Cardiovascular Disease Events and Mortality After Myocardial Infarction Among Black and White Adults: REGARDS Study.
Ontology highlight
ABSTRACT: Background
Despite improvements in prognosis following myocardial infarction (MI), racial disparities persist. The objective of this study was to examine disparities between Black and White adults in cardiovascular disease (CVD), coronary heart disease, stroke, heart failure (HF), and mortality after MI and characteristics that may explain the disparities.Methods
This prospective cohort study included 1122 REGARDS (Reasons for Geographic and Racial Differences in Stroke) study participants with incident MI between 2003 and 2016. We followed participants for subsequent CVD events (MI, stroke, HF hospitalization, or death from CVD; n=431), coronary heart disease events (MI or death from coronary heart disease; (n=277), stroke (n=68), HF events (HF hospitalization or death from HF; n=191), and all-cause mortality (n=527; 3-year median follow-up after MI).Results
Among 1122 participants with incident MI, 37.5% were Black participants, 45.4% were women, and mean age was 73.2 (SD, 9.5) years. The unadjusted hazard ratio for CVD events comparing Black to White participants was 1.42 (95% CI, 1.17-1.71). Adjusting for sociodemographic characteristics did not attenuate the association (1.41 [95% CI, 1.14-1.73]), but further adjusting for pre-MI health status (1.25 [95% CI, 1.00-1.56]) and characteristics of the MI (1.01 [95% CI, 0.80-1.27]) resulted in substantial attenuation. Similar patterns were observed for the other outcomes, although the number of strokes was small.Conclusions
Black individuals had a higher risk of CVD events and mortality after MI than White individuals. The disparities were explained by health status before MI and characteristics of the MI. These findings suggest that both primordial prevention of risk factors and improved acute treatment strategies are needed to reduce disparities in post-MI outcomes.
SUBMITTER: Blackston JW
PROVIDER: S-EPMC7853403 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:BackgroundType 2 myocardial infarction (MI) and myocardial injury are associated with increased short-term mortality. However, data regarding long-term mortality are lacking.ObjectivesThis study compared long-term mortality among young adults with type 1 MI, type 2 MI, or myocardial injury.MethodsAdults age 50 years or younger who presented with troponin >99th percentile or the International Classification of Diseases code for MI over a 17-year period were identified. All cases were adjudicated as type 1 MI, type 2 MI, or myocardial injury based on the Fourth Universal Definition of MI. Cox proportional hazards models were constructed for survival free from all-cause and cardiovascular death.ResultsThe cohort consisted of 3,829 patients (median age 44 years; 30% women); 55% had type 1 MI, 32% had type 2 MI, and 13% had myocardial injury. Over a median follow-up of 10.2 years, mortality was highest for myocardial injury (45.6%), followed by type 2 MI (34.2%) and type 1 MI (12%) (p < 0.001). In an adjusted model, type 2 MI was associated with higher all-cause (hazard ratio: 1.8; 95% confidence interval: 1.2 to 2.7; p = 0.004) and cardiovascular mortality (hazard ratio: 2.7; 95% confidence interval: 1.4 to 5.1; p = 0.003) compared with type 1 MI. Those with type 2 MI or myocardial injury were younger and had fewer cardiovascular risk factors but had more noncardiovascular comorbidities. They were significantly less likely to be prescribed cardiovascular medications at discharge.ConclusionsYoung patients who experience a type 2 MI have higher long-term all-cause and cardiovascular mortality than those who experience type 1 MI, with nearly one-half of patients with myocardial injury and more than one-third of patients with type 2 MI dying within 10 years. These findings emphasize the need to provide more aggressive secondary prevention for patients who experience type 2 MI and myocardial injury.
