Risk Of Acute Myocardial Infarction Research Articles

Causal effect of gallstone disease on the risk of coronary heart disease or acute myocardial infarction: a Mendelian randomization study

Gallstone disease (GSD) is thought to be associated with the risk of coronary heart disease (CHD) or acute myocardial infarction (AMI), which may be due to abnormal cholesterol metabolism. We used multiple Mendelian randomization (MR) methods based on publicly available genome-wide association study data to assess whether this association is genetically causal and to search for loci driving causality. Pooled data for GSD were obtained from FinnGen Biobank and Biobank Japan, while CHD and AMI were obtained as pooled data from the CARDIoGRAMplusC4D consortium. In this MR study, we found a significant negative causal effect of genetic susceptibility to GSD on AMI in the Finnish population, but no causal effect was found on CHD. This causal effect was not confounded by reverse causality and the same findings were obtained in the Japanese population. Furthermore, the negative causal effect of GSD on AMI risk may be driven by the rs4245791-regulated ABCG5/8 protein. In conclusion, the results of this MR study support a negative causal effect of GSD on AMI and suggest that rs4245791 is the causal driver locus of this effect, which provides new ideas and evidence for the prevention and etiologic study of AMI in patients with GSD.

Lipoprotein(a) and Long-Term Recurrent Infarction After an Acute Myocardial Infarction

Lipoprotein(a) (Lp[a]) is an emerging risk factor for incident ischemic heart disease. However, its role in risk stratification in in-hospital survivors to an index acute myocardial infarction (AMI) is scarcer, especially for predicting the risk of long-term recurrent AMI. We aimed to assess the relation between Lp(a) and very long-term recurrent AMI after an index episode of AMI. It is a retrospective analysis that included 1,223 consecutive patients with an AMI discharged from October 2000 to June 2003 in a single-teaching center. Lp(a) was assessed during index admission in all cases. The relation between Lp(a) at discharge and total recurrent AMI was evaluated through negative binomial regression. The mean age of the patients was 67.0 ± 12.3years, 379 (31.0%) were women, and 394 (32.2%) were diabetic. The index event was more frequently non-ST-segment elevation myocardial infarction (66.0%). The median Lp(a) was 28.8 (11.8 to 63.4)mg/100ml. During a median follow-up of 9.9 (4.6 to 15.5)years, 813 (66.6%) deaths and 1,205 AMI in 532 patients (43.5%) occurred. Lp(a) values were not associated with an increased risk of long-term all-cause mortality (p=0.934). However, they were positively and nonlinearly associated with an increased risk of total long-term reinfarction (p=0.016). In the subgroup analysis, there was no evidence of a differential effect for the most prevalent subgroups. In conclusion, after an AMI, elevated Lp(a) values assessed during hospitalization were associated with an increased risk of recurrent reinfarction in the very long term. Further prospective studies are warranted to evaluate their clinical implications.

Cardiovascular Risk Associated with Alpha-1 Antitrypsin Deficiency (AATD) Genotypes: A Meta-Analysis with Meta-Regressions.

