Background: Statin medications reduce the risk of atherosclerotic cardiovascular disease (ASCVD). China's new central government medicine procurement policy lowered statin prices by five-fold or more, which may impact the cost-effectiveness of statin therapy. Objective: To explore the impact of China's 2019 centralized medicine procurement policy on the cost-effectiveness of statins treatment for primary ASCVD prevention. Methods: A microsimulation decision tree analytic model was built using individual participant data from ASCVD-free adults aged 35–64 years (n = 21,265) in the China Multi-provincial Cohort Study. ASCVD incidence, costs (2019 Int$), and quality-adjusted life years (QALYs) over a 10-year period from health-care sector and societal perspectives were estimated. Effect and cost-effectiveness of low-dose statins (equivalent potency regimens of simvastatin 20 mg/day, atorvastatin 10 mg/day, or rosuvastatin 5 mg/day) and moderate-dose (double low dose) statins therapy were simulated. The incremental cost-effectiveness ratio (ICER) of statin treatment was compared with no treatment by category of 10-year ASCVD risk. New lower prices of statins were from the centralized procurement policy bid-winning announcement file. One-way and probabilistic sensitivity analyses quantified model uncertainty. Results: Low-dose statins interventions reduced 10-year ASCVD incidence by 4.1%, 9.7%, and 15.5% among people with low, moderate, and high risk comparing to no treatment. Lowering statin prices to the 2019 central government procurement policy level could lower the ICER of low-dose statins treatment for high-risk people from Int$ 141,000 to Int$ 51,300 per QALY gained from health-care sector perspective. Moderate-dose statin treatment lowered the ICER compared with the low-dose statins treatment in each ASCVD risk category (Int$ 43,100 vs. Int$ 51,300 per QALY gained from the health-care sector perspective for high risk people). Cost-effectiveness improved progressively with increased baseline ASCVD risk. Conclusion: Implementing low central government prices will substantially improve the cost-effectiveness of statins for primary ASCVD prevention in 35–64-year-old Chinese adults.
Aim: The lipoprotein-associated phospholipase A2(Lp-PLA2) level has been shown to be associated with the risk of clinical cardiovascular events. We aimed to investigate whether Lp-PLA2 is associated with the progression of subclinical atherosclerosis in the general population. Methods: The degree of carotid plaque and the maximal intima-media thickness(IMT) were measured twice over a 5-year interval in 913 participants 45 to 74 years of age at baseline in a cohort study. The associations between the plasma Lp-PLA2 activity and the progression of carotid plaque and changes in the IMT level were assessed according to sex after adjusting for traditional risk factors and the high-sensitivity C-reactive protein(hsCRP) level. Results: During the 5-year follow-up period, the progression of plaque was observed in 58.5% of men and 48.3% of women. The median maximal IMT level increased by 0.12 mm in men and 0.09 mm in women per year. The progression of plaque and changes in the IMT level increased according to the quartile of the Lp-PLA2 activity in men(p＜0.05 for trend), but not women. Following adjustment for traditional risk factors and the hsCRP level, the odds ratio for plaque progression associated with an increase in the Lp-PLA2 activity of one standard deviation was 1.28(95% CI=1.09-1.49, p=0.043) in men and 0.92(95% CI=0.78-1.08, p=0.273) in women. The regression coefficient for IMT progression was 0.003(p=0.004) in men and −0.001(p=0.166) in women after adjusting for the other factors. Conclusions: The Lp-PLA2 level is associated with the progression of subclinical atherosclerosis in men. Lp-PLA2 may play an important role in the pathogenesis of atherosclerosis and be a potential target for the early prevention of cardiovascular disease.
