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Background: The association of hypertension (HTN) severity and control with the risk of incident atrial fibrillation (AF) is unclear. Hypothesis: Increased HTN severity and poorer blood pressure control would be associated with an increased risk of incident AF. Methods: This analysis included 9485 participants (mean age 63 ± 8 years; 56% women; 35% Black). Participants were stratified into six mutually exclusive groups at baseline—normotension (n = 1629), prehypertension (n = 704), controlled HTN (n = 2224), uncontrolled HTN (n = 4123), controlled apparent treatment‐resistant hypertension (aTRH) (n = 88), and uncontrolled aTRH (n = 717). Incident AF was ascertained at the follow‐up visit, defined by either electrocardiogram or self‐reported medical history of a physician diagnosis. Multivariable logistic regression analyses adjusted for demographic and clinical variables. Results: Over an average of 9.3 years later, 868 incident AF cases were detected. Compared to those with normotension, incident AF risk was highest for those with aTRH (controlled aTRH: odds ratio (OR) 2.95; 95% confidence interval (CI) 1.60, 5.43, & uncontrolled aTRH: OR 2.47; 95% CI 1.76, 3.48). The increase in AF risk was smaller for those on no more than three antihypertensive agents regardless of their blood pressure control (controlled OR 1.72; 95% CI 1.30, 2.29 and uncontrolled OR 1.56; 95% CI 1.14, 2.13). Conclusions: The risk of developing AF is increased in all individuals with HTN. Risk is highest in those aTRH regardless of blood pressure control. A more aggressive approach that focuses on lifestyle and pharmacologic measures to either prevent HTN or better control HTN during earlier stages may be particularly beneficial in reducing related AF risk. [ABSTRACT FROM AUTHOR]

• CMEC quantifies net movement of cholesterol between cells and HDL. • We determined the association of CMEC with CAC. • Higher CMEC levels were not associated with lower CAC score or higher CAC density. • CV risk associated with HDL CMEC appears unrelated to calcified plaque burden. We assessed the cross-sectional and longitudinal relationships of high-density lipoprotein (HDL)-mediated cholesterol mass efflux capacity (CMEC) with coronary artery calcium (CAC) score and CAC density. CMEC was measured in 1626 Multi-Ethnic Study of Atherosclerosis (MESA) participants in samples obtained between 2000 and 2002 as part of two nested case-control studies, one with cases of incident cardiovascular disease and the other with cases of carotid plaque progression by ultrasound. Cardiac CT examinations for the presence of CAC were performed at baseline and at two additional examinations. CAC scores (Agatston and volume) and density scores (for those with positive CAC) were calculated. Multivariable linear regression modeling per SD increment of CMEC was used to estimate the associations of CMEC with each of these CAC measures. We found no association between higher CMEC and either lower CAC scores or a higher CAC density. We also found no association between higher CMEC and progression of any of these CAC measures. These findings suggest that HDL-mediated cholesterol efflux may be associated with cardiovascular risk via mechanisms unrelated to burden of calcified plaque. [ABSTRACT FROM AUTHOR]

Objective: To characterize the association of preoperative functional performance status based on Eastern Cooperative Oncology Group (ECOG) scoring with the risk of adverse cardiovascular events, vascular events, and mortality in patients undergoing EVAR and TEVAR. Methods: Retrospective review of the Society for Vascular Surgery Vascular Quality Initiative, a large, multi-center, registry database was performed. All individuals undergoing EVAR (n = 18,730) and TEVAR (n = 6595) for non-ruptured aortic pathologies between 2014 and 2018 were eligible for analysis. Multivariable logistic regression was used to determine the association of pre-procedure ECOG functional performance status on risk of in-hospital adverse cardiovascular events, vascular events, and mortality. Results: The number of operations complicated by adverse cardiovascular and vascular events was 480 (2.6%) and 190 (1.0%) for EVAR and 733 (11.1%) and 219 (3.3%) for TEVAR, respectively. There were 118 (0.6%) and 240 (3.6%) in-hospital deaths following EVAR and TEVAR, respectively. Patients with ECOG grades 3 or 4 undergoing EVAR were at increased risk of cardiovascular events (OR = 1.62; 95% CI = 1.09, 2.41) and one-year mortality (HR = 2.62; 95% CI = 1.92, 3.57) compared to those with ECOG grade 0. Patients undergoing TEVAR with ECOG grade 3 or 4 were at increased risk for both inpatient death (OR = 2.77; 95% CI = 1.56, 4.9) and one-year mortality (HR = 3.27, 95% CI = 2.06, 5.21). ECOG status was not associated with an increased risk of adverse vascular events following either EVAR or TEVAR. Conclusions: Poor preoperative functional status as assessed by ECOG score is associated with an increased risk of adverse postoperative cardiovascular events following EVAR and a higher mortality risk following both EVAR and TEVAR. Functional status assessment may be useful for risk stratification and determining procedural candidacy prior to EVAR and TEVAR. [ABSTRACT FROM AUTHOR]