Alpha-1 antitrypsin deficiency (AATD) can result in severe liver and respiratory disorders. The uninhibited elastase activity on the elastic tissue of arterial walls suggests that AATD may also impact vascular health. Thus, we performed a meta-analysis of the studies evaluating cardiovascular risk in individuals with AATD and non-AATD controls. A systematic literature search was conducted in the main scientific databases according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Differences between cases and controls were expressed as odds ratios (OR) with 95% confidence intervals (95%CI). The protocol was registered on PROSPERO under the identification number CRD42023429756. The analysis of eight studies showed that, with a prevented fraction of disease of 15.0% and a corresponding OR of 0.779 (95%CI: 0.665-0.912; p = 0.002), a total of 24,428 individuals with AATD exhibited a significantly lower risk of ischemic heart disease compared to 534,654 non-AATD controls. Accordingly, given a prevented fraction of disease of 19.5%, a lower risk of acute myocardial infarction was documented when analyzing four studies on 21,741 cases and 513,733 controls (OR: 0.774; 95%CI: 0.599-0.999; p = 0.049). Sensitivity and subgroup analyses substantially confirmed results. Meta-regression models suggested that these findings were not influenced by AATD genotypes or prevalence of chronic obstructive pulmonary disease (COPD) among cases and controls, while higher differences in the prevalence of male sex (Z-score: 3.40; p < 0.001), hypertension (Z-score: 2.31; p = 0.021), and diabetes (Z-score: 4.25; p < 0.001) were associated with a lower effect size. Individuals with AATD may exhibit a reduced risk of ischemic heart disease, even in the presence of mild deficiency of the serine protease inhibitor. Although caution is warranted due to the observational nature of the data, future pharmacological and rehabilitation strategies should also take this controversial relationship into account.

Peripheral Inflammatory Factors and Acute Myocardial Infarction Risk: A Mendelian Randomization Study.

Previous observational studies have confirmed the relationship between inflammation and acute myocardial infarction (AMI), but genetic evidence is still lacking. The aim of this study was to explore the bidirectional association of multiple peripheral inflammatory factors with this disease at the genetic level. Summary data for AMI and several peripheral inflammatory factors (such as interleukin-10 and interleukin-18) were collected from published genome-wide correlation studies. Based on the correlation, independence, and exclusivity assumptions, a total of 9 to 110 instrumental variables were selected from these summary data to predict the above traits. Two-sample Mendelian randomization methods, including inverse-variance weighted (IVW), were used to make causal inferences between exposures and outcomes. Sensitivity analyses including Cochran's Q, MR-Egger intercept, leave-one-out, forest plot, and MR-PRESSO were adopted to assess heterogeneity and horizontal pleiotropy. The IVW reported that elevated peripheral levels of interleukin-10 and interleukin-18 were nominally associated with a reduced risk of AMI (OR = 0.876, 95% CI = 0.788 ~ 0.974, P = 0.015; OR = 0.934, 95% CI = 0.875 ~ 0.997, P = 0.040). The IVW also reported that the risk of AMI nominally increased the peripheral level of interleukin-10 (OR = 1.062, 95% CI = 1.003 ~ 1.124, P = 0.040). No significant heterogeneity or horizontal pleiotropy were found by sensitivity analyses. Both interleukin-10 and interleukin-18 were peripheral inflammatory factors genetically associated with AMI. In particular, combined with previous knowledge, interleukin-10 may have a protective effect on the onset, progression, and prognosis of the disease.

Investigating the causal interplay between sleep traits and risk of acute myocardial infarction: a Mendelian randomization study

BackgroundFew studies have investigated the joint effects of sleep traits on the risk of acute myocardial infarction (AMI). No previous study has used factorial Mendelian randomization (MR) which may reduce confounding, reverse causation, and measurement error. Thus, it is prudent to study joint effects using robust methods to propose sleep-targeted interventions which lower the risk of AMI.MethodsThe causal interplay between combinations of two sleep traits (including insomnia symptoms, sleep duration, or chronotype) on the risk of AMI was investigated using factorial MR. Genetic risk scores for each sleep trait were dichotomized at their median in UK Biobank (UKBB) and the second survey of the Trøndelag Health Study (HUNT2). A combination of two sleep traits constituting 4 groups were analyzed to estimate the risk of AMI in each group using a 2×2 factorial MR design.ResultsIn UKBB, participants with high genetic risk for both insomnia symptoms and short sleep had the highest risk of AMI (hazard ratio (HR) 1.10; 95% confidence interval (CI) 1.03, 1.18), although there was no evidence of interaction (relative excess risk due to interaction (RERI) 0.03; 95% CI −0.07, 0.12). These estimates were less precise in HUNT2 (HR 1.02; 95% CI 0.93, 1.13), possibly due to weak instruments and/or small sample size. Participants with high genetic risk for both a morning chronotype and insomnia symptoms (HR 1.09; 95% CI 1.03, 1.17) and a morning chronotype and short sleep (HR 1.11; 95% CI 1.04, 1.19) had the highest risk of AMI in UKBB, although there was no evidence of interaction (RERI 0.03; 95% CI −0.06, 0.12; and RERI 0.05; 95% CI –0.05, 0.14, respectively). Chronotype was not available in HUNT2.ConclusionsThis study reveals no interaction effects between sleep traits on the risk of AMI, but all combinations of sleep traits increased the risk of AMI except those with long sleep. This indicates that the main effects of sleep traits on AMI are likely to be independent of each other.

