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Biomedical subjects

Mary J Roman

Publications and source records attributed to Mary J Roman.

At least 37 records · Page 2Linked to original sources
PubMed2005

C-reactive protein and electrocardiographic ST-segment depression additively predict mortality: the Strong Heart Study.

OBJECTIVES: This study was designed to examine whether high-sensitivity C-reactive protein (CRP) and electrocardiographic (ECG) ST-segment depression (STD) have additive utility for predicting cardiovascular disease (CVD) death and all-cause death (ACD). BACKGROUND: C-reactive protein, a marker of systemic inflammation, and ECG STD, an index of myocardial ischemia and hypertrophy, independently predict mortality. METHODS: Electrocardiograms and CRP levels were examined in 2,155 American Indian participants in the second Strong Heart Study examination. ST-segment depression >/=50 microV (n = 127) and CRP >7.0 mg/l (defining the upper quartile of CRP levels, n = 540) were considered abnormal. RESULTS: After 5.2 +/- 1.2 years follow-up there were 95 CVD deaths and 310 ACD. In univariate Cox analyses, the combination of CRP and ECG STD improved risk stratification compared to either alone, with the presence of both CRP >7.0 and ECG STD associated with a 7.7-fold increased risk of CVD death (95% confidence interval [CI] 3.3 to 18.2) and a 6.5-fold increased risk of ACD (95% CI 4.1 to 10.3). After adjustment for age, gender, and relevant risk factors, the combination of high CRP and STD remained predictive of CVD death and ACD, with the presence of both abnormal CRP and STD associated with the highest risks of CVD death (hazard ratio [HR] 3.2, 95% CI 1.1 to 10.5) and ACD (HR 3.9, 95% CI 2.1 to 7.2) and the presence of either high CRP or abnormal STD associated with intermediate risks of CVD death (HR 2.2, 95% CI 1.4 to 3.4) and ACD (HR 1.5, 95% CI 1.2 to 2.0). CONCLUSIONS: The combination of ECG STD and CRP increases the risk of mortality, demonstrating the additive impacts of active inflammation and preclinical CVD on prognosis.

Aged↗
PubMed2005

Arterial stiffness in chronic inflammatory diseases.

Chronic inflammatory diseases are associated with premature atherosclerosis; however, it is unknown whether arterial stiffness is increased in this setting, possibly as a manifestation of vascular disease preceding and/or independent of atherosclerosis. Carotid ultrasonography and radial applanation tonometry were performed in 101 patients with systemic lupus erythematosus, 80 patients with rheumatoid arthritis, and 105 healthy control subjects. The 3 groups were comparable in age, gender, and carotid artery absolute and relative wall thickness. Atherosclerotic plaque was more common in lupus (46%) and rheumatoid arthritis (38%) patients than in controls (23%) (P<0.003). Although control subjects had higher central and peripheral blood pressures, arterial stiffness was increased in patient groups compared with controls (lupus, rheumatoid arthritis, controls, respectively: beta: 3.36 versus 3.22 versus 2.60, P<0.001; Young's modulus: 441 versus 452 versus 366 mm Hg/cm, P=0.004; Peterson's elastic modulus: 278 versus 273 versus 216 mm Hg, P<0.001) after adjustment for differences in mean brachial pressure. In multivariate analysis involving the entire population, arterial stiffness was independently related to age, serum glucose, and the presence of chronic inflammatory disease. In multivariate analysis restricted to the patients, arterial stiffness was independently related to age at diagnosis, disease duration, serum cholesterol, and C-reactive protein (and IL-6, when substituted for C-reactive protein). When analyses were repeated in the 186 study subjects without carotid plaque, arterial stiffness remained significantly elevated in patient groups after adjustment for differences in age and mean brachial pressure. In conclusion, arterial stiffness is increased in chronic inflammatory disorders independent of the presence of atherosclerosis and is related to disease duration, cholesterol, and the inflammatory mediator C-reactive protein and the cytokine that stimulates its production, IL-6.

Adult↗
PubMed2005

Is high pulse pressure a marker of preclinical cardiovascular disease?

