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In order for the conductance catheter system to accurately measure instantaneous cardiac blood volume, it is necessary to determine and remove the contribution from parallel myocardial tissue. In previous studies, the myocardium has been treated as either purely resistive or purely capacitive when developing methods to estimate the myocardial contribution. We propose that both the capacitive and the resistive properties of the myocardium are substantial, and neither should be ignored. Hence, the measured result should be labeled admittance rather than conductance. We have measured the admittance (magnitude and phase angle) of the left ventricle in the mouse, and have shown that it is measurable and increases with frequency. Further, this more accurate technique suggests that the myocardial contribution to measured admittance varies between end-systole and end-diastole, contrary to previous literature. We have tested these hypotheses both with numerical finite-element models for a mouse left ventricle constructed from magnetic resonance imaging images, and with in vivo admittance measurements in the murine left ventricle. Finally, we propose a new method to determine the instantaneous myocardial contribution to the measured left ventricular admittance that does not require saline injection or other intervention to calibrate. Index Terms--Admittance, conductance catheter, finite-element model, parallel conductance, parallel myocardial admittance, phase angle measurement, ventricular volume.

Although cardiac myocyte apoptosis has been detected in explanted hearts from patients with end-stage dilated and ischemic cardiomyopathy, the relative contribution of apoptotic cell death to left ventricular (LV) remodeling and cardiac decompensation is not known. To determine whether progressive cardiac myocyte apoptosis contributes to the transition from a hypertrophic to a dilated cardiac phenotype that is observed in transgenic myosin heavy chain secreted TNF (MHCsTNF) mice with cardiac restricted overexpression of tumor necrosis factor (TNF), we assessed cardiac myocyte apoptosis (using a DNA ligase technique) in MHCsTNF mice and littermate control mice in relation to serial changes in LV structure, which was assessed using MRI. The prevalence of cardiac myocyte apoptosis increased progressively from 4 to 12 wk as the hearts of the MHCsTNF mice underwent the transition from a concentric hypertrophic to a dilated cardiac phenotype. Treatment of the MHCsTNF mice with the broad-based caspase inhibitor N-[(1,3-dimethylindole-2-carbonyl)-valinyl]-3-amino4-oxo-5-fluoropentanoic acid significantly decreased cardiac myocyte apoptosis and significantly attenuated LV wall thinning and adverse cardiac remodeling. Additional studies suggested that the TNF-induced decrease in Bcl-2 expression and activation of the intrinsic mitochondrial death pathway were responsible for the cardiac myocyte apoptosis observed in the MHCsTNF mice. These studies show that progressive cardiac myocyte apoptosis is sufficient to contribute to adverse cardiac remodeling in the adult mammalian heart through progressive LV wall thinning. tumor necrosis factor; cell death; caspase; congestive heart failure; magnetic resonance imaging

The utility of magnetic resonance imaging (MRI) in the assessment of cardiac hypertrophy is investigated using transgenic mice with hypertension and left ventricular hypertrophy. A gated multislice, multiphase cine MRI was used to assess the size and the mass of the hearts of anesthetized mice. Results were correlated with findings at autopsy. There is an excellent correlation between MRI estimates and heart mass measured at autopsy.

Background: Pectus excavatum is the most common chest wall skeletal deformity. Although commonly evaluated in adolescence, its prevalence in adults is unknown. Methods and findings: Radiographic indices of chest wall shape were analyzed for participants of the first (n = 2687) and second (n = 1780) phases of the population-based Dallas Heart Study and compared to clinical cases of pectus (n = 297). Thoracic computed tomography imaging studies were examined to calculate the Haller index, a measure of thoracic axial shape, and the Correction index, which quantitates the posterior displacement of the sternum relative to the ribs. At the level of the superior xiphoid, 0.5%, 5% and 0.4% of adult Dallas Heart Study subjects have evidence of pectus excavatum using thresholds of Haller index >3.25, Correction index >10%, or both, respectively. Radiographic measures of pectus are more common in females than males and there is a greater prevalence of pectus in women than men. In the general population, the Haller and Correction indices are associated with height and weight, independent of age, gender, and ethnicity. Repeat imaging of a subset of subjects (n = 992) demonstrated decreases in the mean Haller and Correction indices over seven years, suggesting change to a more circular axial thorax, with less sternal depression, over time. Conclusions: To our knowledge, this is the first study estimating the prevalence of pectus in an unselected adult population. Despite the higher reported prevalence of pectus cases in adolescent boys, this study demonstrates a higher prevalence of radiographic indices of pectus in adult females. [ABSTRACT FROM AUTHOR]

