Risk Of Artery Disease Research Articles

ABO blood groups and increased risk for the development of vascular involvement in Behçet's disease.

Inflammatory endothelial activation is a prominent feature of vascular involvement in Behçet's disease (BD), which is usually accompanied by a thrombotic tendency. Recent studies suggest an association between ABO blood groups and thrombotic vascular disease in those carrying non-O (A, B, and AB) groups. This study aimed to analyse the contribution of ABO blood groups to the vascular involvement in BD. In this retrospective study, BD patients with available ABO blood group data and meeting the ISG criteria were included in the study. The presence of vascular involvement, its clinical characteristics, and the data about other manifestations were recorded from the patient charts. This study was conducted in 411 patients; 143 (34.8%) were carrying O and 268 (65.2%) were carrying non-O groups. The vascular involvement was significantly more frequent and the risk for overall vascular and venous events was up to 2-fold higher in the patients with non-O groups. After adjustments for age, sex, and comorbidities, the risk for arterial disease was also found to be increased in association with non-O groups. ABO blood groups were shown to be independent risk factors for vascular BD by multiple regression models based on known predisposing factors. Compared with other non-O blood groups, the patients carrying blood group B had a higher risk for vascular events. The results of this preliminary study show the potential contribution of ABO blood groups to the vascular-BD phenotype and suggest an increased risk for vascular BD in association with non-O blood groups.

Incidence and risk of post-COVID-19 thromboembolic disease and the impact of aspirin prescription; nationwide observational cohort at the US Department of Veteran Affairs.

COVID-19 triggers prothrombotic and proinflammatory changes, with thrombotic disease prevalent in up to 30% SARS-CoV-2 infected patients. Early work suggests that aspirin could prevent COVID-19 related thromboembolic disorders in some studies but not others. This study leverages data from the largest integrated healthcare system in the United States to better understand this association. Our objective was to evaluate the incidence and risk of COVID-19 associated acute thromboembolic disorders and the potential impact of aspirin. This retrospective, observational study utilized national electronic health record data from the Veterans Health Administration. 334,374 Veterans who tested positive for COVID-19 from March 2, 2020, to June 13, 2022, were included, 81,830 of whom had preexisting aspirin prescription prior to their COVID-19 diagnosis. Patients with and without aspirin prescriptions were matched and the odds of post-COVID acute thromboembolic disorders were assessed. 10.1% of Veterans had a documented thromboembolic disorder within 12 months following their COVID-19 diagnosis. Those with specific comorbidities were at greatest risk. Preexisting aspirin prescription was associated with a significant decrease risk of post-COVID-19 thromboembolic disorders, including pulmonary embolism (OR [95% CI]: 0.69 [0.65, 0.74]) and deep vein thrombosis (OR [95% CI]: 0.76 [0.69, 0.83], but an increased risk of acute arterial diseases, including ischemic stroke (OR [95% CI]: 1.54 [1.46, 1.60]) and acute ischemic heart disease (1.33 [1.26, 1.39]). Findings demonstrated that preexisting aspirin prescription prior to COVID-19 diagnosis was associated with significantly decreased risk of venous thromboembolism and pulmonary embolism but increased risk of acute arterial disease. The risk of arterial disease may be associated with increased COVID-19 prothrombotic effects superimposed on preexisting chronic cardiovascular disease for which aspirin was already prescribed. Prospective clinical trials may help to further assess the efficacy of aspirin use prior to COVID-19 diagnosis for the prevention of post-COVID-19 thromboembolic disorders.

Calcification of heart structures in patients with suspected coronary heart disease depending on renal function

