Left ventricular systolic dysfunction in rheumatoid disease.
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Humans↗
Biomedical subjects
Mary J Roman
Publications and source records attributed to Mary J Roman.
Gender differences in left ventricular systolic function in American Indians (from the Strong Heart Study).
Data from population-based studies indicate that men have a higher incidence and worse prognoses of congestive heart failure than women. Echocardiography was used to compare left ventricular (LV) myocardial and chamber contractility between 490 male and 861 female American Indian participants in the second Strong Heart Study examination. After adjusting for fat-free mass, baseline hypertension, diabetes mellitus, coronary heart disease, and alcohol consumption, LV ejection fractions were higher in women than men (66 +/- 8% vs 63 +/- 9%, p = 0.002), as were stress-corrected mid-wall shortening (106 +/- 13% vs 104+/-15%, p = 0.006) and the circumferential end-systolic stress/end-systolic volume index (7.1 x 10(4) +/- 1.9 x 10(4) vs 6.5 x 10(4) +/- 2.1 x 10(4) kdyne/cm3, all p values <0.001). LV ejection fractions were less than the predefined partition value in 4.7% of women and in 16.7% of men (odds ratio 0.25, 95% confidence interval 0.18 to 0.34, p <0.001). Stress-corrected mid-wall shortening was less than the predetermined lower limit of normal in 2.9% of women and in 6.2% of men (odds ratio 0.45, 95% confidence interval 0.29 to 0.70, p <0.001). There was no significant gender difference in supranormal function by either measure of LV systolic function. Estimated mean independent effects of female gender were a 3% greater ejection fraction, 2.7% greater stress-corrected mid-wall shortening, and a 0.4 x 10(4) kdyne/cm3 greater circumferential end-systolic stress/end-systolic volume index. In conclusion, in a population-based sample aged 45 to 74 years, women had greater LV myocardial and chamber function than men. Gender-specific partition values for measures of LV systolic function may be necessary to detect abnormal contractility in clinical and epidemiologic studies.
Aged↗
A quantitative trait loci-specific gene-by-sex interaction on systolic blood pressure among American Indians: the Strong Heart Family Study.
Age-adjusted systolic blood pressure is higher in males than females. Genetic factors may account for this sex-specific variation. To localize sex-specific quantitative trait loci (QTL) influencing blood pressure, we conducted a genome scan of systolic blood pressure, in males and females, separately and combined, and tested for aggregate and QTL-specific genotype-by-sex interaction in American Indian participants of the Strong Heart Family Study. Blood pressure was measured 3 times and the average of the last 2 measures was used for analyses. Systolic blood pressure was adjusted for age and antihypertensive treatment within study center. We performed variance component linkage analysis in the full sample and stratified by sex among 1168 females and 726 males. Marker allele frequencies were derived using maximum likelihood estimates based on all individuals, and multipoint identity-by-descent sharing was estimated using Loki. We detected suggestive evidence of a QTL influencing systolic blood pressure on chromosome 17 at 129 cM between markers D17S784 and D17S928 (logarithm of odds [LOD] = 2.4). This signal substantially improved when accounting for QTL-specific genotype-by-sex interaction (P = 0.04), because we observed an LOD score of 3.3 for systolic blood pressure in women on chromosome 17 at 136 cM. The magnitude of the linkage signal on chromosome 17q25.3 was slightly attenuated when participants taking antihypertensive medications were excluded, although suggestive evidence for linkage was still identified (LOD = 2.8 in women). Accounting for interaction with sex improved our ability to detect QTLs and demonstrated the importance of considering genotype-by-sex interaction in our search for blood pressure genes.
Adult↗
Impact of obesity on cardiac geometry and function in a population of adolescents: the Strong Heart Study.
