Incidence Of Coronary Heart Disease Research Articles

Sex differences in risk factors for coronary heart disease events: a prospective cohort study in Iran

We investigated sex-specific associations and their differences between major cardiovascular risk factors and the risk of incident coronary heart disease (CHD) and hard CHD (defined as nonfatal myocardial infarction and CHD death). A total of 7518 (3377 men) participants from the Tehran Lipid and Glucose Study were included. Cox models were used to estimate the hazard ratios (HRs) and women-to-men ratios of HRs for CHD events associated with each risk factor. During 20 years of follow-up (1999–2018), 1068 (631 men) and 345 (238 men) new cases of CHD and hard CHD, respectively, were documented. In total population, the incidence rates per 1000 person-years were 9.5 (9.0–10.1) and 2.9 (2.6–3.2) for CHD and hard CHD, respectively. Hypertension, diabetes, pre-diabetes, and a high waist-to-hip ratio (WHR) were associated with a greater HR of hard CHD in women than men; the women-to-men HRs were 2.85 [1.36–5.98], 1.92 [1.11–3.31], 2.04 [1.09–3.80] and 1.42 [1.10–1.82], respectively. Diabetes was associated with a higher HR of CHD in women than men (ratio of HRs 1.49 (1.10–2.01). In conclusion, we found that hypertension, diabetes, pre-diabetes, and high WHR conferred a greater excess risk of CHD events in women than in men, suggesting that Iranian women may require greater attention for the prevention of CHD events.

Lipidomics identified novel cholesterol-independent predictors for risk of incident coronary heart disease: Mediation of risk from diabetes and aggravation of risk by ambient air pollution

IntroductionPrevious lipidomics studies have identified various lipid predictors for cardiovascular risk, however, with limited predictive increment, sometimes using too many predictor variables at the expense of practical efficiency. ObjectivesTo search for lipid predictors of future coronary heart disease (CHD) with stronger predictive power and efficiency to guide primary intervention. MethodsWe conducted a prospective nested case-control study involving 1,621 incident CHD cases and 1:1 matched controls. Lipid profiling of 161 lipid species for baseline fasting plasma was performed by liquid chromatography-mass spectrometry. ResultsIn search of CHD predictors, seven lipids were selected by elastic-net regression during over 90% of 1000 cross-validation repetitions, and the derived composite lipid score showed an adjusted odds ratio of 3.75 (95% confidence interval: 3.15, 4.46) per standard deviation increase. Addition of the lipid score into traditional risk model increased c-statistic to 0.736 by an increment of 0.077 (0.063, 0.092). From the seven lipids, we found mediation of CHD risk from baseline diabetes through sphingomyelin (SM) 41:1b with a considerable mediation proportion of 36.97% (P < 0.05). We further found that the positive associations of phosphatidylcholine (PC) 36:0a, SM 41:1b, lysophosphatidylcholine (LPC) 18:0 and LPC 20:3 were more pronounced among participants with higher exposure to fine particulate matter or its certain components, also to ozone for LPC 18:0 and LPC 20:3, while the negative association of cholesteryl ester (CE) 18:2 was attenuated with higher black carbon exposure (P < 0.05). ConclusionWe identified seven lipid species with greatest predictive increment so-far achieved for incident CHD, and also found novel biomarkers for CHD risk stratification among individuals with diabetes or heavy air pollution exposure.

Estimating dose-response relationships for vitamin D with coronary heart disease, stroke, and all-cause mortality: observational and Mendelian randomisation analyses

Randomised trials of vitamin D supplementation for cardiovascular disease and all-cause mortality have generally reported null findings. However, generalisability of results to individuals with low vitamin D status is unclear. We aimed to characterise dose-response relationships between 25-hydroxyvitamin D (25[OH]D) concentrations and risk of coronary heart disease, stroke, and all-cause mortality in observational and Mendelian randomisation frameworks. Observational analyses were undertaken using data from 33 prospective studies comprising 500 962 individuals with no known history of coronary heart disease or stroke at baseline. Mendelian randomisation analyses were performed in four population-based cohort studies (UK Biobank, EPIC-CVD, and two Copenhagen population-based studies) comprising 386 406 middle-aged individuals of European ancestries, including 33 546 people who developed coronary heart disease, 18 166 people who had a stroke, and 27 885 people who died. Primary outcomes were coronary heart disease, defined as fatal ischaemic heart disease (International Classification of Diseases 10th revision code I20-I25) or non-fatal myocardial infarction (I21-I23); stroke, defined as any cerebrovascular disease (I60-I69); and all-cause mortality. Observational analyses suggested inverse associations between incident coronary heart disease, stroke, and all-cause mortality outcomes with 25(OH)D concentration at low 25(OH)D concentrations. In population-wide genetic analyses, there were no associations of genetically predicted 25(OH)D with coronary heart disease (odds ratio [OR] per 10 nmol/L higher genetically-predicted 25(OH)D concentration 0·98, 95% CI 0·95-1·01), stroke (1·01, [0·97-1·05]), or all-cause mortality (0·99, 0·95-1·02). Null findings were also observed in genetic analyses for cause-specific mortality outcomes, and in stratified genetic analyses for all outcomes at all observed levels of 25(OH)D concentrations. Stratified Mendelian randomisation analyses suggest a lack of causal relationship for 25(OH)D concentrations with both cardiovascular and mortality outcomes for individuals at all levels of 25(OH)D. Our findings suggest that substantial reductions in mortality and cardiovascular morbidity due to long-term low-dose vitamin D supplementation are unlikely even if targeted at individuals with low vitamin D status. British Heart Foundation, Medical Research Council, National Institute for Health Research, Health Data Research UK, Cancer Research UK, and International Agency for Research on Cancer.

