Adalimumab in the treatment of cardiac sarcoidosis: Single center case series and narrative literature review.

Background: Tumor necrosis factor (TNF) inhibitors have been used in the treatment of cardiac sarcoidosis, infliximab being the most commonly used. We have previously reported a case of effective treatment of cardiac sarcoidosis using adalimumab. Objective: To describe our experience of using adalimumab in the treatment of cardiac sarcoidosis. Methods: We conducted a retrospective study to evaluate patients with cardiac sarcoidosis who received adalimumab treatment at the University of Illinois Health between 2011 and 2022. The outcome was evaluated by assessing safety, tolerability, and ability to taper systemic corticosteroids therapy following initiation of adalimumab. Results: Seven patients met the inclusion criteria. Clinical responses to adalimumab were universally positive. Corticosteroid therapy was discontinued in five patients and the dose was reduced in two patients. Furthermore, adalimumab was well tolerated, and no adverse events were reported. Conclusion: Adalimumab was safe and well-tolerated in seven patients with cardiac sarcoidosis seen at our medical center and exhibited corticosteroid-sparing effects. Our observation further warrants large prospective studies to evaluate the safety and efficacy of adalimumab in the treatment of cardiac sarcoidosis.

Outcomes of a Pharmacist-Managed Heart Failure Medication Titration Assistance Clinic.

BACKGROUND: National guidelines recommend angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs) and ß-blockers (BBs) at target doses for morbidity and mortality benefits in heart failure with reduced ejection fraction (HFrEF); regardless, titration of these therapies in practice remains suboptimal. We implemented an outpatient pharmacist-managed HFrEF medication titration assistance clinic (MTAC) at one institution to improve titration for general cardiology (GC) patients. OBJECTIVE: To evaluate MTAC impact by determining the proportion of patients on target or maximum tolerated ACE inhibitor/ARB and BB doses. METHODS: A retrospective chart review of adult patients with documented ejection fraction ≤40% managed in the MTAC or GC from 2011 to 2013 was conducted. HFrEF medication regimens were collected at initial visit and months 1, 2, 3, 6, 9, and 12 to assess titration. Target doses were defined per guideline or dose at which ejection fraction recovered during the study. Maximum tolerated doses were defined as the highest dose patients tolerated without physiological limitations. RESULTS: Of 148 patients, the MTAC managed 51 and GC managed 97. At baseline, 90% of MTAC versus 82% of GC patients were prescribed ACE inhibitors/ARBs and BBs. In the MTAC, 4% were at target or maximum tolerated doses compared with 32% of GC patients ( P < 0.001). At 12 months, 95% of patients in the MTAC and 87% in GC were prescribed ACE inhibitors/ARBs and BBs. Of those prescribed ACE inhibitors/ARBs and BBs, 64% in the MTAC versus 40% in GC reached target or maximum tolerated doses ( P = 0.01). CONCLUSIONS: The pharmacist-managed MTAC increased the proportion of patients on optimal HFrEF therapies and are a resource for GC patients.

Coronary artery calcium may stabilize following islet cell transplantation in patients with type 1 diabetes.

Islet cell transplantation can functionally cure type 1 diabetes and also improve carotid intima-media thickness. This study provides a preliminary description of changes in coronary artery calcium following islet transplantation, and associated factors. Coronary artery calcium was measured in 14 patients with type 1 diabetes (11 had measures both pre- and post-transplant [mean 2.3 years]) in the University of Illinois at Chicago's clinical trial. Multivariable mixed-effects linear regression of repeated measures was used to quantify calcium change and determine if this change was longitudinally associated with risk/protective factors. Thirteen of the patients were female, with mean baseline age, diabetes duration, and BMI of 47.6 and 28.7 years, and 23.1, respectively. Over half (57%) had detectable coronary artery calcium pre-transplant. Minimal change (0.39 mm3 /y, P = .02) occurred in coronary artery calcium levels pre- to post-transplant. No patient met criteria for calcium progression. Coronary artery calcium was positively associated with total and small VLDL particles (P ≤ .02), statin dose (P = .02), and urine albumin-to-creatinine ratio (P = .04) and negatively associated with free fatty acids (P = .03), total HDL (P = .03), large HDL particles (P = .005), and tacrolimus dose (P = .02). Islet transplant may stabilize coronary artery calcium, with optimal management of lipids and kidney function remaining key therapeutic targets. [NCT00679041].

