Fatal Coronary Artery Disease Research Articles

Sugar-sweetened or artificially-sweetened beverage consumption, physical activity, and risk of cardiovascular disease in adults: a prospective cohort study

BackgroundWhether physical activity could mitigate the adverse impacts of sugar-sweetened beverages (SSBs) or artificially sweetened beverages (ASBs) on incident cardiovascular disease (CVD) remains uncertain. ObjectivesThis study aimed to examine the independent and joint associations between SSB or ASB consumption and physical activity and risk of CVD, defined as fatal and nonfatal coronary artery disease and stroke, in adults from 2 United States-based prospective cohort studies. MethodsCox proportional hazards models were used to calculate hazard ratios (HRs) and 95% CIs between SSB or ASB intake and physical activity with incident CVD among 65,730 females in the Nurses’ Health Study (1980–2016) and 39,418 males in the Health Professional’s Follow-up Study (1986–2016), who were free from chronic diseases at baseline. SSBs and ASBs were assessed every 4-y and physical activity biannually. ResultsA total of 13,269 CVD events were ascertained during 3,001,213 person-years of follow-up. Compared with those who never/rarely consumed SSBs or ASBs, the HR for CVD for participants consuming ≥2 servings/d was 1.21 (95% CI: 1.12, 1.32; P-trend < 0.001) for SSBs and 1.03 (95% CI: 0.97, 1.09; P-trend = 0.06) for those consuming ≥2 servings/d of ASBs. The HR for CVD per 1 serving increment of SSB per day was 1.18 (95% CI: 1.10, 1.26) and 1.12 (95% CI: 1.04, 1.20) for participants meeting and not meeting physical activity guidelines (≥7.5 compared with <7.5 MET h/wk), respectively. Compared with participants who met physical activity guidelines and never/rarely consumed SSBs, the HR for CVD was 1.47 (95% CI: 1.37, 1.57) for participants not meeting physical activity guidelines and consuming ≥2 servings/wk of SSBs. No significant associations were observed for ASB when stratified by physical activity. ConclusionsHigher SSB intake was associated with CVD risk regardless of physical activity levels. These results support current recommendations to limit the intake of SSBs even for physically active individuals.

Cigarette smoking and air pollution exposure and their effects on cardiovascular diseases.

Cardiovascular disease (CVD) has no socioeconomic, topographical, or sex limitations as reported by the World Health Organization (WHO). The significant drivers of CVD are cardio-metabolic, behavioral, environmental, and social risk factors. However, some significant risk factors for CVD (e.g., a pitiable diet, tobacco smoking, and a lack of physical activities), have also been linked to an elevated risk of cardiovascular disease. Lifestyles and environmental factors are known key variables in cardiovascular disease. The familiarity with smoke goes along with the contact with the environment: air pollution is considered a source of toxins that contribute to the CVD burden. The incidence of myocardial infarction increases in males and females and may lead to fatal coronary artery disease, as confirmed by epidemiological studies. Lipid modification, inflammation, and vasomotor dysfunction are integral components of atherosclerosis development and advancement. These aspects are essential for the identification of atherosclerosis in clinical investigations. This article aims to show the findings on the influence of CVD on the health of individuals and human populations, as well as possible pathology and their involvement in smoking-related cardiovascular diseases. This review also explains lifestyle and environmental factors that are known to contribute to CVD, with indications suggesting an affiliation between cigarette smoking, air pollution, and CVD.

Prognosis of a malignant phenotype of obesity defined by a cardiac biomarker in hypertension: the Japan Morning Surge-Home Blood Pressure study.

