Racial and Ethnic Variation in Lipoprotein (a) Levels among Asian Indian and Chinese Patients

Background. Lipoprotein (a) [Lp(a)] is an independent risk factor for cardiovascular disease (CVD) in Non-Hispanic Whites (NHW). There are known racial/ethnic differences in Lp(a) levels, and the association of Lp(a) with CVD outcomes has not been examined in Asian Americans in the USA. Objective. We hypothesized that Lp(a) levels would differ in Asian Indians and Chinese Americans when compared to NHW and that the relationship between Lp(a) and CVD outcomes would be different in these Asian racial/ethnic subgroups when compared to NHW. Methods. We studied the outpatient electronic health records of 2022 NHW, 295 Asian Indians, and 151 Chinese adults age ≥18 y in Northern California in whom Lp(a) levels were assessed during routine clinical care from 2001 to 2008, excluding those who had received prescriptions for niacin (14.6%). Nonparametric methods were used to compare median Lp(a) levels. Significance was assessed at the P < .0001 level to account for multiple comparisons. CVD outcomes were defined as ischemic heart disease (IHD) (265 events), stroke (122), or peripheral vascular disease (PVD) (87). We used logistic regression to determine the relationship between Lp(a) and CVD outcomes. Results. Both Asian Indians (36 nmol/L) and NHW (29 nmol/L) had higher median Lp(a) levels than Chinese (22 nmol/L, P ≤ .0001 and P = .0032). When stratified by sex, the differences in median Lp(a) between these groups persisted in the 1761 men (AI v CH: P = .001, NHW v CH: P = .0018) but were not statistically significant in the 1130 women (AI v CH: P = .0402, NHW v CH: P = .0761). Asian Indians (OR = 2.0) and Chinese (OR = 4.8) exhibited a trend towards greater risk of IHD with high Lp(a) levels than NHW (OR = 1.4), but no relationship was statistically significant. Conclusion. Asian Indian and NHW men have higher Lp(a) values than Chinese men, with a trend toward, similar associations in women. High Lp(a) may be more strongly associated with IHD in Asian Indians and Chinese, although we did not have a sufficient number of outcomes to confirm this. Further studies should strive to elucidate the relationship between Lp(a) levels, CVD, and race/ethnicity among Asian subgroups in the USA

From Fatalism to Mitigation: a Conceptual Framework for Mitigating Fetal Programming of Chronic Disease by Maternal Obesity

Prenatal development is recognized as a critical period in the etiology of obesity and cardiometabolic disease. Potential strategies to reduce maternal obesity-induced risk later in life have been largely overlooked. In this paper, we first propose a conceptual framework for the role of public health and preventive medicine in mitigating the effects of fetal programming. Second, we review a small but growing body of research (through August 2015) that examines interactive effects of maternal obesity and two public health foci – diet and physical activity – in the offspring. Results of the review support the hypothesis that diet and physical activity after early life can attenuate disease susceptibility induced by maternal obesity, but human evidence is scant. Based on the review, we identify major gaps relevant for prevention research, such as characterizing the type and dose response of dietary and physical activity exposures that modify the adverse effects of maternal obesity in the offspring. Third, we discuss potential implications of interactions between maternal obesity and postnatal dietary and physical activity exposures for interventions to mitigate maternal obesity-induced risk among children. Our conceptual framework, evidence review, and future research directions offer a platform to develop, test, and implement fetal programming mitigation strategies for the current and future generations of children

Metabolic Syndrome and Early-Onset Coronary Artery Disease Is the Whole Greater Than Its Parts?

ObjectivesWe sought to examine the association between the metabolic syndrome (MetS) (defined both by the 2001 National Cholesterol Educational Program Adult Treatment Panel III [ATP-III] definition and the American Heart Association/National Heart, Lung and Blood Institute [AHA/NHLBI] revision incorporating the lower threshold for impaired fasting glucose [IFG]) and early-onset coronary artery disease (CAD).BackgroundThe impact of MetS on premature CAD has not been studied extensively. Lowering the threshold to define the IFG component (from 110 to 100 mg/dl) and the value of the syndrome as a whole versus its individual components are subjects of intense debate.MethodsWe performed a case-control study with 393 early-onset CAD subjects (acute myocardial infarction, angina with ≥50% stenosis, or coronary revascularization) in men under age 46 years or women under age 56 years and 393 control subjects individually matched for gender, age, and race/ethnicity.ResultsBy conditional logistic regression, presence of ATP-III MetS without diabetes (adjusted odds ratio [adj-OR] 4.9; 95% confidence interval [CI] 3.4 to 8.0) and with diabetes (adj-OR 8.0, 95% CI 4.39 to 14.6) was a strong independent determinant of early-onset CAD. Using the AHA/NHLBI revision, these ORs became slightly stronger. However, neither definition of MetS remained significantly associated with early-onset CAD in multivariate models adjusting for individual components.ConclusionsThe presence of MetS imparts a high risk of early-onset clinical CAD, but the prognostic information associated with the syndrome is not greater than the sum of its parts

