Risk Of Myocardial Infarction Mortality Research Articles

Systemic lupus erythematosus patients have unique changes in serum metabolic profiles across age associated with cardiometabolic risk.

Cardiovascular disease through accelerated atherosclerosis is a leading cause of mortality for patients with systemic lupus erythematosus (SLE), likely due to increased chronic inflammation and cardiometabolic defects over age. We investigated age-associated changes in metabolomic profiles of SLE patients and healthy controls (HCs). Serum NMR metabolomic profiles from female SLE patients (n = 164, age = 14-76) and HCs (n = 123, age = 13-72) were assessed across age by linear regression and by age group between patients/HCs (Group-1, age ≤ 25, n = 62/46; Group-2, age = 26-49, n = 50/46; Group-3, age ≥ 50, n = 52/31) using multiple t-tests. The impact of inflammation, disease activity and treatments were assessed, and UK Biobank disease-wide association analysis of metabolites was performed. Age-specific metabolomic profiles were identified in SLE patients vs HCs, including reduced amino acids (Group-1), increased very-low-density lipoproteins (Group-2), and increased low-density lipoproteins (Group-3). Twenty-five metabolites were significantly altered in all SLE age groups, dominated by decreased atheroprotective high-density lipoprotein (HDL) subsets, HDL-bound apolipoprotein(Apo)A1 and increased glycoprotein acetyls (GlycA). Furthermore, ApoA1 and GlycA were differentially associated with disease activity and serological measures, as well as atherosclerosis incidence and myocardial infarction mortality risk through disease-wide association. Separately, glycolysis pathway metabolites (acetone/citrate/creatinine/glycerol/lactate/pyruvate) uniquely increased with age in SLE, significantly influenced by prednisolone (increased pyruvate/lactate) and hydroxychloroquine (decreased citrate/creatinine) treatment and associated with type-1 and type-2 diabetes by disease-wide association. Increasing HDL (ApoA1) levels through therapeutic/nutritional intervention, whilst maintaining low disease activity, in SLE patients from a young age could improve cardiometabolic disease outcomes. Biomarkers from the glycolytic pathway could indicate adverse metabolic effects of current therapies.

3,4-benzo[a]pyrene aggravates myocardial infarction injury by activating NLRP3-related pyroptosis through PINK1/Parkin-mitophagy-mPTP opening axis.

Air pollution is an important and interventionable risk factor for cardiovascular disease. Air pollution exposure, even for a short-term exposure, is conspicuously relevant to increased risk of myocardial infarction (MI) mortality and clinical evidence has shown that air pollution particulate matter (PM) induces the aggravation of AMI. 3,4-benzo[a]pyrene (BaP), an extremely toxic polycyclic aromatic hydrocarbon (PAH) and a common component of PM, is listed as one of the main objects of environmental pollution monitoring. Both epidemiological and toxicological studies suggest that BaP exposure may be associated with cardiovascular disease. Since PM is significantly associated with the increased risk of MI mortality, and BaP is an important component of PM associated with cardiovascular disease, we intend to investigate the effect of BaP on MI models. The MI mouse model and the oxygen and glucose deprivation (OGD) H9C2 cell model were used to investigate the effect of BaP in MI injury. The involvement of mitophagy and pyroptosis in regulating deterioration of cardiac function and aggravation of MI injury induced by BaP was comprehensively evaluated. Our study shows that BaP exacerbates MI injury in vivo and in vitro, a result based on BaP-induced NLRP3-related pyroptosis. In addition, BaP can inhibit PINK1/Parkin dependent mitophagy through the aryl hydrocarbon receptor (AhR), thus the mitochondrial permeability transition pore (mPTP) was induced to open. Our results suggest a role for the BaP from air pollution in MI injury aggravation and reveal that BaP aggravates MI injury by activating NLRP3-related pyroptosis via the PINK1/Parkin-mitophagy-mPTP opening axis.

