Impact of the COVID-19 pandemic on cardiovascular mortality and contrast analysis within subgroups.

Background: An increase in deaths has been perceived during the pandemic, which cannot be explained only by COVID-19. The actual number of deaths far exceeds the recorded data on deaths directly related to SARS-CoV-2 infection. Data from early and short-lived pandemic studies show a dramatic shift in cardiovascular mortality. Grounded in the post-pandemic era, macroscopic big data on cardiovascular mortality during the pandemic need to be further reviewed and studied, which is crucial for cardiovascular disease prevention and control. Methods: We retrieved and collected data associated with cardiovascular disease mortality from the National Vital Statistic System from the Center for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) platform based on the ICD-10 codes. We applied regression analysis to characterize overall cardiovascular disease mortality trends from 2010 to 2023 and built a time series model to predict mortality for 2020-2023 based on mortality data from 2010 to 2019 in order to affirm the existence of the excess deaths by evaluating observed vs. predicted mortality. We also conducted subgroup analyses by sex, age and race/ethnicity for the purpose of obtaining more specific sociodemographic information. Results: All-cause age-standardised mortality rates (ASMRs) for CVD dramatically increased between 2019 and 2021[annual percentage change (APC) 11.27%, p < 0.01], and then decreased in the following 2021-2023(APC: -7.0%, p < 0.01). Subgroup analyses found that the ASMR change was most pronounced in Alaska Indians/Native American people (APC: 16.5% in 2019-2021, -12.5% in 2021-2023, both p < 0.01), Hispanics (APC: 12.1% in 2019-2021, -12.2% in 2021-2023, both p < 0.05) and non-Hispanic Black people (APC:11.8% in 2019-2021, -10.3% in 2021-2023, both p < 0.01)whether during the increasing or declining phase. Similarly, the ASMR change was particularly dramatic for the 25-44 age group (APC:19.8% in 2019-2021, -15.4% in 2021-2023, both p < 0.01) and males (APC: 11.5% in 2019-2021, -7.6% in 2021-2023, both p < 0.01). By the end of 2023, the proportion of COVID-related excess death remained high among the elderly (22.4%), males (42.8%) and Alaska Indians/Native American people(39.7%). In addition, we did not find the presence of excess deaths in the young (25-44) and middle-aged cohort (45-64) in 2023, while excess deaths remained persistent in the elderly. Conclusions: All-cause ASMRs for CVD increased notably during the initial two years of the COVID-19 pandemic and then witnessed a decline in 2021-2023. The cohorts (the young, males and minorities) with the steepest rise in mortality decreased at the fastest rate instead. Previous initiatives to promote cardiovascular health were effective, but further research on cardiovascular healthcare for the elderly and racial disparities should be attached to priority considering the presence of sociodemographic differences in CVD death.

Association between triglyceride glucose-body mass and one-year all-cause mortality of patients with heart failure: a retrospective study utilizing the MIMIC-IV database.

BACKGROUND: The triglyceride glucose-body mass (TyG-BMI) index is acknowledged as both a reliable indicator of the risk of cardiovascular disease and an accurate surrogate biomarker for evaluating insulin resistance (IR). The importance of the TyG-BMI index among people with heart failure (HF), however, requires more investigation. The objective of this study was to inquire about the relationship between HF patients' TyG-BMI index and their risk of 360-day mortality. METHODS: The Medical Information Mart for Intensive Care (MIMIC-IV) database provided the study's patient data, which were divided into quartiles according to their TyG-BMI index. The endpoint was mortality from all causes within 360 days. Kaplan-Meier analysis was used to compare this primary endpoint amongst the four groups indicated above. The association between the TyG-BMI index and the endpoint was investigated using restricted cubic splines and Cox proportional hazards analysis. RESULTS: The study enrolled a total of 423 patients with HF (59.2% male), of whom 70 patients (16.9%) died within 360 days. Patients with higher TyG-BMI indexes had significantly lower mortality risks, according to the Kaplan-Meier analysis (log-rank P = 0.003). Furthermore, the restricted cubic spline analysis illustrated a decrease in the risk of all-cause mortality with an increasing TyG-BMI index. Additionally, multivariable Cox proportional hazards analyses showed that the risk of 360-day death from all causes was considerably higher in the lowest quartile of TyG-BMI. In comparison to the lowest TyG-BMI group, the fully adjusted Cox model yielded a hazard ratio (HR) of 0.24 (95% CI: 0.10, 0.59; p = 0.002) for 360-day mortality. CONCLUSIONS: In patients diagnosed with HF, a lower TyG-BMI index is strongly related to a higher risk of 360-day mortality. This index can be employed to categorize the risk levels of patients with HF and predict their one-year all-cause mortality .

