Background Socioeconomic status ( SES ) is associated with health‐related quality of life ( HRQOL ) for children with critical congenital heart disease; however, literature from newly industrialized countries is scarce. Methods and Results This cross‐sectional study included 2037 surviving patients operated on for critical congenital heart disease at a tertiary hospital in China between May 2012 and December 2015. All eligible patients were aged 2 to 12 years. HRQOL was measured by the Pediatric Quality of Life Inventory 4.0 generic and 3.0 cardiac modules. Family SES was assessed by a composite of household income in the past year and occupation and education level of each parent in the family. Mean scores of major domains in HRQOL were significantly lower in the low‐ SES group than in the medium‐ and high‐ SES groups (total generic scores: 71.2±7.9 versus 75.0±8.0 and 76.0±7.9, respectively [ P <0.001]; psychosocial functioning: 70.8±9.0 versus 74.4±8.4 and 75.3±8.4 [ P <0.001]; physical functioning: 71.6±10.4 versus 76.0±9.7 and 77.1±9.4 [ P <0.001]; heart symptoms: 71.9±11.6 versus 75.7±11.0 and 76.8±10.3 [ P <0.001]; cognitive problems: 65.4±11.1 versus 69.4±12.1 and 74.6±13.6 [ P <0.001]). After adjustment for other clinical and demographic variables in the multivariable linear regression model, family SES significantly affected all dimensions of HRQOL except for treatment barriers, treatment anxiety, physical appearance and communication. Conclusions Family SES is an important factor associated with HRQOL in patients with critical congenital heart disease. Further targeted interventions to improve HRQOL that consider the family and environmental issues confronted by those who are economically disadvantaged might help these patients have better outcomes.

Therapeutic hypothermia is commonly used during cardiopulmonary bypass (CPB) to protect the heart against myocardial injury in cardiac surgery. Patients who suffer from chronic hypoxia (CH), such as those with certain heart or lung conditions, are at high risk of severe myocardial injury after cardiac surgery, but the underlying mechanisms are unknown. This study tested whether CH attenuates hypothermic cardioprotection during CPB. Using a rat model of CPB, we found that hypothermic cardioprotection was impaired in CH rats but was preserved in normoxic rats. Cardiac proteomes showed that cold-inducible RNA binding protein (CIRBP) was significantly (P = 0.03) decreased in CH rats during CPB. Methylation analysis of neonatal rat cardiomyocytes under CH and myocardium specimens from patients with CH showed that CH induced hypermethylation of the Cirbp promoter region, resulting in its depression and failure to respond to cold stress. Cirbp-knockout rats showed attenuated hypothermic cardioprotection, whereas Cirbp-transgenic rats showed an enhanced response. Proteomics analysis revealed that the cardiac ubiquinone biosynthesis pathway was down-regulated during CPB in Cirbp-knockout rats, resulting in a significantly (P = 0.01) decreased concentration of ubiquinone (CoQ10). Consequently, cardiac oxidative stress was aggravated and adenosine 5′-triphosphate production was impaired, leading to increased myocardial injury during CPB. CoQ10-supplemented cardioplegic solution improved cardioprotection in rats exposed to CH, but its effect was limited in normoxic rats. Our study suggests that an individualized cardioprotection strategy should be used to fully compensate for the consequences of epigenetic modification of Cirbp in patients with CH who require therapeutic hypothermia.

Background Congenital heart disease (CHD) is the leading cause of morbidity and mortality from birth defects worldwide. We report an overview of trends in CHD mortality in 204 countries and territories over the past 30 years and associations with age, period, and birth cohort.Methods Cause-specific CHD mortality estimates were derived from the Global Burden of Disease 2019 study. We utilised an age-period-cohort model to estimate overall annual percentage changes in mortality (net drifts), annual percentage changes from 0 to 4 to 65−69 years (local drifts), period and cohort relative risks (period/cohort effects) between 1990 and 2019. This approach allows for the examination and differentiation of age, period, and cohort effects in the mortality trends, with the potential to identify disparities and treatment gaps in cardiac care.Findings CHD is the leading cause of deaths from non-communicable diseases (NCDs) in those under 20 years. Global CHD deaths in 2019 were 217,000 (95% uncertainty interval 177,000−262,000). There were 129 countries with at least 50 deaths. India, China, Pakistan, and Nigeria had the highest mortality, accounting for 39.7% of deaths globally. Between 1990 and 2019, the net drift of CHD mortality ranged from −2.41% per year (95% confidence interval [CI] −2.55, −2.67) in high Socio-demographic Index (SDI) countries to −0.62% per year (95% CI: −0.82, −0.42) in low-SDI countries. Globally, there was an emerging transition in the age distribution of deaths from paediatric to adult populations, except for an increasing trend of mortality in those aged 10−34 years in Mexico and Pakistan. During the past 30 years, favourable mortality reductions were generally found in most high-SDI countries like South Korea (net drift = −4.0% [95% CI −4.8 to −3.1] per year) and the United States (−2.3% [−2.5 to −2.0]), and also in many middle-SDI countries like Brazil (−2.7% [−3.1 to 2.4]) and South Africa (−2.5% [−3.2 to −1.8]). However, 52 of 129 countries had either increasing trends (net drifts ≥0.0%) or stagnated reductions (≥−0.5%) in mortality. The relative risk of mortality generally showed improving trends over time and in successively younger