We investigated the associations of high-sensitivity cardiac Troponin T (hs-cTnT) and N-terminal pro B-type natriuretic peptide (NT-proBNP) levels with risk of developing clinical peripheral artery disease (PAD) or a low ankle–brachial index (ABI). Hs-cTnT and NT-proBNP were measured in 6692 and 5458 participants respectively without baseline PAD between 2000 and 2002 in the Multi-ethnic Study of Atherosclerosis. A significant number also had repeat biomarker measurement between 2004 and 2005. Incident clinical PAD was ascertained through 2017. Incident low ABI, defined as ABI <0.9 and decline of ≥0.15 from baseline, was assessed among 5920 eligible individuals who had an ABI >0.9 at baseline and at least one follow-up ABI measurement 3–10 years later. Multivariable Cox proportional hazards and logistic regression modeling were used to determine the association of these biomarkers with clinical PAD and low ABI, respectively. Overall, 121 clinical PAD and 118 low ABI events occurred. Adjusting for demographic and clinical characteristics, each log unit increment in hs-cTnT and NT-proBNP was associated with a 30% (adjusted hazard ratio (HR) 1.3, 95% confidence interval (CI): 1.1, 1.6) and 50% (HR) 1.5, 95% CI: 1.2, 1.8) higher risk of clinical PAD respectively. No significant associations were observed for incident low ABI. Change in these biomarkers was not associated with either of the PAD outcomes. NT-proBNP and hs-cTnT are independently associated with the development of clinical PAD. Further study should determine whether these biomarkers can help to better identify those at higher risk for PAD. • Hs-cTnT and NT-proBNP levels are associated with an increased risk of PAD in predominantly white populations. • We expanded these findings to a multi-ethnic cohort without baseline cardiovascular disease. • Future studies are needed to determine whether these biomarkers can actually improve PAD risk prediction. [ABSTRACT FROM AUTHOR]

Background: Current literature examining the prospective relation of circulating omega-3 (n-3) and omega-6 (n-6) PUFAs and atrial fibrillation (AF) is limited to predominantly white populations.Objectives: We investigated the association of circulating n-3 and n-6 PUFAs with incident AF in participants from the Multi-Ethnic Study of Atherosclerosis.Methods: A total of 6229 participants (mean age = 62 y; 53% female; 39% white, 27% black, 22% Hispanic, and 12% Chinese) who were free of baseline AF and with plasma phospholipid PUFAs measured at baseline using GC were prospectively followed for the development of AF. Incident AF was ascertained using International Classification of Diseases-9 codes from hospital discharge records and Medicare claims data with follow-up through 2014. Multivariable Cox proportional hazards regression analysis was performed to determine the risk of incident AF.Results: During a median follow-up of 12.9 y, 813 (13%) participants developed AF. Each higher SD increment in arachidonic acid (AA; 20:4n-6) concentrations was associated with an 11% decreased risk of incident AF (HR: 0.89; 95% CI: 0.82, 0.96). Similarly, higher overall n-6 PUFA concentrations were also associated with a reduced AF risk (HR per SD increment: 0.93; 95% CI: 0.87, 1.00). Although no significant overall associations were observed for any individual n-3 PUFAs, higher circulating concentrations of DHA (22:6n-3) and EPA (20:5n-3) were associated with a decreased AF risk in blacks and Hispanics (DHA only) but not whites or Chinese Americans.Conclusions: In a multiethnic cohort of individuals free of baseline cardiovascular disease, higher plasma concentrations of n-6 PUFAs, particularly AA, were associated with a reduced risk of incident AF. Important differences in AF risk were also noted across race/ethnicity for the n-3 PUFAs DHA and EPA. [ABSTRACT FROM AUTHOR]

