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AimElevated pulmonary artery pressure (ePAP) in response to high-altitude hypoxia is a critical physiopathological factor in the hypoxic adaptation that may lead to high-altitude pulmonary edema in the acute phase or high-altitude pulmonary hypertension in the long term. However, the sea-level predictors of risk factors for altitude-induced ePAP have not been examined. Thus, we aimed to identify the baseline systemic blood predictors of ePAP after acute high-altitude exposure.Materials and MethodsA total of 154 participants were transported to a high altitude 3,700 m from sea level within 2 h. Echocardiography examinations were performed to assess the mean pulmonary artery pressure (mPAP) and hemodynamics at both altitudes. All the individuals underwent blood tests to determine the concentrations of vascular regulatory factors. Univariate and adjusted logistic regression analyses were performed to identify the independent predictors of ePAP and factors related to ePAP.ResultsThe mPAP increased significantly from sea level to high altitude (19.79 ± 6.53–27.16 ± 7.16 mmHg, p < 0.05). Increased levels of endothelin (ET-1), Ang (1–7), Ang II, and bradykinin were found after high-altitude exposure, while the levels of nitric oxide (NO), prostaglandin E2 (PEG2), and serotonin decreased sharply (all p-values < 0.05). At high altitude, 52.6% of the subjects exhibited ePAP, and the mPAP was closely correlated with the baseline Ang II level (r = 0.170, p = 0.036) and follow-up levels of NO (r = −0.209, p = 0.009), Ang II (r = 0.246, p = 0.002), and Ang (1–7) (r = −0.222, p = 0.006) and the left atrial inner diameter (LAD, r = 0.270, p < 0.001). Both the baseline and follow-up NO and Ang II levels were significantly different between the ePAP and non-ePAP groups. Finally, we identified the baseline Ang II and NO concentrations as two independent predictors of ePAP (p < 0.05). We also found that two vascular regulatory factors with inverse roles, namely, Ang (1–7) and Ang II, at high altitudes were independently associated with ePAP. Additionally, ET-1, NO, PEG2, and LAD were associated with ePAP.ConclusionThe baseline concentrations of Ang II and NO at sea level are two independent predictors of ePAP after acute high-altitude exposure. Furthermore, Ang (1-7) and Ang II combined with ET-1, NO, PEG2, and LAD at high altitudes may contribute to the development of ePAP.

Hypobaric hypoxia (HH) is the primary challenge at high altitude. Prolonged HH exposure impairs right cardiac function. Mitochondria-associated membrane (MAM) plays a principal role in regulating mitochondrial function under hypoxic conditions, but the mechanism remains poorly understood. In this study, proteomics analysis identified that PACS2, a key protein in MAM, and mitophagy were down-regulated in HH conditions. Metabolomics analysis indicated suppression of aerobic oxidation of glucose and fatty acids. Cardiomyocyte Pacs2 deficiency disrupted MAM formation and endoplasmic reticulum (ER)-mitochondria calcium flux further inhibiting mitophagy and mitochondrial energy metabolism during HH exposure. Overexpression of Pacs2 reversed these effects. Cardiac-specific knockout of Pacs2 exacerbated mitophagy inhibition, cardiomyocyte injury and right cardiac dysfunction induced by HH. Knock-in of Pacs2 recovered HH-induced RV structural and functional impairment. Thus, PACS2 is essential for protecting cardiomyocytes through mechanisms of ER-mitochondria calcium flux, mitophagy, and mitochondrial energy metabolism, thereby maintaining right cardiac function at high altitude.

