Biomedical subjects

Gerardo Heiss

Publications and source records attributed to Gerardo Heiss.

At least 73 records · Page 4Linked to original sources

PubMed2004

Familial aggregation and genome-wide linkage analysis of carotid artery plaque: the NHLBI family heart study.

OBJECTIVE: To evaluate familial and genetic influences on carotid artery plaque, a qualitative marker of the systemic burden of atherosclerosis. METHODS: The design was a cross-sectional study of 2,223 members of 525 randomly-ascertained families and 2,514 members of 589 high coronary heart disease (CHD) risk families from 4 U.S. communities. RESULTS: The prevalence of plaque was 33, 36, and 47%, respectively, among probands with 0, 1, and 2 or more first-degree relatives with a history of CHD. There was evidence of sibling aggregation of plaque in random families (OR = 1.89; 95% CI: 1.44, 2.48), but associations were substantially attenuated when adjusted for major cardiovascular disease risk factors. A genome scan with 420 microsatellite markers revealed no regions of significant or suggestive linkage for plaque in 342 affected sibling pairs, although suggestive linkage (LOD score: 2.43) was found on chromosome 2p11.2 (D2S1790) in pairs aged 55 years or younger. Other markers with nominal evidence for linkage (p < 0.05) were found on chromosomes 2p25, 2q24-q32, 6q21-q23, 7p12-p21, 7q11-q21, 8q24, 12q12-q13, 18p11, 21q21 and Xp11, Xq12, and Xq24. CONCLUSIONS: There was modest familial aggregation of carotid artery plaque, but a genome-wide scan indicated no regions of significant or suggestive linkage.

Adult↗

PubMed2004

Linkage analysis of diabetes status among hypertensive families: the Hypertension Genetic Epidemiology Network study.

Type 2 diabetes susceptibility is determined by multiple genetic and environmental factors. Genome-wide linkage scans have localized common regions, possibly harboring susceptibility genes on chromosomes 1, 2, 12, and 20. Variability in linkage findings underscores the probable genetic heterogeneity of type 2 diabetes. Thus, we conducted a genome scan of diabetes status using maximum likelihood methods that model affection status by a liability threshold model. Hypertensive sibships and their offspring and/or parents in the Hypertension Genetic Epidemiology Network study were recruited from five field centers. The diabetes phenotype was derived using the World Health Organization criteria and adjusted for race/study center, age, age2, sex, and with and without percent body fat. In total, 567 diabetic participants were identified in 437 families. Variance component linkage analysis was performed among 1,545 Caucasians and 1,608 African Americans using race-specific marker allele frequencies. We detected a quantitative trait loci (QTLs) influencing diabetes variance (logarithm of odds = 3.4) on chromosome 22, which overlaps a positive type 2 diabetes finding among Canadian Oji-Cree Indians. We also observed suggestive evidence for linkage on chromosomes 1, 2, 5, 8, 14, 17, and 19. The identification and replication of type 2 diabetes QTLs will bring us closer to the detection of functional genes that influence diabetes susceptibility.

Chromosome Mapping↗

PubMed2004

Adiponectin and the development of type 2 diabetes: the atherosclerosis risk in communities study.

Adipocyte-derived secretory proteins have been increasingly linked to diabetes. To investigate whether adiponectin, a major adipocyte secretory protein, predicts diabetes, we conducted a case-cohort study representing the approximately 9-year experience of the 10,275 middle-aged, U.S. African-American and white participants of the Atherosclerosis Risk in Communities (ARIC) study. Adiponectin was measured on stored plasma of 581 incident diabetes case subjects and 572 noncase subjects. Overall hazard ratios (95% CIs) for developing diabetes, for those in the second, third, and fourth (versus the first) quartile of adiponectin were 0.57 (0.41-0.78), 0.39 (0.27-0.56), and 0.18 (0.11-0.27), respectively, after adjustment for age, sex, ethnicity, study center, parental history of diabetes, and hypertension and 0.72 (0.48-1.09), 0.67 (0.43-1.04), and 0.58 (0.34-0.99), respectively, after additional adjustment for BMI, waist-to-hip ratio, fasting glucose, insulin, and a score composed of six inflammation markers. The association was of similar magnitude in men and women and in whites and African Americans, but was absent in smokers and in those with a greater inflammation score (interaction P < 0.01 for each). In conclusion, in this community-based sample of U.S. adults, higher adiponectin levels were associated with a lower incidence of diabetes.