Background: Endothelial dysfunction is associated with common risk factors for AF and has been implicated in the pathophysiology of atrial fibrillation (AF) through a variety of mechanisms. We determined the prospective association of brachial flow-mediated dilation (FMD) with incident AF among older adults.Methods: We included 2027 Cardiovascular Health Study participants (mean age=78.3 years, male=39%, Black=17%) who underwent brachial FMD measurement at the 1997 to 1998 clinic visit. Incident AF was ascertained by study electrocardiograms, hospital discharge diagnosis coding and Medicare claims data. Cox regression models were used to examine the association between FMD and incident AF.Results: We identified 754 incident of AF cases (37%) over a median follow-up of 11.0 years. After adjusting for age, sex, race, height, weight, cardiovascular disease, cigarette smoking, hypertension, diabetes, kidney function, c-reactive protein, physical activity, alcohol consumption, and statins, the risk of AF did not differ according to brachial FMD response (4th vs 1st quartile hazard ratio (HR)=1.01, 95% confidence interval (CI): 0.81, 1.26; per FMD unit increment HR=1.01, 95% CI: 0.97, 1.05).Conclusion: We found no relationship between brachial FMD and the risk of developing AF in this elderly cohort. Our findings suggest that the utility of brachial FMD as a risk marker for AF in older individuals is minimal. [ABSTRACT FROM AUTHOR]

Aims The detection of cardiac valvular calcification on routine imaging may provide an opportunity to identify individuals at increased risk for peripheral artery disease (PAD). We investigated the associations of aortic valvular calcification (AVC) and mitral annular calcification (MAC) with risk of developing clinical PAD or a low ankle–brachial index (ABI). Methods and results AVC and MAC were measured on cardiac computed tomography in 6778 Multi-Ethnic Study of Atherosclerosis participants without baseline PAD between 2000 and 2002. Clinical PAD was ascertained through 2015. Incident low ABI, defined as ABI <0.9 and decline of ≥0.15, was assessed among 5762 individuals who had an ABI >0.9 at baseline and at least one follow-up ABI measurement 3–10 years later. Adjusted Cox proportional hazards and Poisson regression modelling were used to determine the association of valvular calcification with clinical PAD and low ABI, respectively. There were 117 clinical PAD and 198 low ABI events that occurred over a median follow-up of 14 years and 9.2 years, respectively. The presence of MAC was associated with an increased risk of clinical PAD [hazard ratio 1.79; 95% confidence interval (CI) 1.04–3.05] but not a low ABI (rate ratio 1.28; 95% CI 0.75–2.19). No significant associations were noted for the presence of AVC and risk of either clinical PAD. Conclusion MAC is associated with an increased risk of developing clinical PAD. Future studies are needed to corroborate our findings and better understand whether MAC holds any predictive value as a risk marker for PAD. [ABSTRACT FROM AUTHOR]

Higher levels of hepatocyte growth factor (HGF) have been associated with the presence of peripheral arterial disease (PAD), but prospective associations are unknown. We examined the association of circulating HGF levels with incident PAD. Between 2000 and 2002, HGF was measured in 6742 Multi-Ethnic Study of Atherosclerosis participants without PAD. Incident clinical PAD, adjudicated on the basis of a positive history for the presence of disease-related symptoms or treatment, was ascertained through 2015. Incident low ankle-brachial index (ABI), defined as an ABI < 0.9 and a decline of ≥ 0.15, was assessed among 5736 individuals who had an ABI > 0.9 at baseline and ≥1 follow-up ABI measurement 3 to 10 years later. There were 116 clinical PAD and 197 low ABI events that occurred over a median follow-up of 14 and 9 years, respectively. After adjustment for demographic and clinical variables, a standard deviation increment of HGF (303 ng/L) was associated with an increased risk of clinical PAD (hazard ratio: 1.21; 95% confidence interval [CI]: 1.05-1.39) but not a low ABI (rate ratio: 1.03; 95% CI: 0.85-1.25). In conclusion, higher HGF levels were modestly associated with an increased risk of developing clinical PAD. [ABSTRACT FROM AUTHOR]