Differential impact of obesity on the pathogenesis of RA or preclinical models is contingent on the disease status.

OBJECTIVE: Studies were performed to uncover the significance of obesity in rheumatoid arthritis (RA) and preclinical models. METHODS: Preclinical arthritis models were used to examine the impact of obesity on disease onset and remission. Conditioned media from RA adipose tissues were used to investigate the mechanism contributing to joint neutrophil influx and M1 macrophage differentiation observed in early and remission phases of arthritis. RESULTS: We report that mice fed with high fat diet (HFD) have an earlier onset of collagen-induced arthritis (CIA) compared with mice on regular diet. However, the differences in CIA joint swelling between the two diet groups are lost once disease is established. We found that early arthritis triggered by obesity is due to elevated joint MIP2/interleukin-8 levels detected in CIA as well as in the RA and mouse adipose tissues and the effect of this chemokine on neutrophil recruitment. Although active disease progression is similarly affected in both diet groups, arthritis resolution is accelerated in lean mice while joint inflammation is sustained in obese mice. We document that HFD can prolong toll-like receptor (TLR)4-induced arthritis by increasing joint monocyte migration and further remodelling the recruited cells into M1 macrophages. Consistently, we show that adipose condition media can transform RA and wild-type naïve myeloid cells into M1 macrophages; however, this function is impaired by TLR4 blockade or deficiency. CONCLUSIONS: We conclude that despite established disease being unaffected by obesity, the early and the resolution phases of RA are impacted by obesity through different mechanisms.

Computed Tomography of the Esophagus in Scleroderma and Lung Disease.

Systemic sclerosis, or scleroderma, is a collagen vascular disease characterized by hardening of the skin and involvement of internal organs, most commonly the esophagus. The most frequent cause of death in these patients is lung disease. Esophageal dysfunction has been implicated in the pathogenesis of interstitial lung disease. We previously developed a standard for the esophageal diameter on chest computed tomography (CT) and hypothesized that patients with esophageal dilation would be more likely to have interstitial lung disease than those without. In this study, we test this in 121 systemic sclerosis patients with interstitial lung disease and 48 of those without interstitial lung disease. For controls, we evaluated 121 patients followed at a general pulmonary clinic and the previously studied normal healthy standards. This study demonstrated that esophageal dilation is common in systemic sclerosis patients (66.3% for the maximal esophageal diameter more than or equal to 15 mm), that systemic sclerosis patients with interstitial lung disease have more dilated esophagi than those without interstitial lung disease (median 19.4 mm vs. 14.1 mm), and that esophageal parameters are negatively correlated with pulmonary function. We also found that patients from general pulmonary clinic were more likely to have dilated esophagi than normal controls (median 12.1 mm vs. 9.7 mm). The CT measurement of esophageal diameter may be a useful marker of patients at risk for developing lung disease.

Adverse pregnancy outcomes and subsequent risk of cardiovascular disease in women with systemic lupus erythematosus.

BACKGROUND/OBJECTIVE: Patients with systemic lupus erythematosus (SLE) are at increased risk for adverse pregnancy outcomes and cardiovascular disease (CVD). The objective of this exploratory study was to investigate the association between a history of adverse pregnancy outcomes and subsequent risk of subclinical CVD assessed by imaging studies and verified clinical CVD events in 129 women with SLE. METHODS: The occurrence of adverse pregnancy outcomes, specifically pre-eclampsia, preterm birth and low birth weight was ascertained by questionnaire. Subclinical CVD was assessed by coronary artery calcium (CAC) as measured by electron beam CT and carotid plaque measured by B mode ultrasound. Clinical CVD events were verified by medical record review. Logistic regression was used to estimate the association of pregnancy complications with occurrence of subclinical CVD and clinical CVD with a priori adjustment for age, which is associated with CVD and SLE disease duration as a measure of SLE disease burden. RESULTS: Fifty-six women reported at least one pregnancy complication while 73 had none. Twenty-six women had at least one pregnancy complicated by pre-eclampsia and were more likely to have a CAC score greater than or equal to 10 (adjusted OR=3.7; 95% CI 1.2 to 11.9), but the presence of plaque was not associated with this pregnancy complication, OR=1.1, (95% CI 0.4 to 2.8). Low birth weight and preterm birth were not associated with CAC or plaque. CONCLUSIONS: Patients with SLE with a history of pre-eclampsia had a higher rate of subclinical CVD as measured by CAC score. Future studies are needed to confirm the relationship between adverse pregnancy outcomes and subsequent subclinical CVD and clinical CVD events.

