Risk Of Myocardial Infarction Research Articles

Plasma proteome and incident myocardial infarction: sex-specific differences.

Few population-based cohort studies, including both men and women, have explored circulating proteins associated with incident myocardial infarction (MI). This study investigated the relationships between circulating cardiometabolic-related proteins and MI risk using cohort-based and Mendelian randomization (MR) analyses and explored potential sex-specific differences. The discovery cohort included 11 751 Swedish adults (55-93 years). Data on 259 proteins assessed with Olink proximity extension assays, biochemical, and questionnaire-based information were used. Participants were followed up for incident MI and death over 8 years through linkage to Swedish registers. Replication analyses were conducted on the UK Biobank sample (n = 51 613). In MR analyses, index cis-genetic variants strongly related to the proteins were used as instrumental variables. Genetic association summary statistic data for MI were obtained from the CARDIoGRAMplusC4D consortium and FinnGen. Forty-five proteins were associated with incident MI in discovery and replication samples following adjustment for potential confounders and multiple testing. In the secondary analysis, 13 of the protein associations were sex-specific, with most associations identified among women. In MR analysis, genetically predicted higher levels of renin, follistatin, and retinoic acid receptor responder protein 2 were linked to an increased risk of MI. Tissue factor pathway inhibitor, tumor necrosis factor receptors 1 and 2, placenta growth factor had an inverse association with MI. This study identified both new and confirmed previously established associations between circulating proteins and incident MI and, for the first time, suggested sex-specific patterns in multiple protein-MI associations.

Combination of oral anticoagulant and antiplatelet therapy does not change the 1-year prognosis compared to oral anticoagulant alone in stroke patients with atherosclerosis and atrial fibrillation

This study aims to evaluate the effectiveness of combined antiplatelet and oral anticoagulant (OAC) therapy versus OAC therapy alone on one-year post-stroke outcomes in patients with non-valvular atrial fibrillation (NVAF) and systemic atherosclerosis. A retrospective study was conducted using the recorded data of patients diagnosed with ischemic cerebrovascular disease between January 1, 2022, and January 1, 2023, at the Neurology Clinic, Afyonkarahisar Health Sciences University. Patients with non-valvular atrial fibrillation (NVAF) and systemic atherosclerosis were included in the study. Collected data included demographic information, medical history. Patients were divided into two groups based on the treatment regimen used at discharge: those receiving OAC alone and those receiving a combination of OAC and antiplatelet therapy. Clinical outcomes were evaluated within one year following the stroke. A total of 671 stroke patients were screened, and 565 (84.2%) had ischemic stroke. Among these, 113 (20%) had NVAF, and 53 had both NVAF and systemic atherosclerosis. Data from these 53 patients were analyzed. The mean age was 71.81±11.90 years, with a female gender ratio of 52.8%. Logistic regression analysis showed no statistically significant differences between the two treatment groups in terms of all-cause mortality, bleeding, recurrent stroke, and hemorrhagic stroke (p>0.05 for all comparisons). The combination of antiplatelet and OAC therapy did not demonstrate superiority over OAC therapy alone in reducing the risks of recurrent ischemic stroke, hemorrhagic stroke, myocardial infarction, and mortality in patients with NVAF and systemic atherosclerosis. These findings suggest that OAC therapy alone may provide sufficient protection in this patient population. Prospective studies with larger samples are needed to confirm these results.

Effect of air pollution, genetic susceptibility on the risk of all-cause mortality and cardiovascular outcomes among atrial fibrillation patients