Short-Term Exposure to Ambient Air Pollution and Mortality From Myocardial Infarction

BackgroundShort-term exposure to ambient air pollution has been linked to occurrence of myocardial infarction (MI); however, only a limited number of studies investigated its association with death from MI, and the results remain inconsistent. ObjectivesThis study sought to investigate the association of short-term exposure to air pollution across a wide range of concentrations with MI mortality. MethodsA time-stratified case-crossover study was conducted to investigate 151,608 MI death cases in Hubei province (China) from 2013 to 2018. Based on each case’s home address, exposure to particulate matter with an aerodynamic diameter ≤2.5 μm (PM2.5), particulate matter with an aerodynamic diameter ≤10 μm (PM10), sulfur dioxide, nitrogen dioxide (NO2), carbon monoxide, and ozone on each of the case and control days was assessed as the inverse distance–weighted average concentration at neighboring air quality monitoring stations. Conditional logistic regression models were implemented to quantify exposure-response associations. ResultsExposure to PM2.5, PM10, and NO2 (mean exposure on the same day of death and 1 day prior) was significantly associated with increased odds of MI mortality. The odds associated with PM2.5 and PM10 exposures increased steeply before a breakpoint (PM2.5, 33.3 μg/m3; PM10, 57.3 μg/m3) and flattened out at higher exposure levels, while the association for NO2 exposure was almost linear. Each 10-μg/m3 increase in exposure to PM2.5 (<33.3 μg/m3), PM10 (<57.3 μg/m3), and NO2 was significantly associated with a 4.14% (95% confidence interval [CI]: 1.25% to 7.12%), 2.67% (95% CI: 0.80% to 4.57%), and 1.46% (95% CI: 0.76% to 2.17%) increase in odds of MI mortality, respectively. The association between NO2 exposure and MI mortality was significantly stronger in older adults. ConclusionsShort-term exposure to PM2.5, PM10, and NO2 was associated with increased risk of MI mortality.

Occupational exposure to noise and cold environment and the risk of death due to myocardial infarction and stroke

PurposeThe present study examined a possible association between occupational exposure to noise, working and living in cold conditions, and the risk of mortality in myocardial infarction and stroke.MethodsThe present cohort study consists of 194,501 workers in the Swedish construction industry that participated in health examinations between 1971 and 1993. Noise exposure was defined on a job-exposure matrix based on a survey of the working conditions carried out during the mid 1970s. All workers were categorised into three main regions of Sweden, differing in temperature: Reference (Götaland), colder (Svealand), and coldest (Norrland). Relative risks (RR) were analysed by negative binomial regression adjusting for age, BMI, and smoking habits.ResultsModerate and high noise exposure was associated with increased risk of myocardial infarction (RR 1.10–1.13 with 95% CI over unit) and stroke mortality (RR 1.15 to 1.19 with 95% CI over unit). There was an increased risk for myocardial infarction (RR 1.10, 95% CI 1.01–1.20), but not for stroke mortality (RR 1.09, 95% CI 0.94–1.25) associated with living and working in the coldest region. There was an interaction on the risk of myocardial infarction mortality between different regions and noise exposure (p = 0.016), but not for stroke mortality (p = 0.88).ConclusionsThe study indicates an interaction between working at hazardous noise levels and living and working in cold conditions for increased mortality in myocardial infarction.

Geographic disparities and temporal changes in risk of death from myocardial infarction in Florida, 2000\u20132014

