18 research outputs found
An Audio-Visual Ethnographic Case Study of International, Rural, Nonprofit Public Relations Geared Towards Sustainable Development
No full textThis paper analyzes nonprofit public relations and its relationship to development communication. It evaluates previous attempts to integrate the two fields for development purposes. The author then offers an alternative approach, a so-called public relations for community development (PRCD) model.
The PRCD model is then tested in the form of a case studyùincluding digitally recorded video interviews and observationùon Warm Heart Worldwide, Inc. (WHW), an American-founded and operated nongovernment organization (NGO) in Phrao District, northern Thailand. The study aims to identify which elements of the PRCD approach WHW adheres to, and perceived efficacy of community development as a result.
The data suggest that although WHW does maintain an underlying PRCD philosophy, it does not implement public relations practice as outlined in PRCD. In addition to the paper, the audio-visual data have resulted in a video titled Public Relations for Community Development: Warm Heart Foundation in rural northern Thailand
Comparison of retinal vascular geometry in obese and non-obese children.
No full textChildhood obesity is associated with adult cardiometabolic disease. We postulate that the underlying microvascular dysfunction begins in childhood. We thus aimed to compare retinal vascular parameters between obese and non-obese children.This was a cross-sectional study involving 166 children aged 6 to 12 years old in Malaysia. Ocular examination, biometry, retinal photography, blood pressure and body mass index measurement were performed. Participants were divided into two groups; obese and non-obese. Retinal vascular parameters were measured using validated software.Mean age was 9.58 years. Approximately 51.2% were obese. Obese children had significantly narrower retinal arteriolar caliber (F(1,159) = 6.862, p = 0.010), lower arteriovenous ratio (F(1,159) = 17.412, p < 0.001), higher venular fractal dimension (F(1,159) = 4.313, p = 0.039) and higher venular curvature tortuosity (F(1,158) = 5.166, p = 0.024) than non-obese children, after adjustment for age, gender, blood pressure and axial length.Obese children have abnormal retinal vascular geometry. These findings suggest that childhood obesity is characterized by early microvascular abnormalities that precede development of overt disease. Further research is warranted to determine if these parameters represent viable biomarkers for risk stratification in obesity
Thiazolidinediones associated with recurrent pleural effusions post coronary artery bypass surgery
No full textWe report the case of a patient in which thiazolidinediones (TZDs) were associated with recurrent pleural effusions post coronary artery bypass surgery, in spite of a normal left ventricular function. The potential mechanisms are discussed, particularly in relation to the vascular leak syndrome. This finding has important implications for the management of diabetic patients who are referred for coronary artery bypass surgery and who are on TZDs for glycemic control. © 2005 Elsevier Ireland Ltd. All rights reserved.Emoto M, 2001, DIABETES, V50, P1166, DOI 10.2337-diabetes.50.5.1166; GARG A, 2003, MAYO CLIN P, V78, P1088; Kennedy FP, 2003, MAYO CLIN PROC, V78, P1076; Nesto RW, 2003, CIRCULATION, V108, P2941, DOI 10.1161-01.CIR.0000103683.99399.7E; Tang WHW, 2003, J AM COLL CARDIOL, V41, P1394, DOI 10.1016-S0735-1097(03)00159-121
Device-estimated sleep metrics do not mediate the relation between race and blood pressure dipping in young black and white women
No full textThis article was originally published in Journal of Clinical Hypertension . The version of record is available at: https://doi.org/10.1111/jch.14856
