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Context: Although authoritative bodies have promulgated guidelines for donation after cardiac death (DCD) and the Joint Commission requires hospitals to address DCD, little is known about actual hospital policies.Objective: To characterize DCD policies in children's hospitals and evaluate variation among policies.Design, Setting, and Participants: Mixed-methods analysis of policies collected between November 2007 and January 2008 from hospitals in the United States, Puerto Rico, and Canada in 2 membership categories of the National Association of Children's Hospitals and Related Institutions.Main Outcome Measures: Status of DCD policy development and content of the policies based on coding categories developed in part from authoritative statements.Results: One hundred five of 124 eligible hospitals responded, a response rate of 85%. Seventy-six institutions (72%; 95% confidence interval [CI], 64%-82%) had DCD policies, 20 (19%; 95% CI, 12%-28%) were developing policies; and 7 (7%; 95% CI, 3%-14%) neither had nor were developing policies. We received and analyzed 73 unique, approved policies. Sixty-one policies (84%; 95% CI, 73%-91%) specify criteria or tests for declaring death. Four policies require total waiting periods prior to organ recovery at variance with professional guidelines: 1 less than 2 minutes and 3 longer than 5 minutes. Sixty-four policies (88%; 95% CI, 78%-94%) preclude transplant personnel from declaring death and 37 (51%; 95% CI, 39%-63%) prohibit them from involvement in premortem management. While 65 policies (89%; 95% CI, 80%-95%) indicate the importance of palliative care, only 5 (7%; 95% CI, 2%-15%) recommend or require palliative care consultation. Of 68 policies that indicate where withdrawal of life-sustaining treatment can or should take place, 37 policies (54%; 95% CI, 42%-67%) require it to occur in the operating room and 3 policies (4%; 95% CI, 1%-12%) require it to occur in the intensive care unit.Conclusions: Most children's hospitals have developed or are developing DCD policies. There is, however, considerable variation among policies. [ABSTRACT FROM AUTHOR]

Linkage of creatinine clearance to chromosome 10 in Utah pedigrees replicates a locus for end-stage renal disease in humans and renal failure in the fawn-hooded rat. Background. Renal failure is an important health concern for persons with hypertension and diabetes. In the fawn-hooded rat, a renal failure locus, Rf-1 , has been identified on rat chromosome 1. A study of African American sibpairs with end-stage renal disease (ESRD) replicated this finding on the orthologous region in humans, chromosome 10, with a maximum logarithm of odds (LOD) score of 3.4. An important question is whether this region can be detected in healthy subjects prior to onset of ESRD by examining creatinine clearance as an indicator of early renal damage. Methods. We analyzed 49 Utah Caucasian pedigrees and performed quantitative nonparametric linkage analysis using 21 markers spanning chromosome 10. Pedigree members (mean age of 40 ± 17) were examined up to three different times over 10 years, with creatinine clearance measured at each exam. For examination 1, three overnight, timed, 12-hour urine samples were obtained and averaged. One 12-hour sample was obtained for examinations 2 and 3. Results. Heritabilities of creatinine clearance were 0.33 (N = 1360), 0.36 (N = 1196), and 0.53 (N = 718) for the three examinations, respectively. The nonparametric LOD score for examination 1 was 1.4 at marker D10S677 (∼117 cM). The LOD score at examination 2, an average of 21 /2 years later, was 1.8 at marker D10S1239 (∼123 cM) and 1.9 at marker D10S1425 (∼137 cM). The LOD score at examination 3, an average of 10 years from baseline, was 2.1 at marker D10S2470 (∼113 cM). Thus, there is consistent evidence of linkage to this region from three different examinations spanning a period of 10 years. Conclusions. These linkage results confirm the ESRD linkage and the rat renal failure linkage to this region even though the LOD score is somewhat... [ABSTRACT FROM AUTHOR]