Adiponectin↗

PubMed2003

Lung function and incident coronary heart disease: the Atherosclerosis Risk in Communities Study.

The authors examined the association between lung function, as measured by forced expiratory volume in 1 second (FEV1) and forced vital capacity, and the 10-year incidence of coronary heart disease among 14,480 participants in the Atherosclerosis Risk in Communities Study (1987-1998). Separate proportional hazards models were used for FEV1 and forced vital capacity, with gender-specific lung function quartiles and lung function x gender interaction terms. An association between lung function and coronary heart disease was observed in both genders and was stronger among women. After adjustment for age, race, study center, height, height squared, smoking, and cardiovascular disease risk factors, the hazard ratios for the first (lowest), second, and third quartiles of FEV1 were 3.70 (95% confidence interval (CI): 2.19, 6.24), 2.54 (95% CI: 1.49, 4.32), and 2.25 (95% CI: 1.31, 3.87) for women and 1.51 (95% CI: 1.07, 2.13), 1.59 (95% CI: 1.15, 2.20), and 1.52 (95% CI: 1.10, 2.09) for men. After stratification by smoking status, associations were observed in each smoking group for women, while those in men were weaker and less consistent. Similar results were obtained for forced vital capacity. This analysis indicates an association between lung function and incident coronary heart disease that may be stronger in women than in men.

Black or African American↗

PubMed2003

Hypertension, blood pressure, and heart rate variability: the Atherosclerosis Risk in Communities (ARIC) study.

Dysregulation of the autonomic nervous system has been implicated in the development of hypertension. Heart rate variability is a noninvasive tool to quantitatively estimate cardiac autonomic activity and has been used to document decreased cardiac autonomic activity in hypertension. The ability of decreased heart rate variability to predict incident hypertension has not been well studied, and there are no studies of whether hypertension leads to changes in heart rate variability. We investigated the temporal sequence linking hypertension, blood pressure, and heart rate variability in a population-based cohort of 11 061 individuals aged 45 to 54 years at baseline. Individuals with hypertension had decreased heart rate variability at baseline, and this association was present across the full blood pressure range. Among 7099 individuals without hypertension at baseline, low heart rate variability predicted greater risk of incident hypertension over 9 years of follow-up. The hazard ratio (95% confidence interval [CI]) for the lowest compared with the highest quartile of the standard deviation of normal-to-normal R-R intervals was 1.24 (95% CI, 1.10-1.40), for the root mean square of successive differences in normal-to-normal R-R intervals was 1.36 (95% CI, 1.21-1.54), and for R-R interval was 1.44 (95% CI, 1.27-1.63). Over 9 years, there was no measurable difference in the rate of change in heart rate variability among those with and without hypertension, although the differences in heart rate variability at follow-up were smaller than those at baseline. These findings thus support the thesis that the autonomic nervous system is involved in the development of hypertension, yet suggest that differences in the autonomic profile of hypertensives and normotensives do not increase with time.

Blood Pressure↗

PubMed2003

A genome-wide scan for urinary albumin excretion in hypertensive families.

Albuminuria increases the risk of cardiovascular events in patients with essential hypertension and diabetic subjects. The heritability (h2) of albuminuria in multiplex hypertensive families is unknown. We calculated the familial aggregation of urine albumin:creatinine ratio (ACR) and performed a genome-wide scan to assess for loci contributing to ACR in participants enrolled in the Hypertension Genetic Epidemiology Network (HyperGEN). To perform the genome scan, we analyzed genotype results from 2589 individuals from 805 families in the Family Blood Pressure Program. ACR and covariates were available in 1727 individuals (mean age, 57.1 years). Estimates of h2 were obtained by using variance component methodology as implemented in the SOLAR software package. Linkage was tested between 387 markers spanning the genome at an average interval of 9.32 cM, using SOLAR multipoint analysis. The h2 of log urine ACR was 0.49 (P<1x10(-7)) after controlling for significant main and interactive effects of age, gender, race, body mass index, blood pressure, and use of ACE inhibitors or angiotensin-2 receptor blockers. The genome-wide scan revealed a maximum LOD score of 2.73 on chromosome 19 (robust corrected LOD, 2.40; P=0.0009) at marker D19S591 and a LOD score of 2.0 on chromosome 12 (robust corrected LOD, 1.75; P=0.005) at marker PAH. These analyses demonstrate the marked heritability of urine ACR in families enriched for the presence of members with essential hypertension. They suggest that a gene(s) associated with urinary ACR may be present on human chromosomes 19 and 12.