© 2024 The Author(s). The Journal of Clinical Hypertension published by Wiley Periodicals LLC.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.Short, disturbed, and irregular sleep may contribute to blunted nocturnal blood pressure (BP) dipping, a predictor of cardiovascular disease. Black women (BLW) demonstrate less BP dipping and poorer sleep health than White women (WHW). However, it remains unclear whether device-estimated sleep health metrics mediate the relation between race and BP dipping in young women. We hypothesized that the relation between race and BP dipping would be partly mediated by sleep health metrics of sleep duration, sleep efficiency, and sleep regularity. Participants (20 BLW, 17 WHW) were 18–29 years old, normotensive, nonobese, and without evidence of sleep disorders. Systolic and diastolic BP dipping were derived from 24-h ambulatory BP monitoring. Habitual sleep duration and sleep efficiency were estimated via 14 days of wrist actigraphy. Sleep duration regularity was calculated as the standard deviation (SD) of nightly sleep duration (SDSD). Sleep timing regularity metrics were calculated as the SD of sleep onset and sleep midpoint (SMSD). Mediation analysis tested the mediating effect of each sleep metric on the relation between race and BP dipping. BLW experienced less systolic (P = .02) and diastolic (P = .01) BP dipping. Sleep duration (P = .14) was not different between groups. BLW had lower sleep efficiency (P .38). In conclusion, mediation pathways of sleep health metrics do not explain racial differences in nocturnal BP dipping between young BLW and WHW.The authors thank all the study participants as well as Wendy Nichols, BSN, RN, CCRC, CEN, and the staff at the Nurse Managed Primary Care Center for assistance with blood collections and with the processing of clinical labs for this project. University of Delaware Research Foundation (UDRF)—Strategic Initiative Grant (MAW/FP) and American Heart Association (AHA) Award #831488 (EKH) and the University of Delaware Graduate College Doctoral Fellowship for Excellence
A study of the correlation between stroke and gut microbiota over the last 20years: a bibliometric analysis
No full textPurposeThis study intends to uncover a more thorough knowledge structure, research hotspots, and future trends in the field by presenting an overview of the relationship between stroke and gut microbiota in the past two decades.MethodStudies on stroke and gut microbiota correlations published between 1st January 2002 and 31st December 2021 were retrieved from the Web of Science Core Collection and then visualized and scientometrically analyzed using CiteSpace V.ResultsA total of 660 papers were included in the study, among which the United States, the United Kingdom, and Germany were the leading research centers. Cleveland Clinic, Southern Medical University, and Chinese Academy of Science were the top three institutions. The NATURE was the most frequently co-cited journal. STANLEY L HAZEN was the most published author, and Tang WHW was the most cited one. The co-occurrence analysis revealed eight clusters (i.e., brain-gut microbiota axis, fecal microbiome transplantation, gut microbiota, hypertension, TMAO, ischemic stroke, neuroinflammation, atopobiosis). “gut microbiota,” “Escherichia coli,” “cardiovascular disease,” “risk,” “disease,” “ischemic stroke,” “stroke,” “metabolism,” “inflammation,” and “phosphatidylcholine” were the most recent keyword explosions.ConclusionFindings suggest that in the next 10 years, the number of publications produced annually may increase significantly. Future research trends tend to concentrate on the mechanisms of stroke and gut microbiota, with the inflammation and immunological mechanisms, TMAO, and fecal transplantation as hotspots. And the relationship between these mechanisms and a particular cardiovascular illness may also be a future research trend
Trends in gut-heart axis and heart failure research (1993–2023): A bibliometric and visual analysis