Background: Primary aldosteronism is a nonsuppressible renin-independent aldosterone production that causes hypertension and cardiovascular disease., Objective: To characterize the prevalence of nonsuppressible renin-independent aldosterone production, as well as biochemically overt primary aldosteronism, in relation to blood pressure., Design: Cross-sectional study., Setting: 4 U.S. academic medical centers., Participants: Participants with normotension ( n  = 289), stage 1 hypertension ( n  = 115), stage 2 hypertension ( n  = 203), and resistant hypertension ( n  = 408)., Measurements: Participants completed an oral sodium suppression test, regardless of aldosterone or renin levels, as a confirmatory diagnostic for primary aldosteronism and to quantify the magnitude of renin-independent aldosterone production. Urinary aldosterone was measured in participants in high sodium balance with suppressed renin activity. Biochemically overt primary aldosteronism was diagnosed when urinary aldosterone levels were higher than 12 μg/24 h., Results: Every blood pressure category had a continuum of renin-independent aldosterone production, where greater severity of production was associated with higher blood pressure, kaliuresis, and lower serum potassium levels. Mean adjusted levels of urinary aldosterone were 6.5 μg/24 h (95% CI, 5.2 to 7.7 μg/24 h) in normotension, 7.3 μg/24 h (CI, 5.6 to 8.9 μg/24 h) in stage 1 hypertension, 9.5 μg/24 h (CI, 8.2 to 10.8 μg/24 h) in stage 2 hypertension, and 14.6 μg/24 h (CI, 12.9 to 16.2 μg/24 h) in resistant hypertension; corresponding adjusted prevalence estimates for biochemically overt primary aldosteronism were 11.3% (CI, 5.9% to 16.8%), 15.7% (CI, 8.6% to 22.9%), 21.6% (CI, 16.1% to 27.0%), and 22.0% (CI, 17.2% to 26.8%). The aldosterone-renin ratio had poor sensitivity and negative predictive value for detecting biochemically overt primary aldosteronism., Limitation: Prevalence estimates rely on arbitrary and conventional thresholds, and the study population may not represent nationwide demographics., Conclusion: The prevalence of primary aldosteronism is high and largely unrecognized. Beyond this categorical definition of primary aldosteronism, there is a prevalent continuum of renin-independent aldosterone production that parallels the severity of hypertension. These findings redefine the primary aldosteronism syndrome and implicate it in the pathogenesis of "essential" hypertension., Primary Funding Source: National Institutes of Health.

Background: The scope of plastic surgery is not well understood by people outside the field. Better educating medical students about plastic surgery may improve understanding of the field, establish appropriate referral patterns early on, and assist with career decision-making. The purpose of this study was to assess medical student understanding of plastic surgery and to analyze the impact of prior plastic surgery clinical exposure on this understanding., Methods: An online survey consisting of 24 clinical scenarios was administered to medical students of the University of Utah. After indicating their level of training and whether they had prior clinical exposure to plastic surgery or other surgical subspecialties, students selected one or more appropriate surgical subspecialties to manage each scenario., Results: Of 408 students, 230 (56.4%) responded to the survey. Prior clinical exposure to plastic surgery was reported by 15.8% to 29.4% of students (first to fourth year). Overall, 92% of students chose at least one acceptable surgical specialty for referral. Plastic surgery was selected by only 54% of students for all conditions, and this did not improve throughout medical school. Senior students (third and fourth years) with prior plastic surgery exposure chose plastic surgery more often than those without prior exposure (71% vs. 51%, P < 0.0001). Plastic surgery was chosen most frequently for rhinoplasty and breast reconstruction and less frequently for hand/peripheral nerve surgery and wound surgery., Conclusions: Improved medical student education about the scope of plastic surgery is needed, especially in the areas of hand/peripheral nerve surgery and general reconstructive surgery.