Dental Caries, Race and Incident Ischemic Stroke, Coronary Heart Disease, and Death.

Dental caries is a highly prevalent disease worldwide. In the United States, untreated dental caries is present in >1 in 5 adults. The objective of this study was to determine the relationship between dental caries and incident ischemic stroke, coronary heart disease (CHD) events, and death. The dental cohort (n=6351) of the ARIC study (Atherosclerosis Risk in Communities) was followed for incident ischemic stroke, CHD event, and all-cause mortality. Of all the participants at visit 4 (n=11 656), those who were unable to go through dental examination, or with prevalent ischemic stroke and CHD events, were excluded. The full-mouth dental examination was conducted at visit 4 (1996-1998), assessing dental caries. The dose response of decayed, missing, and filled surfaces due to caries was assessed and related to the outcome. Outcomes were assessed through the end of 2019. Additionally, the effect of regular dental care utilization on dental caries was evaluated. Participants with ≥1 dental caries had an increased risk of stroke (adjusted hazard ratio [HR], 1.40 [95% CI, 1.10-1.79]) and death (adjusted HR, 1.13 [95% CI, 1.01-1.26]) but not for CHD events (adjusted HR, 1.13 [95% CI, 0.93-1.37]). The association of dental caries and ischemic incident stroke was significantly higher in the African American population compared with the White subgroup (interaction term P=0.0001). Increasing decayed, missing, and filled surfaces were significantly associated with stroke (adjusted HR, 1.006 [95% CI, 1.001-1.011]) and death (adjusted HR, 1.003 [95% CI, 1.001-1.005]) but not CHD (adjusted HR, 1.002 [95% CI, 1.000-1.005]). Regular dental care utilization lowered (adjusted odds ratio, 0.19 [95% CI, 0.16-0.22]; P<0.001) the chance of caries. Among the cohort, dental caries was independently associated with the risk of ischemic stroke and death, with the effect higher in African American participants. Regular dental care utilization was associated with a lower chance of caries, emphasizing its relevance in the prevention of these events.

Metabolite Signature of Life's Essential 8 and Risk of Coronary Heart Disease Among Low-Income Black and White Americans.

Life's essential 8 (LE8) is a comprehensive construct of cardiovascular health. Yet, little is known about the LE8 score, its metabolic correlates, and their predictive implications among Black Americans and low-income individuals. In a nested case-control study of coronary heart disease (CHD) among 299 pairs of Black and 298 pairs of White low-income Americans from the Southern Community Cohort Study, we estimated LE8 score and applied untargeted plasma metabolomics and elastic net with leave-one-out cross-validation to identify metabolite signature (MetaSig) of LE8. Associations of LE8 score and MetaSig with incident CHD were examined using conditional logistic regression. The mediation effect of MetaSig on the LE8-CHD association was also examined. The external validity of MetaSig was evaluated in another nested CHD case-control study among 299 pairs of Chinese adults. Higher LE8 score was associated with lower CHD risk (standardized odds ratio, 0.61 [95% CI, 0.53-0.69]). The MetaSig, consisting of 133 metabolites, showed significant correlation with LE8 score (r=0.61) and inverse association with CHD (odds ratio, 0.57 [0.49-0.65]), robust to adjustment for LE8 score and across participants with different sociodemographic and health status ([odds ratios, 0.42-0.69]; all P<0.05). MetaSig mediated a large portion of the LE8-CHD association: 53% (32%-80%). Significant associations of MetaSig with LE8 score and CHD risk were found in validation cohort (r=0.49; odds ratio, 0.57 [0.46-0.69]). Higher LE8 score and its MetaSig were associated with lower CHD risk among low-income Black and White Americans. Metabolomics may offer an objective measure of LE8 and its metabolic phenotype relevant to CHD prevention among diverse populations.