OBJECTIVES: The goal here was to examine left ventricular (LV) geometry and function in a large, unselected group of adolescents with different degrees of abnormal body build, and verify whether possibly higher LV mass is compensatory for increased cardiac workload. BACKGROUND: There is little information on how much the excess of body weight impacts LV geometry and function in populations of adolescents. METHODS: Anthropometric, laboratory, and Doppler echocardiographic parameters of cardiac geometry and function were obtained in 460 adolescent participants (age 14 to 20 years, 245 female participants, 27 hypertensive, 10 with diabetes) from the Strong Heart Study. Body build was classified based on 85th and 95th percentiles of body mass index (BMI)-for-age charts. RESULTS: Range of BMI was 16.3 to 56.5 kg/m2 (28.8 +/- 8.3 kg/m2); 114 participants (24.9%) fell within the 85th percentile of BMI distribution (normal weight [NW]), 113 (24.6%) fell between 85th and 95th percentile (overweight [OW]), and 223 (48.5%) fell above the 95th percentile (obese [OB]). Obese participants were older than OW and NW subjects (p < 0.01), without differences in heart rate. Both OW and OB had greater LV diameter and mass than NW (all p < 0.05). Left ventricular hypertrophy was more prevalent in the OB (33.5%) and OW (12.4%), as compared with NW participants (3.5%; p < 0.001), largely compensating increased cardiac workload. However, OB subjects had four-fold higher probability of carrying an LV mass exceeding values compensatory for their cardiac workload (p < 0.001), a feature associated with lower ejection fraction, myocardial contractility, and greater force developed by left atrium to complete LV filling (all p < 0.05). CONCLUSIONS: While in OW adolescents increased levels of LV mass are appropriate to compensate their higher hemodynamic load, in OB increase in LV mass exceeds this need and is associated with mildly reduced LV myocardial performance and increased left atrial force to contribute to LV filling.
Adaptation, Physiological↗
Aneurysms of the sinuses of Valsalva.
Sinus of Valsalva aneurysms are rare cardiac anomalies which may be acquired or congenital, most commonly involving the right or noncoronary sinuses. The congenital aneurysms are more common and often caused by weakness at the junction of the aortic media and the annulus fibrosus. Acquired aneurysms are caused by conditions affecting the aortic wall, such as infections (syphilis, bacterial endocarditis, or tuberculosis), trauma, or connective tissue disorders. Unruptured aneurysms are usually found incidentally during diagnostic studies. More commonly, sinus of Valsalvaaneurysms are diagnosed after clinical sequelae of rupture. Diagnosis of sinus of Valsalva aneurysm is facilitated by echocardiography, contrast aortography, and more recently, magnetic resonance imaging. Repair is generally required for ruptured aneurysms; unruptured aneurysms encroaching on nearby structures, causing myocardial ischemia, or having the potential to rupture warrant repair. A review of the literature is presented focusing on anatomy, clinical presentation of ruptured and unruptured aneurysms, noninvasive diagnostic modalities, and techniques for repair of this anomaly.
Aortic Aneurysm↗
Preclinical carotid atherosclerosis in patients with rheumatoid arthritis.
BACKGROUND: Rheumatoid arthritis is associated with increased morbidity and mortality because of cardiovascular disease, independent of traditional risk factors. OBJECTIVE: To determine the prevalence of preclinical atherosclerosis in patients with rheumatoid arthritis and to identify clinical and biological markers for atherosclerotic disease in this patient population. DESIGN: Matched, cross-sectional study. SETTING: Hospital for Special Surgery in New York City. PATIENTS: 98 consecutive outpatients with rheumatoid arthritis who were followed by rheumatologists and 98 controls matched on age, sex, and ethnicity. MEASUREMENTS: Cardiovascular risk factor ascertainment and carotid ultrasonography in all participants; disease severity, disease treatment, and inflammatory markers in patients with rheumatoid arthritis. RESULTS: Despite a more favorable risk factor profile, patients with rheumatoid arthritis had a 3-fold increase in carotid atherosclerotic plaque (44% vs. 15%; P < 0.001). The relationship between rheumatoid arthritis and carotid atherosclerotic plaque remained after accounting for age, serum cholesterol levels, smoking history, and hypertensive status; adjusted predicted prevalence was 7.4% (95% CI, 3.4% to 15.2%) for the control group and 38.5% (CI, 25.4% to 53.5%) for patients with rheumatoid arthritis. Age (P < 0.001) and current cigarette use (P < 0.014) were also significantly associated with carotid atherosclerotic plaque. Among patients with rheumatoid arthritis, atherosclerosis was related to age, hypertension status, and use of tumor necrosis factor-alpha inhibitors (a possible marker of disease severity). LIMITATIONS: The study had a cross-sectional design, and inflammatory markers were determined only once. CONCLUSIONS: Patients with rheumatoid arthritis have a high prevalence of preclinical atherosclerosis independent of traditional risk factors, suggesting that chronic inflammation and, possibly, disease severity are atherogenic in this population.