Insufficient cardiorespiratory compensation is closely associated with acute hypoxic symptoms and high-altitude (HA) cardiovascular events. To avoid such adverse events, predicting HA cardiorespiratory fitness impairment (HA-CRFi) is clinically important. However, to date, there is insufficient information regarding the prediction of HA-CRFi. In this study, we aimed to formulate a protocol to predict individuals at risk of HA-CRFi. We recruited 246 volunteers who were transported to Lhasa (HA, 3,700 m) from Chengdu (the sea level [SL], <500 m) through an airplane. Physiological parameters at rest and during post-submaximal exercise, as well as cardiorespiratory fitness at HA and SL, were measured. Logistic regression and receiver operating characteristic (ROC) curve analyses were employed to predict HA-CRFi. We analyzed 66 pulmonary vascular function and hypoxia-inducible factor- (HIF-) related polymorphisms associated with HA-CRFi. To increase the prediction accuracy, we used a combination model including physiological parameters and genetic information to predict HA-CRFi. The oxygen saturation (SpO2) of post-submaximal exercise at SL and EPAS1 rs13419896-A and EGLN1 rs508618-G variants were associated with HA-CRFi (SpO2, area under the curve (AUC) = 0.736, cutoff = 95.5%, p < 0.001; EPAS1 A and EGLN1 G, odds ratio [OR] = 12.02, 95% CI = 4.84–29.85, p < 0.001). A combination model including the two risk factors—post-submaximal exercise SpO2 at SL of <95.5% and the presence of EPAS1 rs13419896-A and EGLN1 rs508618-G variants—was significantly more effective and accurate in predicting HA-CRFi (OR = 19.62, 95% CI = 6.42–59.94, p < 0.001). Our study employed a combination of genetic information and the physiological parameters of post-submaximal exercise at SL to predict HA-CRFi. Based on the optimized prediction model, our findings could identify individuals at a high risk of HA-CRFi in an early stage and reduce cardiovascular events.

继发性二尖瓣反流(SMR)是多种心脏疾病共同的重要合并症,因其改变了血流动力学,不仅加重了原发心脏疾病病情,还导致心血管疾病不良预后.随着以MitraClip为代表的SMR介入治疗技术的飞速发展,SMR的临床诊治已发生了革命性改变.然而,对于心力衰竭继发二尖瓣反流的临床诊治,目前尚无正式的临床诊治指南或共识.2021年,欧洲心脏协会(ESC)的心力衰竭协会(HFA)、欧洲心血管影像协会(EACVI)、欧洲心脏节律协会(EHRA)以及欧洲经皮心血管介入治疗协会(EAPCI)联合发布了《2021 HFA/EACVI/EHRA/EAPCI立场声明:心力衰竭患者继发二尖瓣反流的管理》,这是世界范围内首次对心力衰竭继发二尖瓣反流临床管理进行的正式立场声明.本文从心力衰竭继发二尖瓣反流的临床流行、病理生理学机制、临床初步评价和影像学检查方法、临床管理过程和治疗决策方面对该声明进行详细阐述和解读,以期为心力衰竭继发二尖瓣反流的临床诊治提供实用性的指导.

Hypertension is the most common comorbidity in patients with coronavirus disease 2019 (COVID-19) and increases in-hospital mortality. Day-by-day blood pressure (BP) variability (BPV) is associated with clinical outcomes in hypertensive patients. However, little information is available on the association of BPV with the outcomes of COVID-19 patients with hypertension. This study aimed to demonstrate whether day-by-day in-hospital BPV had prognostic significance in these patients. The authors included 702 COVID-19 patients with hypertension from Huoshenshan Hospital (Wuhan, China), who underwent valid in-hospital BP measurements on at least seven consecutive days. Day-by-day BPV was assessed by standard deviation (SD), coefficient of variation (CV), and variation independent of mean (VIM). Overall, patients with severe COVID-19 and non-survivors had higher BPV than moderate cases and survivors, respectively. Additionally, higher BPV was correlated with greater age and higher levels of C-reactive protein, procalcitonin, high-sensitive cardiac troponin I, and B-type natriuretic peptide. In multivariable Cox regression, SD of systolic BP (SBP) was predictive of mortality [hazard ratio (HR) 1.17, 95% confidence interval (CI) 1.05-1.30] as well as acute respiratory distress syndrome (ARDS) (HR 1.09, 95% CI 1.01-1.16). Similar trends were observed for CV and VIM of SBP, but not indices of diastolic BP variability. The authors demonstrated that day-by-day in-hospital SBP variability can independently predict mortality and ARDS in COVID-19 patients with hypertension. And high BPV might be correlated with severe inflammation and myocardial injury. Further studies are needed to clarify whether early reduction of BPV will improve the prognosis of these patients.