Genetic Polymorphisms and Risk of Cardiovascular Disease

&lt;p&gt;&lt;span style="font-size: 10.0pt; font-family: 'Arial',sans-serif; mso-ascii-theme-font: minor-bidi; mso-fareast-font-family: PMingLiU; mso-hansi-theme-font: minor-bidi; mso-bidi-theme-font: minor-bidi; mso-ansi-language: EN-US; mso-fareast-language: EN-US; mso-bidi-language: EN-US;"&gt;Cardiovascular disease (CVD) is the major cause of death and disability worldwide. Major and well-established cardiovascular disease risk factors include advancing age, male sex, hypertension, smoking, diabetes, elevated total serum low-density lipoprotein (LDL) cholesterol, and decreased high-density lipoprotein (HDL) cholesterol. Genetic polymorphism represents an additional risk factor for cardiovascular disease and is not explored and researched thoroughly. In this review article, a total of 31 scientific articles studying the association between different genetic polymorphisms and the risk of cardiovascular disease were studied. &lt;a name="_Hlk80393453"&gt;&lt;/a&gt;Different genetic polymorphisms were found to be associated with an increased risk of cardiovascular disease and coronary heart disease incidence, and genotyping of these different genetic polymorphisms should be considered as routine screening for cardiovascular disease.&lt;/span&gt;&lt;/p&gt;

Fatty Liver Index as a proxy for non-alcoholic fatty liver disease and the risk of stroke and coronary heart disease: The Suita Study

BackgroundNon-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in developed countries, but its role in predicting cardiovascular disease (CVD) needs further investigation. Herein, we studied the association between NAFLD and the risk of CVD, stroke, and coronary heart disease (CHD) among Japanese people. MethodsThis prospective cohort study analyzed data from 2,517 men and 3,958 women, aged 30-84 years, who were registered in the Suita Study. NAFLD was defined as Fatty Liver Index (FLI) ≥ 60. Cox proportional hazard models were applied to calculate the hazard ratios (HRs) and 95% confidence intervals (95% CIs) of incident CVD, stroke, and CHD events by baseline FLI. The results were adjusted for age, smoking, alcohol consumption, hypertension, diabetes, lipid profile, chronic kidney disease, and cardiac murmur or valvular diseases. ResultsWithin 16.6 years of median follow-up, 590 participants developed CVD (346 stroke events and 244 CHD events). Women with NAFLD (FLI ≥ 60) showed a higher risk of CVD and stroke: HRs (95% CIs) = 1.69 (1.16, 2.46) and 2.06 (1.31, 3.24), respectively. Besides, women in the fourth and fifth (highest) FLI quintiles showed a higher risk of CVD and stroke than those in the third (middle) quintile: HRs (95% CIs) = 1.60 (1.08, 2.36) and 1.67 (1.13, 2.45) for CVD and 1.73 (1.07, 2.79) and 1.90 (1.18, 3.05) for stroke, respectively. No corresponding associations were detected in men. NAFLD was not associated with CHD risk in either sex. ConclusionsNAFLD, diagnosed by FLI, was associated with a higher risk of CVD and stroke in Japanese women. From a preventive perspective, women with NAFLD should be targeted for CVD screenings and interventions.

Coronary Angiographic Findings between Diabetic and nondiabetic Patients in Coronary Artery Disease: A Comparative Study

Background &amp; Objectives: Coronary artery disease (CAD) accounts for the major risk factor of mortality in diabetes. Coronary angiography is the “gold-standard” technique for diagnosing and evaluating CAD. Material and Methods: The present study was undertaken at Border Guard hospital, Dhaka between the periods of November - 2017 to December 2021. Percutaneous coronary angiography (CAG) was performed in 204 consecutive patients with suggestive of ischaemic chest pain. The population consisted of 88 cases which are diabetic and 116 cases nondiabetic Results: We observed angiographic lesion among both groups comparing site &amp; number of vessel(s) involvement and also average percentage of stenosis. The presence of coronary risk factors was not significantly different between the two populations. Total positive angiographic lesion was (61.5%) in both groups. Among the Diabetes mellitus patients positive CAG finding (69.3%). The recognized lesions were single vessel disease (SVD) 23 (26.1%), double vessel disease (DVD) 14 (15.9%), triple vessel disease (TVD) 24 (27.3%) percentage of vessel stenosis 82.63%. On the other hand, total positive angiographic lesion was 70 (53.4%) in non-diabetic group; among them single vessel disease (SVD) 30 (25.9%), double vessel disease (DVD) 15(12.9%), triple vessel disease (TVD) 17 (14.7%). No diffuse lesions was found and average vessel stenosis was 78.03%. The results of the angiographic finding suggest that diabetic patients have a higher incidence of coronary heart disease (CHD), DVD, TVD, diffuse lesion &amp; marked stenosis of coronary vessel than non-diabetic patient. Conclusion: CAD in diabetics had considerably higher percent of severe and unpredictable presentation. This increased frequency of complex lesion morphology is more difficult to treat by definitive intervention like percutaneous transluminal coronary angioplasty (PCI) &amp; coronary artery bypass graft (CABG). Diabetics have a higher risk factor profile and poor clinical outcome. Early diagnosis and appropriate management will reduce the risk of complication after the onset of disease. University Heart Journal 2023; 19(1): 5-9

Associations of pedometer-measured ambulatory activity with incidence of atherosclerotic cardiovascular diseases: Strong heart family study

ObjectiveCoronary heart disease has several risk factors that require a multifactorial community intervention approach in prevention efforts. Prevalence of coronary heart disease and its risk factors have been disproportionately high among American Indians. The objective of this study is to evaluate the impact of ambulatory activity levels on the development of coronary heart disease in this population. MethodsUsing pedometer data and other lifestyle and clinical factors from 2492 participants in the Strong Heart Family Study, we examined the associations of average daily step counts with incident coronary heart disease during an 18 to 20 year follow-up. ResultsAfter adjusting for potential confounders, participants with daily step counts in the 4th quartile (>7282 steps per day) had significantly lower odds of developing coronary heart disease compared to those in the 1st quartile (<3010 steps per day) (p = 0.035). ConclusionsHigher daily step count (over 7282 steps per day) is significantly associated with lower incidence of coronary heart disease among American Indian participants of the Strong Heart Family Study in a 20-year follow-up period.