Adult↗
Recommendations for chamber quantification.
Quantification of cardiac chamber size, ventricular mass and function ranks among the most clinically important and most frequently requested tasks of echocardiography. Over the last decades, echocardiographic methods and techniques have improved and expanded dramatically, due to the introduction of higher frequency transducers, harmonic imaging, fully digital machines, left-sided contrast agents, and other technological advancements. Furthermore, echocardiography due to its portability and versatility is now used in emergency rooms, operating rooms, and intensive care units. Standardization of measurements in echocardiography has been inconsistent and less successful, compared to other imaging techniques and consequently, echocardiographic measurements are sometimes perceived as less reliable. Therefore, the American Society of Echocardiography, working together with the European Association of Echocardiography, a branch of the European Society of Cardiology, has critically reviewed the literature and updated the recommendations for quantifying cardiac chambers using echocardiography. This document reviews the technical aspects on how to perform quantitative chamber measurements of morphology and function, which is a component of every complete echocardiographic examination.
Cardiac Volume↗
Relationship of antiphospholipid antibodies to cardiovascular manifestations of systemic lupus erythematosus.
OBJECTIVE: Although antiphospholipid antibodies (aPL) are associated with arterial and venous thrombosis in systemic lupus erythematosus (SLE), the extent to which they influence other cardiovascular manifestations is either controversial or uncertain. We undertook this study to examine the relationships of aPL with valvular, myocardial, and arterial disease in SLE. METHODS: Two hundred patients in an SLE registry, recruited at the time of outpatient visits, underwent comprehensive interviews, physical examinations, laboratory assessments, echocardiography to assess left ventricular (LV) and valvular status, carotid ultrasonography to detect atherosclerosis (discrete plaque), and radial applanation tonometry to measure arterial stiffness. RESULTS: Antiphospholipid antibodies were present(defined as IgG or IgM anticardiolipin > or =40 IU/ml or the presence of lupus anticoagulant) in 42 patients (21%). Mitral valve nodules and moderate-to-severe mitral regurgitation were more common in aPL-positive patients (both 14.3% versus 4.4%; P = 0.02). Thirty-one percent of patients with high titers of IgG aPL (>80 IU/ml) had mitral valve nodules, compared with 20% of patients with mildly to moderately elevated levels of IgG aPL (16-80 IU/ml) and 4% of patients without IgG aPL (overall P < 0.001). Levels of soluble tumor necrosis factor receptors were higher in the presence of both aPL and mitral valve nodules. LV dimensions, systolic function, and carotid artery stiffness as well as prevalences of Raynaud's phenomenon, pulmonary hypertension, and atherosclerosis were similar in aPL-positive and aPL-negative patients. CONCLUSION: Antiphospholipid antibodies in SLE are associated with mitral valve nodules and significant mitral regurgitation, possibly due to valvular endothelial cell activation. However, in this population, they are not associated with evidence of myocardial hypertrophy, systolic dysfunction, coronary or carotid atherosclerosis, or other vascular abnormalities.
Adult↗
Left atrial diameter as an independent predictor of first clinical cardiovascular events in middle-aged and elderly adults: the Strong Heart Study (SHS).