No full textBackground: The incidence of heart failure, the terminal stage of several cardiovascular diseases, is increasing owing to population growth and aging. Bidirectional crosstalk between the gut and heart plays a significant role in heart failure. This study aimed to analyze the gut-heart axis and heart failure from a bibliometric perspective. Methods: We extracted literature regarding the gut-heart axis and heart failure from the Web of Science Core Collection database (January 1, 1993, to June 30, 2023) and conducted bibliometric and visualization analyses using Microsoft Excel, CiteSpace, VOSviewer, and the R package “bibliometrix.” Results: The final analysis included 1646 articles with an average of 35.38 citations per article. Despite some fluctuations, the number of articles published per year has steadily increased over the past 31 years, particularly since 2018. A total of 9412 authors from 2287 institutions in 86 countries have contributed to this field. The USA and China have been the most productive countries, with the Cleveland Clinic in the USA and Charité-Universitätsmedizin Berlin in Germany being the most active institutions. The cooperation between countries/regions and institutions was relatively close. Professor Tang WHW was the most productive author in the field and the journal Shocks published the highest number of articles. ''Heart failure,'' ''gut microbiota,'' ''trimethylamine N-oxide,'' and ''inflammation'' were the most common keywords, representing the current research hotspots. The keyword burst analysis indicated that ''gut microbiota'' and ''short-chain fatty acids'' are the current frontier research topics in this field. Conclusion: Research on the gut-heart axis and heart failure is increasing. This bibliometric analysis indicated that the mechanisms associated with the gut-heart axis and heart failure, particularly the gut microbiota, trimethylamine N-oxide, inflammation, and short-chain fatty acids, will become hotspots and emerging trends in research in this field. These findings provide valuable insights into current research and future directions
Utilization pattern of mineralocorticoid receptor antagonists in contemporary patients hospitalized with acute decompensated heart failure: A single-center experience
No full textBackground Recent studies have broadened the potential use of mineralocorticoid receptor antagonist (MRA) in patients with systolic heart failure after cardiovascular hospitalization. Real-world data on safety and tolerability of MRA initiation during hospitalization for acute decompensated heart failure (ADHF) are lacking. We examined the patterns of utilization of MRAs in patients admitted for ADHF in contemporary clinical practice. Methods and Results We reviewed consecutive hospitalized patients admitted with a primary diagnosis of ADHF from March to June 2011. The treatment patterns of MRA use or discontinuation before, during, and after hospitalization were reviewed and analyzed retrospectively. In the study cohort of 500 patients, 106 patients (21percent) were on MRAs before admission. During hospitalization, preadmission and newly started MRAs were discontinued in 64 out of 177 (36percent), with worsening renal function being the most common identifiable reason. In a multivariate analysis, high admission creatinine was the only significant predictor of MRA discontinuation during hospitalization (P =.01). Of the 394 patients who did not receive MRA before admission, 81 were eligible for MRAs, but only 17 (21percent) were initiated. After a median follow up of 57 days, 21 additional patients discontinued MRAs; of 72 eligible patients for MRA, 55 patients (76percent) were still appropriately taking it. Conclusions Despite recent data, MRAs are still underutilized in patients admitted with ADHF who are otherwise eligible for it. Elevated serum creatinine and worsening of renal function are the most common cause of in-hospital discontinuation, which highlights the importance of meticulous follow-up after MRA initiation. © 2014 Elsevier Inc. All rights reserved.Albert NM, 2009, JAMA-J AM