Alpha-chlorofatty Acid and coronary artery or aorta calcium scores in women with systemic lupus erythematosus. A pilot study.

OBJECTIVE: Alpha-chlorofatty acid (α-ClFA) is one product of myeloperoxidase activity in vivo during atherogenesis and may be a biomarker for cardiovascular disease (CVD). We investigated if serum α-ClFA is associated with subclinical CVD as measured by coronary artery and aorta calcium scores (CAC and AC, respectively) in women with and without systemic lupus erythematosus (SLE). METHODS: This pilot project analyzed baseline data from 173 women with SLE and 186 women without SLE participating in a 5-year longitudinal investigation of the Study of Lupus Vascular and Bone Long-term Endpoints (SOLVABLE). Data collection included demographic information, CVD and SLE risk factors, and laboratory assessments. Alpha-ClFA was measured in stored serum by liquid chromatography-mass spectrometry. CAC and AC were measured by computed tomography. Outcome measures were CAC and AC present (CAC > 0 or AC > 0) versus absent (CAC = 0 or AC = 0). Associations between risk factors and CAC or AC were tested with descriptive statistics and multivariate analyses. RESULTS: Women with SLE had higher α-ClFA levels than women without SLE (42.0 fmol/25 µl ± 37.3 vs 34.5 fmol/25 µl ± 21.9; p = 0.020). In analyses including individual CVD risk factors, having SLE was independently associated with the presence of CAC (OR 3.42, 95% CI 1.72 to 6.78) but not AC. Alpha-ClFA was not associated with the presence of CAC or AC in patients with SLE. CONCLUSION: SLE, but not serum α-ClFA, was associated with the presence of CAC in this pilot project.

Inflammatory expression profiles in monocyte-to-macrophage differentiation in patients with systemic lupus erythematosus and relationship with atherosclerosis.

INTRODUCTION: Our objectives were to examine mononuclear cell gene expression profiles in patients with systemic lupus erythematosus (SLE) and healthy controls and to compare subsets with and without atherosclerosis to determine which genes' expression is related to atherosclerosis in SLE. METHODS: Monocytes were obtained from 20 patients with SLE and 16 healthy controls and were in vitro-differentiated into macrophages. Subjects also underwent laboratory and imaging studies to evaluate for subclinical atherosclerosis. Whole-genome RNA expression microarray was performed, and gene expression was examined. RESULTS: Gene expression profiling was used to identify gene signatures that differentiated patients from controls and individuals with and without atherosclerosis. In monocytes, 9 out of 20 patients with SLE had an interferon-inducible signature compared with 2 out of 16 controls. By looking at gene expression during monocyte-to-macrophage differentiation, we identified pathways which were differentially regulated between SLE and controls and identified signatures based on relevant intracellular signaling molecules which could differentiate SLE patients with atherosclerosis from controls. Among patients with SLE, we used a previously defined 344-gene atherosclerosis signature in monocyte-to-macrophage differentiation to identify patient subgroups with and without atherosclerosis. Interestingly, this signature further classified patients on the basis of the presence of SLE disease activity and cardiovascular risk factors. CONCLUSIONS: Many genes were differentially regulated during monocyte-to-macrophage differentiation in SLE patients compared with controls. The expression of these genes in mononuclear cells is important in the pathogenesis of SLE, and molecular profiling using gene expression can help stratify SLE patients who may be at risk for development of atherosclerosis.

Risk factors in the progression of subclinical atherosclerosis in women with systemic lupus erythematosus.