BackgroundIdentifying disparities in myocardial infarction (MI) burden and assessing its temporal changes are critical for guiding resource allocation and policies geared towards reducing/eliminating health disparities. Our objectives were to: (a) investigate the spatial distribution and clusters of MI mortality risk in Florida; and (b) assess temporal changes in geographic disparities in MI mortality risks in Florida from 2000 to 2014.MethodsThis is a retrospective ecologic study with county as the spatial unit of analysis. We obtained data for MI deaths occurring among Florida residents between 2000 and 2014 from the Florida Department of Health, and calculated county-level age-adjusted MI mortality risks and Spatial Empirical Bayesian smoothed MI mortality risks. We used Kulldorff’s circular spatial scan statistics and Tango’s flexible spatial scan statistics to identify spatial clusters.ResultsThere was an overall decline of 48% in MI mortality risks between 2000 and 2014. However, we found substantial, persistent disparities in MI mortality risks, with high-risk clusters occurring primarily in rural northern counties and low-risk clusters occurring exclusively in urban southern counties. MI mortality risks declined in both low- and high-risk clusters, but the latter showed more dramatic decreases during the first nine years of the study period. Consequently, the risk difference between the high- and low-risk clusters was smaller at the end than at the beginning of the study period. However, the rates of decline levelled off during the last six years of the study, and there are signs that the risks may be on an upward trend in parts of North Florida. Moreover, MI mortality risks for high-risk clusters at the end of the study period were on par with or above those for low-risk clusters at the beginning of the study period. Thus, high-risk clusters lagged behind low-risk clusters by at least 1.5 decades.ConclusionMyocardial infarction mortality risks have decreased substantially during the last 15 years, but persistent disparities in MI mortality burden still exist across Florida. Efforts to reduce these disparities will need to target prevention programs to counties in the high-risk clusters.

Acute effect of air pollutants (carbon monoxide and ozone) on myocardial infarction mortality in Ningbo

Objective: To explore the effect of carbon monoxide (CO) and ozone (O(3)) in the air on the myocardial infarction mortality in Ningbo, Zhejiang province, from 2011 to 2015. Methods: The data of daily air quality surveillance and the causes of deaths in Ningbo from January 1, 2011 to December 31, 2015 were collected and the time series study using a generalized additive model was conducted to evaluate the relationship between the mortality of myocardial infarction and the air pollutants after adjustment for the long-term trend of death, weather conditions," days of the week" and other confounding factors. Results: The daily average concentrations of CO and O(3) in Ningbo during 2011-2015 were 0.90 (0.02-3.31) mg/m(3) and 82.78 (4-236) μg/m(3), respectively. A total of 5 388 myocardial infarction deaths occurred, with a daily average of 3 deaths. In single-pollutant model, an increase of 0.1 mg/m(3) in average concentration of CO could increase the risk of myocardial infarction mortality by 1.06% (95% CI: 0.29%-1.93%) in general population, and by 1.26% (95% CI:0.28%-2.24%) in aged people aged ≥65 years in lagged 6 days, but the influence was not significant in people aged <65 years. The influence had no significant difference in males, but it increased the risk of myocardial infarction mortality by 1.77% in females (95% CI: 0.44%-3.13%). In multi-pollutant model, CO did remain robust after adjusting for other co-pollutants. Whereas the effect of O(3) had no significant influence. Conclusion: These findings suggested that the increased risk of daily myocardial infarction mortality was associated with the increase of CO concentration, but no such association was found for O(3) in Ningbo.

Radiation-induced coronary artery disease: a second survivorship challenge?

10.2217/FON.15.121 © 2015 Future Medicine Ltd The role of adjuvant mediastinal radiation (RT) in improving disease-free survival in Hodgkin’s disease and breast cancer (BC) is well known. However, this survival advantage is accompanied by the late cardiac sequelae of radiation. Radiationinduced coronary artery disease (RICAD) is a challenging clinical entity and a major contributor to cardiovascular (CV) mortality in cancer survivors. In this review, we discuss the pathophysiology, surveillance and management challenges of RICAD.