Objective: To analyze the association between air pollution, genetic susceptibility, and the risk of all-cause mortality and cardiovascular outcomes in patients with atrial fibrillation (AF). Methods: AF patients aged between 40-69 years old registered in the United Kingdom Biobank from 2006 to 2010 were included. After excluding those lost to follow-up or with incomplete data during follow-up, 5 814 subjects were analyzed. Long-term exposure to air pollution was estimated at the geocoded residential address of each participant. Genetic risk scores for all-cause mortality, cardiovascular disease, heart failure, myocardial infarction, and stroke were constructed separately for each object to assess the corresponding genetic susceptibility. The Cox proportional hazards model was used to analyze the association between air pollution, genetic susceptibility, and the risk of all-cause mortality and cardiovascular outcomes in AF patients. Results: During a median follow-up of 12.4 years, there were 929 of all-cause mortality (15.98%) and 1 772 of cardiovascular events (30.48%). Multivariable-adjusted analyses revealed that higher exposure to PM2.5, PM10, NOx, and NO2 was associated with an increased risk of cardiovascular disease mortality, heart failure, myocardial infarction, and stroke, with hazard ratios (HRs) ranging from 1.26 to 1.48. Specifically, for each interquartile range (IQR) increase in PM2.5 exposure, the HRs for the outcomes mentioned above were 1.33 (95%CI: 1.14-1.54), 1.42 (95%CI: 1.31-1.54), 1.46 (95%CI: 1.30-1.64), and 1.43 (95%CI: 1.27-1.61), respectively. Both NOx and NO2 exposures were associated with a 9% increased risk of all-cause mortality per IQR increment, with corresponding HRs of 1.09 (95%CI: 1.02-1.17) and 1.09 (95%CI: 1.01-1.17), respectively. Individuals with high genetic susceptibility to AF had a higher risk of myocardial infarction and stroke compared to those with low genetic susceptibility, with corresponding HRs of 1.39 (95%CI: 1.04-1.87) and 1.46 (95%CI: 1.09-1.95), respectively. Compared to AF patients with low air pollution exposure, those with high air pollution exposure have adjusted population attributable fractions of up to 33.57% (95%CI: 17.87%-46.26%) for cardiovascular mortality, 28.61% (95%CI: 20.67%-35.75%) for heart failure, 33.35% (95%CI: 20.97%-43.79%) for myocardial infarction, and 42.29% (95%CI: 30.05%-52.71%) for stroke. Furthermore, there was an additive interaction between PM2.5, NOx, and NO2 exposure and high genetic susceptibility on the incidence of myocardial infarction. An additive interaction was also observed between NOx, NO2 exposure, and high genetic susceptibility on the incidence of heart failure (all P<0.05). Conclusions: Both air pollution and genetic susceptibility increase the risk of all-cause mortality and cardiovascular outcomes in AF patients.

Association of serum gamma-glutamyl transferase levels with cardiovascular disease risk in type 2 diabetes patients: a prospective cohort study

To investigate the associations of serum gamma-glutamyl transferase (GGT) levels with the risk of cardiovascular disease (CVD) and its subtypes in patients with type 2 diabetes mellitus (T2DM) in Jiangsu Province. Methods: The participants were enrolled in the Comprehensive Research project regarding 'Prevention and Control of Diabetes' in Jiangsu Province. The baseline survey was conducted from 2013 to 2014, and follow-up until December 31, 2021. After excluding the participants who self-reported with chronic liver disease/stroke/coronary heart disease at baseline survey and those with incomplete information on GGT, a total of 16 147 T2DM patients were included in the final analysis. Cox proportional hazard regression models were used to calculate the hazard ratio (HR) and their 95%CI of GGT for CVD, myocardial infarction, and stroke. Restricted cubic spline models were applied to analyze the dose-response relationship between GGT and the risk of CVD and its subtypes. Results: During the median follow-up time of 8.02 years, 2 860 CVD cases were registered, including 196 cases of myocardial infarction and 2 730 cases of stroke. Multivariate Cox proportional risk regression model indicated that compared to the lowest serum GGT level group, the highest GGT level group had a 24% increased risk of CVD (HR=1.24, 95%CI: 1.09-1.41) and a 23% increased risk of stroke (HR=1.23, 95%CI: 1.08-1.40). The restricted cubic spline model showed a nonlinear dose-response relationship between GGT and the risk of CVD, myocardial infarction, and stroke in T2DM patients. Conclusions: High levels of GGT may be associated with an increased risk of cardiovascular disease in T2DM patients, which needs further exploration and validation in future clinical practice.

COVID-19 Is a Coronary Artery Disease Risk Equivalent and Exhibits a Genetic Interaction With ABO Blood Type.