This study tests the hypothesis that high brachial pulse pressure might constitute preclinical cardiovascular disease, rather than a risk factor. We studied 1250 subjects (472 nonobese normotensive [<135/80 mm Hg] and 778 untreated hypertensive). Central pulse pressure was estimated from brachial pulse pressure and age and divided by stroke volume (PP/SV). Brachial pulse pressure was considered high when >63 mm Hg, and peripheral resistance high when >90th percentile of normal distribution. Among hypertensive subjects, 34% had high resistance; among them, 33% had high brachial pulse pressure, as opposed to 147 of 516 patients (28.5%) with normal resistance (P=not significant). After adjusting for age, sex, race, body mass index, heart rate, and center, left ventricular (LV) internal dimension and mass were lower with high resistance, and higher when brachial pulse pressure was high. PP/SV was 36% higher with high resistance than with normal resistance, and higher when brachial pulse pressure was high (all P<0.0001). Factorial analysis demonstrated that associations of high brachial pulse pressure with both higher PP/SV and LV mass were independent of other pressure components. Thus, because of these associations, our hypothesis is that in hypertension, pulse pressure may be considered as a marker of preclinical cardiovascular disease, similar to LV mass and PP/SV, rather than a cardiovascular risk factor.

Adult↗
PubMed2005

Depressive symptoms are independently predictive of carotid atherosclerosis.

The investigators tested whether depressive symptoms were predictive of carotid atherosclerosis, a marker of coronary atherosclerosis. Healthy participants (n = 219) underwent the baseline assessment of cardiovascular risk factors, including self-reported depressive symptoms, and were assessed for carotid plaque at 10-year follow-up. Adjusting for baseline cardiovascular risk factors, participants with elevated depression scores at baseline were >2 times as likely as those with no depressive symptoms to have carotid plaque.

Adult↗
PubMed2005

Normalization for body size and population-attributable risk of left ventricular hypertrophy: the Strong Heart Study.

BACKGROUND: Left ventricular hypertrophy (LVH) is identified by left ventricular mass (LVM) normalized by body surface area (BSA) or height (in meters) also raised to allometric powers. The presence of LVH detected by these indices predicts increased cardiovascular (CV) events. Whether different indexations of LVH differ in their ability to predict excess risk is unknown. METHODS: A total of 2400 subjects, (1589 women and 811 men), 59 +/- 8 years of age and without prevalent CV disease, valve disease or wall motion abnormalities and high prevalence of obesity were followed for an average of 86 months. Reference values (mean +/- 1.96 SD) for LVM/BSA, LVM/BSA(1.5), LVM/m, LVM/m(2.7), and LVM/m(2.13) were obtained in 251 normal participants and population-attributable risk percent (PAR%) for fatal and nonfatal CV events were calculated from prevalence of LVH and hazard ratios (HR). RESULTS: In the entire population or in hypertensive participants, prevalence of LVH was higher for LVM/m(2.7) (20% and 28%) and LVM/m(2.13) (18% and 25%) than for BSA (7% and 11%). Age and sex-adjusted PAR% for LVM/m(2.7) or LVM/m(2.13) were on average 1.8-fold greater than for LVM/BSA in the entire population, and 1.6-fold greater in hypertensive participants, differences that were statistically significant. CONCLUSIONS: The presence of LVH identified by LVM normalized for height to allometric powers is associated with a higher proportion of incident CV events than is LVH detected by normalization for BSA and is convenient for identification of individuals at high risk and in need of preventive intervention in populations with high prevalence of obesity. Allometric power methods allow detection of prognostically adverse, obesity-related LVH, which is unidentified using BSA.

Body Height↗
PubMed2005

Left atrial systolic force and cardiovascular outcome. The Strong Heart Study.