Cardiovascular disease is the leading cause of death in the world. The use of the coronary artery calcification score (CACS) allows to determine the risk of coronary artery disease (CAD). Chronic kidney disease (CKD) is a one of the major risk factors for coronary artery disease. With a decrease in renal function, impaired calcium-phosphorus metabolism leads to excessive tissue calcification. It is likely that patients with different kidney function experience different types of calcium deposition. The use of CACS is an opportunity to assess the condition of the coronary arteries without using a contrast agent, which is very important for patients with CKD. One of the most accessible and significant research methods for clinical screening use is computed tomography with non-invasive assessment of coronary calcium (quantitative analysis of the calcium index). To evaluate it, the method of A. Agatston is used, which allows to measure calcium in units. Our aim was to investigate the pattern of calcification of heart structures depending on renal function in patients with suspected coronary heart disease. The patients in the presented study had a high incidence of diabetes mellitus (49.4%) and arterial hypertension (83.1%). In patients with suspected coronary artery disease, borderline values of systolic and diastolic blood pressure and total cholesterol were found. In the majority of the patients CACS was 1-100 Agatston units (AU). After the distribution of patients into groups depending on glomerular filtration rate (GFR), it was found that the groups of patients with lower GFR, were of older age. The proportion of patients with total CACS >100 AU was the highest in the group of patients with GFR 30-59 ml/min. There were no significant differences in the structure of general and vascular CACS between patients with GFR 90-120 ml/min and GFR 60-89 ml/min. Valvular CACS was significantly lower in patients with GFR <60 ml/min. In all cases of visual comparison of CACS depending on GFR, significantly higher CACS indices differed in patients with GFR <60 ml/min compared to patients with GFR ≥60 ml/min.

Role of circulating polyunsaturated fatty acids on cardiovascular diseases risk: analysis using Mendelian randomization and fatty acid genetic association data from over 114,000 UK Biobank participants

BackgroundDespite early interest in the health effects of polyunsaturated fatty acids (PUFA), there is still substantial controversy and uncertainty on the evidence linking PUFA to cardiovascular diseases (CVDs). We investigated the effect of plasma concentration of omega-3 PUFA (i.e. docosahexaenoic acid (DHA) and total omega-3 PUFA) and omega-6 PUFA (i.e. linoleic acid and total omega-6 PUFA) on the risk of CVDs using Mendelian randomization.MethodsWe conducted the largest genome-wide association study (GWAS) of circulating PUFA to date including a sample of 114,999 individuals and incorporated these data in a two-sample Mendelian randomization framework to investigate the involvement of circulating PUFA on a wide range of CVDs in up to 1,153,768 individuals of European ancestry (i.e. coronary artery disease, ischemic stroke, haemorrhagic stroke, heart failure, atrial fibrillation, peripheral arterial disease, aortic aneurysm, venous thromboembolism and aortic valve stenosis).ResultsGWAS identified between 46 and 64 SNPs for the four PUFA traits, explaining 4.8–7.9% of circulating PUFA variance and with mean F statistics >100. Higher genetically predicted DHA (and total omega-3 fatty acids) concentration was related to higher risk of some cardiovascular endpoints; however, these findings did not pass our criteria for multiple testing correction and were attenuated when accounting for LDL-cholesterol through multivariable Mendelian randomization or excluding SNPs in the vicinity of the FADS locus. Estimates for the relation between higher genetically predicted linoleic acid (and total omega-6) concentration were inconsistent across different cardiovascular endpoints and Mendelian randomization methods. There was weak evidence of higher genetically predicted linoleic acid being related to lower risk of ischemic stroke and peripheral artery disease when accounting by LDL-cholesterol.ConclusionsWe have conducted the largest GWAS of circulating PUFA to date and the most comprehensive Mendelian randomization analyses. Overall, our Mendelian randomization findings do not support a protective role of circulating PUFA concentration on the risk of CVDs. However, horizontal pleiotropy via lipoprotein-related traits could be a key source of bias in our analyses.

432-P: Single and Joint Impact of Type 2 Diabetes and of Coronary Artery Disease on Albuminuria

Albuminuria is a characteristic feature of diabetic nephropathy, and increased urine albumin excretion is associated with an increased risk of coronary artery disease (CAD) . However, type 2 diabetes (T2DM) and CAD frequently coincide, and the single and joint effects of T2DM and angiographically determined CAD with albuminuria are unclear. This issue therefore was addressed in the present study. We investigated 831 patients with angiographically proven CAD, of whom 261 had T2DM (CAD+/T2DM+) and 570 did not have diabetes (CAD+/T2DM-) and 263 controls without CAD, of whom 63 had T2DM (CAD-/T2DM+) and 200 did not have diabetes (CAD-/T2DM-) . The albumin / creatinine ratio (ACR) was 37±1in CAD-/T2DM- patients. Compared to this group it was higher in CAD-/T2DM+ patients (193±642; p<0,001) , but not in CAD+/T2DM- patients (52±184; p=0,421) , in whom it was significantly lower than in CAD-/T2DM+ patients (p<0.001) . In CAD+/T2DM+ patients the ACR (162±466) was higher than in CAD-/T2DM- (p<0,001) and in CAD+/T2DM- patients (p<0,001) , but did not differ significantly to that in CAD-/T2DM+ patients (p=0,225) . In multivariate analysis of covariance, T2DM but not CAD proved to be an independent predictor of ACR after adjustment for age, sex, body mass index, LDL-C, smoking, hypertension and the use of ACE inhibitors /AT2-antagonists and statins (F=22.06; p<0.0 and F=0.520; p=0.471, respectively) . We conclude that T2DM but not CAD is an independent determinant of albuminuria. Disclosure M.Maechler: None. L.Sprenger: None. A.Mader: None. B.Larcher: None. A.Vonbank: None. A.Leiherer: None. A.Muendlein: None. H.Drexel: None. C.H.Saely: None.