Identification of genetic loci jointly influencing COVID-19 and coronary heart diseases

BackgroundComorbidities of coronavirus disease 2019 (COVID-19)/coronary heart disease (CHD) pose great threats to disease outcomes, yet little is known about their shared pathology. The study aimed to examine whether comorbidities of COVID-19/CHD involved shared genetic pathology, as well as to clarify the shared genetic variants predisposing risks common to COVID-19 severity and CHD risks.MethodsBy leveraging publicly available summary statistics, we assessed the genetically determined causality between COVID-19 and CHD with bidirectional Mendelian randomization. To further quantify the causality contributed by shared genetic variants, we interrogated their genetic correlation with the linkage disequilibrium score regression method. Bayesian colocalization analysis coupled with conditional/conjunctional false discovery rate analysis was applied to decipher the shared causal single nucleotide polymorphisms (SNPs).FindingsBriefly, we observed that the incident CHD risks post COVID-19 infection were partially determined by shared genetic variants. The shared genetic variants contributed to the causality at a proportion of 0.18 (95% CI 0.18–0.19) to 0.23 (95% CI 0.23–0.24). The SNP (rs10490770) located near LZTFL1 suggested direct causality (SNPs → COVID-19 → CHD), and SNPs in ABO (rs579459, rs495828), ILRUN(rs2744961), and CACFD1(rs4962153, rs3094379) may simultaneously influence COVID-19 severity and CHD risks.InterpretationFive SNPs located near LZTFL1 (rs10490770), ABO (rs579459, rs495828), ILRUN (rs2744961), and CACFD1 (rs4962153, rs3094379) may simultaneously influence their risks. The current study suggested that there may be shared mechanisms predisposing to both COVID-19 severity and CHD risks. Genetic predisposition to COVID-19 is a causal risk factor for CHD, supporting that reducing the COVID-19 infection risk or alleviating COVID-19 severity among those with specific genotypes might reduce their subsequent CHD adverse outcomes. Meanwhile, the shared genetic variants identified may be of clinical implications for identifying the target population who are more vulnerable to adverse CHD outcomes post COVID-19 and may also advance treatments of ‘Long COVID-19.’

Sex-specific associations of the difference between 2-hour post-load and fasting plasma glucose with cardiovascular risk in a normoglycemic population

Abstract Background Elevated levels of fasting plasma glucose (FPG) and 2-hour post-load glucose (2hPG) have been established as individual risk factors for cardiovascular disease (CVD), coronary heart disease (CHD), and stroke. However, it is unclear whether the difference between 2hPG and FPG (2hPG-FPG) within normoglycemic influences the cardiovascular risk in women and men. Purpose To investigate the association between 2hPG-FPG and the incidence of CVD, CHD, and stroke among normoglycemic women and men in a large population-based cohort. Methods In this prospective cohort study, a total of 7224 participants with the normoglycemic state (mean age 37±11; women, 57.4%) that had baseline measurements of both FPG and 2hPG values and did not have prior CVD, CHD, or stroke were included and were followed for incidence of outcomes annually until March 2018. The normoglycemic range was defined as FPG&amp;lt; 5.55 and 2 h-PG&amp;lt; 7.77 mmol/L and not taking anti-diabetic medications. CHD was defined as either positive ECG findings and biomarkers, cardiac symptoms accompanied by either positive ECG or biomarker, or angiographic-proven CHD. Stroke was defined based on the WHO criteria. Also, CVD was defined as a composite of CHD and stroke. A Multivariable Cox­-regression model adjusted for age, body mass index, hypertension, hyperlipidemia, FPG, education level, and smoking status was used to assess the association between 2hPG-FPG and incident CVD, CHD, and stroke in women and men. We also used a cumulative incidence curve to illustrate the cumulative sex-specific incidence of CVD, CHD, and stroke during the follow-up time (Figure 1). Results During a median follow-up of 17.9 years (IQR: 13.75-18.46), 487 CVD (174 women), 427 CHD (140 women), and 76 stroke (37 women) events occurred. Among men, 2hPG-FPG was associated with an increased risk of CVD (hazard ratio [HR]:1.11, 95% confidence interval [CI]:1.01-1.22, p=0.03) and CHD (HR:1.11, 95% CI:1.00-1.22, p=0.04 ), but not stroke (HR:1.14, 95% CI:0.88-1.50, p= 0.33). No significant associations among women were found between 2hPG-FPG and the incidence of outcomes, with adjusted HRs of 1.02 (95% CI, 0.88-1.18, p=0.82), 1.00 (0.85-1.17, p=0.99), and 1.10 (0.80-1.52, p=0.54) for incident CVD, CHD, and stroke, respectively (Table 1). Conclusion A greater difference between 2hPG and FPG (2hPG-FPG) within the normoglycemic range was associated with an increased risk for incidence of CVD and CHD in men but not women. Further studies are warranted to explore the potential use of 2hPG-FPG for cardiovascular risk stratification, particularly among those with normal glucose parameters.Association of 2hPG-FPG with CV riskCumulative incidence of CVD, CHD, stroke

Can the association between LDL-Cholesterol and incident coronary heart disease (CHD) be modulated by concomitant Lp(a) levels in the general population?