Introduction: The American Heart Association's Life's Simple 7 includes seven metrics of ideal cardiovascular health to target for cardiovascular disease prevention. This study determined the relationship between Life's Simple 7 and incident peripheral artery disease in a biracial cohort of middle- and older-aged adults.Methods: This analysis included 12,865 participants from the Atherosclerosis Risk in Communities study recruited between 1987 and 1989 (mean age=54years, 55% women, 25% black) and free of peripheral artery disease or other cardiovascular disease at baseline. Overall, Life's Simple 7 score was calculated as the sum of the Life's Simple 7 component scores (two points if ideal, one point if intermediate, and zero if poor) and classified as inadequate (zero to four), average (five to nine), or optimal (ten to 14) cardiovascular health and linked to incident peripheral artery disease identified by hospital discharge diagnosis and leg revascularization. Analysis was conducted in 2017.Results: A total of 434 incident peripheral artery disease cases occurred over a median follow-up of 24.4years. Compared with the inadequate category (n=1,008), participants in the average (n=8,395) and optimal (n=3,462) categories each had a substantially lower risk of developing peripheral artery disease in a Cox proportional hazards model adjusted for potential confounders (hazard ratio=0.36, 95% CI=0.28, 0.46 for average, and hazard ratio=0.09, 95% CI=0.06, 0.15 for optimal). In a similar model, a one-point higher Life's Simple 7 score was associated with a 25% lower risk of incident peripheral artery disease (hazard ratio=0.75, 95% CI=0.72, 0.79).Conclusions: Better cardiovascular health, as defined by higher Life's Simple 7 score, is associated with a substantially lower risk of peripheral artery disease. [ABSTRACT FROM AUTHOR]

Introduction: Brachial flow-mediated dilation (FMD) is a physiologic measure of endothelial function. We determined the prospective association of brachial FMD with incident dementia among older adults.Methods: We included 2777 Cardiovascular Health Study participants who underwent brachial FMD measurement. Incident dementia was ascertained by medication use, International Classification of Diseases-9 codes, requirement for a proxy, and death certificates and calibrated to gold-standard assessments performed in a subset of the cohort.Results: Mean participant age at time of brachial FMD measurement was 77.9 years. We identified 1650 incident dementia cases (median follow-up=10.5 y). After adjusting for age, race, sex, education, clinic site, and baseline arterial diameter, risk of dementia for participants in the highest quartile of percent brachial FMD did not differ from those in lowest quartile (hazard ratio=0.89, 95% confidence interval: 0.77, 1.03).Conclusions: Brachial FMD, measured late in life, is not associated with an increased risk of incident dementia. [ABSTRACT FROM AUTHOR]

Background: Multiple prospective studies have established an association between inflammation and higher risk of atrial fibrillation (AF), but the association between lipoprotein-associated phospholipase A2 (Lp-PLA2) mass and activity and incident AF has not been extensively evaluated.Methods: Using data from 10,794 Atherosclerosis Risk In Communities (ARIC) study participants aged 53-75 years, 5,181 Cardiovascular Health Study (CHS) participants aged 65 to 100 years, and 5,425 Multi-Ethnic Study of Atherosclerosis (MESA) participants aged 45-84 years, we investigated the association between baseline Lp-PLA2 levels and the risk of developing AF. Incident AF was identified in each cohort by follow-up visit electrocardiograms, hospital discharge coding of AF, or Medicare claims data.Results: Over a mean of 13.1, 11.5, and 10.0 years of follow-up, 1,439 (13%), 2,084 (40%), and 615 (11%) incident AF events occurred in ARIC, CHS, and MESA, respectively. In adjusted analyses, each SD increment in Lp-PLA2 activity was associated with incident AF in both ARIC (hazard ratio [HR] 1.13, 95% CI 1.06-1.20) and MESA (HR 1.24, 95% CI 1.05-1.46). Each SD increment in Lp-PLA2 mass was also associated with incident AF in MESA (HR 1.25, 95% CI 1.11-1.41). No significant associations were observed among CHS participants.Conclusions: Although higher Lp-PLA2 mass and activity were associated with development of AF in ARIC and MESA, this relationship was not observed in CHS, a cohort of older individuals. [ABSTRACT FROM AUTHOR]