Abstract 2184: Past use of coal for cooking is associated with all-cause mortality in the prospective Shanghai Women's Health Study

Abstract Introduction: Indoor air pollution (IAP), mostly from coal burning, was responsible for approximately 3.5 million deaths from all-causes and over 100,000 disability-adjusted life years in 2010. The majority of studies conducted in the past have been retrospective, in rural and under developed populations with recent and high levels of exposure. We assessed the association between historic kitchen coal use and various causes of mortality in the prospective Shanghai Women's Health Study cohort. Methods: A cohort of 73,363 women was followed through December 2009 with a combination of in-person surveys every 2-3 years and annual linkage to a vital statistics registry database where all causes of mortality was recorded. A total of 3808 deaths were identified during the follow-up period. Cox proportional hazards models were used to estimate risk of mortality associated with in-home coal use. Models were adjusted for smoking status, family income, environmental tobacco smoke, occupational history, shift work, BMI, hormone therapy, and parity. Results: All-cause mortality was elevated 13% among ever coal users (Hazard Ratio (HR): 1.13; 95% CI: 1.04-1.23) compared to never-coal users. Coal use was most strongly associated with all-cause mortality among women who had more than 15 years of coal use (15-30 years: HR: 1.14; 95% CI: 1.02-1.26; &amp;gt;30 years: HR: 1.15; 95% CI: 1.04-1.26). Women with 15-30 years of coal use had a 21% elevation of cancer mortality (95% CI: 1.04-1.42), but no elevation was observed in women with &amp;gt;30 years of coal use (HR: 1.06; 95% CI: 0.91-1.24) compared to never-coal users. More than 30 years of coal use was associated with a 32% elevated risk of cardiovascular mortality (HR: 1.32; 95% CI: 1.11-1.57), and 62% elevated risk of myocardial infarction mortality (HR: 1.62; 95% CI: 1.01-2.63) compared to never-coal users. All-cause mortality was elevated in women who last lived in a coal burning home up to 20 years ago (&amp;gt;0-10 years: HR: 1.16; 95% CI: 1.04-1.28; &amp;gt;10-20 years: HR: 1.21; 95% CI: 1.09-1.35). Discussion: This is the first study of mortality and in-home coal use in a prospective study after much of Shanghai transitioned into a developed and urban city. Evidence from this study suggests that previous coal use could be related to excess cardiovascular and cancer deaths among women in Shanghai. Citation Format: Christopher Kim, Xiao-Ou Shu, H. Dean Hosgood, Bryan A. Bassig, Wei Jie Seow, Yongbin Xiang, Bu-Tian Ji, Wei Hu, Wong-Ho Chow, Yutang Gao, Nathaniel Rothman, Qing Lan. Past use of coal for cooking is associated with all-cause mortality in the prospective Shanghai Women's Health Study. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2184. doi:10.1158/1538-7445.AM2014-2184

Day of admission and risk of myocardial infarction mortality in a cardiac care unit in Basrah, Iraq.

Among many factors that may affect the in-hospital mortality among acute myocardial infarction (AMI) patients admitted to the cardiac care unit (CCU), the day and time of admission have been reported to play some role, but such relationship is controversial. The objective of the following study is to assess the effect of the day and time of admission on in-hospital mortality of patients with AMI. Retrospective analysis of data of all patients with AMI who were admitted to the CCU in Al-Sadr Teaching Hospital, Basrah, Iraq during 2010 was conducted. A total of 419 patients were included in this analysis. The mean age of patients was 62.4 ± 11.6 years, 64.9% of them were men. Admission during weekdays was greater than that during weekends (63.2% vs. 36.8%). Admission during off hours was greater than that during regular-hours (59.9% vs. 41.1%). Weekend admissions were more likely to be presenting with ST elevation myocardial infarction, complications and hypotension. A likewise pattern of baseline characteristics was found among patients admitted at the off-hours time. The overall in-hospital mortality rate was 16.5%. The weekend admission was associated with a higher unadjusted hospital mortality rate than that for weekday admission (23.4% vs. 12.5%, respectively; odds ratio [OR], 2.14; 95% confidence interval [CI], 1.27-3.61; P = 0.004). In multivariate analyzes, no statistically significant difference in mortality was found between weekend and weekday admissions (OR, 0.658; 95% CI, 0.311-1.392). Whereas, off-hours admission was significantly associated with a higher mortality (25.5% vs. 3%; P < 0.001), adjusted OR, 12.178; 95% CI, 3.846-38.442. Of predictors for the in-hospital outcome of AMI, day of admission had no significant influence on mortality, whereas off-hour admission was associated with an increased risk of AMI in-hospital mortality.