MED ASSOC, V302, P1658, DOI 10.1001-jama.2009.1493; Butler J, 2012, J CARD FAIL, V18, P265, DOI 10.1016-j.cardfail.2012.02.005; Eschalier R, 2013, J AM COLL CARDIOL, V62, P1585, DOI 10.1016-j.jacc.2013.04.086; Ferreira JP, 2014, EUR J INTERN MED, V25, P67, DOI 10.1016-j.ejim.2013.08.711; Goebel Jason A, 2008, Curr Heart Fail Rep, V5, P153, DOI 10.1007-s11897-008-0024-y; Hamaguchi S, 2010, AM HEART J, V160, P1156, DOI 10.1016-j.ahj.2010.08.036; Hernandez AF, 2012, JAMA-J AM MED ASSOC, V308, P2097, DOI 10.1001-jama.2012.14795; Jacob Miriam S, 2011, Curr Heart Fail Rep, V8, P7, DOI 10.1007-s11897-010-0046-0; Krantz MJ, 2011, AM J CARDIOL, V107, P1818, DOI 10.1016-j.amjcard.2011.02.322; Maron BA, 2010, CIRCULATION, V121, P934, DOI 10.1161-CIRCULATIONAHA.109.895235; Pitt B, 2003, NEW ENGL J MED, V348, P1309, DOI 10.1056-NEJMoa030207; Pitt B, 1999, NEW ENGL J MED, V341, P709, DOI 10.1056-NEJM199909023411001; Testani JM, 2010, CIRCULATION, V122, P265, DOI 10.1161-CIRCULATIONAHA.109.933275; Testani JM, 2011, CIRC-HEART FAIL, V4, P685, DOI 10.1161-CIRCHEARTFAILURE.111.963256; Vardeny O, 2012, J AM COLL CARDIOL, V60, P2082, DOI 10.1016-j.jacc.2012.07.048; Yancy CW, 2013, J AM COLL CARDIOL, V62, pE147, DOI 10.1016-j.jacc.2013.05.019; Zannad F, 2011, NEW ENGL J MED, V364, P11, DOI 10.1056-NEJMoa10094923
Relation between echocardiographically estimated and invasively measured filling pressures in constrictive pericarditis
No full textThe ratio of early transmitral flow velocity (E) to mitral annular velocity (E′) is considered a predictor of pulmonary capillary wedge pressure (PCWP). In a previous small study, the paradoxical relation between PCWP and E-E′ ratio has been described in patients with constrictive pericarditis (CP). We sought to test this paradoxical relation in a larger cohort. We retrospectively identified 49 patients with surgically confirmed CP (40 men; mean age 61 ± 10 years) who underwent right-sided cardiac catheterization with PCWP measurement, preceded by an echocardiographic study. Of these, 48 patients underwent either computed tomography or magnetic resonance imaging to measure pericardial thickness on the lateral side of the left ventricular wall. Mean interval time between echocardiogram and right-sided cardiac catheterization was 1.5 ± 3.8 days. There were no significant correlations between mean, medial, or lateral E-E′ and PCWP (r = -0.17, 95percent confidence interval [CI] -0.43 to -0.12; r = -0.17, 95percent CI -0.43 to -0.12; and r = -0.12, 95percent CI -0.39 to -0.17, respectively). Similarly, there was no correlation between mean E-E′ and brain natriuretic peptide (Spearman r = -0.17, p = NS). Patients with increased pericardial thickness (defined as 4 mm) had both lower lateral peak systolic annular velocity (S′) and lower lateral S′ integral (7.8 ± 2.4 vs 9.6 ± 2.4, p = 0.02 and 13.2 ± 4.2 vs 15.9 ± 4.7, p = 0.04, respectively). In patients with CP, there were no correlations between septal, lateral, or mean E-E′ and PCWP. In conclusion, E-E′ is not predictive of filling pressures in patients with CP, and perhaps the annulus paradoxus phenomenon should be revisited. The relation between the mitral annular velocity and thickness of the parietal pericardium may affect this phenomenon. © 2014 Elsevier Inc. All rights reserved.Bertog SC, 2004, J AM COLL CARDIOL, V43, P1445, DOI 10.1016-j.jacc.2003.11.048; Chowdhury UK, 2006, ANN THORAC SURG, V81, P522, DOI 10.1016-j.athoracsur.2005.08.009; DCRUZ IA, 1989, AM HEART J, V118, P128, DOI 10.1016-0002-8703(89)90082-3; Garcia MJ, 1996, J AM COLL CARDIOL, V27, P108, DOI 10.1016-0735-1097(95)00434-3; Geske JB, 2009, J AM SOC ECHOCARDIOG, V22, P961, DOI 10.1016-j.echo.2009.05.003; Ha JW, 2001, CIRCULATION, V104, P976, DOI 10.1161-hc3401.095705; Ioannidis JPA, 2005, PLOS MED, V2, P696, DOI 10.1371-journal.pmed.0020124; Klein AL, 2011, JACC-CARDIOVASC IMAG, V4, P576, DOI 10.1016-j.jcmg.2011.03.012; Klein AL, 2013, J AM SOC ECHOCARDIOG, V26, P965, DOI 10.1016-j.echo.2013.06.023; Kusunose