Obesity with increased high-sensitive cardiac troponin T (hs-cTnT) has been reported to be more likely to progress cardiovascular disease (CVD) events, which suggests that hs-cTnT may identify a "malignant" phenotype of obesity. We classified 3513 hypertensive patients from the Japan Morning Surge-Home Blood Pressure (J-HOP) study into groups based on body mass index (BMI) (normal weight: <25 kg/m2, overweight: 25-29.9 kg/m2, obesity: ≥30 kg/m2) and elevations in biomarker levels (hs-cTnT ≥3 ng/mL: 51.3%, 54.9%, 53.3%, and N-terminal pro-brain natriuretic peptide [NT-ProBNP] ≥55 pg/mL: 51.1%, 40.7%, 36.0% in each BMI category). We evaluated the independent and combined associations of BMI and each hs-cTnT/NT-proBNP or both with CVD events (fatal and nonfatal coronary artery disease, stroke, and hospitalized heart failure). During the mean 6.4 ± 3.9-year follow-up, 232 CVD events occurred. Obesity with elevated hs-cTnT was associated with a risk of CVD events compared to normal weight without elevated hs-cTnT (hazard ratio 3.22, 95% confidence interval: 1.83-5.68). A similar pattern of results was also observed across the status of obesity and elevated NT-proBNP. There was a significant interaction between hs-cTnT and CVD events according to the obesity status (p = 0.039), while this association was marginal in NT-proBNP (p = 0.060). The magnitude of the mediation of hs-cTnT for the association between obesity and CVD risk was 41.2%, and that for NT-proBNP was 8.1%. In this Japanese hypertensive population, the elevation of hs-cTnT identified obese patients at particularly high risk for developing CVD events, suggesting that hs-cTnT may identify a 'malignant' phenotype of obesity.

A rare case of fatal coronary artery disease in a 4 year old child

A rare case of fatal coronary artery disease in a 4 year old child

Identification of Risk of Cardiovascular Disease by Automatic Quantification of Coronary Artery Calcifications on Radiotherapy Planning CT Scans in Patients With Breast Cancer

Cardiovascular disease (CVD) is common in patients treated for breast cancer, especially in patients treated with systemic treatment and radiotherapy and in those with preexisting CVD risk factors. Coronary artery calcium (CAC), a strong independent CVD risk factor, can be automatically quantified on radiotherapy planning computed tomography (CT) scans and may help identify patients at increased CVD risk. To evaluate the association of CAC with CVD and coronary artery disease (CAD) in patients with breast cancer. In this multicenter cohort study of 15 915 patients with breast cancer receiving radiotherapy between 2005 and 2016 who were followed until December 31, 2018, age, calendar year, and treatment-adjusted Cox proportional hazard models were used to evaluate the association of CAC with CVD and CAD. Overall CAC scores were automatically extracted from planning CT scans using a deep learning algorithm. Patients were classified into Agatston risk categories (0, 1-10, 11-100, 101-399, >400 units). Occurrence of fatal and nonfatal CVD and CAD were obtained from national registries. Of the 15 915 participants included in this study, the mean (SD) age at CT scan was 59.0 (11.2; range, 22-95) years, and 15 879 (99.8%) were women. Seventy percent (n = 11 179) had no CAC. Coronary artery calcium scores of 1 to 10, 11 to 100, 101 to 400, and greater than 400 were present in 10.0% (n = 1584), 11.5% (n = 1825), 5.2% (n = 830), and 3.1% (n = 497) respectively. After a median follow-up of 51.2 months, CVD risks increased from 5.2% in patients with no CAC to 28.2% in patients with CAC scores higher than 400. After adjustment, CVD risk increased with higher CAC score (hazard ratio [HR]CAC = 1-10 = 1.1; 95% CI, 0.9-1.4; HRCAC = 11-100 = 1.8; 95% CI, 1.5-2.1; HRCAC = 101-400 = 2.1; 95% CI, 1.7-2.6; and HRCAC>400 = 3.4; 95% CI, 2.8-4.2). Coronary artery calcium was particularly strongly associated with CAD (HRCAC>400 = 7.8; 95% CI, 5.5-11.2). The association between CAC and CVD was strongest in patients treated with anthracyclines (HRCAC>400 = 5.8; 95% CI, 3.0-11.4) and patients who received a radiation boost (HRCAC>400 = 6.1; 95% CI, 3.8-9.7). This cohort study found that coronary artery calcium on breast cancer radiotherapy planning CT scan results was associated with CVD, especially CAD. Automated CAC scoring on radiotherapy planning CT scans may be used as a fast and low-cost tool to identify patients with breast cancer at increased risk of CVD, allowing implementing CVD risk-mitigating strategies with the aim to reduce the risk of CVD burden after breast cancer. ClinicalTrials.gov Identifier: NCT03206333.