325-OR: Associations of Systolic Blood Pressure (SBP) with the Incidence of Heart Failure (HF) According to Glucose Tolerance Status (GTS)

Although a linear relationship between SBP and risk of coronary artery disease or cerebrovascular disease was observed regardless of GTS, this association in HF is little known. We analyzed data from a nationwide claims database from 20to 20on 589,621 individuals. A Cox proportional hazards model identified risks of HF among 5 levels of SBP according to GTS [i.e. normal glucose tolerance (NGT) , prediabetes, diabetes (DM) ]. Incidence of HF per 1,000 person-years was 0.for NGT, 0.18 for prediabetes, and 0.80 for DM. Compared with SBP <1mmHg, hazard ratios (HR) (95% CI) for HF in the 4 higher NGT levels (120-129, 130-139, 140-149, ≥150 mmHg) increased from 1.93 (1.30-2.85) in the second level to 8.66 (5.44-13.39) in the fifth level. For prediabetes or DM, HF risk was significantly increased in the ≥150 mmHg group compared with the ≤1mmHg group. Compared with NGT and SBP ≤1mmHg, prediabetes or DM patients with SBP ≤1mmHg had approximately 2-fold or 5-fold risks of HF, respectively (Table) . Association of SBP with HF differs according to GTS. BP control is essential in those with NGT. The impact of risk factors other than SBP, such as poor glycemic control and physical inactivity, on the development of HF may increase with worsening of glucose status, suggesting that comprehensive management of risk factors other than BP is essential in those with prediabetes and DM to prevent HF. Disclosure K.Fujihara: None. M.H.Yamada: None. M.Yamamoto: None. M.Oe: None. T.Osawa: None. M.Iwanaga: None. T.Yamada: None. S.Kodama: None. H.Sone: Research Support; Astellas Pharma Inc., Eisai Co., Ltd., Kyowa Kirin Co., Ltd., Novo Nordisk, Ono Pharmaceutical Co., Ltd., Taisho Pharmaceutical Holdings Co., Ltd., Takeda Pharmaceutical Company Limited. Funding JSPS (21K11569)

411-P: Potential to Utilize DNA Methylation as a Biomarker to Predict Major Coronary Artery Disease (CAD) Risk in Type 1 Diabetes (T1D)

DNA methylation (DNAme) has been associated with risk of future CAD in the general population and is a potential target for pharmacological intervention. In T1D, DNAme has been associated with microvascular complications but its association with CAD has not been examined in this high risk population. Thus, we performed an epigenome-wide association study (EWAS) of DNAme and 28-year major CAD (CAD death, nonfatal myocardial infarction) incidence in an observational T1D cohort. Whole blood DNAme was assayed via Illumina EPIC beadchip in the Pittsburgh Epidemiology of Diabetes Complications (EDC) study of childhood onset (<17 years) T1D (n=400; mean age 29, T1D duration 21 yrs) . After quality control DNAme at 683,597 CpGs was analyzed in Cox models for time-to-CAD, adjusting for T1D duration, sex, smoking pack-years, estimated blood cell composition, and technical/batch covariates. Over 28 years 102 (25%) developed major CAD. DNAme at two CpGs was associated with lower CAD risk: cg06125996 (Chr 5, NLN; log HR per 5% DNAme= -1.10, p=6.0e-11) and cg051638 (Chr 9, CARD9; log HR= -0.97, p=1.2e-08) . Other associations with FDR<5% included CpGs in MRPS21, ZNF428, PCMTD1, and LYRM4. KEGG pathway analysis of all CpGs with FDR<10% (n=44) suggested enrichment for renin-angiotensin-aldosterone system, lipid metabolism, and immune system pathways. In GWAS we identified methylation quantitative trait loci (QTL) associated with DNAme at cg06125996 and cg05163804, three of which were annotated as expression QTLs in GTEx including SNPs in genes involved in insulin receptor signaling (SIK2) and cytokine activity (CMTM2, CMTM4) , and calcium ion binding (EFHB) . DNAme was not correlated with cross-sectional HbA1c at either CpG and adjusting for baseline HbA1c did not alter CpG-CAD associations. Our results demonstrate that DNAme may be an early marker of CAD risk in T1D, but the potential role of glycemic exposure in this association is unclear and warrants further study. Disclosure R.G.Miller: Stock/Shareholder; Becton, Dickinson and Company. J.Mychaleckyj: None. S.Onengut-gumuscu: None. T.J.Orchard: None. T.Costacou: None. Funding American Diabetes Association (1-19-JDF-109) ; NIH/NIDDK R01-DK034818, Rossi Memorial Fund