Targeted Plasma Metabolomics Reveals Association of Acute Myocardial Infarction Risk with the Dynamic Balance between Trimethylamine-N-oxide, Betaine, and Choline.

The relationship between trimethylamine-N-oxide (TMAO), betaine, and choline with acute myocardial infarction (AMI) end point remains unclear. We analyzed plasma TMAO, betaine, and choline concentrations in AMI cases and non-AMI community-dwelling controls by LC-MS/MS to understand how the balance between these metabolites helps to reduce AMI risk. Results showed that the odds ratio (OR) for the highest versus lowest quartiles of betaine was 0.30 (95% CI, 0.10-0.82) after adjustment for AMI risk factors, and the unadjusted OR for quartile 3 versus quartile 1 of TMAO was 2.47 (95% CI, 1.02-6.17) (p < 0.05). The study populations with "high betaine + low TMAO" had a significant protective effect concerning AMI with a multivariable-adjusted OR of 0.20 (95% CI, 0.07-0.55) (p < 0.01). Multivariate linear regression showed that the chronological age was correlated with TMAO concentrations among AMI patients (95% CI, 0.05-3.24, p < 0.01) but not among the controls. This implies a further potential interplay between age and metabolite combination─AMI risk association.

Bioinformatics analysis of potential common pathogenic mechanisms for systemic lupus erythematosus and acute myocardial infarction.

Systemic lupus erythematosus (SLE) patients have a higher risk of acute myocardial infarction (AMI) compared to the general population. However, the underlying common mechanism of this association is not fully understood. This study aims to investigate the molecular mechanism of this complication. Gene expression profiles of SLE (GSE50772) and AMI (GSE66360) were obtained from the Gene Expression Omnibus (GEO) database. Common differentially expressed genes (DEGs) in SLE and AMI were identified, and functional annotation, protein-protein interaction (PPI) network analysis, module construction, and hub gene identification were performed. Additionally, transcription factor (TF)-gene regulatory network and TF-miRNA regulatory network were constructed for the hub genes. 70 common DEGs (7 downregulated genes and 63 upregulated genes) were identified and were mostly enriched in signaling pathways such as the IL-17 signaling pathway, TNF signaling pathway, lipid metabolism, and atherosclerosis. Using cytoHubba, 12 significant hub genes were identified, including IL1B, TNF, FOS, CXCL8, JUN, PTGS2, FN1, EGR1, CXCL1, DUSP1, MMP9, and ZFP36. This study reveals a common pathogenesis of SLE and AMI and provides new perspectives for further mechanism research. The identified common pathways and hub genes may have important clinical implications for the prevention and treatment of AMI in SLE patients.

Changes in proteinuria and the associated risks of ischemic heart disease, acute myocardial infarction, and angina pectoris in Korean population.

