Increased interstage morbidity and mortality following stage 1 palliation in patients with genetic abnormalities.

BACKGROUND: Hypoplastic left heart syndrome and single ventricle variants with aortic hypoplasia are commonly classified as severe forms of CHD. We hypothesised patients with these severe defects and reported genetic abnormalities have increased morbidity and mortality during the interstage period. METHODS AND RESULTS: This was a retrospective review of the National Pediatric Cardiology Quality Improvement Collaborative Phase I registry. Three patient groups were identified: major syndromes, other genetic abnormalities, and no reported genetic abnormality. Tukey post hoc test was applied for pairwise group comparisons of length of stay, death, and combined outcome of death, not a candidate for stage 2 palliation, and heart transplant. Participating centres received a survey to establish genetic testing and reporting practices. Of the 2182 patients, 110 (5%) had major genetic syndromes, 126 (6%) had other genetic abnormalities, and 1946 (89%) had no genetic abnormality. Those with major genetic syndromes weighed less at birth and stage 1 palliation. Patients with no reported genetic abnormalities reached full oral feeds sooner and discharged earlier. The combined outcome of death, not a candidate for stage 2 palliation, and heart transplant was more common in those with major syndromes. Survey response was low (n = 23, 38%) with only 14 (61%) routinely performing and reporting genetic testing. CONCLUSIONS: Patients with genetic abnormalities experienced greater morbidity and mortality during the interstage period than those with no reported genetic abnormalities. Genetic testing and reporting practices vary significantly between participating centres.

Impact of Shared Plans of Care on Healthcare Utilization by Children with Special Healthcare Needs and Mental Health Diagnoses.

OBJECTIVES: We assessed how shared plans of care (SPoC), a care coordination tool, impact healthcare utilization of a cohort of children with special healthcare needs (CSHCN) and mental health conditions. METHODS: Data, including emergency department (ED) visits, hospitalizations, and primary care visits, were collected through chart review of CSHCN. A Poisson generalized linear mixed model was used to analyze healthcare utilization data for CSHCN. RESULTS: Our results showed a decrease in primary care visits, hospitalizations, and ED visits for CSHCN after SPoC implementation, though only primary care visits reached significance. Mental health care visits were specifically found to decrease by 39% following employment of SPoC. CONCLUSIONS FOR PRACTICE: The use of SPoCs in CSHCN had a positive impact on healthcare utilization suggesting widespread use of this tool improved care coordination in this population.

CaMKII determines mitochondrial stress responses in heart.

Myocardial cell death is initiated by excessive mitochondrial Ca(2+) entry causing Ca(2+) overload, mitochondrial permeability transition pore (mPTP) opening and dissipation of the mitochondrial inner membrane potential (ΔΨm). However, the signalling pathways that control mitochondrial Ca(2+) entry through the inner membrane mitochondrial Ca(2+) uniporter (MCU) are not known. The multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is activated in ischaemia reperfusion, myocardial infarction and neurohumoral injury, common causes of myocardial death and heart failure; these findings suggest that CaMKII could couple disease stress to mitochondrial injury. Here we show that CaMKII promotes mPTP opening and myocardial death by increasing MCU current (I(MCU)). Mitochondrial-targeted CaMKII inhibitory protein or cyclosporin A, an mPTP antagonist with clinical efficacy in ischaemia reperfusion injury, equivalently prevent mPTP opening, ΔΨm deterioration and diminish mitochondrial disruption and programmed cell death in response to ischaemia reperfusion injury. Mice with myocardial and mitochondrial-targeted CaMKII inhibition have reduced I(MCU) and are resistant to ischaemia reperfusion injury, myocardial infarction and neurohumoral injury, suggesting that pathological actions of CaMKII are substantially mediated by increasing I(MCU). Our findings identify CaMKII activity as a central mechanism for mitochondrial Ca(2+) entry in myocardial cell death, and indicate that mitochondrial-targeted CaMKII inhibition could prevent or reduce myocardial death and heart failure in response to common experimental forms of pathophysiological stress.