Background:Pulmonary hypertension (PH) is one of the most common complications associated with end-stage renal disease (ESRD). Though numerous risk factors have been founded, other risk factors remain unidentified, particularly in patients undergoing maintenance hemodialysis with elder age. Soluble Fas (sFas) and its ligand FasL (sFasL) have been reported in chronic renal disease patients; however, they have not been identified in the PH patients of elder hemodialysis patients. We aimed to determine the roles of sFas/sFasL in onset of PH in elder patients undergoing maintenance hemodialysis with ESRD.Methods:Altogether, 163 patients aged 68.00 ± 10.51 years with ESRD who undergoing maintenance hemodialysis in a prospective cohort and were followed-up for a median of 5.5 years. They underwent echocardiography examinations, liver function assessments, residual renal function, and serum ion examinations, before and after dialysis. Furthermore, levels of sFas and sFasL at baseline had also been measured. We compared demographic data, echocardiographic parameters, liver function, ions, and residual renal function as well as serum sFas and sFasL between the PH and non-PH groups. These parameters were correlated with systolic pulmonary artery pressure (sPAP) using Spearman's correlation. Moreover, univariate and adjusted logistic regression analyses have also been conducted.Results:The incidence of PH in the elder dialysis patients was 39.1%. PH populations were demonstrated with significantly higher end-diastolic internal diameters of the left atrium, left ventricle, right ventricle (RV), and pulmonary artery, as well as the left ventricular posterior wall thickness (LVWP; all p < 0.05). A higher baseline serum sFas and sFasL levels have also been identified ( p < 0.001). They also showed lower fractional shortening and left ventricular ejection fraction (LVEF; p < 0.05). Following dialysis, the post-dialysis serum potassium concentration (K+) was significantly higher in the PH group ( p = 0.013). Furthermore, the adjusted regression identified that ratio of sFas/FasL (OR: 1.587, p = 0.004), RV (OR: 1.184, p = 0.014), LVPW (OR: 1.517, p = 0.007), and post-dialysis K+ (OR: 2.717, p = 0.040) was the independent risk factors for PH while LVEF (OR: 0.875, p = 0.040) protects patients from PH.Conclusion:The baseline ratio of sFas/sFasL, RV, LVPW, and post-dialysis K+ was independent risk factors for PH onset, while LVEF was a protective factor for PH.

目的探讨低血钙与COVID-19患者预后不良的关系。 方法回顾性分析2020年2月4日至4月11日在武汉火神山医院就诊的2 651例COVID-19患者资料，对比分析低血钙组患者(n=773)与正常血钙组患者(n=1 878)的人口学基本特征、实验室检查、治疗、并发症和预后结果，采用Cox回归模型分析低血钙是否为COVID-19患者预后不良的独立危险因素。 结果与正常血钙组比较，低血钙组患者机械通气使用率、体外膜肺氧合使用率和重症监护室入住率显著升高(P 结论低血钙是影响COVID-19患者预后不良的独立危险因素，纠正低血钙可能是改善COVID-19患者预后的重要策略。

