The present study highlights the effects of salvianolic acid B (Sal B) on angiotensin II (Ang II)–activated atrial fibroblasts as well as the associated potential mechanism from the metabonomics perspective. Metabolic profile analysis performed an optimal separation of the Ang II and control group, indicating a recovery impact of Sal B on Ang II–activated fibroblasts (FBs). We found that metabolite levels in the Ang II + Sal B group were reversed to normal. Moreover, 23 significant metabolites were identified. Metabolic network analysis indicated that these metabolites participated in purine metabolism and FoxO signaling pathway. We found that Sal B activated AMP-activated protein kinase (AMPK) phosphorylation, which further promoted FoxO1 activation and increased miR-148a-3p level. We further verified that Sal B modulate the abnormal AMP, phosphocreatine, glutathione (GSH), and reactive oxygen species (ROS) production in Ang II–stimulated FBs. Collectively, Sal B can protect the Ang II–activated FBs from fibrosis and oxidative stress via AMPK/FoxO1/miRNA-148a-3p axis. Graphical abstract

Background Pharmacologic challenge test is often used to diagnose Brugada syndrome (BrS) when spontaneous ECGs do not show type I Brugada pattern but reported sensitivity varies. The role of exercise stress test in diagnosing Brugada syndrome is not well-established. Case Summary A patient had a type I Brugada pattern ECG during the recovery phase of exercise stress test but had a negative procainamide challenge test. He had a loop recorder implanted and later survived a ventricular fibrillation (VF) arrest provoked by COVID-19. ECG on arrival showed type 1 Brugada pattern. He was discharged after implantable cardioverter-defibrillator (ICD) implantation. He later underwent genetic testing and was found to be heterozygous for c.844C>G (p.Arg282Gly) mutation in the SCN5A gene. Discussion Type 1 Brugada pattern ECG may be unmasked by ST segment augmentation during recovery from exercise. Exercise stress test may play a role in diagnosis of Brugada syndrome when suspicion for Brugada syndrome remains after a negative procainamide challenge test or if the patient has exercise related symptoms. COVID-19 can unmask BrS and trigger a VF cardiac arrest.

Background In-hospital cardiac arrest (IHCA) carries a high mortality and significant morbidity in survivors. Gastrointestinal bleeding (GIB) can complicate cardiac arrests. We aim to study the association between GIB and the in-hospital outcomes of patients with IHCA. Methods and results The National Inpatient Sample 2016–2018 databases were used. IHCA were identified using ICD-10-PCS code for cardiopulmonary resuscitation. Other diagnoses including GIB were identified using ICD-10-CM codes. Multivariate logistic regression was used to study the effect of GIB on in-hospital mortality. Gamma regression with log link was used to determine the effect of GIB on length of stay and cost of admission. In patients with IHCA, GIB as a secondary diagnosis is associated with an increased in hospital mortality (unadjusted 74.2% vs 68.3%, adjusted OR 1.17, 95% confidence interval [CI] 1.09–1.25, p < 0.001), longer length of stay (unadjusted median 16 vs 10 days, IQR 9–27 vs 5–17 days, exponentiated coefficient 1.45, 95% CI 1.36–1.54, p < 0.001 for survivors; unadjusted median 4 vs 3 days, IQR 1–10 vs 1–7 days, exponentiated coefficient 1.27, 95% CI 1.22–1.34, p < 0.001 for patients who died in hospital), and higher cost for hospital stay (unadjusted median $226065 vs $151459, IQR $117551–434003 vs $76197–287846, exponentiated coefficient 1.40, 95% CI 1.32–1.49, p < 0.001 for survivors; unadjusted median $87996 vs $77056, IQR $42566–186677 vs $34066–149009, exponentiated coefficient 1.26, 95% CI 1.20–1.32, p < 0.001 for patients who died in hospital) adjusted for baseline characteristics and other comorbidities. Conclusions In patients with IHCA, GIB as a secondary diagnosis is associated with a higher in-hospital mortality, longer length of stay and higher cost for the admission.

Introduction Influenza causes significant morbidity and mortality annually in the United States (US) and people with chronic medical conditions are thought to be at higher risk for severe disease and death. Infection is a leading cause of death for patients with end-stage kidney disease (ESKD). We used a national-level inpatient database to study the trend of influenza hospitalizations and in-hospital mortality for patients without and with ESKD. Methods The National Inpatient Sample (NIS) 2010-2019 was used. A primary diagnosis of influenza was identified using ICD-9-CM (487.X, 488.X) and ICD-10-CM codes (J09.X, J10.X, J11.X). ESKD was identified using a validated algorithm identifying patients with a diagnosis of ESKD or procedure code for dialysis and excluding patients with a diagnosis of acute kidney injury. Other diagnoses and procedures were identified using validated algorithms based on ICD-9-CM, ICD-10-CM, and ICD-10-PCS codes. Discharge-level weights were used to estimate the total number of admissions in the NIS universe. Weighted multivariable logistic regression was performed to study the association between ESKD and in-hospital death. Results 131,942 admissions with a primary diagnosis of influenza with 4,647 admissions for ESKD patients among them were included in our analysis. Admissions varied by influenza season and ESKD patients accounted for 2.91% to 3.65% of all influenza admissions each season. 2,081 influenza patients (1.58%) died in the hospital and 115 patients with influenza and ESKD (2.47%) died in the hospital. Age-adjusted in-hospital mortality varied from season to season but was consistently higher in ESKD patients (2.25% vs 1.38%). ESKD was a risk factor for in-hospital death (OR 1.26, 95% CI 1.15-1.38) after adjusting for age, gender, primary payer, heart failure, chronic lung disease, obesity, drug abuse, immunocompromised status, bacterial pneumonia, the Charlson Comorbidity Index, and the influenza season. Conclusion ESKD patients accounted for a significant proportion of influenza hospitalizations in the US from 2010-11 to the 2018-19 influenza season. Among people hospitalized primarily for influenza, age-adjusted in-hospital mortality varied from season to season and was consistently higher in ESKD patients. For people hospitalized primarily for influenza, ESKD was an independent risk factor for in-hospital death.