Abstract Background LDL-cholesterol (LDL-C), quantified by conventional methods, also includes the choles-terol attributable to Lipoprotein (a) (Lp(a)-C) due to their overlapping densities. The clinical relevance of this is still poorly investigated, since current attempts to estimate a true LDL-C (i.e. a LDL-C without its Lp(a)-C content, so called LDL-C-Lp(a)corr) remain challenging. Aims The aims of the present analysis were 1) to compare the association between LDL-C and LDL-C-Lp(a)corr with incident coronary heart disease (CHD) in the general population; 2) to determine the prognostic ability of LDL-C for future CHD events depending on concomitant Lp(a) levels. Methods Data from 68,748 subjects from eight European prospective population-based cohorts, who were free of CHD at baseline were used. LDL-C-Lp(a)corr was calculated as "LDL-C - Lp(a)-C", where Lp(a)-C was estimated as being 30% of the Lp(a) total mass. Fine and Gray competing risk-adjusted models were calculated for the association between LDL-C and LDL-C-Lp(a)corr (in quintiles (Q) with Q1 as REF) and future CHD events in the total study sample, as well as for LDL-C only after categorization of the study population according to Lp(a) mass (&amp;lt;90th percentile (pctl.) (43,5 mg/dL) (n=61,861) and ≥90th pctl. (n=6,887)). Results Similar risk estimates for incident CHD were found for LDL-C and LDL-C-Lp(a)corr with sHRs of 2.69 (95% CI 2.30-3.15) and 2.49 (95% CI 2.13-2.90), respectively (both p&amp;lt;0.001, comparing Q5 vs Q1; fully-adjusted models, including traditional cardiovascular risk factors and hsCRP). Categorization of the study sample according to Lp(a) mass revealed that the association between LDL-C and incident CHD was potentiated by higher Lp(a) mass (≥90th pctl) resulting in a sHR of 4.36 (95% CI 2.05-9.23; p&amp;lt;0.001 for Q5 vs Q1; fully-adjusted model), which was approximately x1.5 higher than the risk estimate found in the total study sample (i.e. without categorization for Lp(a) mass). In contrast, in subjects with Lp(a) mass &amp;lt;90th pctl. sHR for future CHD events was found to be 2.56 (95% CI 2.18-3.02) (for Q5 vs Q1 of LDL-C distribution; fully-adjusted model), being almost identical to the sHR obtained within the overall cohort (p for interaction between the categories of Lp(a) was 0.42). Conclusion Within the present analysis, correction of LDL-C for its Lp(a)-C content did not provide any meaningful additional information on CHD-risk estimation in the general population, thereby not confirming a clinically relevant value of LDL-C-Lp(a)corr. On the other hand, a simple categorization of Lp(a) mass with respect to high (≥90th pctl.) vs low (&amp;lt;90th pctl.) values demonstrated that Lp(a) significantly modulates LDL-C-related risk for future CHD only at higher levels. So, for the vast majority of subjects (&amp;lt;90th pctl. of Lp(a) distribution), no correction of LDL-C for its Lp(a)-C content is required.

Utility of a polygenic risk score for incident CHD: interplay with lifestyle in a multi-ethnic cohort of more than 60,000 individuals

Abstract Background The degree to which benefits of healthy eating, physical activity and not smoking are protective for coronary heart disease (CHD) based on levels of polygenic risk remains an important question. We set out to investigate whether and to what degree a favorable lifestyle could reduce the effect of high genetic risk. Methods We utilized data from the Genetic Epidemiology Resource in Adult Health and Aging (GERA) Multi-Ethnic cohort of 60,682 (mean ± SD age = 59 ± 9 years; 67% female; 18% non-European ancestry) Kaiser Permanente of Northern California (KPNC) members. We characterized the cohort at baseline in 2003-2007 by smoking status (never, former or current smoker), Mediterranean-pattern diet (MedDiet) and meeting current AHA physical activity recommendations (PAR) of at least 150 min of moderate activity or 75 min of vigorous activity per week. We stratified the cohort into three groups of CHD genetic risk (low: quintile 1, intermediate: quintiles 2, 3 and 4 combined, and high: quintile 5) using a validated 12-SNP Polygenic Risk Score (PRS) for CHD (CARDIO inCode-Score, GENinCode Plc). Incident CHD consisted of primary in-patient codes for angina pectoris, myocardial infarction, revascularization procedures or CHD death (n=2,220) through 12/31/2014; mean follow-up was 9.5 years. Results Age-adjusted CHD rates per 10,000 person-years were estimated using Poisson regression (accounting for death and health plan disenrollment) by number of favorable lifestyle factors (LF) and, within each level, by genetic risk groups (see Figure below). Genetic background provided further CHD risk stratification within each lifestyle group. The most favorable lifestyle (never smoking, MedDiet, meeting PAR) reduced the effect of high genetic risk by 59% (age-adjusted rates per 10,000 person-years 40 vs. 99) and similar reductions were observed at intermediate or low genetic risk. Conclusions Our results are consistent with an additive model of genetic risk and lifestyle as determinants of CHD. These results underscore the importance of favorable lifestyle and the need to prioritize those individuals with the highest CHD risk (most unfavorable lifestyle and high genetic risk), who will benefit the most from lifestyle advice.