Objective The development of acute kidney injury (AKI) and its effect on prognosis after lower extremity bypass (LEB) surgery have not been well described. We determined risk factors associated with AKI in patients undergoing infrainguinal LEB surgery and whether individuals with AKI are at increased risk for cardiovascular events and mortality. Methods Data for 12,907 operations entered in the Vascular Quality Initiative (VQI) registry from January 2012 through April 2015 were retrospectively reviewed. Procedures performed on patients not on dialysis before the surgery with perioperative assessments of renal function were eligible for the study. AKI was defined as a postoperative increase in serum creatinine ≥0.5 mg/dL or new dialysis requirement. Logistic regression was performed to determine the effect of AKI on the risk of in-hospital cardiovascular events, including myocardial infarction, stroke, congestive heart failure, or arrhythmias, and mortality. Cox proportional hazards regression was performed to determine the risk of long-term mortality (median follow-up of 11.5 months). Results AKI developed after 507 (4%) of the 12,907 operations performed in 11,859 patients. After adjustment for demographic, clinical, and perioperative variables, AKI was associated with an increased risk of in-hospital cardiovascular events (odds ratio, 2.50; 95% confidence interval [CI], 1.91-3.28) and in-hospital mortality (odds ratio, 6.96; 95% CI, 3.94-12.31). Risk of mortality persisted over the course of follow-up (hazard ratio, 1.98; 95% CI, 1.58-2.47). Conclusions AKI after LEB is associated with an increased risk of cardiovascular events and all-cause mortality. Further study should evaluate whether preoperative interventions before LEB can be effectively applied for at-risk patients to reduce the incidence of AKI and its associated morbidity and mortality. [ABSTRACT FROM AUTHOR]

Prospective studies supporting a relationship between elevated lipoprotein-associated phospholipase A2 (Lp-PLA2) and incident peripheral arterial disease (PAD) are limited. We evaluated the association of Lp-PLA2 with incident PAD in a multi-ethnic cohort without clinical cardiovascular disease. A total of 4622 participants with measurement of Lp-PLA2 mass and Lp-PLA2 activity and an ankle–brachial index (ABI) between 0.9 and 1.4 were followed for the development of PAD (median follow-up = 9.3 years), defined as an ABI ⩽0.9 and decline from baseline ⩾0.15. There were 158 incident PAD events during follow-up. In adjusted logistic regression models, each higher standard deviation of both Lp-PLA2 activity and mass did not confer an increased risk of developing PAD [odds ratios, (95% confidence intervals)]: 0.92 (0.66–1.27) for Lp-PLA2 activity and 1.06 (0.85–1.34) for mass. Additionally, no significant interaction was found according to ethnicity: p=0.43 for Lp-PLA2 activity and p=0.55 for Lp-PLA2 mass. We found no evidence of an association between Lp-PLA2 and incident PAD. [ABSTRACT FROM AUTHOR]