Chocolate consumption and risk of coronary artery disease: the Million Veteran Program

Although previous studies have suggested cocoa products may promote cardiovascular health in the general population, no public data are available from patients receiving care in a national integrated health care system. We tested the hypothesis that regular chocolate consumption is associated with a lower risk of coronary artery disease (CAD) events among participants of the Million Veteran Program (MVP). Secondary analysis examined if the main hypothesis was observed among participants with type 2 diabetes. We analyzed data from MVP participants who completed the food frequency section of the MVP Lifestyle Survey and were free of CAD at the time of survey completion. CAD events during follow-up (International Statistical Classification of Diseases Ninth Revision codes 410-411 and 413-414, and Tenth Revision codes I20-I25 except I25.2) were assessed using electronic health records. We fitted a Cox proportional hazard model to estimate the RR of CAD. Of 188,447 MVP enrollees with survey data, mean ± SD age was 64 ± 12.0 y and 90% were men. For regular chocolate (28.3 g/serving) consumption of <1 serving/mo, 1-3 servings/mo, 1 serving/wk, 2-4 servings/wk, and ≥5 servings/wk, crude incidence rates (per 1000 person-years) for fatal and nonfatal CAD events or coronary procedures were 20.2, 17.5, 16.7, 17.1, and 16.9, respectively, during a mean follow-up of 3.2 y. After adjusting for age, sex, race, and lifestyle factors, the corresponding HRs (95% CIs) were 1.00 (ref), 0.92 (0.87, 0.96), 0.88 (0.83, 0.93), 0.89 (0.84, 0.95), and 0.89 (0.84, 0.96), respectively (P for linear trend < 0.0001). In a secondary analysis of 47,265 diabetics, we did not observe a decreasing trend in CAD mortality among those who consumed ≥1 serving of chocolate a month compared with those who consumed <1 serving/mo. Regular chocolate consumption was associated with a lower risk of CAD among veterans, but was not associated with cardiovascular disease risk in veterans with type 2 diabetes.

Abstract 17106: Prediction of Recurrent Atherosclerotic Cardiovascular Disease Risk Using Machine Learning and Electronic Health Record Data

Introduction: Patients with atherosclerotic cardiovascular disease (ASCVD) have high risk for recurrent ASCVD events despite statin use. Pooled cohort equations (PCE) are used for ASCVD risk prediction in primary prevention but there are no validated models for recurrent risk prediction in secondary prevention. Machine learning (ML) demonstrates promise in developing novel risk prediction models using electronic health record (EHR) data. Methods: We included adults with prior ASCVD from EHR data from an outpatient Northern California system between January 1, 2009 and December 31, 2018 with at least 2 visits at least 1 year apart and 5 years of follow up. The outcome was a recurrent ASCVD event defined as the first myocardial infarction, stroke, or fatal coronary artery disease in the 5 year follow-up period. We trained ML models to predict recurrent ASCVD risk: random forests (RF), gradient boosted machines (GBM), extreme gradient boosted models (XGBoost), and logistic regression with a standard L 2 penalty (LR) and an L 1 penalty (Lasso). We evaluated performance of ML models and the PCE on a 20% held-out test cohort using the areas under the receiver operating characteristic curves (AUCs). Results: Our cohort consisted of 32,192 patients with ASCVD (Mean age 70 years, 46% women, 12% Asian and 6% Hispanic). Less than half (49%) were on guideline directed statins. XGBoost and GBM were the best performing models for recurrent ASCVD risk prediction, while the PCE performed poorly (Figure). The top 20 predictive variables for recurrent ASCVD risk included prior events (ischemic stroke, myocardial infarction), traditional risk factors (age, blood pressure, lipid levels) and socioeconomic factors (income, education). Conclusions: EHR-trained machine learning models facilitated recurrent ASCVD risk prediction in real-world secondary prevention patients. Machine learning models developed from large datasets may help bridge contemporary gaps in ASCVD risk prediction.