ANG II modulation of cardiac growth and remodeling in immature fetal sheep.

ANG II increases fetal blood pressure and stimulates fetal heart growth; however, little is known regarding its direct effects on cardiomyocytes in vivo. We sought to determine whether ANG II stimulates heart growth and cardiomyocyte hypertrophy and/or hyperplasia in utero in the immature fetal heart independent of the effects on cardiac afterload. In twin gestation, fetal sheep at ∼100 days gestation (term 145 days), one fetus received a chronic (6 days) infusion of ANG II alone (50 µg·kg(-1)·min(-1)) or ANG II plus nitroprusside (NTP) to attenuate the increase in blood pressure; noninstrumented twins served as controls. ANG II alone, but not ANG II + NTP resulted in a significant increase in heart mass (left and right ventricle + septum, corrected for body weight) compared with controls. ANG II, but not ANG II+NTP, also significantly increased cardiomyocyte area compared with control and increased the percentage of binucleated myocytes. ANG II with or without concomitant infusion of NTP increased cardiac PCNA expression, a marker of proliferation. Steady-state protein expression of terminal mitogen-activated protein kinases, cyclin B1, cyclin E1, and p21 were similar among groups. We conclude that in vivo, ANG II increases fetal cardiac mass via cardiomyocyte hypertrophy, differentiation, and to a lesser extent hyperplasia. The effects of ANG II on hypertrophy appear dependent upon the increase in blood pressure (mechanical load), whereas effects on proliferation are load-independent.

Evaluating visual perception for assessing reconstructed flap health.

BACKGROUND: Detecting failing tissue flaps before they are clinically apparent has the potential to improve postoperative flap management and salvage rates. This study demonstrates a model to quantitatively compare clinical appearance, as recorded via digital camera, with spatial frequency domain imaging (SFDI), a noninvasive imaging technique using patterned illumination to generate images of total hemoglobin and tissue oxygen saturation (stO2). METHODS: Using a swine pedicle model in which blood flow was carefully controlled with occlusion cuffs and monitored with ultrasound probes, throughput was reduced by 25%, 50%, 75%, and 100% of baseline values in either the artery or the vein of each of the flaps. The color changes recorded by a digital camera were quantified to predict which occlusion levels were visible to the human eye. SFDI was also used to quantify the changes in physiological parameters including total hemoglobin and oxygen saturation associated with each occlusion. RESULTS: There were no statistically significant changes in color above the noticeable perception levels associated with human vision during any of the occlusion levels. However, there were statistically significant changes in total hemoglobin and stO2 levels detected at the 50%, 75%, and 100% occlusion levels for arterial and venous occlusions. CONCLUSIONS: As demonstrated by the color imaging data, visual flap changes are difficult to detect until significant occlusion has occurred. SFDI is capable of detecting changes in total hemoglobin and stO2 as a result of partial occlusions before they are perceivable, thereby potentially improving response times and salvage rates.

Angiotensin II-induced cardiovascular load regulates cardiac remodeling and related gene expression in late-gestation fetal sheep.

BACKGROUND: Angiotensin II (ANG II) stimulates fetal heart growth, although little is known regarding changes in cardiomyocyte endowment or the molecular pathways mediating the response. We measured cardiomyocyte proliferation and morphology in ANG II-treated fetal sheep and assessed transcriptional pathway responses in ANG II and losartan (an ANG II type 1 receptor antagonist) treated fetuses. METHODS: In twin-gestation pregnant sheep, one fetus received ANG II (50 µg/kg/min i.v.) or losartan (20 mg/kg/d i.v.) for 7 d; noninstrumented twins served as controls. RESULTS: ANG II produced increases in heart mass, cardiomyocyte area (left ventricle (LV) and right ventricle mononucleated and LV binucleated cells), and the percentage of Ki-67-positive mononucleated cells in the LV (all P < 0.05). ANG II and losartan produced generally opposing changes in gene expression, affecting an estimated 55% of the represented transcriptome. The most prominent significantly affected biological pathways included those involved in cytoskeletal remodeling and cell cycle activity. CONCLUSION: ANG II produces an increase in fetal cardiac mass via cardiomyocyte hypertrophy and likely hyperplasia, involving transcriptional responses in cytoskeletal remodeling and cell cycle pathways.