BACKGROUND: Echocardiographic left atrial (LA) volume has been documented to be an independent predictor of cardiovascular events. Less is known about the predictive ability of anteroposterior LA diameter, a simpler measure of LA size obtained routinely during echocardiographic evaluation. METHODS: We investigated the prognostic value of LA diameter for incident cardiovascular events in 2804 American Indians free of clinical cardiovascular disease, valvular disease, and atrial fibrillation. Echocardiographic variables were obtained using standardized methods, and previously derived sex-specific partition values were used to define left ventricular (LV) hypertrophy indexed to height(2.7) (in meters) and LA enlargement (> 4.2 cm in men, > 3.8 cm in women). Cardiovascular events included nonfatal stroke, coronary heart disease, congestive heart failure, and fatal cardiovascular disease based on validated definitions. RESULTS: During a median follow-up of 7 years, 368 events occurred. LA diameter, both as a continuous and as a categorical variable, was significantly associated with incident cardiovascular events in unadjusted analyses. In multivariable analyses that adjusted for age, sex, body mass index, hypertension, diabetes, total cholesterol-high-density lipoprotein cholesterol, smoking, renal insufficiency, LV hypertrophy, abnormal LV systolic and diastolic function, mitral annular calcification, fibrinogen, and C-reactive protein, both LA diameter (risk ratio 1.04/mm, 95% CI 1.02-1.07, P < .002) and LA enlargement (risk ratio 1.57, 95% CI 1.17-2.10, P = .002) remained independent predictors of first cardiovascular events. CONCLUSIONS: In this population-based cohort, LA diameter independently predicted incident cardiovascular events after adjustment for established clinical, echocardiographic, and inflammatory risk factors. This simple measure of LA dilatation can identify individuals at heightened risk who may warrant more aggressive risk factor modification.
Aged↗
Examination of lower targets for low-density lipoprotein cholesterol and blood pressure in diabetes--the Stop Atherosclerosis in Native Diabetics Study (SANDS).
Diabetes incidence is increasing rapidly in the United States. Diabetes increases the risk for cardiovascular disease, the major cause of death in diabetic individuals. The conventional cardiovascular risk factors of hyperlipidemia and hypertension worsen diabetic vascular disease. Treatment targets for low-density lipoprotein cholesterol (LDL-C) and blood pressure in diabetic individuals are being debated. The SANDS is a randomized, open-label, 3-year trial to examine the effects of aggressive LDL-C (goal <70 mg/dL) and blood pressure (BP) (goal <115/75 mm Hg) reduction versus the standard goals of <100 mg/dL for LDL-C and <130/85 mm Hg for BP. Five hundred forty-nine American-Indian men and women >40 years old with type 2 diabetes were randomized to 1 of 2 groups. Lipids and BP are managed using Food and Drug Administration-approved medications in an algorithmic approach. The presence and progression of atherosclerosis are evaluated by carotid ultrasonography; echocardiography assesses cardiac function. The primary end point is the composite outcome of change in carotid artery intimal medial thickness and fatal/nonfatal cardiovascular events. These outcomes are combined by using a ranked analysis for carotid thickness and assigning a "worst rank" for a cardiovascular event. Secondary end points include carotid plaque score, left ventricular geometry and function, serum C-reactive protein, and safety measures. Unique aspects of the study design and analysis plan involve the use of a composite outcome and changes during the trial of LDL-C treatment goals for participants with baseline or incident cardiovascular disease in the conventional group because of changes in the standard of care. Study results will further understanding of the effects of aggressive risk factor reduction on atherosclerosis burden and cardiac function in diabetic individuals in US populations and will help determine optimal LDL-C and BP treatment goals for diabetic patients.
Adult↗
Association of pulse pressure with cardiovascular outcome is independent of left ventricular hypertrophy and systolic dysfunction: the Strong Heart Study.