Background: Postprandial lipemia (PPL) is likely a risk factor for cardiovascular disease but these changes have not been well described and characterized in a large cohort. We assessed acute changes in the size and concentration of total and subclasses of LDL, HDL, and VLDL particles in response to a high-fat meal. Participants (n = 1048) from the Genetics of Lipid-Lowering Drugs and Diet Network (GOLDN) Study who ingested a high-fat meal were included in this analysis. Lipids were measured at 0 hr (fasting), 3.5 hr, and 6 hr after a standardized fat meal. Particle size distributions were determined using nuclear magnetic resonance spectroscopy. Analyses were stratified by baseline triglycerides (normal vs. elevated) and gender. The effect of PPL on changes in lipoprotein subclasses was assessed using repeated measures ANOVA., Results: Postprandially, LDL-C, HDL-C, VLDL-C, and triglycerides increased regardless of baseline triglyceride status, with the largest increases in VLDL-C and TG; however, those with elevated triglycerides demonstrated larger magnitude of response. Total LDL particle number decreased over the 6-hour time interval, mostly from a decrease in the number of small LDL particles. Similarly, total VLDL particle number decreased due to reductions in medium and small VLDL particles. Large VLDL particles and chylomicrons demonstrated the largest increase in concentration. HDL particles demonstrated minimal overall changes in total particle number., Conclusions: We have characterized the changes in LDL and VLDL particle number, and their subclass patterns following a high-fat meal.

Background & Aims: Epidemiologic studies have suggested beneficial effects of flavonoids on cardiovascular disease. Cocoa and particularly dark chocolate are rich in flavonoids and recent studies have demonstrated blood pressure lowering effects of dark chocolate. However, limited data are available on the association of chocolate consumption and the risk of coronary heart disease (CHD). We sought to examine the association between chocolate consumption and prevalent CHD., Methods: We studied in a cross-sectional design 4970 participants aged 25-93 years who participated in the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study. Chocolate intake was assessed through a semi-quantitative food frequency questionnaire. We used generalized estimating equations to estimate adjusted odds ratios., Results: Compared to subjects who did not report any chocolate intake, odds ratios (95% CI) for CHD were 1.01 (0.76-1.37), 0.74 (0.56-0.98), and 0.43 (0.28-0.67) for subjects consuming 1-3 times/month, 1-4 times/week, and 5+ times/week, respectively (p for trend <0.0001) adjusting for age, sex, family CHD risk group, energy intake, education, non-chocolate candy intake, linolenic acid intake, smoking, alcohol intake, exercise, and fruit and vegetables. Consumption of non-chocolate candy was associated with a 49% higher prevalence of CHD comparing 5+/week vs. 0/week [OR = 1.49 (0.96-2.32)]., Conclusions: These data suggest that consumption of chocolate is inversely related with prevalent CHD in a general United States population., (Published by Elsevier Ltd.)

Background & Aims: While a diet rich in anti-oxidant has been favorably associated with coronary disease and hypertension, limited data have evaluated the influence of such diet on subclinical disease. Thus, we sought to examine whether chocolate consumption is associated with calcified atherosclerotic plaque in the coronary arteries (CAC)., Methods: In a cross-sectional design, we studied 2217 participants of the NHLBI Family Heart Study. Chocolate consumption was assessed by a semi-quantitative food frequency questionnaire and CAC was measured by cardiac CT. We defined prevalent CAC using an Agatston score of at least 100 and fitted generalized estimating equations to calculate prevalence odds ratios of CAC., Results: There was an inverse association between frequency of chocolate consumption and prevalent CAC. Odds ratios (95% CI) for CAC were 1.0 (reference), 0.94 (0.66-1.35), 0.78 (0.53-1.13), and 0.68 (0.48-0.97) for chocolate consumption of 0, 1-3 times per month, once per week, and 2+ times per week, respectively (p for trend 0.022), adjusting for age, sex, energy intake, waist-hip ratio, education, smoking, alcohol consumption, ratio of total-to-HDL-cholesterol, non-chocolate candy, and diabetes mellitus. Controlling for additional confounders did not alter the findings. Exclusion of subjects with coronary heart disease or diabetes mellitus did not materially change the odds ratio estimates but did modestly decrease the overall significance (p = 0.07)., Conclusions: These data suggest that chocolate consumption might be inversely associated with prevalent CAC., (Published by Elsevier Ltd.)