COVID-19 is associated with acute risk of major adverse cardiac events (MACE), including myocardial infarction, stroke, and mortality (all-cause). However, the duration and underlying determinants of heightened risk of cardiovascular disease and MACE post-COVID-19 are not known. Data from the UK Biobank was used to identify COVID-19 cases (n=10 005) who were positive for polymerase chain reaction (PCR+)-based tests for SARS-CoV-2 infection (n=8062) or received hospital-based International Classification of Diseases version-10 (ICD-10) codes for COVID-19 (n=1943) between February 1, 2020 and December 31, 2020. Population controls (n=217 730) and propensity score-matched controls (n=38 860) were also drawn from the UK Biobank during the same period. Proportional hazard models were used to evaluate COVID-19 for association with long-term (>1000 days) risk of MACE and as a coronary artery disease risk equivalent. Additional analyses examined whether COVID-19 interacted with genetic determinants to affect the risk of MACE and its components. The risk of MACE was elevated in COVID-19 cases at all levels of severity (HR, 2.09 [95% CI, 1.94-2.25]; P<0.0005) and to a greater extent in cases hospitalized for COVID-19 (HR, 3.85 [95% CI, 3.51-4.24]; P<0.0005). Hospitalization for COVID-19 represented a coronary artery disease risk equivalent since incident MACE risk among cases without history of cardiovascular disease was even higher than that observed in patients with cardiovascular disease without COVID-19 (HR, 1.21 [95% CI, 1.08-1.37]; P<0.005). A significant genetic interaction was observed between the ABO locus and hospitalization for COVID-19 (Pinteraction=0.01), with risk of thrombotic events being increased in subjects with non-O blood types (HR, 1.65 [95% CI, 1.29-2.09]; P=4.8×10-5) to a greater extent than subjects with blood type O (HR, 0.96 [95% CI, 0.66-1.39]; P=0.82). Hospitalization for COVID-19 represents a coronary artery disease risk equivalent, with post-acute myocardial infarction and stroke risk particularly heightened in non-O blood types. These results may have important clinical implications and represent, to our knowledge, one of the first examples of a gene-pathogen exposure interaction for thrombotic events.

Familial risk of myocardial infarction with non-obstructive and obstructive coronary arteries -A nation-wide cohort study.

The familial risk among patients with myocardial infarction with non-obstructive coronary arteries (MINOCA) is unknown. Previous studies of family history in myocardial infarction (MI), have not made a distinction between MINOCA and MI due to coronary artery disease (MI-CAD), based on angiographic findings. We therefore sought to investigate familial risk of MI without and with obstructive coronary arteries. Register-based cohort study with a total of 15,462 MINOCA cases, 204,424 MI-CAD cases, 38,220 control subjects without MI and with non-obstructive coronary arteries. First-degree relatives were identified 1995-2020. Cox proportional hazard regression models were used to compare familial risk in MINOCA and MI-CAD with control subjects. During a mean follow-up of 8.1 ± 4.2 years, MINOCA occurred in 1.0% of first-degree relatives with MINOCA whereas MI-CAD occurred in 9.7% of first-degree relatives of MINOCA. The age- and sex-adjusted hazard ratio (HR) for a MINOCA-relative experiencing MINOCA and MI-CAD, compared to control subjects, was 0.99 (95% confidence interval [CI] 0.80-1.23) and 1.10 (95% CI 1.03-1.18), respectively. During a mean follow-up of 8.5 ±4.8 years, MI-CAD occurred in 12.2% of first- degree relatives with MI-CAD with age- and sex-adjusted HR 1.43 (95% CI 1.37-1.49). No increased familial risk of MINOCA was observed for MINOCA-patients whereas there was an increased familial risk for MI-CAD when compared to control subjects. These results may indicate that genetic factors and shared environmental factors within a family leading to CAD are important also for MINOCA, thus MI-CAD and MINOCA could share underlying mechanisms.

Effect of inflammatory factors on myocardial infarction

BackgroundCohort studies have increasingly shown associations between inflammatory markers and myocardial infarction (MI); however, the specific causal relationships between inflammatory markers and the development of MI remain unclear.Methods and resultsBy utilizing publicly accessible genome-wide association studies, we performed a two-sample Mendelian randomization (MR) analysis to explore the causal associations between inflammatory markers and myocardial infarction (MI). A random-effects inverse-variance weighted method was used to calculate effect estimates. The study included a total of 395,795 European participants for MI analysis and various sample sizes for inflammatory factors, ranging from 3,301 to 563,946 participants.Neutrophil count was found to increase the risk of MI (odds ratio [OR] = 1.08; 95% confidence interval [CI], 1.00–1.17; p = 0.04). C-reactive protein levels correlated positively with MI. No associations were observed with IL-1 beta, IL-6, IL-18, procalcitonin, TNF-α, total white cell count, or neutrophil percentage of white cells. Neutrophil count and C-reactive protein were inversely associated with lactate dehydrogenase: neutrophil cell count (OR 0.95; 95% CI, 0.93–0.98; p < 0.01) and C-reactive protein (OR 0.96; 95% CI, 0.92–1.00; p = 0.02). No associations of MI with myoglobin, troponin I, and creatine kinase-MB levels were found.ConclusionsThis two-sample MR analysis revealed a causal positive association of MI with neutrophil count, C-reactive protein level, and the myocardial injury marker lactate dehydrogenase. These results indicate that monitoring C-reactive protein and neutrophil counts may be useful in management of MI patients.