BACKGROUND: Whether increased pulse pressure (PP) predicts cardiovascular (CV) events independent of left ventricular hypertrophy (LVH) and systolic dysfunction is unclear. METHODS: Strong Heart Study adults (2946) without clinically overt coronary heart disease were studied. Echocardiographic LV mass >49.2 g/m(2.7) in men or >46.7 g/m(2.7) in women defined LVH. Clinical, metabolic, and echocardiographic characteristics were evaluated among participants divided in quartiles of PP (cut points: 42, 52, and 64 mm Hg). Mean follow-up for evaluation of all-cause and CV mortality was approximately 7 years. RESULTS: Mean age, proportion of women, and proportion of participants with diabetes increased across quartiles of PP. Partially by definition, the proportion of participants with hypertension was also higher with wider PP. Systolic and mean blood pressure (BP) increased whereas diastolic BP did not differ significantly across quartiles of PP. The LV mass index was higher whereas ejection fraction (EF) tended to be lower with wider PP. The CV mortality and all-cause mortality were higher in the highest quartile of PP. Wider PP predicted CV mortality independently of traditional risk factors, LVH and reduced EF. CONCLUSIONS: Wider PP was associated with a higher hazard ratio of CV mortality independent of traditional CV risk factors, LVH and reduced EF in adults without overt coronary heart disease.
Aged↗
Clinical application of noninvasive vascular ultrasound in cardiovascular risk stratification: a report from the American Society of Echocardiography and the Society of Vascular Medicine and Biology.
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Atherosclerosis↗
Blood pressure normalization is associated with normal left ventricular mass but not carotid geometry: the ICARe Dicomano Study.
OBJECTIVE: While many studies have examined the relation between antihypertensive treatment and ventricular hypertrophy, relatively few data are available regarding changes in arterial structure due to blood pressure reduction. Therefore, we compared normotensive to untreated hypertensive subjects to uncontrolled (treated with elevated blood pressure values) or controlled (treated with normal blood pressure values) hypertensive older subjects. PATIENTS: Community-dwellers (age >or= 65 years) of a small town in Italy (Dicomano) underwent extensive clinical examination, echocardiography, carotid ultrasonography, and applanation tonometry. Of the 614 participants, 173 subjects were normotensive; among the hypertensive subjects, 225 were untreated (51%), 177 (40%) were uncontrolled, and only 39 (9%) were controlled. RESULTS: The majority of treated hypertensive subjects were on monotherapy (82%). Subjects with a history of coronary artery disease or stroke were more frequently treated. Controlled hypertensives had left ventricular mass index similar to normotensives but lower than uncontrolled and untreated hypertensives. There were no differences among the three hypertensive groups in carotid artery structure. Only the pressure-independent stiffness index was reduced in the treated hypertensive subjects compared to untreated hypertensives, with no difference between controlled and uncontrolled subjects. CONCLUSIONS: In our community-based, older population, antihypertensive treatment was associated with a normal left ventricular mass only when blood pressure was well controlled. In contrast, carotid artery remodeling and atherosclerosis were independent of antihypertensive treatment as well as of achievement of satisfactory blood pressure control. However, antihypertensive treatment was associated with significantly higher carotid compliance even in the absence of detectable changes in carotid structure.
Aged↗
Risk factors for arterial hypertension in adults with initial optimal blood pressure: the Strong Heart Study.
Whether metabolic factors and their change over time influence development of arterial hypertension in adults with initially optimal blood pressure (BP) is unknown. We analyzed associations of BP in the optimal range (<120/80 mm Hg), metabolic risk factors, and their changes over 4-year follow-up, with 8-year incident hypertension, in a cohort of American Indians with a high prevalence of obesity. At baseline, 967 participants with optimal BP and no prevalent cardiovascular disease (69.5% women; mean age, 54+/-7 years) were evaluated and reexamined after 4 (second examination) and 8 years to evaluate predictors of 8-year incident arterial hypertension. In participants with normal glucose tolerance, baseline BP and decrease in high-density lipoprotein cholesterol from baseline to the second examination were the most potent predictors of 8-year arterial hypertension (both P<0.0001), with additional effects of baseline waist circumference and its increase, increase in BP, and presence of diabetes at the second examination (all P<0.04). In participants with impaired glucose tolerance or diabetes, the most potent predictor of 8-year incident hypertension was diabetes at the second examination (P<0.0001) followed by a increase in BP and LDL cholesterol over the first 4 years (both P<0.001). Thus, incident arterial hypertension can be predicted by initial metabolic profile and unfavorable metabolic variations over time, in addition to initial BP. At optimal levels of initial BP, increasing abdominal obesity, and abnormal lipid profile are major predictors of development of arterial hypertension. Possible implications of these findings for primary cardiovascular prevention should be tested in prospective studies.