Enhanced cryoprecipitate for skin graft and donor site wound healing in pigs.

Due to similarities in skin characteristics, the authors hypothesise that a pig model would most accurately show the ability of autologous, enhanced cryoprecipitate (eCryo) to improve the wound healing of split-thickness skin grafts (STSGs) and corresponding donor sites. Fifty-two STSGs (5 × 5 cm) were fashioned and treated according to a randomised protocol with an autologous eCryo-treated and a control group. Macroscopic assessment, histological evaluation and cellular composition were completed at days 7, 14, 21 and 28. Thirty-two donor sites were also created and assessed in a similar manner. Histologic analysis showed enhancement of healing over all time points for eCryo-treated donor sites. All other results showed no statistically significant improvement with the use of eCryo. Autologous cryoprecipitate appears to be a safe, inexpensive and easy-to-use alternative to fibrin glue, which carries risks and is, in many cases, prohibitively expensive. Further studies are necessary to evaluate the full potential of eCryo. Interestingly, eCryo application may improve donor site aesthetic appearance. We believe that a pig model most reliably simulates eCryo's behaviour in humans to accurately reflect its future clinical applicability.

Thyroid hormone is required for growth adaptation to pressure load in the ovine fetal heart.

Thyroid hormone exerts broad effects on the adult heart, but little is known regarding the role of thyroid hormone in the regulation of cardiac growth early in development and in response to pathophysiological conditions. To address this issue, we determined the effects of fetal thyroidectomy on cardiac growth and growth-related gene expression in control and pulmonary-artery-banded fetal sheep. Fetal thyroidectomy (THX) and/or placement of a restrictive pulmonary artery band (PAB) were performed at 126 ± 1 days of gestation (term, 145 days). Four groups of animals [n = 5-6 in each group; (i) control; (ii) fetal THX; (iii) fetal PAB; and (iv) fetal PAB + THX] were monitored for 1 week prior to being killed. Fetal heart rate was significantly lower in the two THX groups compared with the non-THX groups, while mean arterial blood pressure was similar among groups. Combined left and right ventricle free wall + septum weight, expressed per kilogram of fetal weight, was significantly increased in PAB (6.27 ± 0.85 g kg(-1)) compared with control animals (4.72 ± 0.12 g kg(-1)). Thyroidectomy significantly attenuated the increase in cardiac mass associated with PAB (4.94 ± 0.13 g kg(-1)), while THX alone had no detectable effect on heart mass (4.95 ± 0.27 g kg(-1)). The percentage of binucleated cardiomyocytes was significantly decreased in THX and PAB +THX groups (∼16%) compared with the non-THX groups (∼27%). No differences in levels of activated Akt, extracellular signal-regulated kinase or c-Jun N-terminal kinase were detected among the groups. Markers of cellular proliferation but not apoptosis or expression of growth-related genes were lower in the THX and THX+ PAB groups relative to thyroid-intact animals. These findings suggest that in the late-gestation fetal heart, thyroid hormone has important cellular growth functions in both physiological and pathophysiological states. Specifically, thyroid hormone is required for adaptive fetal cardiac growth in response to pressure overload.

Novel percutaneous transcatheter intervention for refractory active endocarditis as a bridge to surgery-angiovac aspiration system.

Guidelines for the treatment of active right-sided endocarditis are not well defined. We report the first novel use of an aspiration catheter system for transcatheter therapy of refractory active right sided endocarditis on a bioprosthetic valve in a high-risk surgical patient as a bridge to surgical intervention.

Influenza vaccination during pregnancy and risk of selected major structural congenital heart defects, National Birth Defects Prevention Study 2006-2011.