Mortality from myocardial infarction in relation to exposure to vibration and dust among a cohort of iron-ore miners in Sweden

ObjectivesThe aim of this study was to investigate myocardial infarction (MI) mortality in relation to exposure to hand/arm vibration (HAV) and whole body vibration (WBV) as well as exposure to...

Pesticides and Myocardial Infarction Incidence and Mortality Among Male Pesticide Applicators in the Agricultural Health Study

Acute organophosphate and carbamate pesticide poisonings result in adverse cardiac outcomes. The cardiac effects of chronic low-level pesticide exposure have not been studied. The authors analyzed self-reported lifetime use of pesticides reported at enrollment (1993-1997) and myocardial infarction mortality through 2006 and self-reported nonfatal myocardial infarction through 2003 among male pesticide applicators in the Agricultural Health Study. Using proportional hazard models, the authors estimated the association between lifetime use of 49 pesticides and fatal and nonfatal myocardial infarction. There were 476 deaths from myocardial infarction among 54,069 men enrolled in the study and 839 nonfatal myocardial infarctions among the 32,024 participants who completed the follow-up interview. Fatal and nonfatal myocardial infarctions were associated with commonly reported risk factors, including age and smoking. There was little evidence of an association between having used pesticides, individually or by class, and myocardial infarction mortality (e.g., insecticide hazard ratio (HR) = 0.91, 95% confidence interval (CI): 0.67, 1.24; herbicide HR = 0.74, 95% CI: 0.49, 1.10) or nonfatal myocardial infarction incidence (e.g., insecticide HR = 0.85, 95% CI: 0.66, 1.09; herbicide HR = 0.91, 95% CI: 0.61, 1.36). There was no evidence of a dose response with any pesticide measure. In a population with low risk for myocardial infarction, the authors observed little evidence of increased risk of myocardial infarction mortality or nonfatal myocardial infarction associated with the occupational use of pesticides.

Myocardial Infarction Mortality Risk After Treatment for Hodgkin Disease: A Collaborative British Cohort Study

Myocardial infarction is a major cause of excess long-term mortality in survivors of Hodgkin disease, but limited information exists on the effects of specific chemotherapy regimens used to treat these patients on their risk of death from myocardial infarction. We followed a cohort of 7033 Hodgkin disease patients who were treated in Britain from November 1, 1967, through September 30, 2000, and compared their risk of myocardial infarction mortality with that in the general population of England and Wales. All statistical tests were two-sided. A total of 166 deaths from myocardial infarction occurred in the cohort, statistically significantly more than expected (standardized mortality ratio [SMR] = 2.5, 95% confidence interval [CI] = 2.1 to 2.9), with an absolute excess risk of 125.8 per 100,000 person-years. Standardized mortality ratios decreased sharply with older age at first treatment, but absolute excess risks of death from myocardial infarction increased with older age up to age 65 years at first treatment. The statistically significantly increased risk of myocardial infarction mortality persisted through to 25 years after first treatment. Risks were increased statistically significantly and independently for patients who had been treated with supradiaphragmatic radiotherapy, anthracyclines, or vincristine. Risk was particularly high for patients treated with the doxorubicin, bleomycin, vinblastine, and dacarbazine regimen (SMR = 9.5, 95% CI = 3.5 to 20.6). Risk at 20 or more years after first treatment was particularly great for patients who had received supradiaphragmatic radiotherapy and vincristine without anthracyclines (SMR = 14.8, 95% CI = 4.8 to 34.5). The risk of death from myocardial infarction after treatment for Hodgkin disease remains high for at least 25 years. The increased risks are related to supradiaphragmatic radiotherapy but may also be related to anthracycline and vincristine treatment.