Browsing by Subject "Heart Failure"
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Item Advanced heart failure(2012-01-20) Drazner, Mark H.Item Association of Fitness and Obesity with Right Ventricular Function(2018-03-23) Metzinger, Mark Philip; Berry, Jarett; Das, Sandeep; Rohatgi, AnandBACKGROUND: Low Cardiorespiratory Fitness (CRF) and obesity are well-established risk factors for heart failure (HF). However, the mechanisms through which CRF and BMI influence HF risk remain uncertain especially with regards to the right ventricle. OBJECTIVES: We hypothesized that lower levels of CRF and higher measures of obesity in young adulthood along with greater decline in CRF and greater increase in BMI from young adulthood to middle-age would be associated with greater abnormalities in RV function in middle-age. METHODS: The CARDIA study is a multi-center longitudinal cohort study of young adults. For the present study, 3,433 participants with baseline CRF test and BMI data and echocardiographic examination at year 25 were selected. 2,544 participants with repeat CRF test and BMI data at year 20 were included in secondary analyses. CRF was measured as the maximal treadmill test duration (in seconds) using a graded, symptom-limited maximal treadmill test using a modified Balke protocol. Study participants were stratified into fit/fat groups using median CRF and median BMI as cutoffs. TAPSE (Tricuspid Annular Plane Systolic Excursion) and RVS' (velocity of tricuspid annular systolic motion) were used as measures of RV systolic function with larger values representing better function. PASP (Pulmonary Artery Systolic Pressure) (N = 1,292 with adequate tricuspid regurgitation jet) was used as a measure of pulmonary artery filling pressures. Multivariable adjusted linear regression analyses were performed to evaluate the independent associations of baseline CRF, baseline BMI, % change in CRF ((CRF at year 20 - CRF at year 0)/CRF at year 0 *100), and % change in BMI ((BMI at year 20 - BMI at year 0)/BMI at year 0 *100) with each echocardiographic measure of RV function at year 25. RESULTS: In unadjusted analysis, both TAPSE and RVS' were highest in the high fitness/high BMI group; PASP was highest with higher BMI. In multivariable adjusted linear regression analyses we observed a significant, direct association between baseline BMI and PASP such that higher BMI in young adulthood was associated with higher PA pressures in middle-age (β 0.12, P-value .0002); this remained significant after adjusting for % change in CRF and % change in BMI. A similar result was seen with % change in BMI and PASP. On the other hand, baseline CRF levels were not significantly associated with PASP (β -.0004, P-value 0.99). While there was a significant negative association between % change in CRF and PASP (β -0.08, P-value 0.02), this association became nonsignificant after adjusting for % change in BMI (β -0.05, P-value 0.22). There was a significant, direct association observed between both baseline CRF levels and baseline BMI and measures of RV systolic function (TAPSE and RVS') such that both higher CRF and BMI at baseline were associated with better RV systolic function in middle-age. Similar results were seen in groups stratified by CRF and BMI where greater RVS' and TAPSE were seen in the high fitness/high BMI group while the lowest PASP was seen in the high fitness/low BMI group. CONCLUSIONS: Given that obesity rather than fitness was associated with higher PASP suggests that the risk of HF seen with obesity could move through the pathway of elevated PA filling pressures while the risk seen with decreased fitness moves through an independent pathway. Given that both fitness and BMI moved in the same direction with regards to TAPSE and RVS', measures of RV systolic dysfunction appear to be less helpful in assessing HF risk. This may have important implications in better understanding the contributions of weight loss towards prevention of diseases characterized by RV dysfunction and pulmonary hypertension.Item Cardiac amyloidosis: the zebra is losing its stripes(2019-02-01) Grodin, Justin L.Item Cardiac regeneration: more hope, less hype(2016-02-26) Sadek, Hesham A.Item Cardiac resynchronization therapy: prospect for long lasting heart failure remission(2009-09-25) Joglar, Jose A.Item Cardiogenic diabetes and related puzzles(2006-01-12) Malloy, Craig R.Item Combined heart-liver transplantation: where we have been, where we are going(2022-12-02) Mufti, ArjmandItem Donald W. Seldin, M.D., Research Symposium finalist presentations(2023-05-05) Eleazu, Ijeoma; Ramos, Lisandro Maya; Salcedo Betancourt, Juan; Singh, Sumitabh; Smith, AaronThis edition of the UT Southwestern Internal Medicine Grand Rounds features presentations by the six Foster Fellows selected as finalists from the Eighth Annual Donald W. Seldin, M.D. Research Symposium, which was held on April 28, 2023. These Foster Fellows presented work that spanned the breadth and depth of scholarly