Study of the Association between VEGF Polymorphisms and the Risk of Coronary Artery Disease in Koreans.

Coronary artery disease (CAD), a leading cause of death worldwide, has a complex etiology comprising both traditional risk factors (type 2 diabetes, dyslipidemia, arterial hypertension, and cigarette smoking) and genetic factors. Vascular endothelial growth factor (VEGF) notably contributes to angiogenesis and endothelial homeostasis. However, little is known about the relationship between CAD and VEGF polymorphisms in Koreans. The aim of this study is to investigate the associations of 2 VEGF promoter region polymorphisms (−1154G>A [rs1570360], −1498T>C [rs833061]) and 4 VEGF 3′-UTR polymorphisms (+936C>T [rs3025039], +1451C>T [rs3025040], +1612G>A [rs10434], and +1725G>A [rs3025053]) with CAD susceptibility in Koreans. We studied 885 subjects: 463 CAD patients and 422 controls. Genotyping was conducted with polymerase chain reaction-restriction fragment length polymorphism analysis and TaqMan allelic discrimination assays, and the genotype frequencies were calculated. We then performed haplotype and genotype combination analyses and measured the associations between VEGF polymorphisms and clinical variables in both the CAD patients and control subjects. We detected statistically significant associations between CAD and certain VEGF allele combinations. In the haplotypes of 5 single-nucleotide polymorphisms, the VEGF allele combination −1154A/+936T was associated with a decreased prevalence of CAD (A-T-T-G-G of VEGF −1154G>A/−1498T>C/+936C>T/+1612G>A/+1725G>A, AOR = 0.077, p = 0.021). In contrast, the VEGF allele combinations −1498T/+1725A and −1498T/+1612A/+1725A were associated with an increased prevalence of CAD (G-T-C-C-A of VEGF −1154G>A/−1498T>C/+936C>T/+1451C>T/+1725G>A, AOR = 1.602, p = 0.047; T-C-C-A-A of VEGF −1498T>C/+936C>T/+1451C>T/+1612G>A/+1725G>A, AOR = 1.582, p = 0.045). Gene–environment combinatorial analysis showed that the combination of the VEGF +1725AA genotype and several clinical factors (e.g., body mass index, hemoglobin A1c, and low-density lipoprotein cholesterol) increased the risk of CAD. Therefore, we suggest that VEGF polymorphisms and clinical factors may impact CAD prevalence.

Influence of Proteus sp. on Trimethylamine N- Oxide production via the Choline Metabolism Pathway and the Formulation of a Predictive Model to Assess the Risk of Coronary Artery Disease in Indian Patients

Influence of Proteus sp. on Trimethylamine N- Oxide production via the Choline Metabolism Pathway and the Formulation of a Predictive Model to Assess the Risk of Coronary Artery Disease in Indian Patients

A COMPARATIVE STUDY OF HOMOCYSTEINE, CYANOCOBALAMINE, FOLATE, LIPID PROFILE AND SERUM CREATININE LEVEL IN HYPERTHYROID SUBJECTS BEFORE AND DURING TREATMENT