Adult↗

PubMed2003

Coronary artery disease risk in familial combined hyperlipidemia and familial hypertriglyceridemia: a case-control comparison from the National Heart, Lung, and Blood Institute Family Heart Study.

BACKGROUND: Conventional wisdom suggests that a diagnosis of familial combined hyperlipidemia (FCHL) carries a substantially greater risk of premature coronary artery disease (CAD) than a diagnosis of familial hypertriglyceridemia (FHTG). However, no population-based studies have critically addressed this issue. METHODS AND RESULTS: FCHL and FHTG were diagnosed in 10.2% and 12.3% of 334 random control families and in 16.7% and 20.5% of 293 families with at least one case of premature CAD. The diagnosis of either FCHL or FHTG in an individual was associated with an odds ratio for CAD of 2.0 (P=0.003 and 0.002, respectively). However, odds ratios for premature CAD associated with both lipid disorders decreased substantially and identically with further adjustment for hypertension, diabetes, and especially HDL cholesterol, triglycerides, or apolipoprotein B. Similar results were found for differences in carotid intima-medial thickness and ankle-brachial index. Metabolic syndrome was identified in 65% of FCHL and 71% of FHTG patients compared with 19% in controls without FCHL or FHTG and was associated with an odds ratio of 3.3 (P<0.0001). The increased prevalence of the metabolic syndrome alone could account for the elevated CAD risk associated with both FCHL and FHTG. CONCLUSIONS: FCHL and FHTG appear more alike than dissimilar. Further, the risk of CAD in FCHL and FHTG was strongly related to features of the metabolic syndrome. These findings suggest that the hypertriglyceridemia in FHTG is not benign and may warrant a change in epidemiological, genetic, and clinical approaches to these lipid disorders.

Adult↗

PubMed2003

Effect of estrogen plus progestin on stroke in postmenopausal women: the Women's Health Initiative: a randomized trial.

CONTEXT: The Women's Health Initiative (WHI) trial of estrogen plus progestin was stopped early because of adverse effects, including an increased risk of stroke in the estrogen plus progestin group. OBJECTIVE: To assess the effect of estrogen plus progestin on ischemic and hemorrhagic stroke and in subgroups, and to determine whether the effect of estrogen plus progestin was modified by baseline levels of blood biomarkers. DESIGN: Multicenter double-blind, placebo-controlled, randomized clinical trial involving 16 608 women aged 50 through 79 years with an average follow-up of 5.6 years. Baseline levels of blood-based markers of inflammation, thrombosis, and lipid levels were measured in the first 140 centrally confirmed stroke cases and 513 controls. INTERVENTIONS: Participants received 0.625 mg/d of conjugated equine estrogen plus 2.5 mg/d of medroxyprogesterone acetate (n = 8506) or placebo (n = 8102). MAIN OUTCOME MEASURES: Overall strokes and stroke subtype and severity were centrally adjudicated by stroke neurologists. RESULTS: One hundred fifty-one patients (1.8%) in the estrogen plus progestin and 107 (1.3%) in the placebo groups had strokes. Overall 79.8% of strokes were ischemic. For combined ischemic and hemorrhagic strokes, the intention-to-treat hazard ratio (HR) for estrogen plus progestin vs placebo was 1.31 (95% confidence interval [CI], 1.02-1.68); with adjustment for adherence, the HR was 1.50 (95% CI, 1.08-2.08). The HR for ischemic stroke was 1.44 (95% CI, 1.09-1.90) and for hemorrhagic stroke, 0.82 (95% CI, 0.43-1.56). Point estimates of the HRs indicate that excess risk of all stroke was apparent in all age groups, in all categories of baseline stroke risk, and in women with and without hypertension, prior history of cardiovascular disease, use of hormones, statins, or aspirin. Other risk factors for stroke, including smoking, blood pressure, diabetes, lower use of vitamin C supplements, blood-based biomarkers of inflammation, higher white blood cell count, and higher hematocrit levels did not modify the effect of estrogen plus progestin on stroke risk. CONCLUSIONS: Estrogen plus progestin increases the risk of ischemic stroke in generally healthy postmenopausal women. Excess risk for all strokes attributed to estrogen plus progestin appeared to be present in all subgroups of women examined.

Aged↗

PubMed2003

Relationship between periodontal disease and C-reactive protein among adults in the Atherosclerosis Risk in Communities study.