Proteinuria is widely used to predict cardiovascular risk. However, there is insufficient evidence to predict how changes in proteinuria may affect the incidence of cardiovascular disease. The study included 265,236 Korean adults who underwent health checkups in 2003-2004 and 2007-2008. They were categorized into 4 groups based on changes in proteinuria (negative: negative → negative; resolved: proteinuria ≥1+ → negative; incident: negative → proteinuria ≥1+; persistent: proteinuria ≥1+ → proteinuria ≥1+). We conducted 6 years of follow-up to identify the risks of developing ischemic heart disease (IHD), acute myocardial infarction (AMI), and angina pectoris according to changes in proteinuria. A multivariate Cox proportional-hazards model was used to calculate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for incident IHD, AMI, and angina pectoris. The IHD risk (expressed as HR [95% CI]) was the highest for persistent proteinuria, followed in descending order by incident and resolved proteinuria, compared with negative proteinuria (negative: reference, resolved: 1.211 [95% CI, 1.104 to 1.329], incident: 1.288 [95% CI, 1.184 to 1.400], and persistent: 1.578 [95% CI, 1.324 to 1.881]). The same pattern was associated with AMI (negative: reference, resolved: 1.401 [95% CI, 1.048 to 1.872], incident: 1.606 [95% CI, 1.268 to 2.035], and persistent: 2.069 [95% CI, 1.281 to 3.342]) and angina pectoris (negative: reference, resolved: 1.184 [95% CI, 1.065 to 1.316], incident: 1.275 [95% CI, 1.160 to 1.401], and persistent: 1.554 [95% CI, 1.272 to 1.899]). Experiencing proteinuria increased the risks of IHD, AMI, and angina pectoris even after proteinuria resolved.

Adipokines and Inflammatory Markers in Acute Myocardial Infarction Patients with and without Obstructive Sleep Apnea: A Comparative Analysis.

An association has been suggested between acute myocardial infarction (AMI) and obstructive sleep apnea (OSA). Considering the role of adipose-tissue-derived inflammatory mediators (adipokines) and the shared risk factor of obesity in OSA and AMI, this study aimed to investigate the involvement of adipokines in AMI patients with and without OSA. Serum levels of adipokines and inflammatory mediators were quantified, and home respiratory polygraphy was conducted. A total of 30 AMI patients and 25 controls were included. Patients with AMI exhibited elevated levels of resistin (7.4 vs. 3.7 ng/mL), interleukin-6 (8.8 vs. 1.3 pg/mL), and endothelin-1 (3.31 vs. 1.8 pg/mL). Remarkably, AMI patients with concomitant OSA exhibited higher levels of resistin (7.1 vs. 3.7 ng/mL), interleukin-6 (8.9 vs. 1.3 pg/mL), endothelin-1 (3.2 vs. 1.8 pg/mL), creatin kinase (1430 vs. 377 U/L), creatine kinase-MB (64.6 vs. 9.7 ng/mL), and troponin T (2298 vs. 356 pg/mL) than their non-OSA counterparts. Leptin showed a correlation with OSA severity markers. OSA was associated with greater cardiac damage in AMI patients. Our findings underscore that adipokines alone are not sufficient to discriminate the risk of AMI in the presence of OSA. Further research is necessary to determine the potential mechanisms contributing to exacerbated cardiac damage in patients with both conditions.

Chronic rhinosinusitis is not associated with increased incidence of acute myocardial infarction: A national population-based study.

Chronic rhinosinusitis (CRS) is one of the most prevalent upper respiratory tract diseases. However, little is known the effect of CRS on the cardiovascular aspects of patients. This study aimed to investigate the incidence of acute myocardial infarction (AMI) in patients with CRS compared with that in the general population. This retrospective cohort study was performed using the Korean National Health Insurance Service (NHIS) database. To minimize confounding, age, sex, and cardiovascular risk profiles were adjusted. The primary endpoint was newly diagnosed AMI in patients between January 2005 and December 2018. The relative risk of AMI in patients with CRS was compared with that in controls. Kaplan-Meier survival curves and Cox proportional regression tests were used for statistical analyses. Among 5,179,981 patients from the NHIS database, 996,679 patients with CRS were selected. The control group was 10 times (n = 9,966,790) the number of individuals in the CRS group. The CRS group had better cardiovascular profiles than those of the control group and had an adjusted hazard ratio of 0.99 (95% confidence interval, 0.97-1.02) for AMI. There was no significant association between the two groups regardless of the presence of nasal polyps. This is the first study adjusting cardiovascular risk profiles and analyzing the relationship between CRS and AMI. CRS was not associated with a high incidence of AMI after adjusting for cardiovascular risk factors.