Effect of eicosapentaenoic acid/docosahexaenoic acid on coronary high-intensity plaques detected with non-contrast T1-weighted imaging: subgroup analysis of the AQUAMARINE EPA/DHA study

Abstract Background In the recent the Reduction of Cardiovascular Events with EPA-Intervention Trial (REDUCE-IT), statin therapy plus high-dose eicosapentaenoic acid (EPA) significantly reduced the risk of cardiovascular death in patients with coronary artery disease (CAD) with elevated triglyceride (TG) levels. An epidemiologic study has shown that increasing the intake of long-chain n-3 polyunsaturated fatty acids, especially EPA and docosahexaenoic acid (DHA), are associated with a lower risk of fatal CAD. However, the anti-atherosclerotic effect of high-dose EPA/DHA has not be clarified. We reported that coronary high-intensity plaques (HIPs) detected with non-contrast T1-weighted imaging (T1WI) on cardiac magnetic resonance (CMR), which can be uniquely quantitative assessed using the plaque-to-myocardium signal intensity ratio (PMR) of ≥1.4, are significantly associated with future coronary events. Moreover, we demonstrated that intensive statin therapy reduces the PMR of coronary HIPs by 19% but is unlikely to completely resolve HIP (PMR&amp;lt;1.0). In the AQUAMARINE EPA/DHA study, our goal was to assess the anti-atherogenic effect of EPA/DHA in an exploratory manner by examining the change in PMR of coronary HIPs after 12 months of EPA/DHA therapy in patients with CAD on statin therapy. Methods This study was designed as a single-center, triple-arm, parallel-group, randomized controlled, open-label, superiority trial examining the effect of 12 months of additional EPA/DHA therapy on coronary HIPs in patients with CAD who receiving statin therapy. Eligible subjects are randomly assigned to the 2 g/day EPA/DHA group (n=26), the 4 g/day group (n=23), or the no EPA/DHA (statin-only) group (n=24) between May 2014 and December 2017. The PMR was defined as the signal intensity of the coronary plaque divided by that of nearby left ventricular myocardium. The primary endpoint is the change in PMR after EPA/DHA treatment. Results These 3 groups were well matched at baseline, with no statistically significant differences in age, male sex, conventional coronary risk factors, TG level, medications, and PMR. Figure 1 shows subgroup analysis of patients with high triglyceride levels (&amp;gt;150mg/dl). In the patient-based analysis (A), 12 months of EPA/DHA therapy significantly reduced the PMR of primary lesions. In the segment-based analysis (B), additional reduction of PMR was observed in the high-dose EPA/DHA group compared with the no EPA/DHA treatment group. Discussion The present study of patients with high triglyceride levels demonstrated that EPA/DHA had a dose-dependent anti-atherosclerotic effect. This finding may provide additional information of EPA/DHA for lowering the residual risk in patients with CAD on statin therapy. Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Takeda Pharmaceutical Co., Ltd.

Impact of the new American College of Cardiology/American Heart Association definition of hypertension on atherosclerotic vascular events in systemic lupus erythematosus

BackgroundThe 2017 American College of Cardiology/American Heart Association guidelines defined hypertension at ≥130/80 mm Hg. Studies on patients with connective tissue diseases were not considered. Our aim was to assess...

Supravalvular Aortic Stenosis with Extensive Atherosclerosis and Fatal Premature Coronary Artery Disease Secondary to Homozygous Familial Hypercholesterolemia – So Early But Too Late!!

Supravalvular Aortic Stenosis with Extensive Atherosclerosis and Fatal Premature Coronary Artery Disease Secondary to Homozygous Familial Hypercholesterolemia – So Early But Too Late!!