| S-EPMC7382936 | biostudies-literature
Project description:To determine the validity of uric acid as a potential prognostic marker for long-term outcomes of patients with acute myocardial infarction (AMI) and those with AMI undergoing percutaneous coronary intervention (PCI). Methods: Systematic review and meta-analysis were performed. We retrieved data from retrospective and prospective cohort studies that investigated whether serum uric acid (SUA) level affects the prognosis of patients with AMI.Thirteen studies involving 9371 patients were included. High serum uric acid (HSUA) level increased mid/long-term mortality (risk ratio (RR)=2.32, 95% confidence intervals (CI): 2.00-2.70) and had higher short-term mortality (RR=3.09, 95% CI: 2.58-3.71), higher mid/long-term major adverse cardiovascular events (MACE) risk (RR=1.70, 95% CI: 1.54-1.88), and higher short-term MACE risk (RR=2.47, 95% CI: 2.08-2.92) for patients with AMI. In the PCI subgroup, the HSUA level also increased mid/long-term mortality (RR=2.33, 95% CI: 1.89 to 2.87) and had higher mid/long-term MACE risk (RR=1.64, 95% CI: 1.48-1.82), and higher short-term MACE risk (RR 2.43, 95% CI: 2.02-2.93) for patients who were treated with PCI after AMI. Particularly in the PCI subgroup, a higher short-term mortality (RR=6.70, 95% CI: 3.14-14.31) was presented in the group with lower HSUA cut-off level, and the mortality was higher than the group with higher HSUA cut-off level (RR=2.69, 95% CI: 2.09-3.46). Conclusion: The HSUA level significantly increased the mortality and MACE risk of patients with AMI. Mild elevation of SUA levels (normal range) have started to have a significant impact on the short-term mortality of patients who underwent PCI, and has not received the attention of previous studies. However, this condition should be further investigated.
| S-EPMC5541179 | biostudies-other
Project description:AimsOutcomes after myocardial infarction (MI) improved during recent decades alongside better risk factor management and implementation of guideline-recommended treatments. However, it is unknown whether this applies to stable patients who are event-free 1 year after MI.Methods and resultsUsing nationwide Danish registries, we included all patients with first-time MI during 2000-17 who survived 1 year free from bleeding and cardiovascular events (n = 82 108, median age 64 years, 68.2% male). Follow-up started 1 year after MI and continued through January 2022. Crude risks of mortality, cardiovascular events, and bleeding were estimated in consecutive 3-year periods. Standardized risks were calculated with respect to the distribution of age, sex, comorbidities, and treatments in the latter period. Guideline-recommended treatment use increased during the study period: e.g. statins (68.6-92.5%) and percutaneous coronary intervention (23.9-68.2%). The crude 5-year risks of outcomes decreased (all P-trend <0.001): Mortality, 18.6% (95% confidence interval [CI]: 17.9-19.2) to 12.5% (CI: 11.9-13.1); Recurrent MI, 7.5% (CI: 7.1-8.0) to 5.5% (CI: 5.1-6.0); Bleeding, 3.9% (CI: 3.6-4.3) to 2.7% (CI: 2.4-3.0). Crude 5-year risk of mortality in 2015-17 was as low as 2.6% for patients aged <60 years. Use of guideline-recommended treatments was associated with improved outcomes: After standardization for changes in treatments, 5-year risk of mortality in 2000-02 was 15.5% (CI: 14.9-16.2).ConclusionsFor patients who were event-free 1 year after MI, the long-term risks of mortality, cardiovascular events, and bleeding decreased significantly, along with an improved use of guideline-recommended treatments between 2000 and 2017. In the most recent period, 1 year after MI, the risk of additional events was lower than previously reported.
| S-EPMC9902154 | biostudies-literature
Project description:BackgroundFurin is the key enzyme involved in the cleavage of pro-BNP and plays a critical role in the cardiovascular system through its involvement in lipid metabolism, blood pressure regulation and the formation of atheromatous plaques. NT-proBNP and recently, corin, also a key enzyme in the cleavage of pro-BNP, have been accepted as predictors of prognosis after acute myocardial infarction (AMI). This cohort study was conducted to investigate the relationship between plasma furin and the prognostic outcomes of AMI patients.MethodsIn total, 1100 AMI patients were enrolled in the study and their plasma furin concentrations were measured. The primary endpoint was major adverse cardiac events (MACE), a composite of cardiovascular (CV) death, non-fatal myocardial infarction (MI) and non-fatal stroke. The associations between plasma furin concentration and AMI outcomes were explored using Kaplan-Meier curves and multivariate Cox regression analysis.ResultsThe results showed a slight increase in mean cTNT in patients with higher furin concentrations (P = 0.016). Over a median follow-up of 31 months, multivariate Cox regression analysis indicated that plasma furin was not significantly associated with MACE (HR 1.01; 95% CI 0.93-1.06; P = 0.807) after adjustment for potential conventional risk factors. However, plasma furin was associated with non-fatal MI (HR 1.09; 95% CI 1.01-1.17; P = 0.022) in the fully adjusted model. Subgroup analyses indicated no relationship between plasma furin and MACE in different subgroups.ConclusionsThis study found no association between plasma furin and risk of MACE. Thus, plasma furin may not be a useful predictor of poor prognosis after AMI. However, higher levels of plasma furin may be associated with a higher risk of recurrent non-fatal MI.