Congenital myasthenic syndromes (CMSs) are a group of inherited disorders caused by genetic defects in neuromuscular junctions. Mutations in CHAT, encoding choline acetyltransferase, cause congenital myasthenic syndrome with episodic apnea (CMS-EA), a rare autosomal recessive disease characterized by respiratory insufficiency with cyanosis and apnea after infections, fever, vomiting or excitement. To date, no studies have reported deletions comprised of multiple exons. Here, using next generation sequencing, we identified compound heterozygous mutations, namely a large maternally inherited deletion, including exons 4, 5, and 6, and a paternally inherited missense variant (c.914T>C [p.Ile305Thr]) in CHAT in a Chinese patient with a severe phenotype of CMS-EA. Furthermore, the large deletion was also validated by real-time fluorescence quantitative polymerase chain reaction. The patient was a 10-month-old boy, who presented with a weak cry and feeding difficulties soon after birth, ptosis at 4 months old, episodic apnea after fever at 9 months old, and respiratory insufficiency with cyanosis and apnea that required intubation after a respiratory tract infection at 10 months old. Unfortunately, he died in the Pediatric Intensive Care Unit soon after hospitalization. The patient's elder sister had similar clinical manifestations, and she died prior to the age of 2 months old without a diagnosis. Genotype-phenotype correlation analysis revealed that loss-of-function mutations in exons 4-6 of CHAT might cause more severe CMS-EA. To our knowledge, this is the first study to show compound heterozygous CHAT mutations consisting of a large deletion and missense mutation in a patient with CMS-EA.
Herpes simplex virus (HSV) is a ubiquitous human pathogen that causes a range of diseases from mild uncomplicated mucocutaneous infection to life-threatening conditions.1 HSV-1 is normally associated with orofacial infections, whereas HSV-2 usually causes genital infections and can be transmitted from infected mothers to neonates.2 Less common manifestations of HSV infection, such as meningitis, encephalitis,3, 4 hepatitis,5 and pneumonitis,6, 7 can occur in both children and adults. After primary infection by HSV, the virus establishes a lifelong latent infection in the neuronal district, resulting in reactivation due to various triggering factors. The patient in this fatal case was a one-year-old girl who was born full-term, developed normally, and had no medical history of asthma or pneumonia and no familial history of immunodeficiency. She had a 15-year-old sister and a 13-year-old brother, both of whom were healthy. The patient was admitted to the local hospital due to undergoing more than 20 days of fever, spurting vomit, and convulsions. The symptoms began on 27 April (day 1) with fever (up to 39.8 °C), spurting vomit, and convulsions (4 times), but no cough, runny nose, rash, or diarrhoea presented at that time. Ibuprofen was administered orally, but the patient's body temperature did not decrease. On 28 April (day 2), the patient's blood biochemistry results showed a C-reactive protein (CRP) level of <1 mg/L, and the percentage of neutrophil granulocytes was 75.9%. Additionally, the white blood cell (WBC) count in the patient's cerebrospinal fluid (CSF) was 20×106 cells/L. On 1 May (day 5), brain magnetic resonance (MR) scanning revealed swollen gyri in the bilateral parietal lobes. Together, the above-mentioned findings prompted a diagnosis of viral encephalitis. On 3 May (day 7), the patient's electrocardiogram (ECG) monitoring results were mildly abnormal, with increased δ activities. From 3 May to 5 May, the patient received an intravenous infusion of methyl prednisolone to inhibit inflammatory responses. On 4 May (day 8), the patient's body temperature decreased to a normal level, but her convulsions reappeared. Sodium valproate and prednisone were then administered orally once daily from 6 May to 12 May. On 10 May (day 14), the patient began suffering from a cough and congestion. On 12 May (day 16), the patient's body temperature peaked at 39.8 °C, and cephalosporin was intravenously infused. On 18 May (day 22), a high fever (up to 38.9 °C) and reoccurring spurting vomit persisted in the patient, and she was transferred to our hospital's emergency department. The patient's CSF was tested, revealing a WBC count of 28×106 cells/L, a protein concentration of 1.045 g/L, and a positive Pandy's reaction. A head CT scan showed encephalatrophy in the bilateral cerebral hemisphere and encephalomalacia with cortical laminar necrosis (Figure 1). Most importantly, both the patient's blood and CSF were positive for HSV- specific IgM (Herpes Simplex Virus 1/2 IgM ELISA Kit, Virion/Serion, Germany), and no bacteria or fungi were detected in the blood or