Introduction: Hyperthyroidism disorder results from over production of hormones secreted by thyroid gland itself. The present study plan to delineate influence of thyroxin on homocysteine, folate, cyanocobalamine, lipid profile and serum creatinine in hyperthyroid patients before and during treatment with antithyroid drugs. Material and Method: The present study was conducted on 75 pateints of hyperthyroidism of either sex in department of biochemistry, J.L.N. medical college and hospitals, Ajmer. Serum homocysteine, cyanocobalamine, folate level was measured by ELISA while thyroid function test were evaluated by RIA method. Result and discussion: There were significant change in homocysteine, folate, cyanocobalamine, total cholesterol, HDL-cholesterol and LDL-cholesterol in hyperthyroid subjects before and during treatment (P<0.0001) and these emerging evidence suggest that these parameter are influenced by level of thyroxine hormone which were higher in hyperthyroid subjects before treatment with antithyroid drugs. Conclusion: It is concluded that treatment with antithyroid drug reduces the level of thyroxine hormone in hyperthyroid subject increases level of homocysteine and causes dyslipidemia which increases risk of coronary artery disease, angina pectoris in subclinical hyperthyroidism.

Causal associations of circulating adiponectin with cardiometabolic diseases and osteoporotic fracture

Circulating adiponectin shows some relationships with the occurrence of cardiometabolic diseases and osteoporotic fracture, but little is known about their causal associations. This two-sample Mendelian randomization (MR) study aims to explore the causal roles of circulating adiponectin in cardiometabolic diseases and osteoporotic fracture. We used 15 single nucleotide polymorphisms associated with circulating adiponectin as the instrumental variables. Inverse variance weighted, weighted median and MR-Egger regression methods were applied to study the causal associations. The results found that high circulating adiponectin was causally associated with reduced risk of type 2 diabetes (beta-estimate: −0.030, 95% CI: −0.048 to −0.011, SE: 0.009, P-value = 0.002) and may be the risk factor of coronary artery disease (beta-estimate: 0.012, 95% CI: 0.001 to 0.023, SE: 0.006, P-value = 0.030). No causal associations were seen between circulating adiponectin and other outcomes including heart failure, atrial fibrillation, cerebral ischemia, intracerebral hemorrhage or osteoporotic fracture. This study found the potential causal roles of high circulating adiponectin in reduced risk of type 2 diabetes and increased risk of coronary artery disease, which may help prevent and treat these two diseases.

Abstract MP18: A Multi-ethnic Polygenic Risk Score Is Associated With Hypertension Prevalence And Progression Throughout Adulthood

Background: We used summary statistics from previously-published GWAS of systolic and diastolic BP and of hypertension (HTN) to construct Polygenic Risk Scores (PRS) to predict hypertension across diverse populations. Methods: We used 10,314 participants of diverse ancestry from BioMe to train trait-specific PRS. We implemented a novel approach to select one of multiple potential PRS based on the same GWAS, by optimizing the coefficient of variation across estimated PRS effect sizes in independent subsets of the training dataset. We combined the 3 selected trait-specific PRS as their unweighted sum, called “PRSsum”. We evaluated PRS associations in an independent dataset of 39,035 individuals from eight cohort studies, to select the final, multi-ethnic, HTN-PRS. We estimated its association with prevalent and incident hypertension 4-6 years later. We studied hypertension development within HTN-PRS strata in a longitudinal, six-visit, longitudinal dataset of 3,087 self-identified Black and White participants from the CARDIA study. Finally, we evaluated the HTN-PRS association with clinical outcomes in 40,201 individuals from the MGB Biobank. Results: Compared to other race/ethnic backgrounds, African-Americans had higher average values of the HTN-PRS. The HTN-PRS was associated with prevalent hypertension (OR=1.76, 95% CI [1.70, 1.83], per one standard deviation (SD) of the PRS) across all participants, and in each race/ethnic background, with heterogeneity by background (p-value=1.87x10 -4 ). The lowest estimated effect size was in African Americans (OR=1.49, 95% CI [1.36, 1.61]). The HTN-PRS was associated with new onset hypertension among individuals with normal (respectively, elevated) BP at baseline: OR=1.54, 95% CI [1.43, 1.66] (OR=1.39, 95% CI [1.23, 1.55]). Association was further observed in age-stratified analysis. In CARDIA, Black participants with high HTN-PRS percentiles developed hypertension earlier than White participants with high HTN-PRS percentiles. The HTN-PRS was significantly associated with increased risk of coronary artery disease (OR=1.11), ischemic stroke (OR=1.12), type 2 diabetes (OR=1.16), and chronic kidney disease (OR=1.12), in the MGB Biobank. Conclusions: The multi-ethnic HTN-PRS is associated with both prevalent and incident hypertension at 4-6 years of follow up across adulthood and is associated with clinical outcomes.