BACKGROUND: The force needed to fill the left ventricle (LV) in late diastole (left atrial systolic force [LASF]) is abnormal in diseased hearts. The goal of this study was to determine whether LASF adds to prognostic prediction of other markers of preclinical cardiovascular disease in a population with a high prevalence of hypertension and diabetes. METHODS: Doppler echocardiography was performed on 2808 participants of the Strong Heart Study (age 59.3 +/- 8.0 years, 62.5% women, 43.0% hypertensive, 46.7% diabetic, and 54.1% obese) without valvular abnormalities or previous cardiovascular events. The LASF was estimated from mitral orifice area and mitral peak A velocity. RESULTS: The LASF was correlated with older age, higher BP, body mass index, creatinine, serum glucose, insulin levels, and heart rate. After controlling for clinical covariates, LASF was independently associated with higher LV dimensions, LV mass, stroke volume, and cardiac output (all P < .01). In Cox regression analysis, greater LASF was associated with a higher rate of CV events (HR = 1.033, 95% CI = 1.005 to 1.061; P = .021), independently of demographic characteristics, risk factors, LV geometry, and transmitral diastolic pattern. CONCLUSIONS: In a population-based sample of middle-aged and elderly adults with a high prevalence of hypertension and diabetes and without prevalent cardiovascular disease, LASF was associated with geometric changes of the heart and with increased rate of combined fatal and nonfatal cardiovascular events.

Atrial Function, Left↗
PubMed2005

A genetic and epidemiologic study of cardiovascular disease in Alaska natives (GOCADAN): design and methods.

This article is a report of the design and methods of the Genetics of Coronary Artery Disease in Alaska Natives (GOCADAN) Study. This longitudinal, population-based study was initiated to investigate the genetic determinants of cardiovascular disease and its risk factors. Between October 2000 and April 2004, this family study enrolled 1,214 Eskimos from several coastal villages in the Norton Sound region of Western Alaska. Examinations included a physical, laboratory determinations, and measures of subclinical disease. This study will generate a genome-wide scan for loci influencing cardiovascular disease-related traits. Relations between subclinical atherosclerosis and markers of inflammation will be examined using historic and newly drawn samples. The study will provide data on CVD prevalence, risk factors and the relative contribution of genetic and environmental determinants in Alaska Native peoples. Data from this study will contribute to the delivery of health-care and prevention of CVD in Alaska Eskimos and other populations.

Adult↗
PubMed2005

Ruptured aneurysm of the right sinus of valsalva associated with a ventricular septal defect and an anomalous coronary artery.

Aneurysms of the sinus of Valsalva are extremely rare. Ruptured aneurysms of the sinus of Valsalva are frequently associated with other congenital defects, particularly with ventricular septal defect, aortic valve regurgitation, and bicuspid aortic valve. We describe the case of a 26-year-old man who had a ruptured aneurysm of the right coronary sinus, a ventricular septal defect, and an anomalous origin of the right coronary artery. Successful surgical correction of the aneurysm and ventricular septal defect was performed with patch repair and aortic valve replacement. A review of the English-language medical literature revealed only 1 other case of a sinus of Valsalva aneurysm associated with a ventricular septal defect and an anomalous coronary artery. Previously published reports of the coexistence of a single coronary artery with a sinus of Valsalva aneurysm or with a ventricular septal defect, and their management, are discussed herein.

Adult↗
PubMed2004

Evaluation of concentric left ventricular geometry in humans: evidence for age-related systematic underestimation.

There might be limitations in identifying concentric left ventricular (LV) geometry by ratio of diastolic posterior wall thickness (WT(p)) to cavity radius, defined as relative wall thickness (RWT(p)). This study has been designed to evaluate age effects on RWT(p). WT(p), mean of septal thickness and WT(p) (WT(m)), and cavity radius were cross-sectionally evaluated in 766 1- to 85-year-old, normotensive, nonobese subjects and 331 hypertensive Italians (used as a test series). RWT(p) > or =0.43 defined "traditional" concentric LV geometry. The ratios WT(m)/radius (RWT(m)) and RWT(p) increased by 0.005 and 0.006 per year of age in the age stratum up to 17 years and by 0.002 in the older age stratum (18 years or older; all P<0.0001). Thus, RWT(m) and RWT(p) were normalized to average age in both age strata (10 and 46 years) by age-specific regression coefficients. The 90th and 95th percentiles of age-normalized RWT(p) or RWT(m) were 0.40 and 0.42 or 0.41 and 0.43, respectively, in adults and 0.36 and 0.39 or 0.36 and 0.38, respectively in young subjects. In hypertensive subjects, traditional RWT(p) cutoff identified 74 subjects (22%) with concentric LV geometry; by 95th or 90th normal percentiles, normalized RWT(m) identified 112 (34%), or 149 (45%) subjects with concentric LV geometry, and normalized RWT(p) 29% and 39%, respectively (all P<0.0001 versus unadjusted RWT(p)). Thus, prevalence of concentric LV geometry increases with age-normalized RWT. Accordingly, we suggest that concentric LV hypertrophy be defined by coexistence of high LV mass with age-normalized RWT(m) >0.41 or RWT(p) >0.40. Further studies are required to establish prognostic implications of our findings.