K, 2013, CIRC-CARDIOVASC IMAG, V6, P399, DOI 10.1161-CIRCIMAGING.112.000078; BLAND JM, 1986, LANCET, V1, P307; Motoki H, 2013, J AM SOC ECHOCARDIOG, V26, P640, DOI 10.1016-j.echo.2013.02.014; Mullens W, 2009, CIRCULATION, V119, P62, DOI 10.1161-CIRCULATIONAHA.108.779223; Nagueh SF, 1997, J AM COLL CARDIOL, V30, P1527, DOI 10.1016-S0735-1097(97)00344-6; Popovic ZB, 2011, EUR J ECHOCARDIOGR, V12, P818, DOI 10.1093-ejechocard-jer146; Rajagopalan N, 2001, AM J CARDIOL, V87, P86, DOI 10.1016-S0002-9149(00)01278-9; Reuss CS, 2009, EUR J ECHOCARDIOGR, V10, P372, DOI 10.1093-ejechocard-jen258; Scalia GM, 1997, CIRCULATION, V95, P151; Tang WHW, 2003, CIRCULATION, V108, P2964, DOI 10.1161-01.CIR.0000106903.98196.B6; Troughton RW, 2004, LANCET, V363, P717, DOI 10.1016-S0140-6736(04)15648-1; Veress G, 2011, CIRC-CARDIOVASC IMAG, V4, P399, DOI 10.1161-CIRCIMAGING.110.959619; Verhaert D, 2010, CIRC-CARDIOVASC IMAG, V3, P333, DOI 10.1161-CIRCIMAGING.109.92179113
Sildenafil therapy in thalassemia patients with Doppler-defined risk of pulmonary hypertension
No full textPulmonary hypertension is a common but often overlooked complication associated with thalassemia syndromes. There are limited data on the safety and efficacy of selective pulmonary vasodilators in this at-risk population. We, therefore, designed a 12-week, open-label, phase 1-2, pilot-scale, proof-of-principle trial of sildenafil therapy in 10 patients with β-thalassemia and at increased risk of pulmonary hypertension based on an elevated tricuspid regurgitant jet velocity 2.5 m-s on Doppler-echocardiography. Variables compared at baseline and after 12 weeks of sildenafil treatment included Doppler-echocardiographic parameters, 6-minute walked distance, Borg Dyspnea Score, New York Heart Association functional class, pulmonary function, and laboratory parameters. Treatment with sildenafil resulted in a significant decrease in tricuspid regurgitant jet velocity by 13.3percent (3.0±0.7 versus 2.6±0.5 m-s, P=0.04), improved left ventricular end systolic-diastolic volume, and a trend towards a improved New York Heart Association functional class. No significant change in 6-minute walked distance was noted. Sildenafil was well tolerated, although minor expected adverse events were commonly reported. The total dose of sildenafil (mg) was strongly correlated with percent change in nitric oxide metabolite concentration in the plasma (ρ=0.80, P=0.01). There were also significant increases in plasma and erythrocyte arginine concentrations. Our study suggests that sildenafil is safe and may improve pulmonary hemodynamics in patients at risk of pulmonary hypertension; however, it was not demonstrated to improve the distance walked in 6 minutes. Clinical trials are needed to identify the best treatment strategy for pulmonary hypertension in patients with β-thalassemia. (clinicaltrials.gov identifier: NCT00872170). © 2013 Ferrata Storti Foundation.Aessopos A, 2005, ANN NY ACAD SCI, V1054, P342, DOI 10.1196-annals.1345.041; Aessopos A, 2005, CHEST, V127, P1523, DOI 10.1378-chest.127.5.1523; AESSOPOS A, 1995, CHEST, V107, P50, DOI 10.1378-chest.107.1.50; Aessopos A, 2004, EUR J HAEMATOL, V73, P359, DOI 10.1111-j.1600-0609.2004.00304.x; Atichartakarn V, 2003, INT J HEMATOL, V78, P139, DOI 10.1007-BF02983382; Bunn HF, 2010, BLOOD, V116, P687, DOI 10.1182-blood-2010-02-268193; Derchi G, 2005, HAEMATOL-HEMATOL J, V90, P452; Derchi G, 1999, AM HEART J, V138, P384, DOI 10.1016-S0002-8703(99)70129-8; Du ZD, 1997, AM HEART J, V134, P532, DOI 10.1016-S0002-8703(97)70091-7; Dumitrescu D, 2011, PULMONARY CIRCULATIO, P138; Eldor A, 2002, BLOOD, V99, P36, DOI 10.1182-blood.V99.1.36; El-Hady SBM, 2012, ANN HEMATOL, V91, P1193, DOI 10.1007-s00277-012-1427-0; Erdely A, 2006, AM J PHYSIOL-LUNG C, V290, pL534, DOI 10.1152-ajplung.00326.2005; Farmakis D, 2011, CIRCULATION, V123, P1227, DOI 10.1161-CIRCULATIONAHA.110.988089; Fonseca GH, 2012, EUR RESPIR J, V30, P112; Galie N, 2005, NEW ENGL J MED, V353, P2148, DOI 