Associations of sleep quality and exercise frequency and the risk of coronary heart disease in Chinese urban elderly: a secondary analysis of cross-sectional data

BackgroundSleep quality and exercise frequency are closely associated with coronary heart disease (CHD). Few studies focused on the joint effect of initiating sleep, sleep disorders, and exercise frequency on the risk of CHD in the elderly. We used a secondary data analysis based on Boshan Elderly cross-sectional study. We explored the sleep quality, exercise frequency, and their joint effects on the risk of CHD.MethodsWe collected 678 participants whose age ≥ 60 years old from Boshan District Hospital. We used the Pittsburgh Sleep Quality Index to evaluate the sleep quality and obtained physical examination information from the hospital.ResultsCompared with the non-CHD group, patients with CHD spent more time in initiating sleep (time ≥ 60 min, 34.59% vs. 22.93%, P = 0.025) and less time exercising (exercise frequency < 1 times/week, 23.90% vs. 17.15%, P = 0.024). In multiple logistic regression analysis, sleep latency ≥ 60 min was associated with CHD risk (adjusted OR = 1.83; 95% CI: 1.11, 2.99; P-trend = 0.008). The adjusted OR (95% CI) of CHD was 2.24 (1.16, 4.34) for sleep duration < 5 h versus 5–9 h. Compared with exercise frequency < 1 times/week, the adjusted OR for exercise frequency ≥ 1 times/week was 0.46 (95% CI: 0.26, 0.83; P = 0.010). In addition, the joint effects of long sleep latency (≥ 60 min) and sleep disorders were associated with CHD (adjusted OR = 3.36; 95% CI: 1.41, 8.02). The joint effect of exercise frequency ≥ 1 times/week and sleep onset latency within normal limits (< 30 min) was also associated with CHD, and the adjusted OR (95% CI) was 0.42 (0.21, 0.87).ConclusionsLong sleep latency, high frequency of initiating sleep difficulty, sleep disorders, and short sleep duration were positively associated with CHD. In addition, the joint effects of long sleep latency and sleep disorders were positively correlated with CHD incidence. However, the joint effects of exercise frequency ≥ 1 times/week and normal sleep onset latency were negatively associated CHD.

Abstract 13367: Plasma Lipidomic Markers of Diet Quality Are Associated With Risk of Coronary Heart Disease in American Indians

Background: Diet quality can affect lipid profiles and subsequent risk of coronary heart disease (CHD). Identifying lipidomic markers of diet quality is needed to inform the development of biomarkers of diet, and to understand the mechanisms driving the diet-CHD relation. Objective: To identify lipidomic markers of diet quality and examine whether these lipids are associated with incident CHD. Methods: We studied 1,694 American Indians (aged 18-75, 62% women) who were free of CHD and had lipidomic and dietary data at baseline (2001-2003). Participants were followed for development of CHD through 2020 (mean follow-up: 17.8 years; total incident cases of CHD: 147). Information on past year diet was collected using the Block Food Frequency Questionnaire, and diet quality was assessed using the Alternative Healthy Eating Index-2010 (AHEI). Mixed effects linear regression was used to identify individual lipid species associated with AHEI at baseline. Cox frailty model was used to estimate the hazard ratio of each AHEI-related lipid for CHD risk. All models adjusted for age, sex, center, education, BMI, smoking, alcohol drinking, level of physical activity, energy intake, diabetes, hypertension, and use of lipid-lowering drugs. Results: Among 1,542 lipid species measured, 71 lipid species (23 known) were associated with AHEI at FDR&lt;0.05. Of these, 10 lipids (5 known) were associated with incident CHD (Figure 1 ). The 5 known lipids associated with incident CHD were CE(22:5) B, PC(p-14:0/22:1)/PC(o-14:0/22:1), PC(p-38:3)/PC(o-38:4) B, PE(p-18:0/20:4)/PE(o-18:0/20:4), and SM(d36:2) A. On average, per standard deviation increase in the baseline level of these lipids was associated with 17%-23% increased risk of CHD. These AHEI-related lipids are enriched in glycerophospholipid metabolism. Conclusion: We identified lipidomic markers of diet quality in American Indians. Some diet-related lipids are associated with risk of CHD beyond established risk factors.

