Chest X-ray features facilitate screening for pulmonary hypertension caused by fibrosing mediastinitis.

Background: Misdiagnosis and underdiagnosis of pulmonary hypertension caused by fibrosing mediastinitis (PH-FM) are considerably prevalent due to unspecific symptoms and as well as the lack of awareness of this fatal disease. Objectives: The aim of this study was to evaluate the diagnostic accuracy of the chest X-ray (CXR) for screening the patients with PH-FM from those with pulmonary hypertension (PH). Design: This was a retrospective observational cohort study. Methods: The patients with suspected PH were recruited between October 2014 and October 2020. All the clinical data and CXR findings were collected. The sensitivity, specificity, and likelihood ratio of the CXR features were calculated. Logistic regression was used to identify the factors associated with the CXR characteristics and FM and to generate a prediction model. Finally, the diagnostic efficiency of the prediction model was evaluated using nomogram and internal validation. Results: The patients with PH-FM (n = 36) and PH caused by the diseases other than FM (PH-non-FM, n = 62) were enrolled. The CXR features, including atelectasis, pleural effusion, consolidation, nodules, calcification, interlobular septal thickening, and interstitial reticulation, were more prevalent in patients with PH-FM than in those with PH-non-FM (all p < 0.05). Atelectasis had a specificity of 97%, a sensitivity of 50%, and a greater accuracy for diagnosing of PH-FM [area under the curve (AUC) = 0.720; 95% CI: 0.634-0.806] than the other factors did. The combination of tuberculosis, natural logarithmic NT-proBNP (lnBNP), atelectasis, pleural effusion, and prominent right heart border constituted a prediction model to distinguish the PH-FM from the PH-non-FM, with a sensitivity of 91.7% and a specificity of 83.9%. The model demonstrated good prediction performance by showing an AUC of 0.922 (95% CI: 0.861-0.983) in the internal validation. Conclusion: In this study, atelectasis was the most specific and accurate CXR characteristic for identifying PH-FM in the PH patients. The combination of atelectasis, pleural effusion, prominent right heart border, tuberculosis, and lnBNP constituted a prediction model that distinguished the PH-FM patients from the PH-non-FM ones with good performance.

Pulmonary Hypertension Caused by Fibrosing Mediastinitis.

Pulmonary hypertension (PH) is a progressive and severe disorder in pulmonary hemodynamics. PH can be fatal if not well managed. Fibrosing mediastinitis (FM) is a rare and benign fibroproliferative disease in the mediastinum, which may lead to pulmonary vessel compression and PH. PH caused by FM (PH-FM) is a pathologic condition belonging to group 5 in the World Health Organization PH classification. PH-FM has a poor prognosis because of a lack of effective therapeutic modalities and inappropriate diagnosis. With the development of percutaneous pulmonary vascular interventional therapy, the prognosis of PH-FM has been greatly improved in recent years. This article provides a comprehensive review on the epidemiology, pathophysiologic characteristics, clinical manifestations, diagnostic approaches, and treatment modalities of PH-FM based on data from published reports and our medical center with the goal of facilitating the diagnosis and treatment of this fatal disease.

Neuroprotective Effects of Long-Term Metformin Preconditioning on Rats with Ischemic Brain Injuries.

INTRODUCTION: This study is to analyze the neuroprotective effects of long-term metformin (Met) preconditioning on rats with ischemic brain injuries and the related mechanisms. METHODS: Twenty-five Sprague-Dawley rats were randomly divided into 5 groups: sham group, middle cerebral artery occlusion (MCAO) group, normal saline + MCAO group, pre- Met + MCAO group, and 3-MA + Met + MCAO group. Pathological changes of brain were observed by hematoxylin-eosin staining. Neurobehavior scores were calculated. Infarct area was assessed by 2,3,5-triphenyltetrazolium chloride staining. Apoptosis of neurons was detected by TdT-mediated dUTP Nick-End Labeling (TUNEL). Western blot tested the expression of LC3 (microtubule-associated protein 1 light chain 3), Beclin-1, adenosine 5'-monophosphate ([AMP]-activated protein kinase [AMPK]), and p-AMPK in hippocampal CA1 region. RESULTS: Compared with the sham group, the MCAO group induced severe pathological changes in the brain. The neurobehavior scores and infarct area in the brain were increased in the MCAO group than in the sham group. The apoptosis level in the MCAO group was also higher than in the sham group. However, after pretreatment with Met, the pathological changes in the brain were attenuated. Compared with the MCAO group, the pre-Met + MCAO group also had decreased neurobehavior scores and infarct area in the brain. Additionally, the apoptosis level in the pre-Met + MCAO group was lower than in the MCAO group. Moreover, the MCAO group had increased levels of LC3 and Beclin-1 than in the sham group. In the pre-Met + MCAO group, their levels were decreased than in the MCAO group. The p-AMPK level in the pre-Met + MCAO group was also increased than in the MCAO group, suggesting activation of p-AMPK by Met. CONCLUSION: Long-term Met pretreatment has neuroprotective effect on ischemic brain injury, which may be related to the regulation of autophagy-related protein expression and apoptosis.