OBJECTIVE: To investigate risk factors in subclinical atherosclerosis progression as measured by coronary artery calcium (CAC) and aorta calcium (AC) in women with systemic lupus erythematosus (SLE; cases) and in comparison with a control population. METHODS: A cohort of 149 cases and 124 controls participated in the Study of Lupus Vascular and Bone Long-Term Endpoints. Demographic information, cardiovascular and SLE risk factors, and laboratory assessments were collected at an initial visit. CAC and AC were measured by electron beam computed tomography (CT) or multidetector CT at an initial visit and at a followup visit. Logistic regression models were used to identify predictors of progression in CAC and AC; multivariate models were adjusted for age, hypertension, and total cholesterol to high-density lipoprotein ratio. RESULTS: Higher modified Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index (SDI) score (odds ratio [OR] 2.15, 95% confidence interval [95% CI] 1.33-3.57), use of a corticosteroid (OR 2.93, 95% CI 1.14-7.86), and use of aspirin (OR 4.23, 95% CI 1.53-11.74) were associated with CAC progression in multivariate models. Presence of SLE (OR 2.64, 95% CI 1.26-5.72), lower C3 (OR 0.54, 95% CI 0.33-0.87), lower C4 (OR 0.49, 95% CI 0.27-0.86), use of a corticosteroid (OR 2.73, 95% CI 1.03-7.64), higher corticosteroid dose (OR 1.77, 95% CI 1.12-3.00), higher lipoprotein(a) (OR 1.80, 95% CI 1.11-2.98), and higher homocysteine (OR 2.06, 95% CI 1.06-4.29) were associated with AC progression in multivariate models. CONCLUSION: Higher disease damage at the first study visit, as measured by the modified SDI, may predict increased risk in CAC progression, whereas higher disease activity at the first study visit, as measured by hypocomplementemia and use of corticosteroids, may predict increased risk in AC progression.

25-hydroxyvitamin D and cardiovascular risk factors in women with systemic lupus erythematosus.

OBJECTIVE: Low serum levels of 25-hydroxyvitamin D (25[OH]D; vitamin D) are associated with a higher frequency of cardiovascular disease and risk factors in the general population. Vitamin D deficiency has also been noted in systemic lupus erythematosus (SLE). The objective of this study was to evaluate the associations of serum 25(OH)D levels with cardiovascular risk factors in women with SLE. METHODS: Data collected in 181 women with SLE included demographics, SLE activity and damage assessments, cardiovascular risk factors, medications, and laboratory assessments of inflammatory markers and 25(OH)D levels. Multiple linear and logistic regressions were used to estimate the association of 25(OH)D levels with cardiovascular risk factors. RESULTS: The mean age and disease duration were 43.2 and 11.9 years, respectively. The mean 25(OH)D level was 27.1 ng/ml and 62.2% had 25(OH)D levels <30 ng/ml. In unadjusted analyses, lower 25(OH)D levels were significantly associated with higher diastolic blood pressure, low-density lipoprotein cholesterol, lipoprotein(a), body mass index (BMI), and fibrinogen levels, as well as self-reported hypertension and diabetes mellitus. Lower 25(OH)D levels were also significantly associated with higher SLE disease activity and damage scores. After adjustment for age, seasonal variation, and race/ethnicity, lower 25(OH)D levels were also significantly related to higher fasting serum glucose. With further adjustment for BMI, associations between 25(OH)D and cardiovascular risk factors were no longer significant. CONCLUSION: This study demonstrates that vitamin D levels are low in women with SLE and significant associations exist with selected cardiovascular risk factors, although most of these associations can be explained by BMI.

Cardiovascular events with absent or minimal coronary calcification: the Multi-Ethnic Study of Atherosclerosis (MESA).

BACKGROUND: Elevated coronary artery calcium (CAC) is a marker for increase risk of coronary heart disease (CHD). Although most CHD events occur among individuals with advanced CAC, CHD can also occur in individuals with little or no calcified plaque. In this study, we sought to evaluate the characteristics associated with incident CHD events in the setting of minimal (score

Hypertriglyceridemic waist phenotype predicts increased visceral fat in subjects with type 2 diabetes.