12340 Cardiovascular Risks With Testosterone Replacement Therapy In Patients With Type 2 Diabetes Mellitus

Abstract Disclosure: A. Gupta: None. M. Nassar: None. H. Ghanim: None. Background: Concerns have been raised about testosterone replacement therapy (TRT) in hypogonadism patients, particularly regarding cardiovascular disease (CVD) risk. Despite some studies showing TRT's non-inferiority to placebo in men at high CVD risk, its impact on patients with type 2 diabetes mellitus (T2DM) remains uncertain. This study examines the incidence of cardiovascular events in patients with T2DM on TRT, with a focus on the first four years of treatment. Methods: Utilizing the TriNetX electronic health records network, this retrospective cohort study targeted patients with T2DM with testosterone levels &amp;lt;300 ng/dl or diagnosed hypogonadism. Patients were divided into two main groups based on their CVD history and TRT status. We conducted a comparative analysis between each cohort and a control group of patients who did not get testosterone replacement therapy (TRT). Matching for age, HbA1C, and BMI created balanced cohorts for comparison: 39,589 in each of the non-CVD event cohorts and 16,065 in each of the CVD event cohorts. Results: In patients without prior CVD, TRT significantly reduced the risk of acute myocardial infarction (MI) (risk ratio: 0.765, p &amp;lt;0.0001), with no significant difference in cerebral infarction risk. Conversely, TRT increased the risk of acute MI (risk ratio: 1.164, p &amp;lt; 0.0001) and cerebral infarction (risk ratio: 1.177, p &amp;lt; 0.0001) in patients with a history of CVD.Discussion: TRT may decrease acute MI risk in patients with T2DM without prior CVD but elevate acute MI and stroke risks in those with a CVD history. These findings suggest the need for cautious TRT consideration in patients with T2DM with differing cardiovascular histories. Conclusion: This analysis reveals that TRT is associated with a decreased risk of acute myocardial infarction in patients with T2DM without a history of CVD, suggesting a potential protective effect in this subgroup. However, TRT increases the risk of both myocardial infarction and stroke in patients with a prior history of CVD, indicating the need for careful patient selection and monitoring. These findings highlight the significance of personalized evaluation in the administration of TRT, particularly in patients with T2DM who have different cardiovascular backgrounds, to balance benefits against potential risks. Presentation: 6/2/2024

Weight change and the risk of cardiovascular disease in patients with hypertension: A primary-care cohort study.

Weight control is a cornerstone of hypertension management. Therefore, it is important to understand the relationship of weight change to risk of cardiovascular disease (CVD) among patients with hypertension. We aimed to investigate the association of weight change with the risk of CVD, stroke, and myocardial infarction (MI) among patients with hypertension. We obtained the data from medical records of the Hypertension Health Management Program (HMPH) in Shenzhen, China. The present study included 221 454 individuals with hypertension. Weight change over two years was divided into loss ≥10%, loss 5-10%, stable (-5 ~ 5%), gain 5-10%, and gain >10%. Cox regression analyses were applied to assess the associations of weight change groups with the risk of CVD, stroke, and MI. Compared with the stable weight group (-5 ~ 5%), those with weight loss ≥10% had a higher risk of CVD (hazard ratio (HR) = 1.21; 95% confidence interval (CI) = 1.05-1.40) in the fully adjusted model. Weight gain >10% was significantly associated with a higher risk of CVD (HR = 1.17; 95% CI = 1.04-1.31). In the meanwhile, participants with weight loss ≥10% had significantly higher risks of stroke (HR = 1.20; 95% CI = 1.02-1.41). However, participants with weight gain >10% had an increased risk of MI (HR = 1.45; 95% CI = 1.15-1.82) in the fully adjusted model. Weight loss or weight gain were associated with higher risks of CVD. Management of patients with hypertension requires close monitoring and appropriate interventions to achieve optimal body weight to prevent adverse outcomes.

Exposure to Air Pollutants and Myocardial Infarction Incidence: A UK Biobank Study Exploring Gene-Environment Interaction.