Abstract 18607: Sex-specific Metabolites Associated With Incident Stroke, Incident Coronary Heart Disease, Hypertension, And Chronic Kidney Disease In The Regards Cohort

Sex disparities continue to exist in cardiometabolic diseases. Metabolomic profiling offers the ability to gain insight into disease mechanisms. The purpose of the present analysis was to identify metabolites associated with sex and determine if sex-specific metabolites are associated with incident stoke, incident coronary heart disease (CHD), hypertension (HTN), and chronic kidney disease (CKD). Targeted metabolomics was conducted for 358 metabolites in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) cohort. Weighted logistic regression models were used to test the association between sex and metabolites. Metabolites meeting the Bonferroni-corrected threshold were selected for replication in the Hypertension Genetic Epidemiology Network study. Cox proportional hazard models were used to calculate hazard ratios (HRs) per unit standard deviation (SD) of each replicated metabolite with incident stroke and incident CHD. Weighted logistic regression models were used to calculate odds ratios (ORs) per unit SD of each replicated metabolite with prevalent HTN and prevalent CKD. A total of 1,898 individuals were included in the analysis and 50.47% of the sample was male sex. The mean age was 68.40 ± 10.55 years and 43% of the sample was Black race. Sixteen metabolites were associated with sex, meeting the Bonferroni-adjusted p-value of 1.4 x 10 -4 . These included 8 lipids, 6 amino acids, 1 indole, and 1 quinoline. Of these 16 metabolites, none were associated with incident stroke or incident CHD. Kynurenic acid and leucine were associated with HTN in the base model adjusting for age, sex, and race (kynurenic acid: OR 1.45, 95% CI [1.19, 1.76], p=2.36 x 10 -4 ; leucine: OR 1.41, 95% CI [1.14, 1.76], p=2.03 x 10 -3 ). Indole-3-lactic acid and kynurenic acid were associated with CKD in the full model adjusting for age, sex, race, smoking, alcohol use, and BMI (indole-3-lactic acid: OR 3.83, 95% CI [2.77, 5.29], p=5.93 x 10 -16 ; kynurenic acid: OR 6.63, 95% CI [4.67, 9.41], p=1.50 x 10 -25 ). Our findings shed light on the sexual dimorphism of the metabolome and suggest that differences in biochemical pathways may contribute to sex disparities in cardiometabolic disease risk.

Abstract 14629: Assessing the Contribution of Racial Differences in Elevated Lipoprotein (a) Levels to Disparities in Atherosclerotic Cardiovascular Disease: The Atherosclerosis Risk in Communities (ARIC) Study

Introduction: Racial differences in Lp(a) distributions are well known, with higher levels in Black adults compared to White adults. It is unclear whether the risk implications of higher Lp(a) levels are the same in Black and White adults. Furthermore, the contribution of racial differences in Lp(a) to disparities in ASCVD in the US has not been well characterized in long-term cohort studies. Objective: We evaluated the relative risk associations for higher Lp(a) and estimated the related population-attributable fraction (PAF) for ASCVD in Black and White adults. Methods: We performed a prospective analysis of 9,519 Black and White participants at ARIC Visit 4 (1996-1999) without baseline ASCVD. Plasma Lp(a) was measured from stored Visit 4 plasma samples using an apo(a) isoform-insensitive assay (Denka Seiken). Lp(a) was categorized as &lt;30, ≥30 to &lt;50, 50≥ to &lt;100 and ≥100 mg/dL. We assessed the association of higher Lp(a) categories with incident coronary heart disease (CHD) and ASCVD (CHD and ischemic stroke) overall and stratified by race, with tests for interaction. We calculated the PAF for ASCVD and CHD associated with Lp(a) ≥30 mg/dL, overall, and for Black and White adults. Results: The mean age was 63±6 years, with 59% women and 23% Black adults. There was a higher prevalence of Lp(a) &gt; 30 mg/dL among Black than White adults (54 vs 24%). During a follow-up of 24 years, there were 2,235 ASCVD and 1,715 CHD events. Higher Lp(a) categories were associated with progressively higher risk, with Lp(a) ≥100 mg/dL associated with hazard ratios of 1.71 (95% CI 1.38-2.12) for ASCVD and 1.67 (1.30-2.13) for CHD, with no significant differences by race (Table). The PAF associated with elevated Lp(a) was two times higher in Black than White adults for ASCVD (10.7 vs 4.7%) and CHD (10.5 vs 4.3%). Conclusion: Differences in Lp(a) distributions likely contribute to racial disparities in ASCVD. Evolving therapies targeting Lp(a) lowering could assist in addressing disparities in ASCVD.