Prognostic implications of ST-segment elevation in lead aVR in patients with acute coronary syndrome: A meta-analysis.

BACKGROUND: ST-segment elevation (STE) in lead aVR is a useful tool in recognizing patients with left main or left anterior descending coronary obstruction during acute coronary syndrome (ACS). The prognostic implication of STE in lead aVR on outcomes has not been established. METHODS: We performed a systematic search for clinical studies about STE in lead aVR in four databases including PubMed, EMBASE, Cochrane Library, and Web of Science. Primary outcome was in-hospital mortality. Secondary outcomes included in-hospital (re)infarction, in-hospital heart failure, and 90-day mortality. RESULTS: We included 7 studies with a total of 7,700 patients. The all-cause in-hospital mortality of patients with STE in lead aVR during ACS was significantly higher than that of patients without STE (OR: 4.37, 95% CI 1.63 to 11.68, p = .003). Patients with greater STE (>0.1 mV) in lead aVR had a higher in-hospital mortality when compared to lower STE (0.05-0.1 mV) (OR: 2.00, 95% CI 1.11-3.60, p = .02), However, STE in aVR was not independently associated with in-hospital mortality in ACS patients (OR: 2.72, 95% CI 0.85-8.63, p = .09). The incidence of in-hospital myocardial (re)infarction (OR: 2.77, 95% CI 1.30-5.94, p = .009), in-hospital heart failure (OR: 2.62, 95% CI 1.06-6.50, p = .04), and 90-day mortality (OR: 10.19, 95% CI 5.27-19.71, p < .00001) was also noted to be higher in patients STE in lead aVR. CONCLUSIONS: This contemporary meta-analysis shows STE in lead aVR is a poor prognostic marker in patients with ACS with higher in-hospital mortality, reinfarction, heart failure and 90-day mortality. Greater magnitude of STE portends worse prognosis. Further studies are needed to establish an independent predictive role of STE in aVR for these adverse outcomes.

A rare case of severe right heart failure due to pulmonary artery lymphomatoid granulomatosis.

Lymphomatoid granulomatosis is a rare, vascular-centric, and vessel-destroying lymphoproliferative disease that hardly involves the pulmonary arteries. Herein, we report a case with severe right heart failure and pulmonary arterial stenosis caused by pulmonary artery lymphomatoid granulomatosis. This case was diagnosed by percutaneous transluminal pulmonary artery biopsy and was effectively treated with stent implantation and steroid administration.

Meta-analysis of right ventricular function in patients with aortic stenosis after transfemoral aortic valve replacement or surgical aortic valve replacement.

BACKGROUND: Right ventricular function (RVF) is an independent predictor of prognosis for patients undergoing aortic valve replacement: transcatheter aortic valve replacement (TAVR) or surgical aortic valve replacement (SAVR). The effect of transfemoral aortic valve replacement (TF-TAVR) on RVF is uncertain. We aimed to perform a meta-analysis of the effect of TF-TAVR on RVF in patients with aortic stenosis (AS) and compare the effect of TF-TAVR with SAVR. METHODS: We searched relevant studies from PubMed, Embase, Cochrane Library databases, and Web of Science. Furthermore, two reviewers (Wang AQ and Cao YS) extracted all relevant data, which were then double checked by another two reviewers (Zhang M and Qi GM). We used the forest plot to present results. Tricuspid annular plane systolic excursion (TAPSE) was the primary outcome. RESULTS: This meta-analysis included 11 studies. There were 353 patients who underwent TF-TAVR, and 358 patients who were subjected to SAVR. There was no significant difference in TAPSE at 1 week and 6 months as well as right ventricular ejection fraction (RVEF) at <2 weeks and 6 months after TF-TAVR. For the SAVR group, TAPSE at 1 week and 3 months as well as fractional area change (FAC) at 3 months post procedure were significantly aggravated, while RVEF did not change significantly. Moreover, TAPSE post-TF-TAVR was significantly improved as compared with post-SAVR. The △TAPSE, the difference between TAPSE post-procedure and TAPSE prior to procedure, was also significantly better in the TF-TAVR group than in the SAVR group. CONCLUSION: RVF was maintained post TF-TAVR. For SAVR, discrepancy in the measured parameters exists, as reduced TAPSE indicates compromised longitudinal RVF, while insignificant changes in RVEF implicate maintained RVF post procedure. Collectively, our study suggests that the baseline RV dysfunction and the effect of TF-TAVR versus SAVR on longitudinal RVF may influence the selection of aortic valve intervention.