High altitude (HA) exposure has been considered as a cardiac stress and might impair ventricular diastolic function. Atrial contraction is involved in ventricular passive filling, however the atrial performance to HA exposure is poorly understood. This study aimed to evaluate the effect of short-term HA exposure on bi-atrial function. Physiological and 2D-echocardiographic data were collected in 82 healthy men at sea level (SL, 400 m) and 4100 m after an ascent within 7 days. Atrial function was measured using volumetric and speckle-tracking analyses during reservoir, conduit and contractile phases of cardiac cycle. Following HA exposure, significant decreases of reservoir and conduit function indexes were observed in bi-atria, whereas decreases of contractile function indexes were observed in right atrium (RA), estimated via RA active emptying fraction (SL 41.7 ± 13.9% vs. HA 35.4 ± 12.2%, p = 0.001), strain during the contractile phase [SL 13.5 (11.4, 17.8) % vs. HA 12.3 (9.3, 15.9) %, p = 0.003], and peak strain rate during the contractile phase [SL − 1.76 (− 2.24, − 1.48) s−1 vs. HA − 1.57 (− 2.01, − 1.23) s−1, p = 0.002], but not in left atrium (LA). In conclusion, short-term HA exposure of healthy individuals impairs bi-atrial performance, mostly observed in RA. Especially, atrial contractile function decreases in RA rather than LA, which seems not to compensate for decreased ventricular filling after HA exposure. Our findings may provide a novel evidence for right-sided heart dysfunction to HA exposure.

Background Ascending to high altitude (HA) contribute to the development of acute mountain sickness (AMS). The prevalence, clinical features and relative risks for AMS may dynamically evolve but has not been described. Methods A total of 1,629 healthy men aged from 16 to 45 years were enrolled. A fast ascent cohort (n=1283) ascended to 3700 m by airplane and further ascended to 4400 m by bus; a slow ascent cohort (n=346) ascended to 3450 m by bus and further ascended to 4100 m by bus. AMS was diagnosed by the Lake Louise Scoring (LLS) system. Results As diagnosed by the old LLS and new LLS, the prevalence of AMS was 68.4% and 56.1% at 3700 m, respectively, which decreased to 21.4% and 14.3% after further ascending to 4400 m in the fast ascent cohort; the prevalence of AMS was 30.3% and 25.7% at 3450 m, which increased to 36.6% and 32.2% after further ascending to 4100 m in the slow ascent cohort. Moreover, AMS-related symptoms, such as headache, dizziness and fatigue, were the leading symptoms except at 4400 m in the fast ascent cohort. Fast ascent protocol was a risk factor during the initial ascent but became a protective factor after a further ascent to a higher altitude. Conclusions Ascent protocol was the primary factor that affected the incidence of AMS and related symptoms. These findings imply a novel strategy for high altitude travels or work with a plan to ascend to a higher altitude.

BACKGROUNDHigh altitude exposure induces overload of right-sided heart and may further predispose to supraventricular arrhythmia. It has been reported that atrial mechanical dyssynchrony is associated with atrial arrhythmia. Whether high altitude exposure causes higher right atrial (RA) dyssynchrony is still unknown. The aim of study was to investigate the effect of high altitude exposure on right atrial mechanical synchrony.METHODSIn this study, 98 healthy young men underwent clinical examination and echocardiography at sea level (400 m) and high altitude (4100 m) after an ascent within 7 days. RA dyssynchrony was defined as inhomogeneous timing to peak strain and strain rate using 2D speckle-tracking echocardiography.RESULTSFollowing high altitude exposure, standard deviation of the time to peak strain (SD-TPS) [36.2 (24.5, 48.6) ms vs. 21.7 (12.9, 32.1) ms, p<0.001] and SD-TPS as percentage of R-R' interval (4.6 ± 2.1% vs. 2.5 ± 1.8%, p<0.001) significantly increased. Additionally, subjects with higher SD-TPS (%) at high altitude presented decreased right ventricular global longitudinal strain and RA active emptying fraction, but increased RA minimal volume index, which were not observed in lower group. Multivariable analysis showed that mean pulmonary arterial pressure and tricuspid E/A were independently associated with SD-TPS (%) at high altitude.CONCLUSIONOur data for the first time demonstrated that high altitude exposure causes RA dyssynchrony in healthy young men, which may be secondary to increased pulmonary arterial pressure. In addition, subjects with higher RA dyssynchrony presented worse RA contractile function and right ventricular performance.