Mitophagy-dependent cardioprotection of resistance training on heart failure.

Resistance exercise is an indispensable mode of exercise rehabilitation for heart failure. Here we elucidate the cardiac effects of resistance training alone or combined with different aerobic trainings on heart failure and explore the critical regulation of mitophagy. The chronic heart failure model was constructed by transverse aortic constriction surgery, followed by 8 wk of resistance training (RT), moderate-intensity continuous training combined with resistance training (MRT), and high-intensity interval training combined with resistance training (HRT), and subsequently analyzed the changes of maximum load, cardiac structure and function, and myocardial mitophagic activity. The role and signaling of mitophagy in exercise protection of heart failure were investigated by knockdown of Hif1α and Parkin genes in primary neonatal cardiomyocytes. RT and especially MRT improved maximum load (P < 0.0001), myocardial morphology and fibrosis (P < 0.0001), reduced left ventricular diameter and enhanced left ventricular systolic function (P < 0.01), and enhanced myocardial mitophagic activity and HIF1α expression (P < 0.05) in heart failure mice. However, HRT had no obvious protective effect on ventricular diameter and function or mitophagy. The abilities of exercise stimulation to regulate reactive oxygen species, adenosine triphosphate, and brain natriuretic peptide were impaired after knockdown of Hif1α and Parkin genes inhibited mitophagy in failing cardiomyocytes (P < 0.05). Different exercise modalities provide discrepant cardiovascular effects on heart failure, and MRT exhibits optimal protection. The HIF1α-Parkin-mitophagy pathway is involved in the protection and regulation of exercise on heart failure.NEW & NOTEWORTHY Impaired myocardial mitophagy is implicated in the pathogenesis of heart failure. Resistance training alone or combined with different aerobic trainings provide discrepant cardiovascular effects on heart failure, and the cardioprotective function depends on HIF1α-Parkin-mitophagy pathway.

Exercise training improves cardiac function and regulates myocardial mitophagy differently in ischaemic and pressure-overload heart failure mice.

NEW FINDINGS: What is the central question of this study? What are the cardioprotective effects of different aerobic exercises on chronic heart failure with different aetiologies, and is mitophagy involved? What is the main finding and its importance? Moderate-intensity continuous training may be the 'optimum' modality for improving cardiac structure and function in ischaemic heart failure, while both moderate-intensity continuous training and high-intensity interval training were suitable for pressure-overload heart failure. Various mitophagy pathways, especially parkin-dependent pathways, participated in the protective effects of exercise on heart failure. ABSTRACT: The cardioprotective effects of different aerobic exercises on chronic heart failure with different aetiologies and whether mitophagy is involved remain elusive. In the current research, left anterior descending ligation and transverse aortic constriction surgeries were used to establish mouse models of heart failure, followed by 8 weeks of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT). The results showed that for ischaemic heart failure MICT significantly improved ejection fraction (P < 0.05) and fractional shortening (P < 0.05), mitigated left ventricular end-systolic dimension (P < 0.01), decreased brain natriuretic peptide (P < 0.0001) and mitigated fibrosis (P < 0.0001), while HIIT only decreased brain natriuretic peptide (P < 0.0001) and fibrosis (P < 0.0001). For pressure-overload heart failure, both MICT and HIIT significantly increased ejection fraction (P < 0.0001) and fractional shortening (MICT: P < 0.001, HIIT: P < 0.0001), and reduced left ventricular end-diastolic and end-systolic dimensions, brain natriuretic peptide (P < 0.0001), and fibrosis (MICT: P < 0.01, HIIT: P < 0.0001); HIIT was even better in reducing brain natriuretic peptide. Myocardial autophagy and mitophagy were compromised in heart failure, and the exercises improved myocardial autophagic flux and mitophagy inconsistently in heart failure with different aetiologies. Significant correlations were found between multiple mitophagy pathways and the cardioprotection of the exercises. Collectively, MICT may be the 'optimum' modality for ischaemic heart failure, while both MICT and HIIT (especially HIIT) were suitable for pressure-overload heart failure. Exercises differently improved myocardial autophagy/mitophagy, and multiple mitophagy-related pathways were closely implicated in cardioprotection of exercises for chronic heart failure.