CSF cultures. Therefore, the patient was definitively diagnosed with a central nervous system (CNS) infection and treated with ceftriaxone and acyclovir. Meanwhile, the patient retained a persistent fever, cough, and wheezing due to the retention of phlegm in her throat. Both lungs exhibited rough breathing sounds, and wheezing and coarse rales could be heard. To promote sputum expulsion, ambroxol was intravenously infused and acetylcysteine was used to humidify the patient's trachea. Budesonide and ipratropium bromide were administered via atomized inhalation to alleviate the inflammatory response and expand the bronchi. Mannitol and glycerin fructose were administered to reduce intracranial pressure, and the patient was also intravenously infused with immunoglobulin for four days. On 31 May (day 35), the patient suffered from convulsions on two occasions, but her symptoms were relieved after the administration of midazolam. On 1 June (day 36), the patient's CSF tested weakly positive for Pandy's reaction, and her CSF WBC count was 20×106 cells/L. On 7 June (day 42), both the patient's blood and CSF were positive for HSV-specific IgM and HSV-specific IgG. Polymerase chain reaction (PCR) assays to detect viral DNA were performed on 2 June and 7 June; however, the CSF and blood were negative for both HSV-1- and HSV-2-specific DNA. On 13 June, the patient's CSF tested negative for Pandy's reaction, and her CSF WBC count had decreased to 12×106 cells/L. On 11 June (day 46), the patient's lower respiratory symptoms became aggravated, and severe cough and wheezing were prevalent due to the retention of phlegm in her throat. Chest radiographs showed increased lung markings with patchy shadows in both lungs, and the patient was diagnosed with bronchopneumonia. Cefepime was intravenously infused, and the patient was administered of more frequent doses of budesonide and ipratropium bromide via atomized inhalation. On 16 June (day 51), the patient's pulmonary condition deteriorated further, with wheezy phlegm and moist rales unmistakably observable. Chest radiographs showed obvious increases in the densities of both lungs (Figure 2). The patient was then diagnosed with acute respiratory distress syndrome (ARDS) and admitted to the paediatric intensive care unit (PICU) with nasal continuous positive airway pressure (NCPAP) treatment (FiO2: 100%, PEEP: 5-cm H2O, flow: 12 L/min). The patient's throat swab was negative for 18 common respiratory viruses, as measured by the Luminex xTAG Respiratory Viral Panel Assay, and no bacteria or fungi were detected in the throat swab culture. On 17 June (day 52), the patient died. In summary, this report describes a case of ARDS in an HSV-infected paediatric patient. During hospitalization, both the blood and CSF samples collected from the patient were positive for HSV-specific IgM and IgG. The patient was diagnosed with HSV encephalitis, ARDS, encephalomalacia, encephalatrophy, subdural effusion, symptomatic epilepsy, and pneumonia, and she died 52 days after hospital admission. Herein, we report the case of a one-year-old girl presenting with viral encephalitis, encephalomalacia, encephalatrophy, subdural effusion, and symptomatic epilepsy that was followed by ARDS and pneumonia during hospitalization. HSV infection most likely played a primary role in the dissemination of inflammatory responses into multiple organs, mainly the brain and lungs, which ultimately caused the patient's death. No other encephalotropic or respiratory pathogens were detected in the patient's blood, CSF, or throat swab specimens. Two distinct types of HSV infection of the CNS are currently recognized: (1) herpes simplex encephalitis of older children and adults, which is the most common cause of sporadic fatal encephalitis and is nearly always caused by HSV-1; and (2) neonatal herpes simplex encephalitis, which occurs during the first month of life and is usually caused by HSV-2.4 In the present case, because HSV 1/2 IgM or IgG ELISA kits were used for diagnosis, we cannot definitely assert which HSV subtype was the causative pathogen. HSV-2 typically causes aseptic meningitis and is usually benign.4 However, recent studies indicate that a deviation of the prevalent HSV meningitis from HSV-2 to HSV-1 may be underway. Here, because the patient was not a neonate, the fatal encephalitis and pneumonia were more likely to have been caused by HSV-1. HSV-1 pulmonary infections have recently been reported in critical patients. Such infections were postulated to be due to HSV-1 reactivation in the oropharynx towards the lungs in patients undergoing mechanical ventilation (MV).7-9 We further speculate that HSV-1 encephalitis can induce severe complications in the lower respiratory tract of patients not undergoing prolonged MV; however, the