BACKGROUND: Although results from studies of first-trimester influenza vaccination and congenital heart defects (CHDs) have been reassuring, data are limited for specific CHDs. METHODS: We assessed associations between reported maternal influenza vaccination, 1 month before pregnancy (B1) through end of third pregnancy month (P3), and specific CHDs using data from a multisite, population-based case-control study. Analysis included 2,982 case children diagnosed with a simple CHD (no other cardiac involvement with or without extracardiac defects) and 4,937 control children without a birth defect with estimated delivery dates during 2006-2011. For defects with ≥5 exposed case children, we used logistic regression to estimate propensity score-adjusted odds ratios (aORs) and 95% confidence intervals (CIs), adjusting for estimated delivery year and season; plurality; and maternal age at delivery, race/ethnicity, low folate intake, and smoking and alcohol use during B1P3. RESULTS: Overall, 124 (4.2%) simple CHD case mothers and 197 (4.0%) control mothers reported influenza vaccination from 1 month before through the third pregnancy month. The aOR for any simple CHD was 0.97 (95% CI: 0.76-1.23). Adjusted ORs for specific simple CHDs ranged from 0.62 for hypoplastic left heart syndrome to 2.34 for total anomalous pulmonary venous return (TAPVR). All adjusted CIs included the null except for TAPVR. CONCLUSIONS: Although we cannot fully exclude that exposure misclassification may have masked risks for some CHDs, findings add to existing evidence supporting the safety of inactivated influenza vaccination during pregnancy. The TAPVR result may be due to chance, but it may help inform future studies.

Prepregnancy exposure to dietary arsenic and congenital heart defects.

INTRODUCTION: Arsenic crosses the placenta and accumulates in fetal tissues. In the United States, diet is the predominant route of arsenic exposure, but epidemiologic data are sparse regarding this exposure and development of birth defects. Using data from a large case-control study, we explored associations between maternal dietary arsenic exposure and congenital heart defects (CHDs), the most prevalent birth defects. METHODS: We used maternal self-reported dietary assessments and arsenic concentration estimates in food items to estimate average daily exposure to dietary arsenic during the year before pregnancy for mothers of 10,446 unaffected control children and 6,483 case children diagnosed with CHDs. Using tertiles of dietary exposure to total arsenic (all species) and inorganic arsenic, we applied logistic regression analysis to estimate associations for middle and high tertiles, compared with the low tertile. RESULTS: Positive associations (odds ratio [OR] ≥ 1.2) for total arsenic were observed in both tertiles for perimembranous ventricular septal defect (VSD) and high tertile only for double outlet right ventricle-transposition of the great arteries (DORV-TGA), partial anomalous pulmonary venous return (PAPVR), and tricuspid atresia. Positive associations were also observed in both tertiles (tricuspid atresia) and high tertile only (DORV-TGA, conoventricular VSD, PAPVR, and pulmonary atresia) for inorganic arsenic. Most remaining associations were near or below unity. DISCUSSION: Exploration of maternal dietary exposure to total and inorganic arsenic and CHDs produced few positive associations but was limited by available food item concentrations. Future research requires expanded collection of dietary data, improved estimates of concentrations, and consideration of nondietary sources of arsenic exposure.

Sex-specific programming of hypertension in offspring of late-gestation diabetic rats.