Incidence of cardiovascular disease in familial combined hyperlipidemia: A 15-year follow-up study

Background and aimsFamilial combined hyperlipidemia (FCHL) is a complex dyslipidemia associated with premature cardiovascular disease (CVD). The present study was conducted to 1) determine the incidence of CVD in FCHL in this era of protocolled, primary prevention; and 2) examine whether cardiovascular risk estimation based on the Systemic Coronary Risk Estimation (SCORE) chart, as proposed in the 2016 ESC/EAS guidelines for the management of dyslipidemia, is justified in FCHL. MethodsFCHL patients, their normolipidemic (NL) relatives and spouses originally included in our baseline cohort in 1998–2005 (n = 596) were invited for a follow-up visit to determine the incidence of CVD, defined as (non-)fatal coronary artery disease, ischemic stroke and peripheral artery disease requiring invasive treatment. ResultsFollow-up data (median: 15 years) was acquired for 85% of the original cohort. The cumulative incidence of CVD was significantly higher in FCHL patients than in spouses (23.6% versus 4.7%; hazard ratio (HR): 5.4, 95%CI: 2.0–14.6; HR after adjustment for risk factors included in SCORE: 4.7, 95%CI: 1.6–13.8), but not in NL relatives compared to spouses (5.8% versus 4.7%). The SCORE chart tended to overestimate CVD risk in the spouses (observed [O]/expected [E] ratio:0.2, p = 0.01), but not in FCHL patients (O/E:1.3, p = 0.50). ConclusionsRisk of primary CVD is still substantially increased in FCHL patients, despite preventive measures. The overestimation of CVD risk by the SCORE chart – a nowadays frequently observed phenomenon thanks to improved primary prevention – was not seen in FCHL. These results suggest that more aggressive treatment is justified to avoid excessive CVD in FCHL.

Genetic Tools for Coronary Risk Assessment in Type 2 Diabetes: A Cohort Study From the ACCORD Clinical Trial.

OBJECTIVEWe evaluated whether the increasing number of genetic loci for coronary artery disease (CAD) identified in the general population could be used to predict the risk of major CAD events (MCE) among participants with type 2 diabetes at high cardiovascular risk.RESEARCH DESIGN AND METHODSA weighted genetic risk score (GRS) derived from 204 variants representative of all the 160 CAD loci identified in the general population as of December 2017 was calculated in 5,360 and 1,931 white participants in the Action to Control Cardiovascular Risk in Diabetes (ACCORD) and Outcome Reduction With Initial Glargine Intervention (ORIGIN) studies, respectively. The association between GRS and MCE (combining fatal CAD events, nonfatal myocardial infarction, and unstable angina) was assessed by Cox proportional hazards regression.RESULTSThe GRS was associated with MCE risk in both ACCORD and ORIGIN (hazard ratio [HR] per SD 1.27, 95% CI 1.18–1.37, P = 4 × 10−10, and HR per SD 1.35, 95% CI 1.16–1.58, P = 2 × 10−4, respectively). This association was independent from interventions tested in the trials and persisted, though attenuated, after adjustment for classic cardiovascular risk predictors. Adding the GRS to clinical predictors improved incident MCE risk classification (relative integrated discrimination improvement +8%, P = 7 × 10−4). The performance of this GRS was superior to that of GRS based on the smaller number of CAD loci available in previous years.CONCLUSIONSWhen combined into a GRS, CAD loci identified in the general population are associated with CAD also in type 2 diabetes. This GRS provides a significant improvement in the ability to correctly predict future MCE, which may increase further with the discovery of new CAD loci.

Sympathetic activation in chronic anxiety: not just at the "height" of stress. Editorial Focus on "Relative burst amplitude of muscle sympathetic nerve activity is an indicator of altered sympathetic outflow in chronic anxiety".

Sympathetic activation in chronic anxiety: not just at the "height" of stress. Editorial Focus on "Relative burst amplitude of muscle sympathetic nerve activity is an indicator of altered sympathetic outflow in chronic anxiety".