Unraveling gene-environment interaction can provide a novel insight into early disease prevention. Nevertheless, current understanding of the interplay between genetic predisposition and air pollution in relation to myocardial infarction (MI) risk remains limited. Furthermore, the potential long-term influence of air pollutants on MI incidence risk warrants more conclusive evidence in a community population. We investigated interactions between genetic predisposition and exposure to air pollutants on MI incidence. This study incorporated a sample of 456,354 UK Biobank participants and annual mean air pollution (, , , and ) from the UK Department for Environment, Food and Rural Affairs (2006-2021). The Cox proportional hazards model was employed to explore MI incidence after chronic air pollutants exposure. By quantifying genetic risk through the calculation of polygenic risk score (PRS), this study further examined the interactions between genetic risk and exposure to air pollutants in the development of MI on both additive and multiplicative scales. Among 456,354 participants, 9,114 incident MI events were observed during a median follow-up of 12.08 y. Chronic exposure to air pollutants was linked with an increased risk of MI occurrence. Specifically, the hazard ratios (per interquartile range) were 1.12 (95% CI: 1.10, 1.13) for , 1.20 (95% CI: 1.19, 1.22) for , 1.13 (95% CI: 1.12, 1.15) for , and 1.12 (95% CI: 1.11, 1.13) for . In terms of the joint effects, participants with high PRS and high level of air pollution exposure exhibited the greatest risk of MI among all study participants ( to 324%). Remarkably, both multiplicative and additive interactions were detected in the ambient air pollutants exposure and genetic risk on the incidence of MI. There were interactions between exposure to ambient air pollutants and genetic susceptibility on the risk of MI onset. Moreover, the joint effects of these two exposures were greater than the effect of each factor alone. https://doi.org/10.1289/EHP14291.

Ten-year clinical outcomes after drug-eluting stents implantation according to clinical presentation-Insights from the DECADE cooperation.

Investigations of very long-term outcomes after percutaneous coronary intervention (PCI) with drug-eluting stents (DES) according to clinical presentation are scarce. Here, we investigated the 10-year clinical outcomes of patients undergoing DES-PCI according to clinical presentation. Patient-level data from five randomized trials with 10-year follow-up after DES-PCI were pooled. Patients were dichotomized into acute coronary syndrome (ACS) or chronic coronary syndrome (CCS) groups as per clinical presentation. The primary outcome was all-cause death. Secondary outcomes were cardiovascular death, myocardial infarction (MI), definite stent thrombosis (ST) and repeat revascularization involving the target lesion (TLR), target vessel (TVR) or non-target vessel (nTVR). Of the 9700 patients included in this analysis, 4557 presented with ACS and 5143 with CCS. Compared with CCS patients, ACS patients had a higher risk ofall-cause death and nTVR in the first year, but comparable risk thereafter. In addition, ACS patients had a higher risk of MI [adjusted hazard ratio 1.21, 95% confidence interval (1.04-1.41)] and definite ST [adjusted hazard ratio 1.48, 95% confidence interval (1.14-1.92)], while the risk of TLR and TVR was not significantly different up to 10-year follow-up. Compared to CCS patients, ACS patients treated with PCI and DES implantation have an increased risk of all-cause death and repeat revascularization of remote vessels up to 1 year, with no significant differences thereafter and up to 10-year follow-up. ACS patients have a consistently higher risk of MI and definite ST. Whether these differences persist with current antithrombotic and secondary prevention therapies requires further investigation.

Evaluation of cardiovascular risk in patients with prostate cancer initiating novel hormonal therapy.

301 Background: Cardiovascular risk factor modification is crucial for cancer patients, particularly for those receiving hormonal therapy due to the increased risk of cardiovascular disease (CVD). However, the evaluation of cardiovascular risk in prostate cancer patients undergoing novel hormonal therapy (NHT) remains not well understood. This study aimed to assess the incidence of cardiovascular events in patients with prostate cancer initiating NHT and compare the risk with non-cancer matched controls. Methods: This study is a retrospective cohort analysis that examined electronic medical records from a global federated health research network, TriNetX. The study included male patients with prostate cancer who were 18 years or older and had initiated treatment with abiraterone, enzalutamide, apalutamide, or darolutamide between January 1, 2015, and December 31, 2020. The cohort was stratified based on diabetes mellitus (DM) and prior CVD status. We evaluated the incidence of myocardial infarction (MI) within 1 and 3 years after NHT initiation. MI risk was compared between each strata of cancer patients and propensity score matched non-cancer patients with cox proportional hazards models, with a significance threshold of p&lt;0.05. Results: There were 11,536 patients with prostate cancer receiving NHT, having a mean age of 70.4 years and predominately White (70%). Of this cohort, 22% had DM, 23% had CVD, and 62% had neither condition. One- and 3-year incidence of MI was 5% and 7% amongst all patients; those with DM, CVD, or both had higher incidences of MI at 3 years, with the rates of 13%, 18%, 22% respectively. Adjusted analyses showed that prostate cancer patients initiating NHT had significantly higher hazards of MI compared to matched non-cancer controls (HR: 1.57 [95% CI: 1.32-1.86] for DM, 1.31 [95% CI: 1.14-1.50] for CVD, and 1.29 [95% CI: 1.05-1.57] for both DM and CVD). Conclusions: The incidence of MI is relatively low in prostate cancer patients starting NHT without DM or CVD comorbidities. However, those patients with pre-existing DM and/or CVD are at significantly higher risk of MI, even more than age matched controls without cancer with those co-morbidities. This highlights the need for comprehensive cardiovascular risk stratification and management in high-risk patients with prostate cancer.