activity across the department, and at the close of Grand Rounds, one will be selected as the 2023 Seldin Scholar, in honor of Dr. Donald W. Seldin. The Grand Rounds presentation includes additional award presentations recognizing Clinical Vignettes, as well as the Award for Research in Quality of Care and Education at Parkland Hospital, the Social Impact Award, and the Award for Basic Science (non-GME).Item Donald W. Seldin, M.D., Research Symposium finalist presentations(2020-05-29) Adomako, Emmanuel; Hinkamp, Colin; Liu, Po-Hong (Stuart); McAdams, Meredith; Omar, Wally; Segar, MatthewThis edition of the UT Southwestern Internal Medicine Grand Rounds features presentations by the six Foster Fellows selected as finalists from the Fifth Annual Donald W. Seldin, M.D. Research Symposium, which was held on May 21, 2020. These Foster Fellows presented work that spanned the breadth and depth of scholarly activity across the department, and at the close of Grand Rounds, one will be selected as the 2020 Seldin Scholar, in honor of Dr. Donald W. Seldin. The Grand Rounds presentation also includes additional awards honoring Clinical Vignettes and an award for work in Quality and Education at Parkland Hospital.Item FHL2 Inhibits Calcineurin and Represses Pathological Cardiac Hypertrophy(2010-11-02) Hojayev, Berdymammet; Hill, Joseph A.Stress-induced cardiac hypertrophy is a hallmark feature of pathological remodeling which, left unchecked, predisposes hearts to arrhythmia and failure. FHL2 is a member of the four-and-a-half LIM domain (FHL) family of proteins expressed predominantly in the heart. Targeted disruption of FHL2 leads to an exaggerated response to beta-agonist (isoproterenol)-induced cardiac hypertrophy. Isoproterenol-induced hypertrophy relies on activation of the calcineurin-NFAT pathway, and inhibition of calcineurin is sufficient to block growth in response to isoproterenol. I also observed that FHL2 is up-regulated in mouse hearts after isoproterenol treatment. Based on this, we hypothesized that FHL2 negatively regulates the calcineurin-NFAT pathway and consequently, the hypertrophic growth response. To determine whether calcineurin signaling is enhanced in the absence of FHL2, wild type (WT) and FHL2 knockout (FHL2-/-) mice were treated with isoproterenol (32 mg/kg/day). We observed a significant increase in isoproterenol-induced expression of the NFAT target genes RCAN1.4 and BNP in FHL2-/- hearts as compared to WT. To determine whether the effect of FHL2 on the abundance of NFAT target gene transcripts was mediated by calcineurin-NFAT-dependent transcription, HEK 293 cells were transfected with luciferase reporter constructs containing the NFAT-driven promoters of either RCAN1 or IL-2. Consistent with the in vivo data, knockdown of FHL2 message using siRNA led to increases in both RCAN1 and IL-2 promoter activities elicited by constitutively active calcineurin or the calcium ionophore, ionomycin. Importantly, activation of the RCAN1 promoter by ionomycin, in control and FHL2 knockdown cells, was abolished by the calcineurin inhibitor cyclosporin A, confirming the calcineurin dependence of the response. Over-expression of FHL2 in HEK 293 cells inhibited the activation of both NFAT reporters triggered by either constitutively active calcineurin or ionomycin. Furthermore, neonatal rat ventricular myocytes over-expressing FHL2 exhibited reduced hypertrophic growth in response to constitutively active calcineurin (measured by cell cross-sectional area and fetal gene expression). Finally, immunostaining of adult cardiomyocytes revealed co-localization of FHL2 and calcineurin predominantly at the sarcomere, and activation of calcineurin by endothelin-1 treatment resulted in interaction between FHL2 and calcineurin as demonstrated by coimmunoprecipitation. These observations demonstrate that FHL2 represses calcineurin-NFAT signaling and thereby suppresses hypertrophic cardiac growth at least in part by interacting with calcineurin and inhibiting its activation.Item (Glucose) metabolism a common soil linking diabetes mellitus, heart failure and cancer?(2021-02-05) Abel, E. DaleItem Heart failure with preserved ejection fraction: is there a passage between Scylla and Charybdis?(2008-02-15) Markham, David W.Item Heart failure with preserved ejection fraction: learning from failure(2016-06-10) Sarma, Satyam (Tom)Item It's not always about the heart: a gerocentric approach to heart failure with preserved ejection fraction(2021-05-14) Pandey, AmbarishItem Left ventricular assist device therapy for advanced heart failure: the end is the beginning(2010-06-11) Patel, Parag C.Item [News Release](1969-04-15) Chappell, Frank W., Jr.; Weeks, JohnItem [Southwestern News](1995-09-27) McNeill, Bridgette RoseItem [Southwestern News](1999-09-02) Steeves, Susan A.Item [Southwestern News](2005-10-11) Morales, KatherineItem [Southwestern News](2000-02-29) Steeves, Susan A.; Van Dusen, Gordon
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