Studies have reported a lower burden of calcified atherosclerotic plaque in coronary arteries in African-Americans than in whites. Findings from autopsy studies of sudden cardiac death have suggested a link between left ventricular hypertrophy and severity of coronary atherosclerosis. Echocardiograms and cardiac computed tomograms were analyzed in 334 African-American (84% hypertensive) and 196 white (66% hypertensive) adults with no history of coronary heart disease or revascularization procedures at study entry. The relation of coronary artery calcium (CAC) score to left ventricular mass and left ventricular mass indexed to body surface area was assessed by Spearman's correlations and mixed linear models. Covariates included age, gender, field center, weight, height, systolic blood pressure, number of antihypertensive medications, diabetes, total and high-density lipoprotein cholesterol levels, and current smoking and alcohol consumption. In African-Americans, a significant and independent association between CAC score and left ventricular mass or left ventricular mass indexed to body surface area was present with the 2 analytic strategies. Spearman's correlation coefficients for CAC score with left ventricular mass and left ventricular mass indexed to body surface area were 0.14 (p = 0.015) and 0.13 (p = 0.025), respectively, after multivariable adjustment. In whites, the associations of CAC score with measurements of left ventricular mass were weaker and only marginally significant in mixed linear models. In conclusion, these findings suggest that CAC reflects a different risk burden between African-Americans and whites, and future studies examining the prognostic implications of CAC in African-Americans should consider the potential association between CAC and left ventricular hypertrophy.

The metabolic syndrome is a clustering of low levels of high-density lipoprotein cholesterol, hyperglycemia, high waist circumference, hypertension, and elevated triglycerides, and is associated with cardiovascular disease. Calcified atherosclerotic plaque in the coronary arteries (CAC), measured by cardiac tomographic scans, is a marker for atherosclerosis and relates to mortality. The investigators examined the relation of the metabolic syndrome, and each of its components, to the prevalence of CAC, measured from 2002 to 2004 in 3,166 white and African-American subjects in the National Heart, Lung, & Blood Institute Family Heart Study. Adjusting for age, race, center, smoking, and alcohol consumption, odds ratios and 95% confidence intervals (CI) for a CAC score >100 for subjects with metabolic syndrome were 1.7 (95% CI 1.3 to 2.3) for men and 1.6 (95% CI 1.2 to 2.1) for women. Associations were found for most of the components of the metabolic syndrome with CAC. Associations with the metabolic syndrome were similar for calcified atherosclerotic plaque in the abdominal aorta among 3,173 subjects, with adjusted odds ratios for a score >1,000 of 2.1 (95% CI 1.5 to 3.1) for men and 1.8 (95% CI 1.4 to 2.4) for women. We conclude that the metabolic syndrome and most of its components are associated with a higher prevalence of calcified atherosclerotic plaque in the coronary arteries and abdominal aorta in white and African-American men and women.

The degree to which ethnic differences in left ventricular structure among hypertensive adults are independent of clinical and hemodynamic factors remains uncertain. We assessed whether left ventricular mass and geometry differ between black and white hypertensives after accounting for differences in such factors. Our study group comprised 1060 black and 580 white hypertensive participants free of valvular or coronary disease in a population-based cohort. Blood pressure was measured during a clinic visit and echocardiography was performed using standardized protocols. After controlling for clinical and hemodynamic parameters (cardiac index, peripheral resistance index, and pulse pressure/stroke index), both left ventricular mass and relative wall thickness were higher in blacks than whites (173.9+/-30.9 versus 168.3+/-24.3 grams, P=0.006, and 0.355+/-0.055 versus 0.340+/-0.055 grams, P<0.001). Similarly, the adjusted risk of having left ventricular hypertrophy, whether indexed by height(2.7) or by body surface area, was greater for blacks than for whites (odds ratio: 1.80; 95% CI: 1.29 to 2.51; and odds ratio: 2.50; 95% CI: 1.58 to 3.96, respectively), and this was also true for concentric geometry (odds ratio: 2.28; 95% CI: 1.22 to 4.25). Further adjustment for relatedness in this genetic epidemiological study did not attenuate these differences. Our findings confirm the strong association between black ethnicity and increased left ventricular mass and relative wall thickness in hypertensive adults and demonstrate that these differences are independent of standard clinical and hemodynamic parameters. Whether such differences relate to distinct ambulatory pressure profiles or an ethnic propensity to cardiac hypertrophy requires further investigation.