Abstract 15377: Traditional Cardiovascular Risk Factors Do Not Fully Explain the Risk of CAD Population in Colombia

Introduction: Major cardiovascular events occur even having reached LDL-C goals. Tolima department has the highest rate of cardiovascular mortality within Colombia. Hypothesis: in patients who underwent percutaneous coronary intervention (PCI) in a healthcare institution in Ibague Colombia, there is an increasing cardiovascular risk regardless of traditional risk factors. Methods: Descriptive, retrospective analysis of a cohort of patients with coronary artery disease (CAD) with PCI between 2020-2023. A multiple logistic regression model was developed, adjusted for predictors of CAD (Figure 1). Data was analyzed through R-4.3.0, JASP0.17.1 and Python3.11. Results: A sample size of 463 patients who underwent PCI was assessed (Table 1). Dyslipidemia was the most prevalent risk factor 43.2%(n=200). Mean LDL-C was 102, mean HDL was 38 and mean triglycerides was 186. The most incident coronary heart disease was NSTEMI 50.5%(n=234). Data was fitted into a logistic regression model accounting for comorbidities, risk factors and lipid profile values. Regression coefficients computed for CAD were around 0.07. Independent variables explain approximately 7 up to 16.1% of the variance observed in the dependent variable (Figure 1). Conclusions: In primary and secondary prevention for CAD, there is a high prevalence of risk factors. Although risk factors impact the outcome, they account for a relatively little variability within the model. Results imply that there are other key factors that contribute to the outcome and may not be measured currently. Further studies must be developed to evaluate markers in residual risk that may have an impact on the prognosis of patients with CAD.

Abstract 18742: Matrilysin (MMP7) as a Robust Predictor of Hypertension Incidence and Complications: Findings From a Proteomic Analysis in the Atherosclerosis Risk in Communities (ARIC) Study

Introduction: Proteomic techniques can be applied for the discovery of common pathways underlying both incident hypertension and hypertension-related cardiovascular outcomes. Research Questions: To identify and validate proteins associated with incident hypertension and to examine the association of these validated proteins with hypertension-related cardiovascular events. Methods: We quantified the association of 4,955 plasma proteins (measured by SomaScan® Version 4 Assay) with incident hypertension (defined as systolic blood pressure (BP) ≥140, diastolic BP ≥ 90 mmHg, or hypertension medication use) in participants free of hypertension at ARIC visit 3 (1993-95) using Cox regression models adjusted for demographics, clinical characteristics and baseline BP. Significant associations were validated using proteomic measurements at ARIC visit 2 (1990-92). We then examined the association of validated proteins with incident coronary heart disease (CHD), stroke, and heart failure (HF) among participants with hypertension at visit 3 using Cox regression models additionally adjusted for hypertension duration and treatment. Results: There were 5,080 participants in the discovery cohort (mean age 59y, 13% Black, 54% women, median follow up 11 y) and 6,810 in the validation cohort (median follow up 3.1y). Four proteins were significantly associated with incident hypertension in the discovery cohort. One protein, Matrilysin (MMP7), remained significantly associated in the validation cohort (HR 1.22 [1.11-1.34]) (Figure1A). MMP7 was also significantly associated with all hypertension-related complications (Figure 1B-D). Conclusions: MMP7, a protein involved in extracellular matrix degradation, was robustly associated with incident hypertension and cardiovascular events. Future research examining the pathophysiologic mechanism of MMP7 could potentially yield drug targets for the prevention and treatment of hypertension.

Abstract 14635: Prognostic Value of Heart Rate Variability in Black Americans: The Jackson Heart Study

Background: The prognostic value of heart rate variability (HRV) in Black Americans (BAs), who have distinct cardiac risk profiles, is not well studied. We aimed to investigate the association between HRV, all-cause mortality, and cardiovascular events in the Jackson Heart Study (JHS). Methods: We analyzed data from JHS participants who had HRV readings at baseline (2000-2004). HRV was measured as the standard deviation between subsequent R-waves on a 12-lead EKG. Data were analyzed up to December 31, 2014. Outcomes of interest were all-cause mortality and cardiovascular events (composite of incident stroke and coronary heart disease). Cox regression models were used to estimate hazard ratios (HRs) for the hazard of events in participants with an HRV below the median versus those with an HRV above the median. Restricted cubic splines (RCS) were used to explore non-linear interactions. All analyses were adjusted for age, sex, smoking, clinically relevant comorbidities, and risk factors. Results: Among the 3627 participants (mean age: 55.1 years; female: 62.4%), the median [IQR] HRV was 22.3ms [13.7, 36.1]. At baseline, participants with HRV below the median had a higher prevalence of several cardiometabolic diseases. Adjusted Cox regression showed that HRV below the median was associated with a 32% increased hazard of all-cause mortality (HR: 1.32 [1.09, 1.60]; P = 0.005) and a non-significant increase in incident cardiovascular events (HR: 1.28 [0.99, 1.66]; P = 0.059); Figure 1A . RCS suggested HRV has a non-linear relationship with all-cause mortality (P-nonlinearity: 0.0076) and cardiovascular events (P-nonlinearity: 0.0162), with the hazard of events beginning to increase sharply at HRV &amp;lt;25ms ( Figure 1B ). Conclusion: BAs had a higher mortality hazard associated with lower HRV readings, specifically &amp;lt;25ms. Consumer wearable sensors commonly record HRV, and our findings suggest that HRV could serve as a practical prognostic tool for this population.