Objective To investigate whether hypocalcemia is associated with poor prognosis in COVID-19 patients. Methods A retrospective analysis was performed on 2 651 COVID-19 patients admitted to Wuhan Huoshenshan Hospital from February 4, 2020 to April 11, 2020. They were divided into low and normal calcium groups according to their serum calcium level lower than 2.11 mmol/L or not. Their basic demographic characteristics, results of laboratory tests, treatment, complications and outcomes were analyzed and compared between the 2 groups. COX regression model was used to analyze whether low calcium is an independent risk factors for poor outcomes in COVID-19 patients. Results The low calcium group had significantly higher ratios of mechanical ventilation, extracorporeal membrane oxygenation (ECMO) and ICU occupancy (P < 0.05); obviously higher incidences of sepsis, shock, hypoproteinemia, respiratory failure, coagulation disorders, acute kidney injury, acute myocardial injury, acute respiratory distress syndrome (ARDS), and even mortality (P < 0.05); and remarkably longer length of hospital stay (P < 0.001) when compared with the normal calcium group. The blood calcium level of mild and common, severe, and critical COVID-19 patients was 2.17 (2.11, 2.24), 2.13 (2.04, 2.21), and 2.03 (1.89, 2.18) mmol/L, respectively, and significant differences were seen among the patients (P < 0.05). The calcium level was in a decreasing trend with the severity of COVID-19 (P < 0.05). The calcium level was statistically lower in the dead patients than those survival [1.97 (1.87, 2.03) vs 2.17 (2.09, 2.23), P < 0.001]. Multivariate Cox regression analysis indicated that serum calcium concentration < 2.11 mmol/L was an independent risk factor for poor prognosis of COVID-19 (HR=5.695, 95%CI : 2.363~13.725, P < 0.001). Conclusion Low blood calcium level is an independent risk factor for poor prognosis in COVID-19 patients. Correction for hypocalcemia may be an important strategy to improve the prognosis of COVID-19 patients.

Background: Acute mountain sickness (AMS) may cause life-threatening conditions. This study aimed to screen echocardiographic parameters at sea level (SL) to identify predictors of AMS development. Methods: Overall, 106 healthy men were recruited at SL and ascended to 4100 m within 7 days by bus. Basic characteristics, physiological data, and echocardiographic parameters were collected both at SL and 4100 m above SL. AMS was identified by 2018 Lake Louise Questionnaire Score. Results: After acute high altitude exposure (AHAE), 33 subjects were diagnosed with AMS and exhibited lower lateral mitral valve tissue motion annular displacement (MV TMADlateral) at SL than AMS-free subjects (13.09 vs. 13.89 mm, p = 0.022). MV TMADlateral at SL was significantly correlated with AMS occurrence (OR = 0.717, 95% CI: 0.534-0.964, p = 0.028). The MV TMADlateral<13.30-mm group showed over 4-fold risk for AMS development versus the MV TMADlateral >= 13.30-mm group. After AHAE, the MV TMADlateral<13.30-mm group had increased HR (64 vs. 74 bpm, p = 0.001) and right-ventricular myocardial performance index (0.54 vs. 0.69, p = 0.009) and decreased left ventricular global longitudinal strain (-21.50 vs. -20.23%, p = 0.002), tricuspid valve E/A ratio (2.11 vs. 1.89, p = 0.019), and MV E-wave deceleration time (169.60 vs. 156.90 ms, p = 0.035). Conclusion: MV TMADlateral at SL was a potential predictor of AMS occurrence and might be associated with differential alterations of ventricular systolic and diastolic functions in subjects with different MV TMADlateral levels at SL after AHAE.