Differentiated approach to glycemic management in type 2 diabetic patients during inpatient treatment of acute myocardial infarction: glycemic control and long-term prognosis

BACKGROUND: The risk of acute myocardial infarction (AMI) in patients with type 2 diabetes mellitus (T2DM) is 2 times higher than without DM. Previously an association between the time in the target range of glycemia during hospitalization of AMI in patients with T2DM (hTIR — «hospital time in range») and long-term prognosis was found. It is supposed that a differentiated approach to glycemic management will help to achieve a higher level of hTIR and will lead to an improved prognosis.AIM: To evaluate the effectiveness of differentiated approach to glycemic management in patients with T2DM during inpatient treatment of AMI and impact on long-term prognosis.MATERIALS AND METHODS: The study included patients with T2DM who were hospitalized with AMI with ST-segment elevation and underwent percutaneous coronary intervention. A total amount of patients was 161; 102 were in the main group, 59 in the control group. There was a differentiated approach to glycemia management based on phenotype determination in the main group. Insulin therapy was prescribed to patients with the 1st phenotype during the entire inpatient treatment. Patients with the second phenotype received insulin therapy followed by switching oral antidiabetic drugs (OAD). Patients of the 3rd phenotype were prescribed only OAD. In the control group, therapy of T2DM was prescribed according to the standard hospital procedures based on current clinical recommendations.RESULTS: In the main group, 22 patients (22%) were in the 1st phenotype, 54 (53%) –in the 2nd, 26 (25%) –in the 3rd. The average glycemia during hospitalization in the main group was lower than in the control group: 9.4±1.7 mmol/l vs 10.3±2.3 mmol/l (p=0.006). The hTIR in the main group was 58 [53; 71]% vs 46 [33; 63]% in the control group (p&lt;0.001). It was shown that when hTIR &gt; 55% is reached, the risk of cardiovascular death within a year after hospitalization is reduced by 80%.CONCLUSION: The differentiated approach to glycemic management in patients with T2DM leads to an improvement in glycemic control during inpatient treatment of AMI and is accompanied by a tendency to a lower incidence of cardiovascular death within a year after hospitalization. Achieving hTIR &gt; 55% is associated with a multifold reduction of the risk of cardiovascular death in a year. About 25% of patients with DM2 during inpatient treatment of AMI do not need the insulin therapy.

Appendectomy Mitigates Coxsackievirus B3-Induced Viral Myocarditis.

Appendix has a distinct abundance of lymphatic cells and serves as a reservoir of microbiota which helps to replenish the large intestine with healthy flora. And it is the primary site of IgA induction, which shapes the composition of the intestinal microbiota. Recent population-based cohort studies report that appendectomy is associated with an increased risk of acute myocardial infarction and ischemic heart disease. Here, whether appendectomy has an effect on the occurrence and development of coxsackievirus B3 (CVB3)-induced viral myocarditis is studied. 103 TCID50 CVB3 was inoculated i.p. into appendectomized and sham-operated mice. RNA levels of viral load and pro-inflammatory cytokines in the hearts and the intestine were detected by RT-PCR. Compared to sham-operated mice, appendectomized mice exhibited attenuated cardiac inflammation and improved cardiac function, which is associated with a systemic reduced viral load. Appendectomized mice also displayed a reduction in cardiac neutrophil and macrophage infiltration and pro-inflammatory cytokine production. Mechanistically, we found that CVB3 induced an early and potent IL-10 production in the cecal patch at 2 days post infection. Appendectomy significantly decreased intestinal IL-10 and IL-10+ CD4+ Treg frequency which led to a marked increase in intestinal (primary entry site for CVB3) anti-viral IFN-γ+ CD4+ T and IFN-γ+ CD8+ T response and viral restriction, eventually resulting in improved myocarditis. Our results suggest that appendix modulates cardiac infection and inflammation through regulating intestinal IL-10+ Treg response.