Statin therapy is the standard of care for patients with carotid artery stenosis given its proven cardiovascular benefits. However, the impact of statin therapy on outcomes in patients undergoing carotid revascularization in the Vascular Quality Initiative has not yet been evaluated. Therefore, our aim was to investigate the association of statin therapy with outcomes following carotid endarterectomy (CEA), transfemoral carotid artery stenting (tfCAS), and transcarotid artery revascularization (TCAR). We identified all patients who underwent CEA, tfCAS, or TCAR in the Vascular Quality Initiative registry from January 2016 to September 2021. To compare outcomes, we stratified patients by procedure type and created 1:1 propensity score-matched cohorts of patients who received no preoperative statin therapy (within 36 hours of procedure) versus those who received preoperative statin therapy. Propensity scores incorporated demographic characteristics, comorbidities, carotid symptom status, preoperative medications, and physician and hospital procedural experience. The primary outcome was a composite end point of in-hospital stroke and/or death. As a secondary analysis, we performed repeat propensity score-matching by postoperative statin use (prescribed at discharge) and assessed 5-year mortality. Relative risks (RR) and hazard ratios (HR) were calculated using log binomial regression and Cox regression, respectively. Among 97,835 CEA, 20,303 tfCAS, and 22,371 TCAR patients, 15%, 17%, and 10% of patients did not receive preoperative statin therapy, respectively. Compared with statin use, no statin use was associated with a higher risk of in-hospital stroke or death among 13,434 matched CEA patients (no statin, 1.7% vs statin, 1.4%; RR, 1.2; 95% confidence interval [CI], 1.02-1.5) and among 2707 matched tfCAS patients (4.8% vs 2.8%; RR, 1.7; 95% CI, 1.3-2.3). However, there was no difference for this outcome by statin use among 2089 matched TCAR patients (1.8% vs 1.6%; RR, 1.1; 95% CI, 0.7-1.8). At 5 years, no statin therapy at discharge was associated with higher 5-year mortality after CEA (15% vs 10%; HR, 1.8; 95% CI, 1.6-2) and tfCAS (18% vs 14%; HR, 1.5; 95% CI, 1.2-1.8), but there was no difference after TCAR (14% vs 11%; HR, 1.3; 95% CI, 0.9-1.8). Compared with statin use, no statin use was associated with a higher risk of in-hospital stroke or death and 5-year mortality among CEA and tfCAS patients. Although there was no significant difference in outcomes among TCAR patients, this may in part be due to lower statistical power in this cohort. Overall, statin therapy is essential in the short- and long-term management of patients undergoing carotid revascularization. Our findings not only support current Society for Vascular Surgery recommendations for statin therapy in patients undergoing carotid revascularization, but they also highlight an important opportunity for quality improvement. [Display omitted] [ABSTRACT FROM AUTHOR]

Prior studies evaluating metabolic syndrome (MetS) and incident peripheral artery disease (PAD) have been limited by use of modified MetS criteria and restriction to clinical PAD end points. We investigated MetS and risk of developing a low ankle-brachial index (ABI) and clinical PAD in the Cardiovascular Health Study, a population-based cohort of adults aged ≥65 years. Participants with MetS met at least 3 of 5 Adult Treatment Panel III criteria. Baseline C-reactive protein-MetS or fibrinogen-MetS were defined as presence of 3 of 6 components, with elevated C-reactive protein (>3 mg/L) or fibrinogen (>341 mg/dL) as a sixth component. Incident low ABI, defined as ABI <0.9 and decline of ≥0.15, was assessed among a subset of 1899 individuals with 2 ABI measurements 6 years apart. Over a median follow-up of 13.7 years, 4632 individuals were followed up for clinical PAD, defined as revascularization or diagnosed claudication. Adult Treatment Panel III MetS was associated with both incident low ABI (risk ratio, 1.26; 95% confidence interval [CI], 1.00-1.58) and clinical PAD (hazard ratio, 1.47; 95% CI, 1.11-1.94). Incorporating C-reactive protein or fibrinogen into Adult Treatment Panel III criteria identified an additional 16% to 20% of individuals as having MetS, and both C-reactive protein-MetS and fibrinogen-MetS were associated with incident low ABI (risk ratio, 1.36; 95% CI, 1.07-1.72 and risk ratio, 1.43; 95% CI, 1.13-1.81, respectively) and clinical PAD (hazard ratio, 1.56; 95% CI, 1.17-2.08 and hazard ratio, 1.55; 95% CI, 1.17-2.07, respectively). Among Adult Treatment Panel III MetS criteria, risk of PAD was most strongly associated with hypertension. [ABSTRACT FROM AUTHOR]