BACKGROUND: The intrauterine environment strongly influences adult disease susceptibility. We used a rat model of third-trimester maternal diabetes to test the hypothesis that adult offspring exposed to hyperglycemia in utero display increased blood pressure and alterations in vascular responsiveness. METHODS: Diabetes was induced by streptozotocin injection to pregnant rats on gestation day 13 (term 21 d) and partially controlled with insulin injections. Hemodynamic function was evaluated in 6-12-mo-old offspring. RESULTS: Male but not female offspring of diabetic mothers (ODM) had significantly increased blood pressure as compared with controls; heart rate (HR) was similar. For both sexes, HR baroreflex responses were similar as were in vivo hemodynamic responses to angiotensin II, nitric oxide synthase inhibition, and ganglionic blockade. Aortic contractility to angiotensin II was similar in the two groups. Nitric oxide synthase inhibition and the Cu/Zn superoxide dismutase inhibitor diethyldithiocarbamate, but not the superoxide dismutase-mimetic Tempol, significantly increased contractile responses to angiotensin II in controls but not ODM. Reduced nicotinamide adenine dinucleotide phosphate-stimulated superoxide production was greater in male ODM than in controls (P < 0.05). CONCLUSION: Exposure to hyperglycemia in utero results in sex-specific cardiovascular changes in adult offspring. Impaired nitric oxide-reactive oxygen species signaling may play a significant role in the hemodynamic phenotype of ODM.

Essential roles of an intercalated disc protein, mXinbeta, in postnatal heart growth and survival.

RATIONALE: The Xin repeat-containing proteins mXinalpha and mXinbeta localize to the intercalated disc of mouse heart and are implicated in cardiac development and function. The mXinalpha directly interacts with beta-catenin, p120-catenin, and actin filaments. Ablation of mXinalpha results in adult late-onset cardiomyopathy with conduction defects. An upregulation of the mXinbeta in mXinalpha-deficient hearts suggests a partial compensation. OBJECTIVE: The essential roles of mXinbeta in cardiac development and intercalated disc maturation were investigated. METHODS AND RESULTS: Ablation of mXinbeta led to abnormal heart shape, ventricular septal defects, severe growth retardation, and postnatal lethality with no upregulation of the mXinalpha. Postnatal upregulation of mXinbeta in wild-type hearts, as well as altered apoptosis and proliferation in mXinbeta-null hearts, suggests that mXinbeta is required for postnatal heart remodeling. The mXinbeta-null hearts exhibited a misorganized myocardium as detected by histological and electron microscopic studies and an impaired diastolic function, as suggested by echocardiography and a delay in switching off the slow skeletal troponin I. Loss of mXinbeta resulted in the failure of forming mature intercalated discs and the mislocalization of mXinalpha and N-cadherin. The mXinbeta-null hearts showed upregulation of active Stat3 (signal transducer and activator of transcription 3) and downregulation of the activities of Rac1, insulin-like growth factor 1 receptor, protein kinase B, and extracellular signal-regulated kinases 1 and 2. CONCLUSIONS: These findings identify not only an essential role of mXinbeta in the intercalated disc maturation but also mechanisms of mXinbeta modulating N-cadherin-mediated adhesion signaling and its crosstalk signaling for postnatal heart growth and animal survival.

Immunological demyelination enhances nerve regeneration after acute transection injury in the adult rat sciatic nerve.

INTRODUCTION: Our recent experiments demonstrate that demyelination enhances peripheral nerve regeneration after contusion injury in the adult rat sciatic nerve. The role of demyelination in peripheral nerve regeneration in a sciatic nerve transection model has yet to be elucidated. We hypothesize that (1) axon regeneration within a region of injury increases after experimental, immunologic demyelination, and (2) regenerated axons are partially derived from the proximal motor axons. METHODS: Sciatic nerves of adult female Sprague-Dawley rats (n = 20) were injected with a demyelinating agent immediately after transection injury. The sciatic nerves were harvested 1 month (n = 5) and 2 months (n = 5) after surgery. In the control groups, the cut nerves were reapproximated without demyelination therapy. The lesion containing length of nerve was cut into 1-mm transverse blocks and processed to preserve orientation. Specimens were evaluated using structural and immunohistochemical analyses. RESULTS: A single epineural injection of complement proteins plus antibodies to galactocerebroside resulted in demyelination followed by Schwann cell remyelination. At 1 month, remyelination was clearly shown throughout the injured sciatic nerve segment. At 2 months, there was a statistically significant increase in peripheral nerve regeneration following demyelination therapy as evidenced by total axon count, axon density, and fiber diameter. CONCLUSION: This study demonstrates enhanced histomorphologic nerve regeneration in the rat sciatic nerve after local delivery of experimental, immunologic demyelination following transection injury. It highlights the utility of demyelination in peripheral nerve regeneration. This therapy may be applicable for tissue-engineered constructs, cell-based systems, and nerve transfers to improve outcomes in peripheral nervous system injuries.