High-Sensitivity Cardiac Troponin Assays: Ready for Prime Time!

Rapid and accurate triage of patients presenting with chest pain to an emergency department (ED) is critical to prevent ED overcrowding and unnecessary resource use in individuals at low risk of acute myocardial infarction (AMI) and to efficiently and effectively guide patients at high risk to definite therapy. The use of biomarkers for rule-out or rule-in of suspected AMI has evolved substantially over the last several decades. Previously well-established biomarkers have been replaced by cardiac troponin (cTn). High-sensitivity cTn (hs-cTn) assays represent the newest generation of cTn assays and offer tremendous advantages, including improved sensitivity and precision. Still, implementation of these assays in the United States lags behind several other areas of the world. Within this educational review, we discuss the evolution of biomarker testing for detection of myocardial injury, address the specifics of hs-cTn assays and their recommended use within triage algorithms, and highlight potential challenges in their use. Ultimately, we focus on implementation strategies for hs-cTn assays, as they are now clearly ready for prime time.

Climate Change Adaptation: Exploring the Risk of Acute Myocardial Infarction in Hot Climate Naïve Population Immigrating to Hot Climate Country

Climate Change Adaptation: Exploring the Risk of Acute Myocardial Infarction in Hot Climate Naïve Population Immigrating to Hot Climate Country

Impact of Chronic Coronary Artery Disease and Revascularization Strategy in Patients with Severe Aortic Stenosis Who Underwent Transcatheter Aortic Valve Implantation

The prognostic impact of coronary artery disease (CAD) after transcatheter aortic valve implantation (TAVI) is controversial. The aim of this study is to investigate the impact of CAD and different revascularization strategies on clinical outcomes in patients who underwent TAVI with third generation devices. Patients enrolled in the national observational Observational Study of Effectiveness of SAVR-TAVI Procedures for Severe Aortic Stenosis Treatment II study were stratified according to the presence of CAD (CAD+, n=1,130) versus no CAD (CAD-, n=1,505), and compared using a propensity matched analysis. CAD+ group was further stratified according to the revascularization strategy: no revascularization (n=331), revascularization performed >90days before index-TAVI (n=417) and coronary revascularization performed <90days before index-TAVI or during TAVI (n=382). In-hospital, 30-day and 1-year clinical outcomes were estimated. The mean age of the overall population was 81.8years; 54.9% of patients were female. Propensity score matching yielded 813 pairs and their 30-day all-cause mortality was comparable (p=0.480). Major periprocedural adverse events were also similar between the groups. At 1-year follow-up, the rate of major adverse cardiac and cerebrovascular events (MACCEs) and all-cause mortality were similar between the groups (p=0.732 and p=0.633, respectively). Conversely, patients with CAD experienced more often myocardial infarction and need for percutaneous coronary intervention at 1year (p=0.007 and p=0.001, respectively). Neither CAD nor revascularization strategy were independent predictors of 1-year MACCE. About 40% of patients presenting with severe AS and who underwent TAVI had concomitant CAD. The presence of CAD had no impact on all-cause mortality and MACCE 1-year after TAVR. However, CAD carries a higher risk for acute myocardial infarction and need of percutaneous coronary intervention during follow-up.

A novel metabolic reprogramming strategy for the treatment of targeting to heart injury-mediated macrophages.