Quantitative Extent of Atherosclerotic Plaque in the Major Epicardial Coronary Arteries in Patients with Fatal Coronary Heart Disease, in Coronary Endarterectomy Specimens, in Aorta-Coronary Saphenous Venous Conduits, and Means to Prevent the Plaques: A Review after Studying the Coronary Arteries for 50 Years

This review tries to answer the following 15 questions: Is atherosclerosis a systemic or a regional disease? Is atherosclerosis in any particular region focal or diffuse? What is the quantity of atherosclerotic plaques in endarterectomy specimens of the right coronary artery in patients undergoing coronary artery bypass grafting (CABG) compared to that in the right coronary artery in patients with fatal coronary artery disease? How do the units used for measuring arterial narrowing by angiography compare to the units used for measuring arterial narrowing at necropsy? What do atherosclerotic plaques consist of in coronary arteries in patients with fatal coronary disease? What is the quantity of atherosclerotic plaque in bypassed -vs- non-bypassed native coronary arteries in patients dying early (<60 days) or late (>60 days) after coronary artery bypass grafting? What is the frequency of acute coronary lesions and multi-luminal channels at necropsy in patients with unstable angina pectoris, sudden coronary death, and acute myocardial infarction? What is the mechanism of luminal widening by angioplasty in the coronary arteries? What observations suggest that atherosclerotic plaques are the result at least in part of organization of thrombi? Is atherosclerosis a multifactoral or a unifactoral disease? What characteristics distinguish carnivores and herbivores? What are reasonable guidelines for whom to treat with lipid-altering agents? What is the rule of 5 and the rule of 7 in statin therapy? What is the effect of lipid lowering drug therapy on coronary luminal narrowing? What are some requisites for a healthy life?

Frequency of Coronary Endarterectomy in Patients Undergoing Coronary Artery Bypass Grafting at a Single Tertiary Texas Hospital 2010 to 2016 With Morphologic Studies of the Operatively Excised Specimens

This study examines the frequency of coronary endarterectomy (CE) procedures during coronary artery bypass grafting (CABG), and determines the quantity of plaque in the specimens. Of the 2,268 CABG operations performed from January 2010 to June 2016, 35 patients had CE during CABG. The specimens were incised into 5-mm cross sections, stained by the Movat method, and examined. The number of CEs performed ranged from 0.21% to 4.01%. A total of 140 cm of specimens were examined, and all 140 cm contained considerable quantities of atherosclerotic plaque and narrowed lumens. The quantity of plaque present was similar to or greater than that observed in previously studied patients with fatal coronary artery disease. The frequency of CE during CABG varies greatly in surgeons. The quantity of plaque is enormous, and the lumens are severely narrowed.

Eicosapentaenoic acid prevents arterial calcification in klotho mutant mice.

BackgroundThe klotho gene was identified as an “aging-suppressor” gene that accelerates arterial calcification when disrupted. Serum and vascular klotho levels are reduced in patients with chronic kidney disease, and the reduced levels are associated with arterial calcification. Intake of eicosapentaenoic acid (EPA), an n-3 fatty acid, reduces the risk of fatal coronary artery disease. However, the effects of EPA on arterial calcification have not been fully elucidated. The aim of this study was to determine the effect of EPA on arterial calcification in klotho mutant mice.Methods and resultsFour-week-old klotho mutant mice and wild-type (WT) mice were given a diet containing 5% EPA (EPA food, klotho and WT: n = 12, each) or not containing EPA (control food, klotho and WT: n = 12, each) for 4 weeks. Calcium volume scores of thoracic and abdominal aortas assessed by computed tomography were significantly elevated in klotho mice after 4 weeks of control food, but they were not elevated in klotho mice after EPA food or in WT mice. Serum levels of EPA and resolvin E1, an active metabolite of EPA, in EPA food-fed mice were significantly increased compared to those in control food-fed mice. An oxidative stress PCR array followed by quantitative PCR revealed that NADPH oxidase-4 (NOX4), an enzyme that generates superoxide, gene expression was up-regulated in arterial smooth muscle cells (SMCs) of klotho mice. Activity of NOX was also significantly higher in SMCs of klotho mice than in those of WT mice. EPA decreased expression levels of the NOX4 gene and NOX activity. GPR120, a receptor of n-3 fatty acids, gene knockdown by siRNA canceled effects of EPA on NOX4 gene expression and NOX activity in arterial SMCs of klotho mice.ConclusionsEPA prevents arterial calcification together with reduction of NOX gene expression and activity via GPR120 in klotho mutant mice.