Dual antiplatelet therapy duration and stent type in patients with high bleeding risk: A systematic review and network meta-analysis

BackgroundIt is uncertain whether the efficacy and safety of dual antiplatelet therapy (DAPT) in patients with high bleeding risk (HBR) vary according to DAPT duration and stent type (e.g., durable polymer drug-eluting stents (DP-DESs), biodegradable polymer DESs (BP-DESs), or polymer-free drug-coated stents (PF-DCSs)). We aimed to study the stent type and DAPT duration appropriate for patients with HBR. MethodsPubMed and EMBASE were searched until October 2023. Randomized controlled trials (RCTs) involving patients with HBR that compared standard DAPT (6-12 months) with DP- or BP-DES versus short DAPT (≤3 months) with DP- or BP-DES or PF-DCS or bare-metal stent (BMS) were identified. The primary efficacy outcome was major adverse cardiovascular events (MACEs), defined as cardiovascular death, myocardial infarction (MI), and stroke. The primary safety outcome was major bleeding. Secondary outcomes included MI and stent thrombosis (ST). We performed a network meta-analysis using a random effects model. ResultsThirteen RCTs with a total of 19,418 patients with HBR were included. Compared to standard DAPT with DP-DES, short DAPT with BMS was associated with a higher risk of MACE and MI. For major bleeding, short DAPT strategies were associated with a lower risk than standard DAPT strategies (e.g. short DAPT with DP-DES versus standard DAPT with DP-DES; HR[95% CI]: 0.48[0.28-0.82]). Interestingly, the use of BP-DES was associated with a higher risk of ST than DP-DES (e.g. standard DAPT with BP-DES versus short DAPT with DP-DES; HR[95% CI]: 2.65[1.03-6.79]). ConclusionsIn patients with HBR who underwent percutaneous coronary intervention, a short DAPT strategy with DP-DES should be used since it offers the best combination of efficacy and safety.

Clinical Outcomes After Percutaneous Coronary Intervention for Left Main Coronary Artery Disease in Patients of Diverse Race/Ethnicity

Data on percutaneous coronary intervention (PCI) for left main coronary artery (LMCA) disease in patients of diverse race/ethnicity is scant. The aim of the study was to assess the impact of race/ethnicity on clinical outcomes at 12-month follow-up of patients with LMCA disease undergoing PCI with drug-eluting stent implantation. All patients undergoing PCI for LMCA disease between 2010 and 2019 at a tertiary care center were prospectively enrolled. Clinical outcomes were assessed per each race/ethnic group. The primary endpoint was the composite of all-cause death, myocardial infarction (MI), or stroke at 12 months. A total of 774 consecutive patients with known race/ethnicity were prospectively enrolled, 62.1% (n=481) Caucasians, 17.2% (n=133) Hispanics, 12.7% (n=98) Asians and 8.0% (n=62) African Americans. Compared with Caucasians, the hazard rate of the primary endpoint tended to be lower in Asian patients (6.1% vs 14.2%; hazard ratio [HR]: 0.41; 95% confidence interval [CI]: 0.16-1.03), and similar in African American (13.7% vs 14.2%; HR: 0.93; 95% CI: 0.40-2.16) and Hispanic patients (14.2% vs 14.2%; HR: 1.02; 95% CI: 0.58-1.78). Hazard rates of target vessel or lesion revascularization were comparable in the four groups. Cox multivariable regression adjustment confirmed consistent findings and revealed higher hazard rate of post-discharge bleeding in African Americans vs. Caucasians (HR: 5.89; 95% CI: 1.00-34.5). In conclusion, within a racially/ethnically diverse cohort of patients undergoing PCI for LMCA disease, when compared with Caucasians, Asians are at lower risk of all-cause death, MI or stroke, while African Americans are at increased risk of post-discharge bleeding.