Adolescent↗
PubMed2004

Prevalence of hypertrophic cardiomyopathy in a population-based sample of American Indians aged 51 to 77 years (the Strong Heart Study).

Recognition of the frequency with which hypertrophic cardiomyopathy (HC) occurs in the general population is critical to understanding its demographics and public health implications. However, few data are available for estimating HC prevalence in large populations of different age strata and ethnic or racial groups. The Strong Heart Study is a prospective, population-based epidemiologic survey of cardiovascular disease in residents of 13 geographically diverse American Indian communities. The study population was comprised of 3,501 subjects with echocardiograms performed in 1993 and 1995 to determine the prevalence of HC in middle-aged and older adult populations. Evidence of the HC phenotype was present in 8 previously undiagnosed patients (0.23%; 2 of 1,000) based on a left ventricular (LV) wall thickness >/=15 mm and a nondilated cavity that was not associated with another cardiac disease and was sufficient to produce the magnitude of hypertrophy evident. Ages were 51 to 77 years (mean 64 +/- 9). Four subjects were men and 4 were women, with prevalences by gender of 0.3% (3 of 1,000) and 0.18% (1.8 of 1,000), respectively. Maximum LV thicknesses were 19 to 29 mm (mean 21 +/- 3). Two subjects had mitral valve systolic anterior motion, which was sufficient to produce LV outflow obstruction at rest in 1 patient. Different electrocardiographic abnormalities were present in 5 subjects. In conclusion, clinically unrecognized HC was present in 1:500 of an aging American Indian cohort. This prevalence was similar to that reported in other general populations comprised of younger subjects of other races, offering evidence that HC is a relatively common genetic disease with widespread occurrence within the United States.

Aged↗
PubMed2004

Combined echocardiographic left ventricular hypertrophy and electrocardiographic ST depression improve prediction of mortality in American Indians: the Strong Heart Study.

Echocardiographic left ventricular hypertrophy (Echo-LVH) and ST segment depression (STD) on the ECG have each been demonstrated to predict cardiovascular (CV) and all-cause (AC) mortality. However, the prognostic value of combining Echo-LVH and ECG-STD has not been examined. ECGs and echocardiograms were examined in 2193 American Indian participants in the second Strong Heart Study examination. STD was measured by computer and was considered abnormal if > or =50 microV. Echo-LVH was defined by indexed LV mass >116 g/m2 in men and >104 g/m2 in women. After a mean follow-up of 3.1+/-0.7 years, there were 57 CV and 169 AC deaths. In univariate Cox analyses, Echo-LVH (chi2=54.2 and chi2=68.5) and ECG-STD (chi2=35.9 and chi2=46.3, all P<0.001) predicted CV and AC mortality, respectively. The combination of Echo-LVH and ECG-STD improved risk stratification compared with either alone for both CV death (chi2=74.4, P<0.001) and AC death (chi2=102.0, P<0.001), with presence of both ECG-STD and Echo-LVH associated with the greatest risks. After adjustment for age, sex, and relevant risk factors, combined Echo-LVH and ECG-STD remained predictive of CV mortality (chi2=19.7, P<0.001) and AC mortality (chi2=24.9, P<0.001), with the presence of both Echo-LVH and ECG-STD associated with a 6.3-fold increased risk of CV death (95% CI: 2.8 to 14.2) and a 4.6-fold increased risk of AC mortality (95% CI: 2.5 to 8.5). ECG-STD and Echo-LVH additively increase the risk of both CV mortality and AC mortality. These findings support the value of combining Echo-LVH and ECG-STD to improve risk stratification. These findings require verification in other populations.