M1 macrophages polarization has been reported as the direct risk of acute myocardial infarction (AMI) occurrence and worsen AMI prognosis, especially for hyperinflammation-associated AMI. However, clinic treatments remain challenges, including off-target and side-effects. The development of enzyme mimetics could provide effective treatments for a wide variety of diseases. Herein, nanomaterials were used to create artificial hybrid nanozymes. In this study, we synthesized in situ zeolitic imidazolate framework nanozyme (ZIF-8zyme) with anti-oxidative and anti-inflammatory ability to repair microenvironment via reprogramming M1 macrophages polarization. In vitro study reported that a metabolic reprogramming strategy that the improvement of glucose import and glycolysis with ZIF-8zyme via inhibiting ROS levels led to a metabolic crisis within the macrophages. ZIF-8zyme shifted the polarization of M1 macrophages toward higher production of M2 phenotype, decreased proinflammatory cytokines secretion, and promoted significant survival of cardiomyocytes under hyperinflammation condition. Moreover, ZIF-8zyme elicits more potent macrophages-polarizing effects under hyperinflammation condition. Therefore, metabolic reprogramming strategy based on ZIF-8zyme is a promising AMI therapy, especially for hyperinflammation-associated AMI.

The Incidence and Risk Factors of Acute Myocardial Infarction Among Patients with Gastrointestinal bleeding: A Retrospective Study.

Patients with gastrointestinal bleeding (GIB) and acute myocardial infarction (AMI) have higher mortality than that with either GIB or AMI alone. The aims of this study were to determine the incidence and risk factors of AMI in patients with GIB. From January 2015 to January 2018, we retrospectively studied 1287 patients with GIB in Renmin Hospital of Wuhan University. Various demographic, laboratory and outcome data were reviewed by charts. Thirty-seven patients had AMI and were placed in AMI group and the rest 1250 patients were in non-AMI group. Patients with AMI were more likely to be older than 70 years, have hypertension, coronary heart disease, chronic kidney disease, and have the recent history of taking aspirin before admission. The ROC curve of hemoglobin (HB) on admission showed area under curve was 0.762, the optimal cut-off value is 76.5g/L. Logistic regression analysis showed that age ≥ 70 years old, coronary heart disease and HB < 76.5g/L on admission were independent risk factors of AMI in patients with GIB. The mortality of patients during hospitalization in AMI group and in non-AMI group were 45.95% and 5.48%, respectively. Patients who displayed a history of liver disease and HB < 76.5g/L on admission had a higher death rate. GIB increased the risk of subsequent AMI, especially in patients over 70 years old, with history of coronary heart disease and HB < 76.5g/L on admission. Patients with GIB and AMI who had history of liver disease and HB < 76.5g/L on admission had a higher mortality rate. Clinicians should identify the high-risk patients of AMI among the GIB population early and prevent AMI.

Association of systemic immune inflammation index and system inflammation response index with clinical risk of acute myocardial infarction.

Systemic immune inflammatory index (SII) and systemic inflammatory response index (SIRI) are combinations of non-specific inflammatory and adaptive immune response impairments associated with cardiovascular disease. Yet little analysis has been done on SII, SIRI and acute myocardial infarction (AMI) prognosis. The purpose of this study was to investigate the correlation of SII and SIRI with clinical risk factors such as GRACE, Gensini, and QTc after acute myocardial infarction. This study enrolled 310 patients with AMI from February 1, 2018, to December 31, 2022, at our institution. Routine blood items calculated SII and SIRI. Two groups were divided according to whether MACE occurred: the MACE group (81 cases) and the NMACE group (229 cases); each group was divided into three groups according to the SII and SIRI tertiles. The relationship between SII, SIRI and MACE was analyzed using multifactorial logistic regression analysis after adjusting for confounders; ROC curves were plotted to examine the predictive value of SII and SIRI for MACE. The correlation between SII and SIRI and potential risk factors such as Gensini, QTc and GRACE was further analyzed. The study enrolled 310 patients, comprising 248 men (80%, mean age 60.73 ± 13.695 years) and 62 women (20%, mean age 69.79 ± 11.555 years). In the regression model completely adjusted for confounders, the risk of MACE was higher in AMI patients with SII > 11.00 [OR = 1.061,95% CI (1.018,1.105)] than in SII < 5.98; the risk of MACE was 115.3% higher in AMI patients with SIRI (1.72-3.68) [OR = 2.153, 95% CI (1.251, 3.705)] was 115.3% higher in AMI patients with SIRI < 1.72 and the risk of MACE was 25.1% higher in AMI patients with SIRI > 3.68 [OR = 1.251, 95% CI (1.123, 1.394)] than in AMI patients with SIRI < 1.72. In addition, SII, SIRI, and potential post-infarction risk factors (Gensini, QTc, and GRACE) were also associated. SII and SIRI have been significantly associated with post-myocardial infarction MACE and the predictive potential clinically integrated risk factors in AMI patients, for which more attention should be paid to targeted anti-inflammatory therapy in AMI patients to further reduce the incidence of prognostic MACE in AMI patients.