Objective: The contribution of salt intake to the pathogenesis of hypertension holds longstanding interest. Recent studies employed the sensitivity of blood pressure (BP) to salt intake as an intermediate phenotype. The validity of this approach relative to the homogeneity of sodium-sensitive hypertension was investigated while simultaneously controlling multiple putative factors., Methods: Blood pressure responses to shifts in salt intake were measured in 274 individuals with essential hypertension in steady-state sodium balance on high (200 mEq) and low (10 mEq) sodium intakes. Univariate and multivariate analyses predicted systolic and diastolic sodium sensitivity based on interactions among demographic factors (age, gender, race, body mass index) and hypertensive type [low-renin (LR), modulator (M), non-modulator (NM)]., Results: The influence of hypertension type on systolic salt sensitivity (SSS) depended on gender (P = 0.03). In females, highest SSS was in LR (21, 14, 13 mmHg for LR, M, NM, P = 0.02), while in males highest SSS was in NM (11, 10, 16 mmHg for LR, M, NM, P = 0.07). Age predicted SSS without interacting with other factors, producing a 2.4 mmHg increase per decade (P = 0.02). Hypertension type affected diastolic salt sensitivity (DSS) (P = 0.002) without interacting with other factors. M had less DSS (6 mmHg) than LR (9 mmHg) and NM (11 mmHg) (P < 0.01)., Conclusions: For subjects in sodium balance, the distributions of SSS and DSS were unimodal and the mechanisms mediating SSS and DSS were different. Controlling for multiple demographic factors, at least two hypertensive types have largest BP responses to sodium intake, reducing the usefulness of blood pressure sensitivity to salt intake as an intermediate phenotype.

Although several studies indicate that there are gender differences in left ventricular (LV) systolic function, it remains unclear whether similar differences exist with regard to diastolic function. Accordingly, Doppler echocardiograms were analyzed in 515 male and 839 female, mostly treated (95%) hypertensive participants enrolled in the Hypertension Genetic Epidemiology Network (HyperGEN) study with no evidence of abnormal wall motion or significant valvular heart disease. There was no difference in age between genders, but after adjusting for age and race, men had lower body mass indexes (29.8 +/- 5.2 vs 32.3 +/- 7.6 kg/m(2)) and heart rates (67 +/- 12 vs 69 +/- 11 beats/min) and higher systolic and diastolic blood pressures (BP) than women (134 +/- 20 vs 130 +/- 21 and 80 +/- 11 vs 72 +/- 11 mm Hg, all p <0.001). LV mass/height(2.7) was slightly greater in women than in men (43 +/- 10 vs 42 +/- 9 g/m(2.7), p <0.05). After adjusting for age, race, systolic BP, body mass index, heart rate, and LV hypertrophy, both mitral E-wave (70 +/- 18 vs 77 +/- 19) and A-wave (74 +/- 15 vs 79 +/- 17, both p <0.001) velocities were lower in men than in women, but the mitral E/A ratio and atrial filling fraction were nearly identical in both genders. Deceleration time (221 +/- 55 vs 214 +/- 46 cm/s, p = 0.018) and isovolumic relaxation time (IVRT) were longer in men than in women (85 +/- 18 vs 81 +/- 17 cm/s, p <0.001). Prolonged IVRT was present in more men than women (14% vs 7%, p <0.05). In analyses of covariance, adjusting for age, race, systolic BP, body mass index, heart rate, and medications, male gender remained related to prolonged deceleration time and IVRT. Thus, in this population-based sample of hypertensive adults, men had evidence of slower early diastolic LV filling than women. This gender difference in diastolic function may provide insight into gender differences in congestive heart failure and other specific cardiovascular diseases.