Acute myocardial infarction and transient elevated anticardiolipin antibody in a young adult with possible familial hypercholesterolemia: a case report : Anticardiolipin antibody and myocardial infarction.

BACKGROUND: Familial hypercholesterolemia (FH) can lead to premature coronary heart disease. Anticardiolipin antibody may be a contributor for thrombosis. Here, we report an adult with possible FH suffered from premature myocardial infarction that may be triggered by transient increased anticardiolipin antibody. CASE PRESENTATION: A 29-year-old male had presented with a history of 2-h chest pain and numbness of left upper arm before 5 days. The electrocardiogram (ECG) had demonstrated inferior wall myocardial infarction (MI). Five days later he was admitted to our hospital and diagnosed as acute MI and possible FH (premature coronary heart disease, low density lipoprotein cholesterol of 5.90 mmol/L) with increased anticardiolipin antibody (up to 120 RU/ml). Other auto-antibodies including ß2-glicoprotein antibodies IgM, IgA, IgG, lupus anticoagulant (LA), antinuclear antibodies, anti-myocardial antibody were normal. Coronary artery angiography (CAG) showed right coronary artery was total occlusion from the middle segment. Then he underwent percutaneous coronary intervention with a stent. Four days later, he was discharged with complete recovery. CAG showed intra-stent restenosis and anticardiolipin antibody level was normal and the patient had no any symptoms at 6-month follow-up. CONCLUSIONS: Transient elevated anticardiolipin antibody may be a trigger or biomarker of cardiac thrombotic events in younger atherosclerotic patients.

Autologous bone marrow stem cell therapy for patients undergoing coronary artery bypass grafting: A meta-analysis of 14 randomized controlled trials.

Autologous bone marrow stem cell (BMSC) therapy is a novel option for regenerative therapy in patients with ischemic heart disease. The aim of the present meta-analysis was to evaluate the effectiveness of BMSCs combined with coronary artery bypass grafting (CABG). The PubMed, Cochrane Library, EMBASE and Web of Science databases were searched from inception to November 22, 2017 for randomized controlled trials on BMSC therapy combined with CABG. Finally, 14 trials with a total of 596 participants were included. Data were analyzed using a random-effects model. Compared with the control group, the BMSC therapy group exhibited an improvement in the left ventricular (LV) ejection fraction from baseline to follow-up [mean difference (MD)=4.36%; 95% confidence interval (CI): 1.90-6.81%; P<0.01]. Analysis of the pooled results revealed non-significant differences in the LV end-diastolic volume (MD=-6.27 ml; 95% CI: -22.34 to 9.80 ml; P=0.44), LV end-diastolic volume index (MD=-15.11 ml/m2; 95% CI: -31.53 to 1.30 ml/m2; P=0.07), LV end-systolic volume (MD=-11.52 ml; 95% CI: -26.97 to 3.93 ml; P=0.14) and LV end-systolic volume index (MD=-16.56 ml/m2; 95% CI: -37.75 to 4.63 ml/m2; P=0.13) between the BMSC and CABG alone groups. Therefore, autologous BMSC therapy for patients undergoing CABG appears to be associated with an improvement in LV function compared with CABG alone.

Prognostic value of serum proadrenomedullin in catheter-related bloodstream infection in the intensive care unit: A prospective observational study.