Aged↗
PubMed2004

Comparison of cardiac structure and function in American Indians with and without the metabolic syndrome (the Strong Heart Study).

The metabolic syndrome (MS) is linked to cardiovascular risk. Recently, the Adult Treatment Panel (ATP) III provided new criteria for the definition of the MS. We analyzed the impact of the MS on cardiac structure and function and the independent association of the 5 different components of the ATP III-defined MS with cardiac markers of preclinical disease. Echocardiographic examination was performed in 612 nondiabetic participants with ATP III-defined MS and in 824 participants without the MS. Participants with the MS were more often women (p <0.001) and had similar ages compared with those without the MS. After controlling for confounders, participants with the MS had greater left ventricular (LV) dimension, mass, and relative wall thickness, and left atrial diameter (all p </=0.01), and a higher prevalence of LV hypertrophy (p <0.001), with lower ejection fraction (p <0.05), midwall shortening (p <0.001), and mitral E/A ratio (p <0.05) than participants who did not have the MS. In multiple regression modeling, high blood pressure (BP) and abdominal obesity were the only components of the MS associated with increased LV diameter; only high BP was associated with increased LV mass and prevalence of LV hypertrophy (both p <0.001). When high to normal BP was present in the absence of hypertension, the MS exhibited LV geometry similar to hypertensive participants without the MS. Therefore, abnormal LV geometry and function are related to the MS. Increased BP is the component of the MS most strongly associated with cardiac markers of preclinical disease, even in the absence of traditionally defined hypertension.

Aged↗
PubMed2004

Mechanisms of verbal memory impairment in four neurodevelopmental disorders.

Profiles of verbal learning and memory performance were compared for typically developing children and for four developmental disorders characterized by different patterns of language functioning: specific language impairment, early focal brain damage, Williams Syndrome, and Down Syndrome. A list-learning task was used that allowed a detailed examination of the process of verbal learning, recall, and recognition (California Verbal Learning Test--Children's Version). Distinct patterns of performance characterized the four disorders. These patterns were consistent with the language deficits typically seen in the disorders, with the exception of a dissociation seen in Williams Syndrome.

Adolescent↗
PubMed2004

Heritability of left ventricular dimensions and mass in American Indians: The Strong Heart Study.

OBJECTIVE: We sought to determine the heritability of left ventricular dimensions and mass in adult American Indians. METHODS: Echocardiograms were analysed in 1373 American Indian participants, from 445 families, in the Strong Heart Study (SHS) to determine the heritability of left ventricular dimensions and mass. Heritability calculations were performed using variance component analysis in SOLAR, a computer analysis program. RESULTS: The SHS participants analysed in this study included 1305 relative pairs, predominantly (n = 1077) sib-pairs. After simultaneously adjusting for sex, age and centre, the proportion of the residual phenotypic variance due to additive genetic effects or heritability (h2) of left ventricular mass was 0.27 (SE = 0.08, P < 0.001). Addition of body weight, height, systolic blood pressure, heart rate, medications and diabetes into the polygenic model attenuated the residual h2 of left ventricular mass to 0.17 (SE = 0.09, P < 0.05). The residual h2 for left ventricular end-diastolic chamber diameter (LVID), after simultaneously adjusting for sex, age and centre was 0.36 (SE = 0.08, P < 0.001) for the analysed families. The residual h2 for interventricular septal wall thickness was 0.26 (SE = 0.07), while that of left ventricular posterior wall thickness was 0.19 (SE = 0.08, both P < 0.001). While adjustment for body weight, height, systolic blood pressure, heart rate, medications and diabetes reduced the h2 of LVID to 0.33 (SE = 0.09, P < 0.001), the h2 of septal (0.12, SE = 0.10) and posterior wall thickness (0.09, SE = 0.09) were no longer significant after similar adjustment. The residual h2 for relative wall thickness, a measure of left ventricular geometry, was 0.22 (SE = 0.07, P < 0.001) after adjusting for sex, age and centre, and 0.17 (SE = 0.08, P < 0.05) after additional adjustment for body weight, height, systolic blood pressure, heart rate, medications and diabetes. CONCLUSIONS: A substantial proportion of the variance of left ventricular dimensions and mass can be explained by heredity, independent of the effects of sex, age, body size, blood pressure, heart rate, medications and diabetes. Identification of genes influencing left ventricular size and geometry may provide mechanistic and therapeutic targets to prevent left ventricular hypertrophy.