Maternal antioxidant blocks programmed cardiovascular and behavioural stress responses in adult mice.

Intra-uterine growth restriction is an independent risk factor for adult psychiatric and cardiovascular diseases. In humans, intra-uterine growth restriction is associated with increased placental and fetal oxidative stress, as well as down-regulation of placental 11ß-HSD (11ß-hydroxysteroid dehydrogenase). Decreased placental 11ß-HSD activity increases fetal exposure to maternal glucocorticoids, further increasing fetal oxidative stress. To explore the developmental origins of co-morbid hypertension and anxiety disorders, we increased fetal glucocorticoid exposure by administering the 11ß-HSD inhibitor CBX (carbenoxolone; 12 mg·kg-1 of body weight·day-1) during the final week of murine gestation. We hypothesized that maternal antioxidant (tempol throughout pregnancy) would block glucocorticoid-programmed anxiety, vascular dysfunction and hypertension. Anxiety-related behaviour (conditioned fear) and the haemodynamic response to stress were measured in adult mice. Maternal CBX administration significantly increased conditioned fear responses of adult females. Among the offspring of CBX-injected dams, maternal tempol markedly attenuated the behavioural and cardiovascular responses to psychological stress. Compared with offspring of undisturbed dams, male offspring of dams that received daily third trimester saline injections had increased stress-evoked pressure responses that were blocked by maternal tempol. In contrast, tempol did not block CBX-induced aortic dysfunction in female mice (measured by myography and lucigenin-enhanced chemiluminescence). We conclude that maternal stress and exaggerated fetal glucocorticoid exposure enhance sex-specific stress responses, as well as alterations in aortic reactivity. Because concurrent tempol attenuated conditioned fear and stress reactivity even among the offspring of saline-injected dams, we speculate that antenatal stressors programme offspring stress reactivity in a cycle that may be broken by antenatal antioxidant therapy.

Transfusion effects on cardiomyocyte growth and proliferation in fetal sheep after chronic anemia.

Chronic fetal anemia results in significant cardiac remodeling. The capacity to reverse these effects is unknown. We examined the effects of transfusion on cardiomyocyte adaptations after chronic anemia in fetal sheep subjected to daily hemorrhage beginning at 109-d GA (term ∼145 d). After 10 d of anemia, one group was killed for comparison with age-matched controls. A separate group of anemic fetuses was transfused with red blood cells at 119-d GA for comparison with controls at 129-d GA. Anemia significantly increased the heart-to-body weight ratio, an effect partially ameliorated after transfusion. Cardiomyocyte dimensions were similar among all groups, suggesting an absence of hypertrophy. The percentages of mono- and binucleated cardiomyocytes were similar between groups at 119-d GA, although the percentage of binucleated cells was significantly less in transfused fetuses compared with controls at 129-d GA. Protein levels of mitogen-activated protein kinases and protein kinase B were similar between controls and their respective intervention groups, except for a significant increase in phosphorylated c-Jun N-terminal kinase 1/2 in transfused fetuses. Thus, cardiomyocyte proliferation but not hypertrophy contributes to cardiac enlargement during fetal anemia. Transfusion results in slowing but not cessation of cardiac growth after anemia.

The effect of adrenalectomy on the cardiac response to subacute fetal anemia.