Recommendations for Providers on Person-Centered Approaches to Assess and Improve Medication Adherence

Medication non-adherence is a significant clinical challenge that adversely affects psychosocial factors, costs, and outcomes that are shared by patients, family members, providers, healthcare systems, payers, and society. Patient-centered care (i.e., involving patients and their families in planning their health care) is increasingly emphasized as a promising approach for improving medication adherence, but clinician education around what this might look like in a busy primary care environment is lacking. We use a case study to demonstrate key skills such as motivational interviewing, counseling, and shared decision-making for clinicians interested in providing patient-centered care in efforts to improve medication adherence. Such patient-centered approaches hold considerable promise for addressing the high rates of non-adherence to medications for chronic conditions

Failure to replicate an association of SNPs in the oxidized LDL receptor gene (OLR1) with CAD

Abstract Background The lectin-like oxidized LDL receptor LOX-1 (encoded by OLR1) is believed to play a key role in atherogenesis and some reports suggest an association of OLR1 polymorphisms with myocardial infarction (MI). We tested whether single nucleotide polymorphisms (SNPs) in OLR1 are associated with clinically significant CAD in the Atherosclerotic Disease, VAscular FuNction, & Geneti C Epidemiology (ADVANCE) study. Methods ADVANCE is a population-based case-control study of subjects receiving care within Kaiser Permanente of Northern California including a subset of participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study. We first resequenced the promoter, exonic, and splice site regions of OLR1 and then genotyped four single nucleotide polymorphisms (SNPs), including a non-synonymous SNP (rs11053646, Lys167Asn) as well as an intronic SNP (rs3736232) previously associated with CAD. Results In 1,809 cases with clinical CAD and 1,734 controls, the minor allele of the coding SNP was nominally associated with a lower odds ratio (OR) of CAD across all ethnic groups studied (minimally adjusted OR 0.8, P = 0.007; fully adjusted OR 0.8, P = 0.01). The intronic SNP was nominally associated with an increased risk of CAD (minimally adjusted OR 1.12, p = 0.03; fully adjusted OR 1.13, P = 0.03). However, these associations were not replicated in over 13,200 individuals (including 1,470 cases) in the Atherosclerosis Risk in Communities (ARIC) study. Conclusion Our results do not support the presence of an association between selected common SNPs in OLR1 and the risk of clinical CAD.http://deepblue.lib.umich.edu/bitstream/2027.42/112726/1/12881_2008_Article_317.pd

Peroxisome Proliferator-Activated Receptor Gamma Polymorphisms and Coronary Heart Disease

Single nucleotide polymorphisms (SNPs) in the peroxisome proliferator-activated receptor γ (PPARG) gene have been associated with cardiovascular risk factors, particularly obesity and diabetes. We assessed the relationship between 4 PPARG SNPs (C-681G, C-689T, Pro12Ala, and C1431T) and coronary heart disease (CHD) in the PRIME (249 cases/494 controls, only men) and ADVANCE (1,076 cases/805 controls, men or women) studies. In PRIME, homozygote individuals for the minor allele of the PPARG C-689T, Pro12Ala, and C1431T SNPs tended to have a higher risk of CHD than homozygote individuals for the frequent allele (adjusted OR [95% CI] = 3.43 [0.96–12.27], P = .058, 3.41 [0.95–12.22], P = .060 and 5.10 [0.99–26.37], P = .050, resp.). No such association could be detected in ADVANCE. Haplotype distributions were similar in cases and control in both studies. A meta-analysis on the Pro12Ala SNP, based on our data and 11 other published association studies (6,898 CHD cases/11,287 controls), revealed that there was no evidence for a significant association under the dominant model (OR = 0.99 [0.92–1.07], P = .82). However, there was a borderline association under the recessive model (OR = 1.29 [0.99–1.67], P = .06) that became significant when considering men only (OR = 1.73 [1.20–2.48], P = .003). In conclusion, the PPARG Ala12Ala genotype might be associated with a higher CHD risk in men but further confirmation studies are needed

Trends in Incidence of Hospitalized Acute Myocardial Infarction in the Cardiovascular Research Network (CVRN)

Monitoring trends in cardiovascular events can provide key insights into the effectiveness of prevention efforts. Leveraging data from electronic health records provides a unique opportunity to examine contemporary, community-based trends in acute myocardial infarction hospitalizations

Right coronary wall cmr in the older asymptomatic advance cohort: positive remodeling and associations with type 2 diabetes and coronary calcium