Background: To contain the outbreak of coronavirus disease 2019 in China, many unprecedented intervention measures are adopted by the government. However, these measures may interfere in the normal medical service. We sought to model the trend of COVID-19 and estimate the restoration of operational capability of metropolitan medical service in China.Methods: Real-time data of COVID-19 and population mobility data were extracted from open sources. SEIR (Susceptible, Exposed, Infectious, Recovered) and neural network models (NNs) were built to model disease trends in Wuhan, Beijing, Shanghai and Guangzhou. Combined with public transportation data, Autoregressive Integrated Moving Average (ARIMA) model was used to estimate the accumulated demands for nonlocal hospitalization during the epidemic period in Beijing, Shanghai and Guangzhou. Results: The number of infected people and deaths would increase by 45% and 567% respectively, given that the government only has implemented traffic control in Wuhan without additional medical professionals. The epidemic of Wuhan (measured by cumulative confirmed cases) was predicted to reach turning point at the end of March and end in later April, 2020. The outbreak in Beijing, Shanghai and Guangzhou was predicted to end at the end of March and the medical service could be fully back to normal in middle of April. During the epidemic, the number of nonlocal inpatient hospitalizations decreased by 69.86%, 57.41% and 66.85% in Beijing, Shanghai and Guangzhou respectively. After the end of epidemic, medical centers located in these metropolises may face 58,799 (95% CI 48926-67,232) additional hospitalization needs in the first month.

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Background: Cyanotic congenital heart disease (CCHD) is a complex pathophysiological condition involving systemic chronic hypoxia (CH). Some CCHD patients are unoperated due to various reasons and remain chronically hypoxic throughout their lives, which heightens the risk of heart failure as they age. Hypoxia activates cellular metabolic adaptation to balance energy demands by accumulating hypoxia-inducible factor 1-α (HIF-1α). This study aims to determine the effect of CH on cardiac metabolism and function in CCHD patients and its association with age. The role of HIF-1α in this process was investigated and potential therapeutic targets were explored. Methods: CCHD patients ( n = 25) were evaluated for cardiac metabolism and function using positron-emission tomography/computed tomography and magnetic resonance imaging. Heart tissue samples were subjected to metabolomic and protein analyses. CH rodent models were generated to enable continuous observation of changes in cardiac metabolism and function. The role of HIF-1α in cardiac metabolic adaptation to CH was investigated using genetically modified animals and isotope-labeled metabolomic-pathway tracing studies. Results: Prepubertal CCHD patients had glucose-dominant cardiac metabolism and normal cardiac function. By comparison, among patients who had entered puberty, the levels of myocardial glucose uptake and glycolytic intermediates were significantly decreased, but fatty acids were significantly increased, along with decreased left-ventricular ejection fraction. These clinical phenotypes were replicated in CH rodent models. In CCHD patients and animals exposed to CH, myocardial HIF-1α was upregulated prior to puberty, but was significantly downregulated during puberty. In cardiomyocyte-specific Hif-1α -knockout mice, CH failed to initiate the switch of myocardial substrates from fatty acids to glucose, thereby inhibiting ATP production and impairing cardiac function. Increased insulin resistance (IR) during puberty suppressed myocardial HIF-1α and was responsible for cardiac metabolic maladaptation in animals exposed to CH. Pioglitazone significantly reduced myocardial IR, restored glucose metabolism, and improved cardiac function in pubertal CH animals. Conclusions: In CCHD patients, maladaptation of cardiac metabolism occurred during puberty, along with impaired cardiac function. HIF-1α was identified as the key regulator of cardiac metabolic adaptation in animals exposed to CH, and pubertal IR could suppress its expression. Pioglitazone administration during puberty might help improve cardiac function in CCHD patients.

ObjectivesIdentifying high-risk patients in the intensive care unit (ICU) is important given the high mortality rate. However, existing scoring systems lack easily accessible, low-cost and effective inflammatory markers. We aimed to identify inflammatory markers in routine blood tests to predict mortality in ICU patients and evaluate their predictive power.DesignRetrospective case–control study.SettingSingle secondary care centre.ParticipantsWe analysed data from the Medical Information Mart for Intensive Care III database. A total of 21 822 ICU patients were enrolled and divided into survival and death groups based on in-hospital mortality.Primary and secondary outcome measuresThe predictive values of potential inflammatory markers were evaluated and compared using receiver operating characteristic curve analysis. After identifying the neutrophil-to-lymphocyte ratio (NLR) as having the best predictive ability, patients were redivided into low (≤1), medium (1–6) and high (>6) NLR groups. Univariate and multivariate logistic regression analyses were performed to evaluate the association between the NLR and mortality. The area under the curve (AUC), net reclassification improvement (NRI) and integrated discrimination improvement (IDI) were used to assess whether incorporating the NLR could improve the predictive power of existing scoring systems.ResultsThe NLR had the best predictive ability (AUC: 0.609; p<0.001). In-hospital mortality rates were significantly higher in the low (OR (OR): 2.09; 95% CI 1.64 to 2.66) and high (OR 1.64; 95% CI 1.50 to 1.80) NLR groups than in the medium NLR group. Adding the NLR to the Simplified Acute Physiology Score II improved the AUC from 0.789 to 0.798, with an NRI and IDI of 16.64% and 0.27%, respectively.ConclusionsThe NLR predicted mortality in ICU patients well. Both low and high NLRs were associated with elevated mortality rates, including the NLR may improve the predictive power of the Simplified Acute Physiology Score II.

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