Elevated blood urea nitrogen-to-creatinine ratio increased the risk of Coronary Artery Disease in patients living with type 2 diabetes mellitus

BackgroundHigh Blood Urea Nitrogen (BUN) and high Serum Creatinine (SCr) levels are risk factors for Coronary Artery Disease (CAD). However, the relationship between the Blood Urea Nitrogen to Creatinine (BUN/SCr) ratio (UCR) and the risk of CAD in patients living with new-onset diabetes is unclear. This study aimed to examine the relationship between blood UCR and the risk of CAD in patients living with new-onset type 2 diabetes mellitus (T2DM).MethodsWe analyzed the data from the cohort of 12,299 patients living with type 2 diabetes mellitus. Primary endpoints were the events of CAD. The ANOVA test (continuous indicators) and χ2 test (categorical indicators) were used to assess the differences of baseline characteristics across the groups of UCR. In order to understand the correlation between variables, we performed correlation analysis on variables that have significant differences between CAD group and non-CAD group. Multivariate-adjusted Cox proportional hazard regression models were applied to estimate the association of the blood UCR with the risk of CAD in patients living with T2DM. The Kaplan–Meier survival function plotting and the log-rank test were used to evaluate the event-free survival according to the groups of UCR. The restricted cubic spline model was used to show the adjusted association between blood UCR and risk of CAD in patients living with T2DM.ResultsDuring a median follow-up of 2.66 years, 1173 CAD were recorded with an event rate of 28.49 events per 1000 person-years. In multivariate-adjusted Cox regression models, elevated blood urea nitrogen to creatinine ratio (UCR) was associated with higher risk of CAD in patients living with T2DM [hazard ratio (HR), 1.782; 95% confidence interval (CI), 1.237–2.567]. The Kaplan–Meier survival curves indicated that the high group of UCR tended to have a lower event-free survival than the low group and medium group. There was a nonlinear trend toward increasing risk of CAD across the groups of UCR. And cubic spline function graph suggested that the influence of UCR level on HR for CAD increased significantly at UCR levels above 6.67.ConclusionsAn elevated UCR was significantly associated with an increased risk for CAD in patients living with T2DM.

Abstract TMP22: Genetic Predisposition To Cardiovascular Disease Is Associated With Higher Risk Of Stroke In Persons With COVID-19

Background and Purpose: Stroke is a serious complication of COVID-19. However, the risk factors for this complication are poorly understood. We hypothesize that genetic predisposition to cardio- and cerebrovascular disease (CVD) leads to an increased risk of stroke in patients with COVID-19 infection. Methods: We evaluated data from a nested cohort study conducted within the UK Biobank focused on persons with documented COVID-19. Incident strokes (ischemic and hemorrhagic) were identified by combining inpatient data (including critical care and discharge diagnostic codes) and primary care data, the latter entered by providers within 30 days of a positive COVID-19 test. Genetic predisposition to CVD was evaluated through a polygenic risk score that integrated genomic information on 2,176 independent genetic risk variants for stroke, coronary artery disease and cardiometabolic risk factors. This score was divided into low (0-20 th percentile), intermediate (20 th -80 th percentile), and high (80 th -100 th percentile) genetic risk. Results: A total of 11,882 study participants (mean age 65.8, SD [8.6], female sex 6,306 [53.1%]) with documented COVID-19 infection were included in this study, including 99 (0.8%) persons that sustained a stroke during the infection. Compared to persons with low genetic predisposition to CVD, those with intermediate and high genetic risk had 35% (OR 1.35, 95%CI 1.14-1.55) and 2.4-fold (OR 2.38, 95% CI 1.71-3.05) higher risk of stroke (test for trend p=0.004). Sub-scoring analyses evaluating one polygenic risk score per CVD trait of interest indicated that genetic predisposition to hypertension (p=0.017) and smoking (p=0.03) were the most important genetic risk factors. Conclusions: Genetic predisposition to CVD is associated with a higher risk of stroke in persons with acute COVID-19 infection. Genetic risk factors for hypertension and smoking appear to mediate a significant portion of this association. Genetic information should be considered in the multiple ongoing efforts to create risk-stratification strategies to identify COVID-19 patients at high risk of stroke.