Aged↗
PubMed2003

Prevalence and correlates of accelerated atherosclerosis in systemic lupus erythematosus.

BACKGROUND: Although systemic lupus erythematosus is associated with premature myocardial infarction, the prevalence of underlying atherosclerosis and its relation to traditional risk factors for cardiovascular disease and lupus-related factors have not been examined in a case-control study. METHODS: In 197 patients with lupus and 197 matched controls, we performed carotid ultrasonography, echocardiography, and an assessment for risk factors for cardiovascular disease. The patients were also evaluated with respect to their clinical and serologic features, inflammatory mediators, and disease treatment. RESULTS: The risk factors for cardiovascular disease were similar among patients and controls. Atherosclerosis (carotid plaque) was more prevalent among patients than the controls (37.1 percent vs. 15.2 percent, P<0.001). In multivariate analysis, only older age, the presence of systemic lupus erythematosus (odds ratio, 4.8; 95 percent confidence interval, 2.6 to 8.7), and a higher serum cholesterol level were independently related to the presence of plaque. As compared with patients without plaque, patients with plaque were older, had a longer duration of disease and more disease-related damage, and were less likely to have multiple autoantibodies or to have been treated with prednisone, cyclophosphamide, or hydroxychloroquine. In multivariate analyses including patients with lupus, independent predictors of plaque were a longer duration of disease, a higher damage-index score, a lower incidence of the use of cyclophosphamide, and the absence of anti-Smith antibodies. CONCLUSIONS: Atherosclerosis occurs prematurely in patients with systemic lupus erythematosus and is independent of traditional risk factors for cardiovascular disease. The clinical profile of patients with lupus and atherosclerosis suggests a role for disease-related factors in atherogenesis and underscores the need for trials of more focused and effective antiinflammatory therapy.

Adrenal Cortex Hormones↗
PubMed2003

Association of albuminuria with systolic and diastolic left ventricular dysfunction in type 2 diabetes: the Strong Heart Study.

OBJECTIVES: We sought to compare systolic and diastolic function in American Indians with diabetes mellitus (DM) based on albuminuria status. BACKGROUND: Albuminuria has been shown to predict cardiovascular disease (CVD) in populations with DM. However, the mechanism of the association of albuminuria and CVD is unclear. METHODS: We compared echo-derived indices of left ventricular (LV) systolic and diastolic function in three groups of American Indians with DM based on albuminuria status: I = no albuminuria (<30 mg albumin/g creatinine); II = microalbuminuria (30 to 300 mg/g); and III = macroalbuminuria (>300 mg/g). RESULTS: Group II and III were slightly older than Group I with no significant gender difference between groups. Systolic blood pressure increased and body mass index decreased from Group I to Group III. Left ventricular systolic function was lower in the groups with albuminuria with step-wise decreases in ejection fraction and stress-corrected midwall shortening (MWS) from Group I to Group III. Similar findings were noted in diastolic LV filling with lower mitral E/A ratios and longer deceleration times in groups with albuminuria. The proportion of participants with abnormal MWS and abnormal LV diastolic relaxation showed step-wise increases from no albuminuria to macroalbuminuria. In multivariate analysis, albuminuria status remained independently associated with both systolic and diastolic dysfunction after adjusting for age, gender, body mass index, systolic blood pressure, duration of diabetes, coronary artery disease, and LV mass. CONCLUSIONS: Albuminuria is independently associated with LV systolic and diastolic dysfunction in type 2 DM; this may explain in part the relationship of albuminuria to increased cardiovascular (CV) events in the DM population. Screening for albuminuria identifies individuals with high CV risk and possible cardiac dysfunction.

Aged↗