Introduction Pulmonary artery pressure (PAP) is increased and right ventricular (RV) function is well preserved in healthy subjects upon exposure to high altitude (HA). An increase in PAP may trigger notching of the right ventricular outflow tract Doppler flow velocity envelope (RVOT notch), which is associated with impaired RV function in patients with pulmonary hypertension. However, whether HA exposure can induce RVOT notch formation and the subsequent impact on cardiac function in healthy subjects remains unclear. Methods A total of 99 subjects (69 males and 30 females) with a median age of 25 years were enrolled in this study; they traveled from 500 to 4100 m by bus over a 2-day period. All subjects underwent a comprehensive physiological and echocardiographic examination 1 day before ascension at low altitude and 15 ± 3 h after arrival at HA. The RVOT notch was determined by the presence of a notched shape in the RVOT Doppler flow velocity envelope. The systolic PAP (SPAP) was calculated as Bernoulli equation SPAP = 4 × (maximum tricuspid regurgitation velocity)2+5 and mean PAP (mPAP) = 0.61 × SPAP+2. Cardiac output was calculated as stroke volume × heart rate. Pulmonary capillary wedge pressure (PCWP) was calculated as 1.9+1.24 × mitral E/e’. Pulmonary vascular resistance (PVR) was calculated as (mPAP-PCWP)/CO. Results After HA exposure, 20 (20.2%) subjects had an RVOT notch [notch (+)], and 79 (79.8%) subjects did not have an RVOT notch [notch (−)]. In the multivariate logistic regression analysis, the SPAP, right ventricular global longitude strain (RV GLS), and tricuspid E/A were independently associated with the RVOT notch. The SPAP, mPAP, PVR, standard deviations of the times to peak systolic strain in the four mid-basal RV segments (RVSD4), peak velocity of the isovolumic contraction period (ICV), and the peak systolic velocity (s’) at the mitral/tricuspid annulus were increased in all subjects. Conversely, the pulse oxygen saturation (SpO2), RV GLS, and tricuspid annulus plane systolic excursion (TAPSE)/SPAP were decreased. However, the increases of SPAP, mPAP, PVR, and RVSD4 and the decreases of SpO2, RV GLS, and TAPSE/SPAP were more pronounced in the notch (+) group than in the notch (−) group. Additionally, increased tricuspid ICV and mitral/tricuspid s’ were found only in the notch (−) group. Conclusion HA exposure-induced RVOT notch formation is associated with impaired RV function, including no increase in the tricuspid ICV or s’, reduction of RV deformation, deterioration in RV-pulmonary artery coupling, and RV intraventricular synchrony.

Male novel coronavirus disease (COVID-19) patients tend to have poorer clinical outcomes than female patients, while the myocardial injury is strongly associated with COVID-19-related adverse events. Owing to a lack of corresponding data, we aimed to investigate the sex differences in the incidence of myocardial injury in COVID-19 patients and to identify the potential underlying mechanisms, which may partly account for the sex bias in the incidence of adverse events. This retrospective study included 1,157 COVID-19 patients who were hospitalized in Huoshenshan Hospital from 12 March 2020 to 11 April 2020. Data on the patients’ demographic characteristics, initial symptoms, comorbidities and laboratory tests were collected. Totally, 571 (49.4%) female and 586 (50.6%) male COVID-19 patients were enrolled. The incidence of myocardial injury was higher among men than women (9.2 vs. 4.9%, p = 0.004). In the logistic regression analysis, age, and chronic kidney disease were associated with myocardial injury in both sexes. However, hypertension [odds ratio (OR) = 2.25, 95% confidence interval (CI) 1.20–4.22], coronary artery disease (OR = 2.46, 95% CI 1.14–5.34), leucocyte counts (OR = 3.13, 95% CI 1.24–7.86), hs-CRP (OR = 4.45, 95% CI 1.33–14.83), and D-dimer [OR = 3.93 (1.27–12.19), 95% CI 1.27–12.19] were independent risk factors only in the men. The correlations of hs-CRP and D-dimer with hs-cTnI and BNP were stronger in the men. The incidence of myocardial injury in COVID-19 patients is sex-dependent, predominantly in association with a greater degree of inflammation and coagulation disorders in men. Our findings can be used to improve the quality of clinical management in such settings.