BACKGROUND: In the conventional paradigm of the progression of left ventricular hypertrophy, a thick-walled left ventricle (LV) ultimately transitions to a dilated cardiomyopathy. There are scant data in humans demonstrating whether this transition occurs commonly without an interval myocardial infarction. METHODS AND RESULTS: Participants (n=1282) from the Dallas Heart Study underwent serial cardiac magnetic resonance ≈7 years apart. Those with interval cardiovascular events and a dilated LV (increased LV end-diastolic volume [EDV] indexed to body surface area) at baseline were excluded. Multivariable linear regression models tested the association of concentric hypertrophy (increased LV mass and LV mass/volume0.67) with change in LVEDV. The study cohort had a median age of 44 years, 57% women, 43% black, and 11% (n=142) baseline concentric hypertrophy. The change in LVEDV in those with versus without concentric hypertrophy was 1 mL (-9 to 12) versus -2 mL (-11 to 7), respectively, P<0.01. In multivariable linear regression models, concentric hypertrophy was associated with larger follow-up LVEDV (P≤0.01). The progression to a dilated LV was uncommon (2%, n=25). CONCLUSIONS: In the absence of interval myocardial infarction, concentric hypertrophy was associated with a small, but signifcantly greater, increase in LVEDV after 7-year follow-up. However, the degree of LV enlargement was minimal, and few participants developed a dilated LV. These data suggest that if concentric hypertrophy does progress to a dilated cardiomyopathy, such a transition would occur over a much longer timeframe (eg, decades) and may be less common than previously thought. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifer: NCT00344903. [ABSTRACT FROM AUTHOR]

The aim of this study was to assess characteristic impedance (Zc) of the proximal aorta in young and middle-aged individuals with isolated systolic hypertension (ISH). Zc is an index of aortic stiffness relative to aortic size. In the Dallas Heart Study, 2001 untreated participants 18 to 64 years of age (mean age: 42.3 years; 44% black race) were divided into the following groups based on office blood pressure (BP) measurements: (1) optimal BP (systolic BP [SBP] <120 mm Hg and diastolic BP [DBP] <80 mm Hg; n=837); (2) prehypertension (SBP 120-139 mm Hg and DBP 80-89 mm Hg; n=821); (3) ISH (SBP ≥140 mm Hg and DBP <90 mm Hg; n=121); (4) isolated diastolic hypertension (SBP <140 mm Hg and DBP ≥90 mm Hg; n=44); and (5) systolic-diastolic hypertension (SBP ≥140 mm Hg and DBP ≥90 mm Hg; n=178). Zc, aortic arch pulse wave velocity, and minimum ascending aortic size were quantified using cardiovascular magnetic resonance. In multivariable-adjusted linear models, Zc was highest in the ISH group compared with the optimal BP, isolated diastolic hypertension, or systolic-diastolic hypertension groups (103.2±4.0 versus 68.3±2.1, 75.4±6.0, and 88.9±4.8 dyne*seconds/cm5, respectively; all P<0.05). The Zc-ISH association did not differ by race. Aortic pulse wave velocity was highest in the ISH group compared with the optimal BP, isolated diastolic hypertension, or systolic-diastolic hypertension groups (6.3±0.3 versus 4.3±0.1, 4.4±0.4 and 5.5±0.3 m/s, respectively; all P<0.05), whereas aortic size was similar across groups (all P>0.2). Results were similar in a subgroup of 1551 participants 18 to 49 years of age. In a multiracial population-based sample, we found evidence of a mismatch between proximal aortic stiffness and diameter in young and middle-aged adults with ISH. [ABSTRACT FROM AUTHOR]