BACKGROUND: Moderately elevated serum C-reactive protein (CRP) concentration is a systemic marker of inflammation and a documented risk factor for cardiovascular disease in otherwise healthy persons. Unrecognized infections, such as periodontal disease, may induce an acute-phase response, elevating CRP levels. We evaluated the association between periodontal disease and CRP levels in adults in the Atherosclerosis Risk in Communities study. METHODS: Oral examinations were conducted between January 1, 1996, and December 31, 1998, on 5552 ARIC participants (aged 52-74 years) from 4 US communities. Periodontal disease was quantified as the percentage of periodontal sites with pocket depth of 4 mm or more. Serum CRP concentration was quantified in milligrams per liter using an enzyme-linked immunosorbent assay. RESULTS: Mean (SE) CRP level was 7.6 (0.6) mg/L among people with extensive periodontal pockets (>30% of sites with pocket depth > or =4 mm), approximately one-third greater than that for people with less extensive periodontal pockets (5.7 [0.1] mg/L). In a multivariable linear regression model that controlled for age, sex, diabetes mellitus, cigarette use, and nonsteroidal anti-inflammatory drug use, the association of extensive periodontal pockets with CRP concentration was modified by body mass index (BMI; calculated as weight in kilograms divided by the square of height in meters). For people with a BMI of 20, the model predicted a 2-fold difference in mean CRP concentration between periodontal pocket groups (7.5 vs 3.6 mg/L), but the difference decreased with increasing BMI and was negligible when BMI equaled 35. CONCLUSIONS: Extensive periodontal disease and BMI are jointly associated with increased CRP levels in otherwise healthy, middle-aged adults, suggesting the need for medical and dental diagnoses when evaluating sources of acute-phase response in some patients.

Acute-Phase Reaction↗

PubMed2003

Glutathione-S-transferase genotypes, smoking, and their association with markers of inflammation, hemostasis, and endothelial function: the atherosclerosis risk in communities (ARIC) study.

Recent epidemiologic studies suggest that polymorphisms of glutathione-S-transferases M1 and T1 (GSTM1/GSTT1) modify the effects of cigarette smoking on risk of coronary heart disease (CHD). Since GSTs are able to detoxify numerous toxic compounds and products of oxidative stress, it is possible that GST genotypes may also modify the capacity of smoking to invoke a chronic inflammatory response. A cross-sectional analysis, using a subset of participants (n = 989) in a large (n = 15, 792) biracial cohort, was used to evaluate levels of nine markers of inflammation, hemostasis, and endothelial function by different combinations of GST genotypes and cigarette smoking status. Participants with the GSTM1 null (GSTM1-0) genotype and > or = 20 pack-years of smoking had the highest mean levels of CRP, fibrinogen, von Willebrand factor, ICAM-1, and VCAM-1 and lowest mean levels of albumin compared to other combinations of genotype and smoking. However, a formal test for interaction between GSTM1 genotype and smoking was statistically significant only for albumin. By contrast, participants who had the functional GSTT1 genotype (GSTT1-1) and smoked > or = 20 pack-years had the highest mean levels of only CRP and fibrinogen. The results of this study provide some limited evidence that GSTM1 and GSTT1 polymorphisms modify the effect of smoking on inflammation, hemostasis, and endothelial function.

Cohort Studies↗

PubMed2003

Prospective association between hormone replacement therapy, heart rate, and heart rate variability. The Atherosclerosis risk in communities study.

Hormone replacement therapy is universally associated with coronary heart disease (CHD) in observational studies, but it is unknown whether this association is mediated by the autonomic nervous system. We tested the hypothesis that postmenopausal hormone replacement therapy was associated with more favorable heart rate (HR) and heart rate variability (HRV) in a population sample of women (n=2,621). Hormone therapy use was measured at four examinations beginning in 1987. Supine HR and HRV indices were measured for 6 minutes at the final examination (1996-1998). In unadjusted linear regression models, hormone therapy was associated with lower HR (hormone use=64.7 vs. never=65.7 beats/min, P=.01) and higher HRV. However, following adjustment for age and CHD risk factors, both associations were eliminated. Results from this observational study suggest that hormone therapy is not associated with HR or HRV. These analyses should be replicated in a randomized trial.

Autonomic Nervous System↗

PubMed2003

A genome-wide affected sibpair linkage analysis of hypertension: the HyperGEN network.