Heart rate reactivity mediates the relationship between trait gratitude and acute myocardial infarction

ObjectiveThis study examines the relationship between trait gratitude and acute myocardial infarction. A burgeoning body of literature suggests that gratitude can play a role in regulating individual’s cardiovascular responses to stress which in turn, may reduce the incidence of cardiovascular disease such as acute myocardial infarction. However, to date no research has examined these effects. MethodThis study used the Mid-Life in the United States dataset (MIDUS; N = 1031) to assess these relationships. Participants completed a standardised cardiovascular stress-testing laboratory protocol and were assessed at a second time-point; on average 6.7 years later. ResultsResults from logistic parallel mediation models suggest that trait gratitude was found to be significantly associated with reduced risk of acute myocardial infarction through the mechanism of increased heart rate reactivity, β = −0.098, 95%CI [− 0.331, − 0.010]. However, neither systolic nor diastolic blood pressure reactivity mediated this relationship. ConclusionsThese findings suggest that gratitude may be associated with certain aspects of physical health. Specifically, our study reveals a potential link between gratitude and cardiovascular reactivity, which could be a mechanism through which trait gratitude contributes to reductions in the risk of myocardial infarction. As such, this study highlights the potential utility of positive psychological factors, such as gratitude, in promoting cardiovascular health.

Cold Spells and the Onset of Acute Myocardial Infarction: A Nationwide Case-Crossover Study in 323 Chinese Cities.

Few studies have explored the relationships between cold spells and acute myocardial infarction (AMI) using the information of symptom onset. We assessed the impact of cold spells on AMI onset and the potential effect modifiers. We conducted a time-stratified case-crossover study among 456,051 eligible patients with AMI from 2,054 hospitals in 323 Chinese cities between January 2015 and June 2021 during cold seasons (November to March). Nine definitions of cold spells were used by combining three relative temperature thresholds (i.e., lower than the 7.5th, 5th, and 2.5th percentiles) and three durations of at least 2-4 consecutive d. Conditional logistic regressions with distributed lag models were applied to evaluate the cumulated effects of cold spells on AMI onset over lags 0-6 d, after adjusting for daily mean temperature. The associations generally appeared on lag 1 d, peaked on lag 3 d, and became nonsignificant approximately on lag 5 d. Cold spells defined by more stringent thresholds of temperature were associated with higher risks of AMI onset. For cold spell days defined by a daily mean temperature of percentile and durations of , , and , the percentage changes in AMI risk were 4.24% [95% confidence interval (CI): 2.31%, 6.20%], 3.48% (95% CI: 1.62%, 5.38%), and 2.82% (95% CI: 0.98%, 4.70%), respectively. Significant AMI risks associated with cold spells were observed among cases from regions without centralized heating, whereas null or much weaker risks were found among those from regions with centralized heating. Patients years of age were more susceptible to cold spells. This national case-crossover study presents compelling evidence that cold spells could significantly increase the risk of AMI onset. https://doi.org/10.1289/EHP11841.