Objectives This study aims to compare ethnic difference in proximal aortic pulse wave velocity (PWV) and characteristic impedance (Zc). Background Increased aortic stiffness is an independent predictor of target organ damage, incident hypertension, and all-cause mortality. However, previous studies have not directly assessed proximal aortic function in Blacks, the ethnic population with disproportionately high risk for incident hypertension and target organ complications. Methods We evaluated the multiethnic, population-based DHS (Dallas Heart Study) participants (N = 2,544, 54.2% women, 49.7% Black) who underwent cardiac magnetic resonance at 1.5-T. Aortic stiffness and Zc were determined from aortic arch PWV and lumen area measurements. Linear regression was used to evaluate ethnic differences in proximal aortic wall stiffness using aortic arch PWV and Zc as dependent variables with and without adjustment for traditional cardiovascular risk factors. Because cardiac output was significantly higher in Blacks compared to Whites and Hispanics, additional comparisons of PWV and Zc were performed after adjustment for cardiac output and peripheral vascular resistance. Results Compared with Whites, both Blacks and Hispanics had higher levels of aortic arch PWV (4.25, 95% confidence interval [CI]: 4.15 to 4.35 m/s, vs. 4.72, 95% CI: 4.64 to 4.81 m/s, vs. 4.48, 95% CI: 4.33 to 4.63 m/s, respectively, both p < 0.05 vs. White), and Zc (64.9, 95% CI: 63.3 to 66.6 dyne·s/cm 5 , vs. 75.6, 95% CI: 74.0 to 77.2 dyne·s/cm 5 , vs. 70.1, 95% CI: 67.6 to 72.8 dyne·s/cm 5 , respectively, both p < 0.01 vs. White) after adjustment for age, age squared, sex, body mass index, height, mean arterial blood pressure, antihypertensive treatment, heart rate, total cholesterol, diabetes mellitus, and smoking. Compared with Hispanics, Blacks also had higher level of both PWV and Zc (both p < 0.01). Ethnic differences in PWV and Zc persisted after adjustment for cardiac output and peripheral vascular resistance. Conclusions In a multiethnic population-based-sample, Blacks and Hispanics had higher proximal aortic stiffness compared with Whites independent of blood pressure and relevant risk factors. [ABSTRACT FROM AUTHOR]

Introduction:Asthma is associated with an increased risk of mild cognitive impairment and dementia. Depression and oral corticosteroid use are associated with atrophy of the hippocampus and are common in asthma. However, minimal neuroimaging data are available in asthma patients.Methods:We conducted a retrospective analysis of 1,287 adult participants from the Dallas Heart Study, an epidemiological sample of Dallas County residents. Study outcome variables were hippocampal volumes measured by FreeSurfer. ANOVA was used to examine a gender difference in hippocampal volumes. General Linear Models (GLM) were conducted to examine asthma diagnosis association with hippocampal volumes.Results:The prevalence rate of asthma among our study sample was 10.8% with 9.6% in males and 11.7% in females. After controlling for demographic characteristics, participants with asthma had significantly smaller total, right, and left hippocampal volumes than those without asthma. The association of asthma with smaller hippocampal volume was significant among males but not among females.Conclusion:Hippocampal volume in a large and diverse sample of adults was significantly smaller in people with asthma as compared to those without asthma. These findings suggest that asthma may be associated with structural brain differences. Thus, medical illnesses without obvious direct neurodegenerative or even vascular involvement can be associated with brain changes. Because the hippocampus is a brain region involved in memory formation, these findings may have implications for treatment adherence that could have important implications for asthma treatment. Study limitations are the reliance on a self-reported asthma diagnosis and lack of additional asthma clinical information. [ABSTRACT FROM AUTHOR]