Background and Aim Tricuspid regurgitation (TR) is a frequent complication in various cardiovascular diseases. However, few studies have reported the prevalence of TR especially the moderate to severe or significant TR (ms-TR) maintenance dialysis patients. Thus, we aimed to identify the prevalence of ms-TR and its associated factors. Methods A total of 491 maintenance dialysis patients underwent echocardiographic examinations, while a subgroup (n = 283) also received routine blood tests, renal function examinations, and electrolyte analysis. We first compared the differences in abovementioned parameters among groups with various TR areas (TRAs). Finally, univariate and adjusted regression were also used to identify factors that were independently associated with ms-TR. Results The incidence of TR jets was 62.6%, which included a mildly increased TRA (47.8%), moderately increased TRA (10.4%), and severely increased TRA (3.5%). Most of the cardiac structures and functional parameters, such as the end-diastolic internal diameters of the left atrium (LA), left ventricle (LVDD), right atrium (RA), right ventricle (RV), left ventricular ejection fraction (LVEF), and fractional shortening (FS), were significantly associated with ms-TR. Among serum ions, only total CO2 (TCO2; r = -0.141, p = 0.047) was negatively correlated with TRA. After adjusted, only Na+ [odds ratio (OR): 0.871 0.888, p = 0.048], RA (OR: 1.370, p < 0.001), and FS (OR: 0.887, p < 0.001) were independently associated with ms-TR. Conclusion Tricuspid regurgitation occurs in maintenance hemodialysis patients with ESRD. Na+ FS and RA were independently associated with ms-TR, and these parameters may be potential risk factors/predictors for ms-TR.

Aim: To determine the prevalence of pulmonary hypertension (PH) and its associated factors among end-stage renal disease (ESRD) patients who underwent maintenance dialysis. Methods: A total of 491 patients received echocardiography examinations and underwent pulmonary artery systolic pressure (PASP) assessments. A subgroup of 283 patients were subjected to plasma creatinine (Cr) and blood urea nitrogen concentration (BUN) tests, routine blood examinations and electrolyte analysis. First, we compared the differences in echocardiographic, Cr and BUN, blood routine and electrolyte parameters between PH and non-PH groups. The correlations between PASP and the parameters mentioned above were also analyzed. Furthermore, univariate and adjusted logistic regression analyses were performed to identify the independent associated factors. Results: The incidence of PH among ESRD patients who were treated with maintenance dialysis was 34.6%. Most of the echocardiographic parameters, including end-diastolic internal diameters of the left atrium, left ventricle, right atrium, and pulmonary artery, as well as interventricular septum mobility, left ventricular posterior wall mobility, fractional shortening, stroke volume and left ventricle ejection fraction (LVEF), were associated with PH. Furthermore, Mg 2+ ( p = 0.037) and Cl − ( p = 0.043) were significantly associated with PASP. However, after adjustments were made in the regression analysis, only internal diameters of the left atrium, right atrium, and LVEF were independently associated with PH. Conclusion: PH is prevalent, with a relatively high incidence among ESRD patients who undergo maintenance dialysis. The sizes of the left and right atria as well as LVEF were independently associated with PH, but further cohort and basic mechanistic studies are needed to confirm this finding.

Objective: this study aimed to explore the impacts of myocardial injury on the clinical severity and outcomes in patients with Coronavirus Disease 2019 (COVID-19). Methods: we analyzed the electronic medical records of 1646 COVID-19 inpatients in Wuhan Huoshenshan Hospital. Results: 327 (19.9%) developed into severe cases, 23 (1.4%) died. In comparison to common cases, severe cases showed older age, more comorbidities, abnormal immune responses, as well as liver, renal, cardiac and coagulation disorders. Multivariable logistic regression identified that older age , combining with arrhythmia, abnormal lymphocyte percentage, elevated hypersensitive C reactive protein (hs-CRP) and myocardial injury were the independent risk factors for the incidence of severe cases. Moreover, Kaplan-Meier survival analysis showed that patients with myocardial injury had increasing risks of mortality, incidence of severe cases, acute respiratory distress syndrome (ARDS), and intensive care unit (ICU) admission. Particularly, myocardial injury patients co-existed with any other risk factor further deteriorated the clinical outcomes. Conclusion: The presence of myocardial injury and its co-existing with older age, arrhythmia, abnormal lymphocyte percentage, or elevated hs-CRP were greatly associated with the incidence of severe patients and poor clinical outcomes.