Implications of fasting plasma glucose variability on the risk of incident peripheral artery disease in a population without diabetes: a nationwide population-based cohort study

BackgroundDiabetes have been known as a traditional risk factor of developing peripheral artery disease (PAD). However, the study evaluating the impact of long-term glycemic variability on the risk of developing PAD is limited, especially in a general population without diabetes.MethodsWe included 152,931 individuals without diabetes from the Korean National Health Insurance Service–Health Screening Cohort. Fasting plasma glucose (FPG) variability was measured using coefficient variance (FPG-CV), standard deviation (FPG-SD), and variability independent of the mean (FPG-VIM).ResultsA total of 16,863 (11.0%) incident cases of PAD were identified during a median follow-up of 8.3 years. Kaplan–Meier curves showed a progressively increasing risk of PAD in the higher quartile group of FPG variability than in the lowest quartile group (log rank P < 0.001). Multivariable Cox proportional hazard analysis showed the hazard ratio for PAD prevalence as 1.11 (95% CI 1.07–1.16, P < 0.001) in the highest FPG-CV quartile than in the lowest FPG-CV quartile after adjusting for confounding variables, including mean FPG. Similar degree of association was shown in the FPG-SD and FPG-VIM. In sensitivity analysis, the association between FPG variability and the risk of developing PAD persisted even after the participants were excluded based on previously diagnosed diseases, including stroke, coronary artery disease, congestive heart failure, chronic kidney disease, or current smokers or drinkers. Subgroup analysis demonstrated that the effects of FPG variability on the risk of PAD were more powerful in subgroups of younger age, regular exercisers, and those with higher income.ConclusionsIncreased long-term glycemic variability may have a significant prognostic effect for incident PAD in individuals without diabetes.Graphical

Study to Evaluate Coronary Artery Disease Prevalence and Risk Factors in Heart Failure Patients with Reduced Ejection Fraction

Introduction: Even though heart failure (HF) is a major global health problem, studies on the prevalence and etiology of HF in Nepal are scant. The aim of this study was to assess the prevalence and risk factors of coronary artery disease (CAD) in HF with reduced ejection fraction (HFrEF) using invasive coronary angiography (CAG).&#x0D; Methods: This was a prospective, cross-sectional, descriptive observational study conducted from July 2020 to September 2021. All consecutive patients with HFrEF who met the inclusion criteria underwent CAG at Manipal Teaching Hospital were evaluated and analyzed using various statistical tools.&#x0D; Results: Total 108 patients with a male to female ratio of 2.02:1 were assessed. The mean age of patients was 63+6.08 years. The prevalence of CAD was 72% of which 42% were having significant CAD (stenosis &gt;50%) with 45%, 32% and 23% having triple (TVD), double (DVD) and single vessel disease (SVD) respectively Smoking was the commonest risk factor (61%) followed by hypertension (52%), dyslipidemia (27%) and diabetes (22%). The prevalence of CAD increased with increase in the number of risk factors. There was significant association of smoking (OR: 11.5, P: 0.005), hypertension (OR: 8.5, P: 0.002) and diabetes (OR: 10, P: 0.001) for occurrence of significant CAD.&#x0D; Conclusion: In our study, otherwise unexplained HFrEF showed overall 72% of CAD with 42% having significant CAD (stenosis &gt;50%). Conventional risk factors like smoking, hypertension and diabetes were significantly associated with development of CAD.

A New Risk Score for Patients With Acute Chest Pain and Normal High Sensitivity Troponin.

Objective: To investigate a new risk score for patients who suffered from acute chest pain with normal high-sensitivity troponin I (hs-TnI) levels.Methods: In this study, patients with acute chest pain who were admitted to the emergency department (ED) of our hospital had been recruited. Hs-TnI was measured in serum samples drawn on admission to the ED. The end point was the occurrence of major adverse cardiac events (MACE) within 3 months. Predictor variables were selected by logistic regression analysis, and external validity was assessed in this study. Furthermore, validation was performed in an independent cohort, i.e., 352 patients (validation cohort).Results: A total of 724 patients were included in the derivation cohort. The results showed that four predictor variables were significant in the regression analysis—male, a history of chest pain, 60 years of age or older and with three or more coronary artery disease (CAD) risk factors. A total of 105 patients in the validation cohort had serious adverse cardiac events. The validation cohort showed a homogenous pattern with the derivation cohort when patients were stratified by score. The area under the curve (AUC) of the receiver operating characteristic (ROC) in the derivation cohort was 0.80 (95% CI: 0.76–0.83), while in the validation cohort, it was 0.79 (95% CI: 0.75–0.82).Conclusion: A new risk score was developed for acute chest pain patients without known CAD and ST-segment deviation and with normal hs-TnI and may aid MACE risk assessment and patient triage in the ED.

