Growing evidence indicates that severe tricuspid regurgitation (TR) is independently associated with adverse clinical outcomes. The prognostic benefit of isolated TR surgery remains unclear, and medical therapy for decompensated right heart failure alone cannot delay disease progression. TR assessment and management have substantially evolved in recent years. Currently, minimally invasive catheter-based techniques have emerged as a feasible and effective option for TR treatment in high-risk surgical patients. Transcatheter tricuspid valve edge-to-edge repair (T-TEER) has been proposed and applied as an interventional treatment for TR, and has yielded promising preliminary results. This review provides an overview of the current state of T-TEER.
To probe into changes of cerebral vascular hemodynamics indexes (CVHI) from normal population to different clinical stage before and after occurring of stroke.Participants were selected from 25,355 stroke cohort study population aged 35 years and over in Northeast of China and 55 acute stroke patients were selected from Fuzhou PLA General Hospital. CVHI indexes were checked during baseline investigation or within one week after acute stroke. Participant enlisted in the study were divided into following 5 groups, normal population, high risk population, individuals before stroke, acute stroke patients and convalescence stroke patients. Characteristics of CVHI indexes in different population were analyzed and compared.V(min) of cerebral vascular in previous defined 5 group participants were 11.39 +/- 3.27, 9.66 +/- 3.18, 6.71 +/- 3.30, 4.13 +/- 1.27, 6.78 +/- 3.09, respectively. V(mean) and V(max) were with the same decreasing trends as V(min). However, RV in 5 group participants were 62.35 +/- 21.11, 82.32 +/- 31.16, 122.72 +/- 52.73, 137.46 +/- 49.56 and 115.89 +/- 55.51, respectively. Zcv, WV, DR and CP were also with the same increasing trends as RV. Abnormal rate of CVHI score (< 75 points) from normal population to convalescence stroke patients were 13.3%, 34.7%, 74.1%, 100% and 66.7%, respectively.From normal population to clinical stage of stroke, cerebral vascular velocity showed decreasing trends while other indexes, such as RV, Zcv, WV, DR and CP were increasing.
Abstract Myocardial infarction (MI) is one of the leading causes of heart failure with highly complicated pathogeneses. miR-654-3p has been recognized as a pivotal regulator of controlling cell survival. However, the function of miR-654-3p in cardiomyocytes and MI has yet to be reported. This study aimed to identify the role of miR-654-3p in the regulation of myocardial infarction. To understand the contribution of miR-654-3p on heart function, we generated cardiac-specific knockdown and overexpression mice using AAV9 technology in MI injury. Mechanically, we combined cellular and molecular techniques, pharmaceutical treatment, RNA sequencing, and functional testing to elucidate the potential pathological mechanisms. We identified that mice subjected to MI decreased the expression of miR-654-3p in the border and infarcted area. Mice lacking miR-654-3p in the heart showed some inflammation infiltration and myocardial fibrosis, resulting in a mild cardiac injury. Furthermore, we found a deficiency of miR-654-3p in cardiomyocytes resulted in pyroptotic cell death but not other programmed cell death. Intriguingly, miR-654-3p deficiency aggravated MI-induced cardiac dysfunction, accompanied by higher myocardial fibrosis and cardiac enzymes and augmented pyroptosis activation. Cardiac elevating miR-654-3p prevented myocardial fibrosis and inflammation infiltration and decreased pyroptosis profile, thereby attenuating MI-induced cardiac damage. Using RNA sequence and molecular biological approaches, we found overexpression of miR-654-3p in the heart promoted the metabolic ability of the cardiomyocytes by promoting mitochondrial metabolism and mitochondrial respiration function. Our finding identified the character of miR-654-3p in protecting against MI damage by mediating pyroptosis and mitochondrial metabolism. These findings provide a new mechanism for miR-654-3p involvement in the pathogenesis of MI and reveal novel therapeutic targets.
Provisional stenting using drug-eluting stent is effective for simple coronary bifurcation lesions. Kissing balloon inflation using conventional non-compliant balloon is the primary treatment of side branch (SB) after main vessel (MV) stenting. Drug-coating balloon (DCB) is reported to be associated with less frequent clinical events in in-stent restenosis and small vessel disease. The importance of DCB in bifurcation treatment is understudied. Accordingly, this trial is designed to investigate the superiority of DCB to non-compliant balloon angioplasty for SB after provisional stenting in patients with true coronary bifurcation lesions.
By taking advantage of the anisotropy of AuNRs, we design different bifunctional PEG molecules to selectively bind to either the end or side face and simultaneously protect other faces of individual AuNRs. In this way, we successfully achieve orientation-controllable assemblies of AuNRs into side-by-side (SS), end-to-end (EE) and end-to-side (ES) orientations based on the electrostatic interaction between carboxylic PEG and CTAB capping on AuNRs. Furthermore, we find that the different orientations of assembled motifs in these three types of AuNRs assemblies exhibited different near field coupling between the surface plasma of the neighboring AuNRs, leading to different surface-enhanced Raman signals. Undoubtedly, the current rational design of oriented assembly can be potentially useful for directing anisotropic nanoparticles into well-defined orientations, which provides a powerful route in designing families of novel nanodevices and nanomaterials with programmable electrical and optical properties.
Short-term exposure to ambient air pollution has been linked with daily hospitalization and mortality from acute coronary syndrome (ACS); however, the associations of subdaily (hourly) levels of criteria air pollutants with the onset of ACS and its subtypes have rarely been evaluated. We conducted a time-stratified case-crossover study among 1 292 880 patients with ACS from 2239 hospitals in 318 Chinese cities between January 1, 2015, and September 30, 2020. Hourly concentrations of fine particulate matter (PM2.5), coarse particulate matter (PM2.5-10), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon monoxide (CO), and ozone (O3) were collected. Hourly onset data of ACS and its subtypes, including ST-segment-elevation myocardial infarction, non-ST-segment-elevation myocardial infarction, and unstable angina, were also obtained. Conditional logistic regressions combined with polynomial distributed lag models were applied. Acute exposures to PM2.5, NO2, SO2, and CO were each associated with the onset of ACS and its subtypes. These associations were strongest in the concurrent hour of exposure and were attenuated thereafter, with the weakest effects observed after 15 to 29 hours. There were no apparent thresholds in the concentration-response curves. An interquartile range increase in concentrations of PM2.5 (36.0 μg/m3), NO2 (29.0 µg/m3), SO2 (9.0 µg/m3), and CO (0.6 mg/m3) over the 0 to 24 hours before onset was significantly associated with 1.32%, 3.89%, 0.67%, and 1.55% higher risks of ACS onset, respectively. For a given pollutant, the associations were comparable in magnitude across different subtypes of ACS. NO2 showed the strongest associations with all 3 subtypes, followed by PM2.5, CO, and SO2. Greater magnitude of associations was observed among patients older than 65 years and in the cold season. Null associations of exposure to either PM2.5-10 or O3 with ACS onset were observed. The results suggest that transient exposure to the air pollutants PM2.5, NO2, SO2, or CO, but not PM2.5-10 or O3, may trigger the onset of ACS, even at concentrations below the World Health Organization air quality guidelines.
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