Abdominal Fat↗
Mitral annular calcification, aortic valve sclerosis, and incident stroke in adults free of clinical cardiovascular disease: the Strong Heart Study.
BACKGROUND AND PURPOSE: Mitral annular calcification (MAC) and aortic valve (AV) sclerosis have each been linked to cardiovascular disease. Whether MAC and AV sclerosis are risk factors for stroke independent of other echocardiographic or laboratory predictors has not been established. We evaluated the relationship between MAC, AV sclerosis, and first stroke events in a population-based cohort. METHODS: Our study cohort consisted of 2723 American Indians participating in the Strong Heart Study who were free of prevalent cardiovascular disease. Participants underwent standardized clinical, echocardiographic, and laboratory evaluation, and incident stroke was ascertained using validated methods. RESULTS: During a median follow-up of 7 years, 86 strokes occurred. Age- and sex-adjusted incidence rates of stroke were significantly increased for MAC (rate ratio [RR], 3.12; 95% CI, 1.77 to 5.25) but not for AV sclerosis (RR, 1.15; 95% CI, 0.45 to 2.49). MAC was also associated with a reduced time to first stroke events after adjustment for clinical variables and the inflammatory markers C-reactive protein and fibrinogen (hazard ratio [HR], 2.42; 95% CI, 1.39 to 4.21) or the echocardiographic covariates left ventricular hypertrophy and left atrial enlargement (HR, 1.89; 95% CI, 1.04 to 3.41). Individuals with and without AV sclerosis showed no significant difference in stroke-free survival in unadjusted analyses (P=0.698). Crossing of the survival curves precluded multivariable analysis using Cox models. CONCLUSIONS: In this cohort of American Indians without clinical cardiovascular disease, the presence of MAC, but not AV sclerosis, proved to be a strong risk factor for incident stroke after extensive adjustment for other predictors. Individuals exhibiting MAC may benefit from aggressive risk factor modification, but this will require further investigation.
Aged↗
Prognostic impact of systolic hypertension on asymptomatic patients with chronic severe aortic regurgitation and initially normal left ventricular performance at rest.
The influence of systolic hypertension (SH) on the natural history of chronic aortic regurgitation (AR) and the clinical effect of antihypertensive medication on patients who have hypertension and AR are incompletely defined. Therefore, we reviewed the clinical course of 80 unoperated patients who were entered prospectively into an assessment of natural history of AR and its predictors and were asymptomatic with normal left ventricular ejection fraction (LVEF) at rest at study entry; 30 of 80 patients had SH (systolic blood pressure >140 mm Hg); 20 of 80 patients (16 had SH) used antihypertensive drugs for the long term (not mandated by protocol). During an average 7.2-year event-free follow-up, 24 patients developed symptoms alone (n = 14), subnormal LVEF with or without symptoms (n = 8), or died suddenly (n = 2). SH tripled the average annual risk of cardiac events (8.47% vs 2.85%, p = 0.004). The effect of systolic blood pressure was independent of age, gender, diastolic blood pressure, LV diastolic dimension, fractional shortening, and LVEF at rest (p = 0.004 to <0.008). However, positive prognostic interactions existed between systolic blood pressure and pulse pressure (p <0.001), LVEF during exercise (p <0.001), change in LVEF from rest to exercise (p <0.001), and the contractility index (p <0.02). Among patients who had SH, antihypertensive therapy predicted increased event risk (average annual risk 15.46% vs 3.98%, p <0.02) and remained predictive when analysis was adjusted for potentially confounding subgroup variations at study entry (p <0.03, all models). In conclusion, SH portends poor clinical outcome in chronic severe AR. As a group, antihypertensive drugs do not mitigate outcome, although the effect of individual drugs is uncertain and at least some may be deleterious. The theoretically based practice of giving antihypertensive drugs to patients who have AR requires reexamination.
Adult↗
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↗
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↗