The mechanisms that stimulate fetal heart growth during anemia are unknown. To examine the hypothesis that adrenal hormones contribute to this process, we determined the effects of adrenalectomy (Adx) on heart growth and the activation of cardiac mitogen-activated protein kinases (MAPKs) in the presence and absence of fetal anemia. To identify mechanisms contributing to the initiation of cardiac growth, the duration of anemia was limited to a period shorter than that previously described to result in increased cardiac mass. Four groups of fetal sheep were studied (Adx-Anemic, Adx-Control, Intact-Anemic, Intact-Control). Anemia was created by daily controlled hemorrhage for 5 days; hearts were collected for analysis at 133 d gestation (term 145 d). Cardiomyocyte morphometry, immunohistochemistry for Ki-67 (proliferation marker), and Western blotting for protein levels of MAPKs and proliferating cell nuclear antigen (PCNA) were performed. Blood pressure, heart rate, heart weight-to-body weight ratio, and cardiomyocyte length and width remained similar among groups throughout the study. PCNA levels in the Adx-Anemic group were twice as high as in any other group (both ventricles, p < 0.05). Levels of phosphorylated extracellular signal-regulated kinase (ERK) were ~60% higher in the Intact-Anemic and Adx-Anemic groups, compared with the Intact-Control and Adx-Control groups (p < 0.02). These results suggest that adrenal hormones may attenuate fetal cardiomyocyte proliferation in response to anemia (as evidenced by the increased PCNA in Adx-Anemic fetuses) and that phosphorylation of myocardial ERK results from fetal anemia, irrespective of the status of the fetal adrenal gland.

What patients look for when choosing a plastic surgeon: an assessment of patient preference by conjoint analysis.

The knowledge of patient preference is crucial for plastic surgeons to determine optimal marketing strategies. Conjoint analysis is a statistical technique whereby research participants make a series of trade-offs. Analysis of these trade-offs reveals the relative importance of component attributes. This study will evaluate the relative importance of attributes that influence the selection and decision-making process when choosing a plastic surgeon. A questionnaire consisting of 18 plastic surgeon profiles was rated by 111 patients. Attributes analyzed were as follows: travel distance, number of years in practice, board certification status, method of referral, office décor, and procedure cost. A traditional full-profile conjoint analysis was performed. Subjects consisted of 10 men and 101 women (n = 111). Median age was 51 years (range, 19-72). The "mean importance" of the attributes are as follows: board certification status, 39.7%; method of referral, 23.5%; distance from home to office, 13.2%; office décor, 9.0%; number of years in practice, 7.5%; and cost of procedure, 7.2%. Internal validity checks showed a high correlation (Pearson ρ = 0.995; P < 0.001). This pilot study demonstrates that conjoint analysis is a very powerful tool for market research in the health care system. The level of importance for each attribute reliably helps plastic surgeons to understand the preferences of their patients, thus being able to improve marketing strategies for private practices and institutions. The present study indicates that the most important attributes were board certification and method of referral.

Quantitative assessment of the entire thoracic aorta from magnetic resonance images.

OBJECTIVES: Although magnetic resonance imaging is a primary modality for following patients with connective tissue diseases, only a limited amount of the image data is utilised. The purpose of this study was to show the clinical applicability of an automated four-dimensional analysis method of magnetic resonance images of the aorta and develop normative data for the cross-sectional area of the entire thoracic aorta. STUDY DESIGN: Magnetic resonance imaging was obtained serially over 3 years from 32 healthy individuals and 24 patients with aortopathy and a personal or family history of connective tissue disorder. Graph theory-based segmentation was used to determine the cross-sectional area for the thoracic aorta. Healthy individual data were used to construct a nomogram representing the maximum cross-sectional area 5th-95th percentile along the entire thoracic aorta. Aortic root diameters calculated from the cross-sectional area were compared to measured diameters from echocardiographic data. The cross-sectional area of the entire thoracic aorta in patients was compared to healthy individuals. RESULTS: Calculated aortic root diameters correlated with measured diameters from echo data - correlation coefficient was 0.74-0.87. The cross-sectional area in patients was significantly greater in the aortic root, ascending aorta, and descending aorta compared to healthy individuals. CONCLUSION: The presentation of the dimensional data for the entire thoracic aorta shows an important clinical tool for following patients with connective tissue disorders and aortopathy.