Increased Proximal Aortic Diameter is Associated With Risk of Cardiovascular Events and All-Cause Mortality in Blacks The Jackson Heart Study.

BackgroundEnlargement of the proximal aorta is associated with aortic wall tissue remodeling, including fragmentation of the elastin fibers, increased synthesis of collagen, and calcification, all of which are associated with aortic wall stiffening. We hypothesized that the proximal aortic diameter (AoD) is associated with cardiovascular events in a community‐based cohort of blacks.Methods and ResultsWe investigated the associations between AoD and cardiovascular events among 3018 black participants (mean age, 55.9 years; 69% women) without past history of cardiovascular disease in the Jackson Heart Study. AoD was measured using echocardiography at the level of the sinuses of Valsalva at end diastole. Cardiovascular event was defined as incident myocardial infarction, fatal coronary artery disease, stroke, or heart failure hospitalization. Cox proportional hazards regression models were used to evaluate the association between baseline AoD and cardiovascular events. Over a median follow‐up of 8.3 years, there were 258 cardiovascular events (incident rate, 10.5 per 1000 person‐years). After adjustment for traditional risk factors, increased AoD was significantly associated with cardiovascular events (hazard ratio per 1‐cm increase, 1.72; 95% CI, 1.10–2.69; P<0.05). Participants in the top AoD quintile had a higher incidence of cardiovascular events compared to those not in the top quintile (hazard ratio, 1.47; 95% CI, 1.11–1.94; P<0.005) after adjustment for risk factors.ConclusionsGreater AoD was associated with an increased risk of cardiovascular events in a community‐based cohort of blacks. AoD may be useful as a predictor of incident cardiovascular events and further investigation is warranted.

Low-Dose Aspirin for Primary Prevention of Cardiovascular Events in Patients With Type 2 Diabetes Mellitus: 10-Year Follow-Up of a Randomized Controlled Trial.

The long-term efficacy and safety of low-dose aspirin for primary prevention of cardiovascular events in patients with type 2 diabetes mellitus are still inconclusive. The JPAD trial (Japanese Primary Prevention of Atherosclerosis With Aspirin for Diabetes) was a randomized, open-label, standard care-controlled trial examining whether low-dose aspirin affected cardiovascular events in 2539 Japanese patients with type 2 diabetes mellitus and without preexisting cardiovascular disease. Patients were randomly allocated to receive aspirin (81 or 100 mg daily; aspirin group) or no aspirin (no-aspirin group) in the JPAD trial. After that trial ended in 2008, we followed up with the patients until 2015, with no attempt to change the previously assigned therapy. Primary end points were cardiovascular events, including sudden death, fatal or nonfatal coronary artery disease, fatal or nonfatal stroke, and peripheral vascular disease. For the safety analysis, hemorrhagic events, consisting of gastrointestinal bleeding, hemorrhagic stroke, and bleeding from any other sites, were also analyzed. The primary analysis was conducted for cardiovascular events among patients who retained their original allocation (a per-protocol cohort). Analyses on an intention-to-treat cohort were conducted for hemorrhagic events and statistical sensitivity. The median follow-up period was 10.3 years; 1621 patients (64%) were followed up throughout the study; and 2160 patients (85%) retained their original allocation. Low-dose aspirin did not reduce cardiovascular events in the per-protocol cohort (hazard ratio, 1.14; 95% confidence interval, 0.91-1.42). Multivariable Cox proportional hazard model adjusted for age, sex, glycemic control, kidney function, smoking status, hypertension, and dyslipidemia showed similar results (hazard ratio, 1.04; 95% confidence interval, 0.83-1.30), with no heterogeneity of efficacy in subgroup analyses stratified by each of these factors (all interaction P>0.05). Sensitivity analyses on the intention-to-treat cohort yielded consistent results (hazard ratio, 1.01; 95% confidence interval, 0.82-1.25). Gastrointestinal bleeding occurred in 25 patients (2%) in the aspirin group and 12 (0.9%) in the no-aspirin group (P=0.03), and the incidence of hemorrhagic stroke was not different between groups. Low-dose aspirin did not affect the risk for cardiovascular events but increased risk for gastrointestinal bleeding in patients with type 2 diabetes mellitus in a primary prevention setting. URL: http://www.clinicaltrials.gov. Unique identifier: NCT00110448.