detailed mechanism underlying this phenomenon remains unclear. Warren et al. speculated that HSV may reach the lower respiratory tract via aspiration from the upper respiratory tract or via reactivation of the virus in the lungs or trachea, depending on the presence of the virus in the superior cervical and vagal ganglia.10 Interestingly, Astuto et al7 reported a similar case of a disseminating HSV-1 infection in which a 44-year-old man presented with seizures followed by an acute respiratory illness with a fatal outcome. In that case, the pulmonary infection preceded the herpes simplex encephalitis, unlike in the present case in which the order of infection was reversed. Therefore, we speculate that severe lower respiratory tract infection and HSV encephalitis are possible triggers for each other during HSV infection. One limitation of this report is that throughout the hospitalization period only HSV-specific IgM and IgG, but not viral DNA, was measured in both blood and CSF specimens. Rimerio et al reported the detection of infection with various herpesvirus strains in plasma and CSF using nested PCR. Notably, they found that the sensitivity of this method was low for HSV-1 and EBV, and its positive predictive value (PPV) was low for HSV-1 and HSV-2.11 Thus, low molecular detection sensitivity may be the main reason for the negative HSV DNA results from blood and CSF in our report. The high CRP levels and chest radiographs during the patient's ARDS period suggest the presence of a pulmonary infection. However, molecular detection of HSV based on the patient's throat swab was also negative, perhaps because nasopharyngeal aspirates and bronchoalveolar lavage fluid may be more suitable for the detection of pathogens from the lower respiratory tract. In summary, this report presented the case of an HSV- infected paediatric patient with ARDS. HSV encephalitis may have triggered the severe pneumonia and fatal outcome that followed. We hope that the case reported herein can provide a better understanding of HSV infection in critical patients to aid the management of future similar cases. The authors have no potential conflicts of interest.
Despite advances in the treatment of ST-segment elevation myocardial infarction (STEMI), little is known about how this evolving knowledge is applied in current clinical practice in China.
Objective
To evaluate hospital performance and temporal trends in the management of STEMI.
Design, Setting, and Participants
This study used data from the Improving Care for Cardiovascular Disease in China–Acute Coronary Syndrome Project, a nationwide quality improvement registry, in collaboration with the American Heart Association and the Chinese Society of Cardiology. Participants included patients with STEMI admitted to 143 tertiary hospitals across China from November 2014 to July 2019, and data were analyzed from November 2020 to December 2021.
Main Outcomes and Measures
Levels, hospital-level variations, and trends for utilization rates of the 9 management strategies with Class I recommendations in Chinese and US guidelines.
Results
A total of 57 560 hospitalizations with STEMI were included. Overall, 20.0% of patients received all the care according to the 9 guideline-recommended strategies. The performance rate of quality measures was low for reperfusion therapy (61.0%, 35 115/57 560 patients), β-blocker at discharge (68.3%, 37 750/55 285 patients), angiotensin-converting enzyme inhibitor or angiotensin receptor blocker at discharge (55.1%, 2524/4578 patients), and smoking cessation counseling (36.5%, 9586/26 265 patients) among those who were eligible. Of 25 563 patients who underwent primary percutaneous coronary intervention (PCI), 66.8% underwent this procedure within 90 minutes of hospital arrival. Of 1128 patients who underwent fibrinolysis therapy, 253 (22.4%) underwent this treatment within 30 minutes of hospital arrival. Measures with high performance rates included receipt of dual antiplatelet therapy within 24 hours (95.5%, 54 263/56 848 patients) and at discharge (91.8%, 51 452/56 019 patients) and receipt of statin at discharge (93.0%, 52 214/56 141 patients) for those eligible. There was significant variation between hospitals in all-or-none score (ranging from 0 to 61.9%) and performance of individual measures. The quality of care improved during the study period, especially for reperfusion therapy, primary PCI within the first 90 minutes of hospital arrival, and smoking cessation counseling.
Conclusions and Relevance
The quality of care for patients hospitalized with STEMI does not meet guideline-recommended strategies in China, with only 1 in 5 patients receiving all the care according to the 9 guideline-recommended strategies. Large disparities in the quality of care exist across hospitals.