S633 Gastroesophageal Reflux Disease (GERD) and Risk of Incident Acute Myocardial Infarction: A Systematic Review and Meta-analysis of Cohort Studies

S633 Gastroesophageal Reflux Disease (GERD) and Risk of Incident Acute Myocardial Infarction: A Systematic Review and Meta-analysis of Cohort Studies

Impact of Systolic and Diastolic Blood Pressure on Cardiovascular Health Outcomes

Background: One well-known risk factor for cardiovascular (CV) disease that significantly raises morbidity and mortality rates globally is hypertension. Optimising treatment options requires an understanding of the distinct effects of diastolic and systolic blood pressure on CV outcomes. The study aims to examine into how the effects of both systolic hypertension (SH) and diastolic hypertension (DH) affected the frequency of major CV events, such as hemorrhagic, ischemic, and myocardial infarction (MI). Methods: A retrospective cohort research comprising 180 patients was carried out, with automated oscillometric cuffs being used to measure blood pressure. The burdens of SH and DH, which were determined as continuous variables from weighted average blood pressure, were the main predictors. A composite of ischemic stroke, MI, or hemorrhagic stroke was the main result. Logistic regression and bivariate and multivariable Cox survival analyses were included in the statistical studies. Results: The study population had average age of 65.4 years, with 52% males and 48% females. During the observation period, 45 composite outcome events occurred (25% incidence rate). Bivariate Cox analysis showed significant associations between SH burden (HR: 1.45, p&lt;0.001) and diastolic hypertension burden (HR: 1.30, p=0.015) with the composite outcome. Multivariable analysis confirmed these associations, with consistent findings in logistic regression models. Conclusion: Both SH and DH burdens are significant predictors of adverse CV outcomes. Effective management of both blood pressure components is essential for reducing the risk of ischemic stroke, MI, and hemorrhagic stroke. Recommendations: To lower the risk of significant CV events, clinicians should monitor and treat both systolic and diastolic blood pressure in individuals with hypertension. Subsequent studies ought to investigate the underlying mechanisms of these correlations and assess the effectiveness of focused interventions. Keywords: Hypertension, Cardiovascular Outcomes, Diastolic Blood Pressure, Systolic Blood Pressure.

Patient-Specific Myocardial Infarction Risk Thresholds From AI-Enabled Coronary Plaque Analysis

BACKGROUND: Plaque quantification from coronary computed tomography angiography has emerged as a valuable predictor of cardiovascular risk. Deep learning can provide automated quantification of coronary plaque from computed tomography angiography. We determined per-patient age- and sex-specific distributions of deep learning–based plaque measurements and further evaluated their risk prediction for myocardial infarction in external samples. METHODS: In this international, multicenter study of 2803 patients, a previously validated deep learning system was used to quantify coronary plaque from computed tomography angiography. Age- and sex-specific distributions of coronary plaque volume were determined from 956 patients undergoing computed tomography angiography for stable coronary artery disease from 5 cohorts. Multicenter external samples were used to evaluate associations between coronary plaque percentiles and myocardial infarction. RESULTS: Quantitative deep learning plaque volumes increased with age and were higher in male patients. In the combined external sample (n=1847), patients in the ≥75th percentile of total plaque volume (unadjusted hazard ratio, 2.65 [95% CI, 1.47–4.78]; P =0.001) were at increased risk of myocardial infarction compared with patients below the 50th percentile. Similar relationships were seen for most plaque volumes and persisted in multivariable analyses adjusting for clinical characteristics, coronary artery calcium, stenosis, and plaque volume, with adjusted hazard ratios ranging from 2.38 to 2.50 for patients in the ≥75th percentile of total plaque volume. CONCLUSIONS: Per-patient age- and sex-specific distributions for deep learning–based coronary plaque volumes are strongly predictive of myocardial infarction, with the highest risk seen in patients with coronary plaque volumes in the ≥75th percentile.

Association of monocyte-lymphocyte ratio and myocardial infarction in the U.S. population with diabetes.

The monocyte-to-lymphocyte ratio (MLR) has emerged as a novel inflammatory biomarker; however, its relationship with myocardial infarction (MI) in diabetic populations remains unclear. This study aimed to elucidate the association between MLR and MI prevalence in this unique population. This cross-sectional study used data from the National Health and Nutrition Examination Survey (NHANES), 2015-2018. MLR was utilized as both a continuous and categorical factor to examine its correlation with MI in individuals diagnosed with DM. Subgroup and sensitivity analyses were also performed. In this study, 1,295 individuals with DM were enrolled, among whom 148 (11.4%) were diagnosed with MI. Patients with MI showed a greater MLR. Using a smoothed curve-fitting analysis, a linear relationship was observed between MLR and MI (pfor non-linearity = 0.27). Multivariate logistic regression analysis showed that MLR * 10 was positively correlated with the risk of MI (OR = 1.14, 95% CI 1.01∼1.29, p = 0.041). Compared with the lowest quartile, the OR for Q2, Q3, and Q4 were 2.13 (95% CI: 1.01∼4.47), 2.95 (95% CI: 1.45∼6.00), and 2.74 (95% CI: 1.32∼5.69), respectively. Subgroup analyses showed no significant interaction for MLR in any subgroup (all P > 0.05). The receiver operating characteristic (ROC) curve indicated that the area under the curve (AUCs) of MLR for predicting MI was 0.661 (95% CI: 0.617-0.706; P < 0.05). Our study demonstrated that MLR is significantly correlated with MI in patients with DM.