OBJECTIVE: Greater accumulation of visceral fat is strongly linked to risk of cardiovascular disease. However, elevated waist circumference by itself does not always identify individuals with increased visceral fat. RESEARCH DESIGN AND METHODS: We examined 375 subjects with type 2 diabetes from the CHICAGO cohort for presence of hypertriglyceridemic waist phenotype (waist circumference >90 cm in men or >85 cm in women, in conjunction with a plasma triglyceride concentration of > or =177 mg/dl) to determine its usefulness for identifying subjects with increased amounts of visceral fat. We divided subjects into three groups: group 1 (low waist circumference and low triglycerides; waist circumference < or =90 cm in men or < or =85 cm in women and triglyceride <177 mg/dl, n = 18), group 2 (high waist circumference and low triglycerides; waist circumference >90 cm in men or >85 cm in women and triglycerides <177 mg/dl, n = 230), and group 3 (high waist circumference and high triglycerides; waist circumference >90 cm in men or >85 cm in women and triglycerides > or =177 mg/dl, n = 127). RESULTS: Subjects in group 3 had significantly higher visceral fat (P < 0.0001), A1C (P < 0.01), and coronary artery calcium (P < 0.05) compared with group 2, despite similar age, BMI, and waist circumference. The relationship of the phenotype to atherosclerosis, however, was attenuated by adjustment for HDL cholesterol, triglyceride-rich lipoprotein cholesterol, apolipoprotein B, or LDL particle number. CONCLUSIONS: The presence of hypertriglyceridemic waist phenotype in subjects with type 2 diabetes identifies a subset with greater degree of visceral adiposity. This subset also has greater degree of subclinical atherosclerosis that may be related to the proatherogenic lipoprotein changes.

Relation of abdominal fat depots to systemic markers of inflammation in type 2 diabetes.

OBJECTIVE: Both visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) have been linked to systemic inflammation in nondiabetic cohorts. We examined the relationships between VAT and SAT and systemic inflammatory markers in a large well-characterized cohort of subjects with type 2 diabetes. RESEARCH DESIGN AND METHODS: Three hundred eighty-two subjects with type 2 diabetes in the CHICAGO (Carotid Intima-Media Thickness in Atherosclerosis Using Pioglitazone) study cohort underwent abdominal computed tomography to determine SAT and VAT distribution. Fasting blood was obtained for measurement of inflammatory markers. The relationships between inflammatory markers and BMI, SAT, and VAT were examined using regression models adjusted for age, sex, diabetes treatment, duration of diabetes, smoking, statin use, and A1C. RESULTS: VAT was positively related to CRP, monocyte chemoattractant protein (MCP), intracellular adhesion molecule (ICAM)-1, and plasminogen activator inhibitor type 1 (PAI-1) antigen before adjustment for BMI. After adjustment for BMI, the relationship to CRP was lost but positive associations with MCP (P < 0.01), PAI-1 (P < 0.0001), ICAM-1 (P < 0.01), and vascular cell adhesion molecule (P = 0.01) were evident. BMI was positively related to CRP (P < 0.0001) and IL-6 (P < 0.01) even after adjustment for VAT and SAT. SAT was not related to any inflammatory marker after adjustment for BMI. CONCLUSIONS: In this large group of subjects with type 2 diabetes, BMI was most strongly associated with CRP and IL-6 levels. SAT was not associated with markers of systemic inflammation. The size of the VAT depot provided information additional to that provided by BMI regarding inflammatory markers that are strongly related to vascular wall remodeling and coagulation. Our findings suggest that adipose tissue distribution remains an important determinant of systemic inflammation in type 2 diabetes.

Differences in subclinical cardiovascular disease between African American and Caucasian women with systemic lupus erythematosus.