Causes of Death and Heart Weights in Adults at Necropsy in a Tertiary Texas Hospital, 2013-2015

The causes of death and heart weights at death appear to be quite different in the USA today than in the first few decades of the last century. We determined the causes of death and heart weights at necropsy in 231 adults and compared the heart weights to those reported in several studies in the first half of the 20th century. Of the 231 patients, 91 (39%) died of a cardiovascular (CV) condition, and 140 (61%), of a non-CV condition. Of the 91 fatal CV disease cases, 48 had fatal coronary artery disease (CAD); of the remaining 183 cases without fatal CAD, 25 had narrowing >75% of 1 or more major epicardial coronary arteries. Thus, 73 of the 231 (32%) patients at necropsy had severe CAD. Comparison between the fatal CV and fatal non-CV cases disclosed variable age (mean 64years vs mean 57years) and heart weight (529 g vs 449 g) to be significantly different. Heart weight was found to be the only significantly variable between men and women. Comparison of the heart weights in this study to those recorded as "normal" hearts 75 to 115years earlier showed that today's "average" heart is much larger than those reported earlier. In contrast to the earlier studies, heart weight presently appears to increase with age and with an increase in body mass index. In conclusion, early studies in heart weight did not take into account today's longer survival and therefore a high prevalence of systemic hypertension, diabetes mellitus, obesity (and cardiac adiposity), and the presence of atherosclerotic CAD. Additionally, the cause of death (CV vs non-CV) was rarely considered in the early studies of heart weight.

Food quality score and the risk of coronary artery disease: a prospective analysis in 3 cohorts

Currently, there are few diet quality assessment tools that are predictive of coronary artery disease (CAD) risk that do not require nutrient analysis and substantial time to administer in clinical settings. To inform the development of such a tool, we prospectively examined the association between a food-based diet quality score and risk of CAD in 3 separate large US cohort studies. Between 1984 and 2012, 71,415 women (aged 43-63 y in 1984), 42,945 men (aged 40-75 y in 1986), and 93,131 younger women (aged 27-44 y in 1991) without a history of cardiovascular disease were followed up to 28 y. Diet was assessed ≤7 times by using repeated food-frequency questionnaires. We computed the Food Quality Score (FQS) for each individual based on food groups previously associated with less weight gain. A higher score represented a healthier diet. The FQS and CAD association was modeled with the Cox proportional hazard model, controlling for potential confounders. We also compared the magnitude of association with CAD for the FQS and other diet quality scores. We ascertained 6817 incident total CAD events, with 4588 cases of nonfatal myocardial infarction and 2131 fatal CAD events. Comparing top to bottom deciles, pooled RRs of the FQS were 0.61 (95% CI: 0.54, 0.69; P-trend < 0.001) for total CAD. These associations were independent of established cardiovascular disease risk factors including body weight, physical activity, and smoking. The magnitude of the RR for 1 SD of the FQS and CAD was generally similar to established diet scores that require detailed nutrient analysis, including the Alternate Healthy Eating Index-2010, the Dietary Approaches to Stop Hypertension score, and the alternate Mediterranean diet score. A higher food-based diet quality score was associated with lower risk of CAD and was comparable with established diet scores.