Electroconvulsive therapy (ECT) is an effective somatic treatment, but it may be limited by cognitive adverse effects. The existing cognitive screening instruments often lack specificity to ECT-associated cognitive deficits. The ElectroConvulsive Therapy Cognitive Assessment was developed and validated in a clinical setting, but the reliability and validity of the Chinese version of ElectroConvulsive Therapy Cognitive Assessment (ECCA-C) have not been studied in a large clinical sample.The ECCA-C and the Montreal Cognitive Assessment (MoCA) were administered to patients with major depressive disorder (MDD) undergoing ECT at 3 time points: pretreatment (baseline), before the fifth treatment, and 1 week posttreatment. The instruments were also administered to a sample of healthy subjects.Sixty-five patients with MDD and 50 age- and sex-matched healthy controls were recruited in this study. Overall, the patient group had statistically significantly lower MoCA and ECCA-C scores than the control group (both P values <0.001). The Cronbach α of the ECCA-C was 0.88 at baseline. Statistically significant decreases over time were observed in ECCA-C: pre-ECT (23.9 ± 4.0) > mid-ECT (21.3 ± 3.4) > post-ECT (18.7 ± 4.8) (all P values <0.001), whereas no statistically significant changes in MoCA scores were found at these 3 time points (F = 1.86, P = 0.165). A cutoff score of 26.5 on the ECCA-C was found to best differentiate between MDD patients and healthy controls.The ECCA-C showed satisfactory psychometric properties and may be a more sensitive instrument than the MoCA to assess cognitive impairment associated with ECT.
Background Baseline thrombocytopenia is commonly observed in patients with acute coronary syndrome (ACS) requiring percutaneous coronary intervention (PCI). Aim The purpose of this analysis was to investigate safety and effectiveness of PCI in ACS patients with baseline mild-to-moderate thrombocytopenia. Methods The data were collected from the Improving Care for Cardiovascular Disease in China–Acute Coronary Syndrome project. A total of 50,009 ACS patients were recruited between July 2017 and December 2019. Among them, there were 6,413 patients with mild-to-moderate thrombocytopenia, defined as a platelet count of ≥50 × 109/L and <150 × 109/L on admission. The primary outcome was in-hospital net adverse clinical events (NACE), consisting of major adverse cardiac events (MACE) and major bleeding events. The associations between PCI and in-hospital outcomes were analyzed by inverse probability treatment weighting (IPTW) method. Results PCI was performed in 4,023 of 6,413 patients (62.7%). The IPTW analysis showed that PCI was significantly associated with a reduced risk of in-hospital MACE (odd ratio [OR]: 0.45; 95% confidence interval [CI]: 0.31–0.67; p < 0.01) and NACE (OR: 0.59; 95% CI: 0.42–0.83; p < 0.01). PCI was also associated with an increased risk of any bleeding (OR: 1.56; 95% CI: 1.09–2.22; p = 0.01) and minor bleeding (OR: 1.52; 95% CI: 1.00–2.30; p = 0.05), but not major bleeding (OR: 1.51; 95% CI: 0.76–2.98; p = 0.24). Conclusion Compared with medical therapy alone, PCI is associated with better in-hospital outcomes in ACS patients with mild-to-moderate thrombocytopenia. Further studies with long-term prognosis are needed.
Abstract Background: Renal insufficiency (RI) is a frequent comorbidity among patients with acute coronary syndrome (ACS). We aimed to evaluate the attributable risk associated with mild RI for the in-hospital outcomes in patients with ACS. Methods: The Improving Care for Cardiovascular Disease in China-ACS (CCC-ACS) Project was a collaborative study of the American Heart Association and the Chinese Society of Cardiology. A total of 92509 inpatients with a discharge diagnosis of ACS were included. The attributable risk was calculated to investigate the effect of mild RI (eGFR 60-89 ml / min · 1.73 m 2 ) on major adverse cardiovascular events (MACE) during hospitalization. Results: The average age of these ACS patients was 63 years, and 73.9% were men. The proportion of patients with mild RI was 36.17%. After adjusting for other possible risk factors, mild RI was still an independent risk factor for MACE in ACS patients. In the ACS patients, the attributable risk of eGFR 60-89ml/min·1.73m 2 to MACE was 8.96%, 5.59% of eGFR 45-59 ml/min·1.73m 2 ,5.31% of eGFR 30-44 ml/min·1.73m 2 , and 4.03% of eGFR＜30 ml/min·1.73m 2 . Conclusion: Compared with moderate to severe RI, mild RI has higher attributable risk to MACE during hospitalization in Chinese ACS population.
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