Racial differences exist in disease rates and mortality in both cardiovascular disease (CVD) and systemic lupus erythematosus (SLE). The objective of this cross-sectional study was to compare the frequency and risk factors for subclinical CVD in African American (AA) and Caucasian women with SLE and no prior CVD events. Traditional CVD risk factors and SLE-related factors were assessed in 309 SLE women. Subclinical CVD was assessed by carotid ultrasound to measure intimamedial thickness (IMT) and plaque, and electron beam computed tomography (EBCT) was used to measure coronary artery calcium (CAC). AA women had less education and higher levels of body mass index, blood pressure, lipoprotein(a), C-reactive protein (CRP), fibrinogen, and erythrocyte sedimentation rate (ESR). However, AA women had lower albumin, more and longer duration of corticosteroid use, higher SLE disease activity and damage, and more dsDNA antibodies compared with Caucasian women after adjustment for age and study site. More AA women had carotid plaque (adjusted odds ratio [OR], 1.94; 95% confidence interval [CI], 1.03-3.65) and higher carotid IMT (0.620 vs 0.605 mm, P = 0.07) but similar CAC compared with Caucasians. A multivariate analysis revealed that the following risk factor variables were significantly different between the racial groups and associated with plaque: blood pressure, current corticosteroid use, SLE disease activity, and SLE damage. All factors contributed to the result, but no individual risk factor fully accounted for the association between race and plaque. In conclusion, the presence of carotid plaque was higher in AA compared with Caucasian women with SLE, in contrast to studies of non-SLE subjects, in which AA have similar or less plaque than Caucasians. A combination of SLE-related and traditional CVD risk factors explained the racial difference in plaque burden.

Coronary calcium predicts events better with absolute calcium scores than age-sex-race/ethnicity percentiles: MESA (Multi-Ethnic Study of Atherosclerosis).

OBJECTIVES: In this study, we aimed to establish whether age-sex-specific percentiles of coronary artery calcium (CAC) predict cardiovascular outcomes better than the actual (absolute) CAC score. BACKGROUND: The presence and extent of CAC correlates with the overall magnitude of coronary atherosclerotic plaque burden and with the development of subsequent coronary events. METHODS: MESA (Multi-Ethnic Study of Atherosclerosis) is a prospective cohort study of 6,814 asymptomatic participants followed for coronary heart disease (CHD) events including myocardial infarction, angina, resuscitated cardiac arrest, or CHD death. Time to incident CHD was modeled with Cox regression, and we compared models with percentiles based on age, sex, and/or race/ethnicity to categories commonly used (0, 1 to 100, 101 to 400, 400+ Agatston units). RESULTS: There were 163 (2.4%) incident CHD events (median follow-up 3.75 years). Expressing CAC in terms of age- and sex-specific percentiles had significantly lower area under the receiver-operating characteristic curve (AUC) than when using absolute scores (women: AUC 0.73 versus 0.76, p = 0.044; men: AUC 0.73 versus 0.77, p < 0.001). Akaike's information criterion indicated better model fit with the overall score. Both methods robustly predicted events (>90th percentile associated with a hazard ratio [HR] of 16.4, 95% confidence interval [CI]: 9.30 to 28.9, and score >400 associated with HR of 20.6, 95% CI: 11.8 to 36.0). Within groups based on age-, sex-, and race/ethnicity-specific percentiles there remains a clear trend of increasing risk across levels of the absolute CAC groups. In contrast, once absolute CAC category is fixed, there is no increasing trend across levels of age-, sex-, and race/ethnicity-specific categories. Patients with low absolute scores are low-risk, regardless of age-, sex-, and race/ethnicity-specific percentile rank. Persons with an absolute CAC score of >400 are high risk, regardless of percentile rank. CONCLUSIONS: Using absolute CAC in standard groups performed better than age-, sex-, and race/ethnicity-specific percentiles in terms of model fit and discrimination. We recommend using cut points based on the absolute CAC amount, and the common CAC cut points of 100 and 400 seem to perform well.

CT of the normal esophagus to define the normal air column and its extent and distribution.