Patients with catheter-related bloodstream infection (CRBSI) have a poor prognosis. Proadrenomedullin (pro-ADM) has emerged as a valuable marker of sepsis. The potential role of pro-ADM in predicting the prognosis of CRBSI was evaluated. We enrolled 25 CRBSI patients and pro-ADM level was measured within 24 hours after each admission. Survival was assessed after 28 days. Among 25 patients with CRBSI, 14 patients survived. Pro-ADM in survivors was significantly lower than that in non-survivors (3.71 ±â€Š1.30 vs 5.58 ±â€Š1.18 nmol/L). The area under the curve (AUC) for pro-ADM was 0.87 (95% CI 0.68-0.97) with a cut-off value of 4.67 nmol/L, providing sensitivity of 85.7% and specificity of 81.8%. The AUCs for PCT, WBC, and CRP were 0.76 (95% CI 0.55-0.90), 0.72 (95% CI 0.50-0.88), and 0.69 (95% CI 0.48-0.86), respectively. Kaplan-Meier survival curves showed pro-ADM ≥ 4.67 nmol/L was associated with higher mortality (log-rank p = 0.001). Moreover, the pro-ADM level was significantly higher in patients with septic shock than those without shock (5.44 ±â€Š1.17 vs 3.54 ±â€Š1.18nmol/L). The mortality of patients with septic shock was higher than that of patients without shock (69.2% vs 16.7%, P = .008). In conclusion, pro-ADM could be used as a prognostic marker of CRBSI in critically ill patients.

Trimedazidine alleviates pulmonary artery banding-induced acute right heart dysfunction and activates PRAS40 in rats.

The molecular mechanism underlying acute right heart failure (RHF) is poorly understood. We used pulmonary artery banding (PAB) to induce acute RHF characterized by a rapid rise of right ventricular pressure, and then a decrease in right ventricular pressure along with a decrease in blood pressure right after banding. We found higher brain natriuretic peptide (BNP) and beta-myosin heavy chain (ßMHC) levels and lower alpha-myosin heavy chain (αMHC) levels in RHF rats than sham-operated rats. Hemodynamic indexes in rats with acute RHF were slightly improved by trimedazidine TMZ, a key inhibitor of fatty acid (FA) oxidation. TMZ also reversed downregulation of peroxisome proliferator-activated receptor gamma coactivator 1-beta (PGC-1ß) and peroxisome proliferator-activated receptor alpha (PPARα) by PAB and up-regulates peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), peroxisome proliferator-activated receptor delta (PPARδ) and pyruvate dehydrogenase kinase isoform 4 (PDK4). In addition, TMZ reversed upregulation of phosphorylated Akt by PAB and increased phosphorylated proline-rich Akt-substrate 40 (PRAS40). Autophagy and apoptosis were not modified by PAB or TMZ. An acute RHF model was established in rats through 70% constriction of the pulmonary artery. TMZ treatment alleviated PAB-induced acute RHF by activating PRAS40 and upregulatingPGC-1α, PGC-1ß, PPARα, PPARδ, and PDK4.

A female patient with hypokalaemia-induced J wave syndrome: An unusual case report.

RATIONALE: Prominent J waves can be seen in life-threatening cardiac arrhythmias such as Brugada syndrome, early repolarization syndrome, and ventricular fibrillation. We herein present an unusual case report of hypokalemia-induced J wave syndrome and ST (a part of ECG) segment elevation. PATIENTS CONCERNS: A 52-year-old woman with chief complaints of chest pain for 2 hours and diarrhea showed a marked hypokalemia (2.8 mmol/L) and slightly elevated creatine kinase-MB (CK-MB) (57.5 U/L). The electrocardiographic (ECG) recording was normal upon admission and computed tomography (CT) aorta angiography excluded an aorta dissection. ECG done 17 hours after admission showed ST segment elevation and elevated J wave in leads II, III and aVF, and fusion of T and U wave in all leads. DIAGNOSIS: We first thought that the diagnosis of this patient was acute myocardial syndrome. INTERVENTION: Potassium chloride and oflocaxin treatment was given to the patient. OUTCOMES: Laboratory test showed the level of serum potassium ion increased to 3.4 mmol/L and CK-MB did not have any significant change. The infusion of potassium chloride-induced disappearance of the elevated J wave, although QT (a part of ECG) intervals were still longer than that upon admission. LESSONS: This case tells us that hypokalaemia might induce J wave and elevated ST segments which should be distinguished from acute myocardial syndrome.