Results are reported here from a genome-wide linkage analysis of hypertension in a large sample of hypertensive (affected) sibpairs (650 African American and 915 white sibpairs) recruited by the HyperGEN Network of the National Heart, Lung and Blood Institute (NHLBI) Family Blood Pressure Program (FBPP). Analysis using MAPMAKER/SIBS suggests one interesting region with a LOD score of 2.08 at 63 cM from the p telomere on chromosome 2 in the African American sibpairs, which may harbor hypertension susceptibility genes.

Black or African American↗

PubMed2003

A prospective evaluation of the risk of QT prolongation with hormone replacement therapy: the atherosclerosis risk in communities study.

PURPOSE: Prolongation of the QT interval is associated with an increased risk of arrhythmia, coronary heart disease (CHD), and mortality. Estrogens and androgens have been proposed as a causal factor in QT lengthening. We tested whether postmenopausal hormone replacement therapy was associated with prolonged QT intervals in a healthy population sample of women (mean age=54). METHODS: Women (n=3103) were asked about estrogen (ERT) and progestin plus estrogen (PERT) replacement therapy use at 4 examinations over 9 years. Electrocardiographic QT intervals were measured and corrected for heart rate using the QT Index (QTI) and Bazett's correction. QT prolongation was defined as QTI>110% and a change from baseline of >or=4%. RESULTS: Heart rate corrected QT length was moderately but significantly (p<0.01) greater, and the risk of QT prolongation was nearly twice (Odds Ratio=1.9, 95% Confidence Interval: 1.2-2.0) that in women who used ERT compared with never users. PERT use was not significantly associated with QT length. CONCLUSIONS: The potential for slight increases in QT length over time, and an increased risk of QT prolongation with ERT use identified in this observational study, are important concerns that should be further explored in randomized trials.

Arteriosclerosis↗

PubMed2003

Inflammation markers predict increased weight gain in smoking quitters.

OBJECTIVE: Undesirable weight gain often follows smoking cessation. We investigated whether weight gain after smoking cessation is greater in those with higher levels of inflammatory markers. RESEARCH METHODS AND PROCEDURES: We studied weight gain and risk of a large gain (> or = 90th percentile) over 3 years in a cohort study of 11,687 U.S. men and women, 45 to 64 years old, with focus on the 2664 who continued and the 493 who quit smoking. RESULTS: Among new quitters, adjusted weight gain for those in the highest (vs. lowest) quartile of leukocytes was 0.56 kg/yr more (95% confidence interval, 0.17 to 0.95); for those in the highest (vs. lowest) quartile of fibrinogen, 0.60 kg/yr more (95% confidence interval, 0.27 to 0.92; p = 0.02 and 0.001 for adjusted smoking status by leukocyte and smoking status by fibrinogen interaction terms, respectively). In adjusted analyses, the odds ratio for a large gain associated with quitting (vs. continuing) was 6.2 for those in the highest quartile of leukocytes vs. 2.2 for those in the lowest leukocyte quartile (p = 0.03 for smoking status by inflammatory marker interaction). Similarly, the odds ratio for a large gain associated with quitting was 4.5 in the highest fibrinogen quartile vs. 2.5 in the lowest (p = 0. 09 for the interaction term). DISCUSSION: Weight gain after smoking cessation is increased in those with higher baseline levels of leukocytes and fibrinogen. These findings suggest a close relationship between inflammatory mediators and regulators of energy balance that may have important clinical implications.

Biomarkers↗

PubMed2003

Low-grade systemic inflammation and the development of type 2 diabetes: the atherosclerosis risk in communities study.

To examine the association of low-grade systemic inflammation with diabetes, as well as its heterogeneity across subgroups, we designed a case-cohort study representing the approximately 9-year experience of 10,275 Atherosclerosis Risk in Communities Study participants. Analytes were measured on stored plasma of 581 incident cases of diabetes and 572 noncases. Statistically significant hazard ratios of developing diabetes for those in the fourth (versus first) quartile of inflammation markers, adjusted for age, sex, ethnicity, study center, parental history of diabetes, and hypertension, ranged from 1.9 to 2.8 for sialic acid, orosomucoid, interleukin-6, and C-reactive protein. After additional adjustment for BMI, waist-to-hip ratio, and fasting glucose and insulin, only the interleukin-6 association remained statistically significant (HR = 1.6, 1.01-2.7). Exclusion of GAD antibody-positive individuals changed associations minimally. An overall inflammation score based on these four markers plus white cell count and fibrinogen predicted diabetes in whites but not African Americans (interaction P = 0.005) and in nonsmokers but not smokers (interaction P = 0.13). The fully adjusted hazard ratio comparing white nonsmokers with score extremes was 3.7 (P for linear trend = 0.008). In conclusion, a low-grade inflammation predicts incident type 2 diabetes. The association is absent in smokers and African-Americans.