| S-EPMC8477572 | biostudies-literature
Project description:Background Previous studies have found associations between fine particulate matter <2.5 µm in diameter (PM2.5) and increased risk of cardiovascular disease (CVD) among populations with no CVD history. Less is understood about susceptibility of adults with a history of CVD and subsequent PM2.5-related CVD events and whether current regulation levels for PM2.5 are protective for this population. Methods and Results This retrospective cohort study included 96 582 Kaiser Permanente Northern California adults with a history of stroke or acute myocardial infarction. Outcome, covariate, and address data obtained from electronic health records were linked to time-varying 1-year mean PM2.5 exposure estimates based on residential locations. Cox proportional hazard models estimated risks of stroke, acute myocardial infarction, and cardiovascular mortality associated with PM2.5 exposure, adjusting for multiple covariates. Secondary analyses estimated risks below federal and state regulation levels (12 µg/m3 for 1-year mean PM2.5). A 10-µg/m3 increase in 1-year mean PM2.5 exposure was associated with an increase in risk of cardiovascular mortality (hazard ratio [HR], 1.20; 95% CI, 1.11-1.30), but no increase in risk of stroke or acute myocardial infarction. Analyses of <12 µg/m3 showed increased risk for CVD mortality (HR, 2.31; 95% CI, 1.96-2.71), stroke (HR, 1.41; 95% CI, 1.09-1.83]), and acute myocardial infarction (HR, 1.51; 95% CI, 1.21-1.89) per 10-µg/m3 increase in 1-year mean PM2.5. Conclusions Adults with a history of CVD are susceptible to the effects of PM2.5 exposure, particularly on CVD mortality. Increased risks observed at exposure levels <12 µg/m3 highlight that current PM2.5 regulation levels may not be protective for this susceptible population.
| S-EPMC8200700 | biostudies-literature
Project description:ImportanceChronic stress has been posited to contribute to racial disparities in cardiovascular health. Investigation of whether neighborhood- and individual-level stressors mediate this disparity is needed.ObjectiveTo examine whether racial differences in ideal cardiovascular health (ICH) are attenuated by experiences with neighborhood- and individual-level stressors within a racially and geographically diverse population sample.Design, setting, and participantsThis cross-sectional study examined data from 7720 participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study who completed the second in-home visit (2013-2016). The REGARDS study is a population-based, longitudinal study of 30 239 non-Hispanic Black and non-Hispanic White adults aged 45 years or older at baseline (2003-2007). Data for the present study were analyzed from June to July 2021 and in March 2022.ExposuresNeighborhood physical environment (eg, excessive noise, violence; scored from 7-28, with higher scores indicating more problems), neighborhood safety (scored as very safe, safe, or not safe), neighborhood social cohesion (eg, shared values; scored from 5-25, with higher scores indicating higher cohesion), perceived stress (eg, coping; scored from 0-16, with higher scores indicating greater perceived stress), and the experience of discrimination (yes or no).Main outcomes and measuresIdeal cardiovascular health (ICH), measured as a composite of 4 health behaviors (cigarette smoking, diet, physical activity, body mass index) and 3 health factors (blood pressure, cholesterol, and glucose levels).ResultsThe sample included 7720 participants (mean [SD] age, 71.9 [8.3] years; 4390 women [56.9%]; 2074 Black participants [26.9%]; and 5646 White participants [73.1%]). Black participants compared with White participants reported higher perceived stress (mean [SD] score, 3.2 [2.8] vs 2.8 [2.7]) and more often reported discrimination (77.0% vs 24.0%). Black participants also reported poorer neighborhood physical environment (mean [SD] score, 11.2 [3.8] vs 9.8 [2.9]) and social cohesion (mean [SD] score, 15.5 [2.0] vs 15.7 [1.9]) and more often reported their neighborhoods were unsafe (54.7% vs 24.3%). The odds of having a high total ICH score (ie, closer to ideal) were lower for Black adults compared with White adults, both overall (adjusted odds ratio [AOR], 0.53; 95% CI, 0.45-0.61) and by gender (men: AOR, 0.73 [95% CI, 0.57-0.93]; women: AOR, 0.45 [95% CI, 0.37-0.54]). In mediation analyses, the racial disparity in total ICH score was attenuated by neighborhood physical environment (5.14%), neighborhood safety (6.27%), neighborhood social cohesion (1.41%), and discrimination (11.01%). In stratified analyses, the factors that most attenuated the racial disparity in total ICH scores were neighborhood safety among men (12.32%) and discrimination among women (14.37%). Perceived stress did not attenuate the racial disparity in total ICH scores.Conclusions and relevanceIn this cross-sectional study of Black and White US adults aged 45 years and older, neighborhood-level factors, including safety and physical and social environments, and individual-level factors, including discrimination, attenuated racial disparities in cardiovascular health. Interventional approaches to improve ICH that separately target neighborhood context and discrimination by gender and race are warranted.
| S-EPMC10543067 | biostudies-literature
Project description:Despite improved treatment of myocardial infarction (MI), real-world patients still suffer substantial risk for subsequent cardiovascular events. Little is known about coagulation activity shortly after MI and whether coagulation activity markers may identify patients at increased risk despite contemporary treatment.To evaluate D-dimer concentration and thrombin generation potential shortly after discharge after MI and evaluate if these markers could predict the risk of future cardiovascular and bleeding events.Unselected MI patients (n?=?421) were included in the observational REBUS study (NCT01102933) and followed for two years. D-dimer concentrations, thrombin peak, and endogenous thrombin potential (ETP) were analyzed at inclusion (3-5 days after MI) and at early follow-up (after 2-3 weeks).Seventy-five patients (17.8%) experienced the composite endpoint (all-cause death, MI, congestive heart failure, or all-cause stroke), and 31 patients (7.4%) experienced a clinically relevant bleeding event. D-dimer concentrations at early follow-up were associated with the composite endpoint (HR [per SD increase] 1.51 [95% CI 1.22-1.87]) and with clinically relevant bleeding (HR [per SD increase] 1.80 [95% CI 1.32-2.44]). Thrombin generation potential was not significantly associated with either the composite endpoint or with clinically relevant bleeding. Higher thrombin peak and ETP at early follow-up were both inversely associated with stroke (HR [per SD increase] 0.50 [95% CI 0.30-0.81] and 0.43 [95% CI 0.22-0.83], respectively).In unselected MI patients treated according to contemporary guidelines, D-dimer measurements may identify patients at increased risk of new cardiovascular and bleeding events. The inverse association of thrombin generation potential and risk of stroke has to be further investigated.
| S-EPMC5810226 | biostudies-literature
Project description:BackgroundAPOL1 renal risk variants are strongly associated with chronic kidney disease in Black adults, but reported associations with cardiovascular disease (CVD) have been conflicting.MethodsWe examined associations of APOL1 with incident coronary heart disease (n=323), ischemic stroke (n=331), and the composite CVD outcome (n=500) in 10 605 Black participants of the REGARDS study (Reasons for Geographic and Racial Differences in Stroke). Primary analyses compared individuals with APOL1 high-risk genotypes to APOL1 low-risk genotypes in Cox proportional hazards models adjusted for CVD risk factors and African ancestry.ResultsAPOL1 high-risk participants were younger and more likely to have albuminuria at baseline than APOL1 low-risk participants. The risk of incident stroke, coronary heart disease, or composite CVD end point did not significantly differ by APOL1 genotype status in multivariable models. The association of APOL1 genotype with incident composite CVD differed by diabetes mellitus status (Pinteraction=0.004). In those without diabetes mellitus, APOL1 high-risk genotypes associated with greater risk of incident composite CVD (hazard ratio, 1.67; 95% confidence interval, 1.12-2.47) compared with those with APOL1 low-risk genotypes in multivariable adjusted models. This latter association was driven by ischemic strokes (hazard ratio, 2.32; 95% confidence interval, 1.33-4.07), in particular, those related to small vessel disease (hazard ratio, 5.10; 95% confidence interval, 1.55-16.56). There was no statistically significant association of APOL1 genotypes with incident CVD in subjects with diabetes mellitus. The APOL1 high-risk genotype was associated with higher stroke risk in individuals without but not those with chronic kidney disease in fully adjusted models.ConclusionsAPOL1 high-risk status is associated with CVD events in community-dwelling Black adults without diabetes mellitus.