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Extrapulmonary vein focal sources have been recognized as the source of atrial fibrillation in some cases, and empiric electric isolation of the left atrial appendage has been proposed for long-standing persistent atrial fibrillation by some. Here, we present a case of redo ablation of long-standing persistent atrial fibrillation in which the left atrial appendage played a key role in maintaining AF during ablation, and atrial fibrillation was terminated by electrical isolation of the LAA. During the ablation, a rare phenomenon of half of the atria in atrial fibrillation while the other half of the atria in atrial flutter was seen.

Despite advances in medical therapy, patients with Sickle Cell Disease (SCD) continue to die prematurely, especially from cardiopulmonary disease. Despite the potential for SCD to cause cardiac arrest and sudden cardiac death, few studies have examined this association. Here we study the SCD patients who developed in-hospital cardiac arrest (IHCA) to better characterize this patient population.METHODS: National Inpatient Sample 2016-2018 was queried using ICD-10-PCS codes for cardiopulmonary resuscitation to identify the patients with cardiac arrest. Sickle cell disease, shockable arrest rhythm, and associated comorbidities were identified. Logistic regression was used to adjust for possible confounding variables such as age, gender, race, socioeconomic status (median household income), arrest rhythm, and individual groups of the Charlson Comorbidity Index (CCI). RESULTS:We identified a total of 71002 cardiac arrest hospitalizations from 2016 to 2018. Among them 132 had SCD. SCD patients are younger (median age 41 vs 67, interquartile range [IQR] 29-54 vs 55-77 years, p <0.01), and are more likely to be in the lowest income quartile (52.3% vs 34.5%, p < 0.01). SCD patients have higher mortality (Odds ratio 2.74, p<0.0001). There is a trend towards a lower percentage of shockable arrest rhythm (18.9% vs 26.6%, p¼0.58). They have fewer co-morbidities (median CCI 1 vs 2, IQR 0-2 vs 1-4, p<0.01) and are less likely to have a diagnosis of myocardial infarction (13.6% vs 27.4%, p<0.01), stroke (5.3% vs 14.3%, p<0.01), or cancer (2.3% vs 10.0%, p<0.01).CONCLUSIONS: SCD patients who developed IHCA were younger, have lesser co-morbidities, more likely to have a lower income, and have higher mortality.CLINICAL IMPLICATIONS: It is important for the physicians to recognize that SCD patients can develop cardiac arrest despite the absence of traditional risk factors. Identifying this group early in the disease course is vital to prevent premature cardiac deaths.

Mechanical ventilation (MV) is known to be an independent risk factor of venous thromboembolism (VTE). Together with other thrombosis risk factors, VTE can lead to unfavorable outcomes. We seek to investigate the outcomes of Hereditary thrombophilia (HT) in patients required mechanical ventilation (MV), which is relatively unknown. METHODS:This was a retrospective study of MV-associated adult (age at least 18-year-old) hospitalizations from the 2016-2018 National Inpatient Sample. International Classification of Diseases 10 th Revision was used to identify MV, HT, VTE, and other conditions. Comorbidities were evaluated with Charlson Comorbidity Index (CCI). Continuous variables were compared using Welch two sample T-test. Categorical variables were analyzed with Pearson's Chi-squared test. The possible associated variables and confounders were adjusted with the generalized linear model.RESULTS: There were 616,717 adult MV hospitalizations identified. 5,024 cases had at least one HT diagnosis. The patients with HT were significantly younger (mean age 59.4 vs 61.7, p value <10-15 ). Female and Caucasian ratio were higher in the HT group (46.7% vs 44.5%, p value <0.002; 66.0% vs 63.3%, p value<10 ^-6 ). CCI was slightly higher in HT group (5.09 vs 4.94, p value<0.005). HT was independently associated with higher mortality (Odds ratio (OR): 1.16; p value<0.000005) after adjusted for age, gender, ethnicity, VTE, myocardial infarction, ischemic stroke, and other covariates. HT patients also had significantly higher risk of developing pulmonary embolism (PE) and deep vein thrombosis (DVT) (OR: 2.86 and 2.09 respectively; both p value <10 -15 ). Further subgroup analysis revealed that among all types of HT, only antithrombin III deficiency (ATIII deficiency) was associated with significantly higher mortality (OR: 1.67, p value<10 -15 ). This association of ATIII deficiency and mortality was stronger in young adults and less prominent among older population (<40-year-old OR: 2.81, p value<10 -11 ; >=65-year-old OR: 1.53, p value<10 -7 ). ATIII deficiency patients also had higher risk of developing severe sepsis (OR: 1.52, p value<10 -14 ).CONCLUSIONS: MV patients with HT had increased risk of PE and DVT. Among HT, only ATIII deficiency significantly increased the risk of mortality. This effect was stronger among young adults. ATIII deficiency patients also had higher chance of developing severe sepsis. It was unclear why ATIII deficiency was associated with poor prognosis. The reason could be that ATIII is part of a crucial immune response in critically ill patients. More research needs to be done to fully elucidate this finding.CLINICAL IMPLICATIONS: HT is an independent risk factor of VTE in MV patients. ATIII deficiency could increase the risk of severe sepsis and mortality.