Black People↗

PubMed2002

A genome-wide screen reveals evidence for a locus on chromosome 11 influencing variation in LDL cholesterol in the NHLBI Family Heart Study.

A genome scan was performed for low-density lipoprotein cholesterol concentration (LDL-C) in white subjects who were ascertained through the NHLBI Family Heart Study (FHS). The NIH Mammalian Genotyping Service (Marshfield, Wis.) genotyped 401 autosomal markers spaced at approximate 10-cM intervals. Additional FHS families were genotyped by the FHS Molecular Laboratory at the University of Utah for 243 markers; 645 subjects were typed in both laboratories so that a combined map of the 644 markers from the two screening sets (average distance of 5.46 cM) could be produced. Analyses were done on 2,799 genotyped subjects in 500 families where at least two genotyped persons in the family had measured LDL-C levels (average number of genotyped family members=5.95). The variance components method was used as implemented in GeneHunter (Kruglyak et al. 1996). Prior to analysis, each phenotype was adjusted, within sex, for age, age squared, body mass index, waist-hip ratio, alcohol, smoking, medication status for diabetes and hypertension, estrogen use, and field center location. Linkage analyses were performed, first excluding 305 subjects on lipid-lowering medications, then again including the data from these subjects. The highest peak was on chromosome 11 at 56.3-56.4 cM, with a maximum lod score of 3.72. Two genome scans of lipid traits in other populations have found peaks in this region. Other scores at or above 1.9 occurred on chromosomes 5 (lod=1.89 at 1.6 cM), 10 (lod=2.47 at 127.1 cM), 17 (lod=2.33 at 116.3 cM), and 21 (lod=2.74 at 45.2 cM).

Cholesterol, LDL↗

PubMed2002

Risk factors for progression of common carotid atherosclerosis: the Atherosclerosis Risk in Communities Study, 1987-1998.

Intima-media thickness of the common carotid arteries is a marker of atherosclerosis and has been shown to be associated with prevalent and incident coronary heart disease and with coronary heart disease risk factors. The authors examined the association of baseline risk factors or change in risk factors with change in intima-media thickness over follow-up (1987-1998) in the Atherosclerosis Risk in Communities (ARIC) population-based cohort (baseline: age 45-64 years, n = 15,792). Subjects were members of households sampled in four areas of the United States. Either not adjusting for baseline intima-media thickness or doing so with correction for its measurement error resulted in statistically significant associations of change in intima-media thickness with baseline diabetes, current smoking, high density lipoprotein cholesterol, pulse pressure, white blood cell count, and fibrinogen. The associations were of a similar order of magnitude as anticipated from the authors' cross-sectional findings. Statistically significant associations were found between change in intima-media thickness and change in low density lipoprotein cholesterol and triglycerides and with onset of diabetes and hypertension. In summary, established risk factors for coronary heart disease are associated with the rate of change of subclinical atherosclerosis.

Carotid Artery Diseases↗

PubMed2002

Does the cardiac autonomic response to postural change predict incident coronary heart disease and mortality? The Atherosclerosis Risk in Communities Study.

This study evaluated whether small shifts in cardiac autonomic balance with standing, as measured by heart rate variability (HRV), were prospectively associated with incident coronary heart disease (CHD) and mortality. Both Black and White men and women aged 45-64 years from the Atherosclerosis Risk in Communities Study (n = 9,267) were followed from 1987 to 1997 for myocardial infarction (n = 296), fatal CHD (n = 63), and non-CHD mortality (n = 533). HRV indices and mean R-R interval length (inverse of heart rate) were measured in the supine and standing positions for 2 minutes each; HRV shift was calculated as the difference between positions. After adjustment for demographic characteristics and medication use, HRV in each position was significantly inversely related to events in Cox proportional hazards models. With the exception of R-R interval length shift and myocardial infarction (hazard ratio = 1.42, 95% confidence interval: 1.02, 1.98 for the smallest vs. the largest quartile), there was no association between HRV shift and the other events. Despite clinical research suggesting that HRV shift with standing is a more sensitive measure of autonomic balance than is HRV in one position, simple measures such as heart rate change and supine and standing HRV were better predictors of events.

Autonomic Nervous System↗