower in patients with a high HMGB1post level than in those with a low HMGB1post level (hazard ratio: 3.81 [1.49-9.75], p = .005).In pAF patients who under went CBA, the level of HMGB1 after CBA was associated with AF recurrence and demonstrated a moderate predictive power. Thus, we offer a potential biomarker to identify pAF patients at high risk of AF recurrence.

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

Complete left bundle branch block (cLBBB) is an electrical conduction disorder associated with cardiac disease. Septal flash (SF) involves septal leftward contraction during early systole followed by a lengthening motion toward the right ventricle and affects several patients with cLBBB. It has been revealed that cLBBB patients with SF may be at risk of cardiac function reduction and poor prognosis. Therefore, accurate identification of SF may play a vital role in counseling patients about their prognosis. Generally, Septal flash is identified by echocardiography using visual "eyeballing". However, this conventional method is subjective as it depends on operator experience. In this study, we build a linear attention cascaded net (LACNet) capable of processing echocardiography to identify SF automatically. The proposed method consists of a cascaded CNN-based encoder and an LSTM-based decoder, which extract spatial and temporal features simultaneously. A spatial transformer network (STN) module is employed to avoid image inconsistency and linear attention layers are implemented to reduce data complexity. Moreover, the left ventricle (LV) area-time curve calculated from segmentation results can be considered as a new independent disease predictor as SF phenomenon leads to transient left ventricle area enlargement. Therefore, we added the left ventricle area-time curve to LACNet to enrich input data diversity. The result shows the possibility of using echocardiography to diagnose cLBBB with SF automatically.

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.

This article first proposes an adaptive traffic scheduling strategy for optoelectronic hybrid data centers. The strategy is composed of a deep bidirectional LSTM-based traffic prediction model and a prediction-assisted traffic scheduling method. The simulation results confirm that the presented method can achieve non-congested intra-data center traffic scheduling and higher network performance even under heavy traffic conditions.

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