| S-EPMC6339526 | biostudies-literature
Project description:BackgroundThe epigenetic landscape underlying cardiovascular disease (CVD) is not completely understood and the clinical value of the identified biomarkers is still limited. We aimed to identify differentially methylated loci associated with acute myocardial infarction (AMI) and assess their validity as predictive and causal biomarkers.ResultsWe designed a case-control, two-stage, epigenome-wide association study on AMI (ndiscovery = 391, nvalidation = 204). DNA methylation was assessed using the Infinium MethylationEPIC BeadChip. We performed a fixed-effects meta-analysis of the two samples. 34 CpGs were associated with AMI. Only 12 of them were available in two independent cohort studies (n ~ 1800 and n ~ 2500) with incident coronary and cardiovascular disease (CHD and CVD, respectively). The Infinium HumanMethylation450 BeadChip was used in those two studies. Four of the 12 CpGs were validated in association with incident CHD: AHRR-mapping cg05575921, PTCD2-mapping cg25769469, intergenic cg21566642 and MPO-mapping cg04988978. We then assessed whether methylation risk scores based on those CpGs improved the predictive capacity of the Framingham risk function, but they did not. Finally, we aimed to study the causality of those associations using a Mendelian randomization approach but only one of the CpGs had a genetic influence and therefore the results were not conclusive.ConclusionsWe have identified 34 CpGs related to AMI. These loci highlight the relevance of smoking, lipid metabolism, and inflammation in the biological mechanisms related to AMI. Four were additionally associated with incident CHD and CVD but did not provide additional predictive information.
| S-EPMC8061080 | biostudies-literature
Project description:Racial disparities in acute myocardial infarction treatment may be due to differences in admitting hospitals. Little is known about factors associated with hospital selection for black and white acute myocardial infarction patients.We identified black and white Medicare beneficiaries with acute myocardial infarction in 63 hospital referral regions with at least 50 black admissions during 2005 (n=65,633). We calculated distance from patient home to hospital referral region hospitals using ZIP code centroids. We assessed hospital quality using a composite score made up of hospital risk-adjusted 30-day mortality and acute myocardial infarction performance measures. Hospitals with a score in the top 20% were categorized as high quality, and those in the lowest 20% as low quality. We used conditional multinomial logit models to examine differences in hospital selection for blacks and whites. On average, blacks lived closer to revascularization hospitals (mean, 3.8 versus 6.8 miles; P<0.001) and to high-quality hospitals (mean, 5.6 versus 9.7 miles; P<0.001). After distance was accounted for, blacks were relatively less likely (P<0.001) to be admitted to revascularization hospitals (risk ratio [RR], 0.87; 95% confidence interval [CI], 0.80 to 0.95) and to high-quality hospitals (RR, 0.88; 95% CI, 0.801 to 0.95) but more likely (P<0.001) to be admitted to low-quality hospitals (RR, 1.17; 95% CI, 1.05 to 1.29). In analyses matched by home ZIP code, differences in admissions to revascularization (RR, 0.92; 95% CI, 0.80 to 1.05), high-quality (RR, 0.94; 95% CI, 0.81 to 1.07), and low-quality (RR, 1.15; 95% CI, 0.94 to 1.35) hospitals were not significant.Differences in admissions to revascularization and high-quality hospitals may contribute to disparities in acute myocardial infarction care. These differences may be due in part to residential ZIP code characteristics.
| S-EPMC3142883 | biostudies-literature