OBJECTIVE: This study was designed to quantify and characterize the air-containing thoracic esophagus on CT to help diagnose diseases and facilitate correlation with lung diseases that may be associated with aspiration. SUBJECTS AND METHODS: The maximal air-containing esophageal lumina on each section of standard CT scans of 110 subjects were measured. These subjects came from a cohort of 10,132 self-reported healthy individuals who underwent CT for measurement of coronary artery calcium. Measurements were interpolated to account for variation in the length of the thoraces. RESULTS: Greater than 60% of the esophageal segments contained no air. On average the maximum air column was 10.5 (SD, 5.0) mm. Only 7.9% of the lumina were > 10 mm. Only 2% were > 15 mm, and only 0.2% were > 20 mm. The average number of lumina > 10 mm as a proportion of the entire esophageal length was 8% (14%). The average size at the carina was 2.6 (4.1) mm. In the upper 30% and from 61% to 75% down the length of the esophagus, < 5% of the lumina were > 10 mm. Less than 3% of subjects had air in the lowest two sections, indicating that the normal lower esophageal sphincter was closed. CONCLUSION: Esophageal air of > 10 mm should be considered abnormal in all segments except between the cardiac ventricles and lower esophageal sphincter. In this area, > 15 mm should be considered abnormal. An air-fluid level is abnormal.

Women and non-cardiac chest pain: gender differences in symptom presentation.

A substantial number of individuals evaluated for complaints of chest pain do not suffer from coronary heart disease (CHD). Studies show that many patients who complain of symptoms that might be caused by CHD, such as shortness of breath or chest pain, may actually have an anxiety disorder. Gender differences in how patients present with these symptoms have not been adequately explored. The purpose of this study was to explore possible gender differences in the presentation of patients with CHD-like symptoms. Two groups were examined, one comprising 6,381 individuals self-referred for electron beam tomography (EBT) studies and a subset of these individuals who defined a "low-risk" group based on the absence of risk factors for CHD and low coronary artery calcium (CAC) scores. We explored gender differences in symptom presentation in each group after controlling for relevant variables by using logistic regression models. These analyses showed that women were significantly more likely than men to endorse CHD symptoms that might also be caused by an anxiety disorder. Women in the low risk group reported CHD symptoms also referable to anxiety more often than men, but unlike men did not complain primarily of chest pain. Women were also more likely to have been prescribed antianxiety or antidepressant medication. In previous studies, non-cardiac chest pain has been considered a hallmark of anxiety in individuals seen in medical settings. This study suggests that in individuals with low risk for CHD chest pain was not related to gender, but other anxiety-related symptoms including heart flutter, lightheadedness, nausea, and shortness of breath were more likely to be reported in women than in men.

Relationship of abdominal visceral and subcutaneous adipose tissue with lipoprotein particle number and size in type 2 diabetes.

OBJECTIVE: Insulin resistance and type 2 diabetes are associated with an atherogenic lipoprotein profile. We examined the role of visceral and subcutaneous fat depots, independent of BMI, on the dyslipidemia associated with type 2 diabetes. RESEARCH DESIGN AND METHODS: A total of 382 subjects with type 2 diabetes underwent abdominal computed tomography to evaluate subcutaneous (SAT) and visceral adipose tissue (VAT) distribution and had anthropometric measurements to determine BMI and waist and hip circumference. Fasting blood was obtained for lipoprotein particle number and size using nuclear magnetic resonance spectroscopy. The relationship of lipoprotein particle number and size with BMI, SAT, and VAT was examined using multivariable regression models adjusted for age, sex, diabetes therapy, duration of diabetes, smoking, statin use, and A1C levels. The relation of VAT to lipoprotein particle number and size was further evaluated after the addition of BMI, BMI plus SAT, or BMI plus homeostatis is model assessment of insulin resistance (HOMA-IR) to the model. RESULTS: VAT was positively related to VLDL particle number (P < 0.0001), LDL particle number (P < 0.01), and VLDL size (P < 0.0001) and negatively related to LDL size (P < 0.0001) and HDL size (P < 0.0001). These relationships remained unchanged after addition of BMI and SAT to the model. After addition of HOMA-IR, VAT remained positively related to VLDL particle number (P < 0.0001) and size (P < 0.01) and negatively related to LDL and HDL particle size (P < 0.0001 for both comparisons). Neither BMI nor SAT was independently related to lipoprotein parameters. CONCLUSIONS: In patients with type 2 diabetes, higher VAT independent of BMI was associated with higher VLDL and LDL particle number, larger VLDL particles, and smaller LDL and HDL particles. This lipoprotein pattern has been associated with increased risk for atherosclerosis and cardiovascular disease.