Self-reported smoking status and exhaled carbon monoxide in secondary preventive follow-up after coronary heart events: Do our patients tell the truth?

Smoking cessation reduces the risk of myocardial infarctions (MI) and death in patients with coronary heart disease. Smoking status is frequently assessed based on self-report. The aims of this study were to compare self-reported and objectively measured (exhaled carbon monoxide [eCO]) smoking status after MI, percutaneous coronary intervention (PCI), and coronary artery bypass grafting (CABG), and to assess whether assumed wrongly declared smoking cessation was associated to poorer achievement of other treatment targets for secondary prevention. This study was a sub-analysis from a randomized controlled trial at Sorlandet Hospital, Arendal, Norway, 2007-2022, including patients hospitalized due to MI or after scheduled PCI/CABG, and primarily aimed at comparing secondary preventive follow-up in the outpatient clinic versus primary healthcare. Participants were followed up after the index event through outpatient consultations. Smoking status was assessed by self-report and by eCO (Smokerlyzer, Bedfont, UK) with concentration values ≥6 ppm interpreted as suggesting smoking. A total of 1540 participants aged 18-80 years were included in the main study. Self-reported smoking status and concomitant eCO measurement one year after the index event were available in 1291 (84%) participants. In all, Brussels, Belgium, from the 12th to the 13th of September 2024. The concentration of eCO was ≥6 ppm one year after the index event in 285 (22%) patients, and 72 (25%) of these patients reported non-smoking. Fewer patients with elevated eCO reporting non-smoking achieved the treatment target for blood pressure (<140/90 mmHg) in comparison to those reporting smoking (53% vs 68%, p=0.02). No differences for the other treatment targets for secondary prevention were found. The study indicates a need for objective measures for smoking cessation both in clinical studies and in clinical practice, and may indicate a lack of truthfulness regarding smoking habits. The study is registered on the official website of ClinicalTrials.gov. ID NCT00679237.

Comparing E-Cigarettes and Traditional Cigarettes in Relation to Myocardial Infarction, Arrhythmias, and Sudden Cardiac Death: A Systematic Review and Meta-Analysis.

The use of electronic cigarettes (e-cigarettes) as a perceived safer alternative to traditional cigarettes has grown rapidly. However, the cardiovascular risks associated with e-cigarettes compared to regular cigarettes remain unclear. To systematically review and compare the cardiovascular outcomes of e-cigarette use versus traditional cigarette use, focusing on the risks of myocardial infarction, arrhythmias, and sudden death. A systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Peer-reviewed studies published in English were included if they reported cardiovascular outcomes related to e-cigarette or traditional cigarette use. A total of 20 studies were included, covering observational and interventional studies focusing on heart rate variability, myocardial infarction, arrhythmias, and sudden cardiac events. The quality of the evidence was assessed using the GRADE criteria, and data were extracted and analyzed based on the PICOS (Population, Interventions, Comparisons, Outcomes, and Study designs) framework. The systematic review found that both e-cigarettes and traditional cigarettes pose significant cardiovascular risks, with traditional cigarettes linked to a higher incidence of myocardial infarction, arrhythmias, and sudden cardiac death. E-cigarette users also face increased risks of arrhythmias and myocardial infarction compared to non-smokers, primarily due to the constituents of aerosolized e-liquid, including nicotine and flavorings, which contribute to adverse cardiac effects. Regular e-cigarette use, particularly in combination with traditional cigarette use, was associated with a heightened risk of myocardial infarction. Studies also reported heart function abnormalities, such as systolic and diastolic dysfunction, and reduced ejection fractions. Additionally, changes in heart rate variability, heart rate, and blood pressure were observed, indicating both acute and chronic effects of e-cigarettes on cardiovascular autonomic regulation. While e-cigarettes may present a lower cardiovascular risk compared to traditional cigarettes, they are not without harm. Both products are linked to increased risks of myocardial infarction and arrhythmias, though traditional cigarettes pose a higher overall threat. Given the limitations in the current evidence base, particularly concerning the long-term effects of e-cigarette use, further research is needed to clarify these cardiovascular risks and inform public health guidelines.