Background: Travelling to high altitude (HA) presents a risk of the high levels of pulmonary artery pressure (PAP) at altitude, which is associated with impaired exercise capacity and fatal HA pulmonary oedema. However, prediction of high levels of PAP at altitude is still unclear. Methods: Echocardiography and pulmonary function tests were performed on 121 healthy men at low altitude (LA) and 4100 m (5 +/- 2 h after a 7 day ascent). Results: HA exposure increased the levels of FEV1/FVC ratio, FEF25%, 50%, 75%, MMEF, mPAP, total pulmonary vascular resistance (PVR) and systolic pulmonary arterial pressure (SPAP). More smokers and lower forced expiratory flow at 25% of forced vital capacity (FEF25%) at LA were observed in subjects with mPAP >= 30 mmHg than those with mPAP<30 mmHg at HA. Multivariate logistic regression identified that FEF25% at LA [odds ratio (OR) 0.50, 95%CI 0.33-0.76, p = 0.001] and smoking (OR 3.09, 95%CI 1.31-7.27, p = 0.010) were the independent predictors for identifying subjects with mPAP >= 30 mmHg at HA. Moreover, FEF25% at LA was linearly correlated with mPAP at HA (r = -0.31, p < 0.001), which mainly existed in smokers. Compared to subjects with FEF25% >= 7.55 L/sec at LA, those with FEF25% <7.55 L/sec at LA showed higher levels of mPAP, and total PVR, and a multivariable OR of 11.16 (95%CI, 3.48-35.81) for developing mPAP >= 30 mmHg at HA. However, there was no significant difference in the incidences of AMS and its related clinical symptoms in subjects with different levels of FEF25%. Conclusions: Thus, these findings suggest that subjects with low FEF25% values at LA are susceptible to high levels of PAP at altitude but not the incidence of AMS following short-term HA exposure, especially in smokers.

The aims of this study were to explore the effect of high-altitude (HA) exposure on the incidence, determinants, and impacts of right ventricular dyssynchrony (RVD). In our study, 108 healthy young men were enrolled, and physiological and echocardiographic variables were recorded at both sea level and 4,100 m. By using two-dimensional speckle-tracking echocardiography, RVD was evaluated by calculating the R-R interval-corrected standard deviation of the time-to-peak systolic strain for the four mid-basal RV segments (RVSD4) and defined by RVSD4 > 18.7 ms. After HA exposure, RVSD4 was significantly increased, and the incidence of RVD was approximately 32.4%. Subjects with RVD showed lower oxygen saturation (SaO(2)) and RV global longitudinal strain and higher systolic pulmonary artery pressure than those without RVD. Moreover, myocardial acceleration during isovolumic contraction was increased in all subjects and those without RVD, but not in those with RVD. Multivariate logistic regression revealed that SaO(2)is an independent determinant of RVD at HA (odds ratio: 0.72, 95% CI: 0.56-0.92;P= 0.009). However, the mean pulmonary artery pressure was linearly correlated with the magnitude of RVD in the presence of Notch. No changes were found in RV fractional area change, tricuspid annular motion, or tricuspids' velocity between subjects with and without RVD. Collectively, we demonstrated for the first time that HA exposure could induce RVD in healthy subjects, which may be mainly attributed to the decline in SaO(2)as well as RV overload; the incidence of RVD was associated with reduced RV regional function and blunted myocardial acceleration.