Endothelin 1 gene variant rs5370 and risk of coronary artery disease in the local population of Pakistan, a case-control study

Endothelin 1 gene variant rs5370 and risk of coronary artery disease in the local population of Pakistan, a case-control study

Development and Validation of Decision Rules Models to Stratify Coronary Artery Disease, Diabetes, and Hypertension Risk in Preventive Care: Cohort Study of Returning UK Biobank Participants.

Many predictive models exist that predict risk of common cardiometabolic conditions. However, a vast majority of these models do not include genetic risk scores and do not distinguish between clinical risk requiring medical or pharmacological interventions and pre-clinical risk, where lifestyle interventions could be first-choice therapy. In this study, we developed, validated, and compared the performance of three decision rule algorithms including biomarkers, physical measurements, and genetic risk scores for incident coronary artery disease (CAD), diabetes (T2D), and hypertension against commonly used clinical risk scores in 60,782 UK Biobank participants. The rules models were tested for an association with incident CAD, T2D, and hypertension, and hazard ratios (with 95% confidence interval) were calculated from survival models. Model performance was assessed using the area under the receiver operating characteristic curve (AUROC), and Net Reclassification Index (NRI). The higher risk group in the decision rules model had a 40-, 40.9-, and 21.6-fold increased risk of CAD, T2D, and hypertension, respectively (p < 0.001 for all). Risk increased significantly between the three strata for all three conditions (p < 0.05). Based on genetic risk alone, we identified not only a high-risk group, but also a group at elevated risk for all health conditions. These decision rule models comprising blood biomarkers, physical measurements, and polygenic risk scores moderately improve commonly used clinical risk scores at identifying individuals likely to benefit from lifestyle intervention for three of the most common lifestyle-related chronic health conditions. Their utility as part of digital data or digital therapeutics platforms to support the implementation of lifestyle interventions in preventive and primary care should be further validated.

Falsely normalized ankle-brachial index despite the presence of lower-extremity peripheral artery disease: two\xa0case reports\xa0

BackgroundThe ankle-brachial index measurement is used for screening and diagnosis of lower-extremity peripheral artery disease and cardiovascular risk assessment. However, the value is occasionally unreliable since the oscillometric ankle-brachial index can be elevated and falsely normalized despite the presence of lower-extremity peripheral artery disease because of the incompressibility of infrapopliteal arteries at the ankle, potentially leading to a missed diagnosis of lower-extremity peripheral artery disease or underestimation of cardiovascular risk.Case presentationWe report two cases of lower extremity peripheral artery disease with normal ankle-brachial index (a 76-year-old Asian man and a 66-year-old Asian man). In both cases, the ankle-brachial index was within the normal range (1.00–1.40) despite the presence of lower-extremity peripheral artery disease, whereas upstroke time at the ankle calculated from the pulse volume waveform simultaneously obtained by plethysmography during the ankle-brachial index measurement was prolonged (≥ 180 milliseconds). Diagnostic imaging tests revealed the presence of occlusive arterial disease in the lower extremity and severe calcification of infrapopliteal arteries.ConclusionsIn both cases, the oscillometric ankle-brachial index might have been falsely normalized despite the presence of lower-extremity peripheral artery disease because of calcified incompressible infrapopliteal arteries. Sole reliance on the ankle-brachial index value may lead to a missed diagnosis of lower-extremity peripheral artery disease or underestimation of cardiovascular risk. Upstroke time at the ankle was helpful for suspecting the presence of lower-extremity peripheral artery disease in both patients with normal ankle-brachial index. In addition to history-taking and vascular examination, upstroke time at the ankle should be carefully checked for accurate diagnosis of peripheral artery disease and cardiovascular risk assessment in patients with normal ankle-brachial index.