<p>Abstract</p> <p>Background</p> <p>Coronary wall cardiovascular magnetic resonance (CMR) is a promising noninvasive approach to assess subclinical atherosclerosis, but data are limited in subjects over 60 years old, who are at increased risk. The purpose of the study was to evaluate coronary wall CMR in an asymptomatic older cohort.</p> <p>Results</p> <p>Cross-sectional images of the proximal right coronary artery (RCA) were acquired using spiral black-blood coronary CMR (0.7 mm resolution) in 223 older, community-based patients without a history of cardiovascular disease (age 60-72 years old, 38% female). Coronary measurements (total vessel area, lumen area, wall area, and wall thickness) had small intra- and inter-observer variabilities (r = 0.93~0.99, all p < 0.0001), though one-third of these older subjects had suboptimal image quality. Increased coronary wall thickness correlated with increased coronary vessel area (p < 0.0001), consistent with positive remodeling. On multivariate analysis, type 2 diabetes was the only risk factor associated with increased coronary wall area and thickness (p = 0.03 and p = 0.007, respectively). Coronary wall CMR measures were also associated with coronary calcification (p = 0.01-0.03).</p> <p>Conclusions</p> <p>Right coronary wall CMR in asymptomatic older subjects showed increased coronary atherosclerosis in subjects with type 2 diabetes as well as coronary calcification. Coronary wall CMR may contribute to the noninvasive assessment of subclinical coronary atherosclerosis in older, at-risk patient groups.</p

Markers of inflammation and cardiovascular disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association

In 1998, the American Heart Association convened Prevention Conference V to examine strategies for the identification of high-risk patients who need primary prevention. Among the strategies discussed was the measurement of markers of inflammation.1 The Conference concluded that “many of these markers (including inflammatory markers) are not yet considered applicable for routine risk assessment because of: (1) lack of measurement standardization, (2) lack of consistency in epidemiological findings from prospective studies with endpoints, and (3) lack of evidence that the novel marker adds to risk prediction over and above that already achievable through the use of established risk factors.” The National Cholesterol Education Program Adult Treatment Panel III Guidelines identified these markers as emerging risk factors,1a which could be used as an optional risk factor measurement to adjust estimates of absolute risk obtained using standard risk factors. Since these publications, a large number of peer-reviewed scientific reports have been published relating inflammatory markers to cardiovascular disease (CVD). Several commercial assays for inflammatory markers have become available. As a consequence of the expanding research base and availability of assays, the number of inflammatory marker tests ordered by clinicians for CVD risk prediction has grown rapidly. Despite this, there has been no consensus from professional societies or governmental agencies as to how these assays of markers of inflammation should be used in clinical practice

AHA Guidelines for Primary Prevention of Cardiovascular Disease and Stroke: 2002 Update: Consensus panel guide to comprehensive risk reduction for adult patients without coronary or other atherosclerotic vascular diseases

"The initial Guide to the Primary Prevention of Cardiovascular Diseases was published in 1997 as an aid to healthcare professionals and their patients without established coronary artery disease or other atherosclerotic diseases.1 It was intended to complement the American Heart Association (AHA)/American College of Cardiology (ACC) Guidelines for Preventing Heart Attack and Death in Patients with Atherosclerotic Cardiovascular Disease (updated2) and to provide the healthcare professional with a comprehensive approach to patients across a wide spectrum of risk. The imperative to prevent the first episode of coronary disease or stroke or the development of aortic aneurysm and peripheral arterial disease remains as strong as ever because of the still-high rate of first events that are fatal or disabling or require expensive intensive medical care. The evidence that most cardiovascular disease is preventable continues to grow. Results of long-term prospective studies consistently identify persons with low levels of risk factors as having lifelong low levels of heart disease and stroke.3,4⇓ Moreover, these low levels of risk factors are related to healthy lifestyles. Data from the Nurses Health Study,5 for example, suggest that in women, maintaining a desirable body weight, eating a healthy diet, exercising regularly, not smoking, and consuming a moderate amount of alcohol could account for an 84% reduction in risk, yet only 3% of the women studied were in that category. Clearly, the majority of the causes of cardiovascular disease are known and modifiable. This 2002 update of the Guide acknowledges a number of advances in the field of primary prevention since 1997. Research continues to refine the recommendations on detection and management of established risk factors, including evidence against the safety and efficacy of interventions once thought promising (eg, antioxidant vitamins).6 This, in turn, has stimulated a large number of additional guidelines for specific demographic groups (eg, women), on individual risk factors (eg, diabetes, smoking), and for the primary prevention of stroke. In all of these guidelines, there is an increasing emphasis on further stratifying patients by level of risk and matching the intensity of interventions to the hazard for cardiovascular disease events.7