10.1056-NEJMoa050010; Gladwin MT, 2004, NEW ENGL J MED, V350, P886, DOI 10.1056-NEJMoa035477; Gladwin MT, 2010, BLOOD, V116, P852, DOI 10.1182-blood-2010-04-282095; GRISARU D, 1990, CHEST, V98, P1138, DOI 10.1378-chest.98.5.1138; Guazzi M, 2004, J AM COLL CARDIOL, V44, P2339, DOI 10.1016-j.jacc.2004.09.041; Guazzi M, 2011, CIRC-HEART FAIL, V4, P8, DOI 10.1161-CIRCHEARTFAILURE.110.944694; Hagar RW, 2006, BRIT J HAEMATOL, V133, P433, DOI 10.1111-j.1365-2141.2006.06053.x; Hahalis G, 2005, AM J MED, V118, P957, DOI 10.1016-j.amjmed.2005.02.021; Karimi M, 2011, EUR J INTERN MED, V22, P607, DOI 10.1016-j.ejim.2011.05.013; Kato GJ, 2012, PEDIATR BLOOD CANCER, V58, P831, DOI 10.1002-pbc.23399; Lalande S, 2009, EUR J APPL PHYSIOL, V106, P509, DOI 10.1007-s00421-009-1042-5; Littera R, 2002, BLOOD, V100, P1516, DOI 10.1182-blood-2002-04-1171; Machado RF, 2011, BLOOD, V118, P855, DOI 10.1182-blood-2010-09-306167; Machado RF, 2010, CHEST, V137, p30S, DOI 10.1378-chest.09-3057; McLaughlin VV, 2009, CIRCULATION, V119, P2250, DOI 10.1161-CIRCULATIONAHA.109.192230; Mehari A, 2012, JAMA-J AM MED ASSOC, V307, P1254, DOI 10.1001-jama.2012.358; Michelakis E, 2002, CIRCULATION, V105, P2398, DOI 10.1161-01.CIR.0000016641.12984.DC; Morris CR, 2003, AM J RESP CRIT CARE, V168, P63, DOI 10.1164-rccm.200308-967OC; Morris CR, 2007, ADV PULM HYPERTENS, V5, P31; Morris CR, 2010, ANN NY ACAD SCI, V1202, P205, DOI 10.1111-j.1749-6632.2010.05580.x; Morris CR, 2008, HEMATOL-AM SOC HEMAT, V2003, P177; Morris CR, 2011, PULMONARY CIRCULATIO, P271; Morris CR, 2011, BLOOD, V118, P3794, DOI 10.1182-blood-2010-11-319152; Morris CR, 2005, ANN NY ACAD SCI, V1054, P481, DOI 10.1196-annals.1345.058; Musallam KM, 2011, HAEMATOL-HEMATOL J, V96, P1605, DOI 10.3324-haematol.2011.047852; NEBES VL, 1988, MOL ENDOCRINOL, V2, P444; Parent F, 2011, NEW ENGL J MED, V365, P44, DOI 10.1056-NEJMoa1005565; Phrommintikul A, 2006, HEART, V92, P1467, DOI 10.1136-hrt.2005.079970; Quinones MA, 2002, J AM SOC ECHOCARDIOG, V15, P167, DOI 10.1067-mje.2002.120202; Sebkhi A, 2003, CIRCULATION, V107, P3230, DOI 10.1161-01.CIR.0000074226.20466.B1; Sheth A, 2005, VASC PHARMACOL, V42, P41, DOI 10.1016-j.vph.2004.11.005; Simonneau G, 2009, J AM COLL CARDIOL, V54, pS43, DOI 10.1016-j.jacc.2009.04.012; Singer ST, 2006, AM J HEMATOL, V81, P670, DOI 10.1002-ajh.20640; Sourij H, 2011, ATHEROSCLEROSIS, V218, P220, DOI 10.1016-j.atherosclerosis.2011.04.041; Tam DH, 2006, AM J HEMATOL, V81, P443, DOI 10.1002-ajh.20603; Tang WHW, 2009, J AM COLL CARDIOL, V53, P2061, DOI 10.1016-j.jacc.2009.02.036; Villagra J, 2007, BLOOD, V110, P2166, DOI 10.1182-blood-2006-12-061697; Wu KH, 2004, ANN HEMATOL, V83, P779, DOI 10.1007-s00277-004-0954-8; Zakynthinos E, 2001, THORAX, V56, P737, DOI 10.1136-thorax.56.9.73753
Prognostic role of pulmonary arterial capacitance in advanced heart failure
No full textBackground-Right ventricular (RV) dysfunction frequently occurs and independently prognosticates in left-sided heart failure. It is not clear which RV afterload measure has the greatest impact on RV function and prognosis. We examined the determinants, prognostic role, and response to treatment of pulmonary arterial capacitance (PAC, ratio of stroke volume over pulmonary pulse pressure), in relation to pulmonary vascular resistance (PVR) in heart failure. Methods and Results-We reviewed 724 consecutive patients with heart failure who underwent right heart catheterization between 2000 and 2005. Changes in PAC were explored in an independent cohort of 75 subjects treated for acute decompensated heart failure. PAC showed a strong inverse relation with PVR (r=-0.64) and wedge pressure (r=-0.73), and provides stronger prediction of significant RV failure than PVR (area under the curve ROC 0.74 versus 0.67, respectively, P=0.003). During a mean follow-up of 3.2±2.2 years, both lower PAC (P0.0001) and higher PVR (P0.0001) portend more adverse clinical events (all-cause mortality and cardiac transplantation). In multivariate analysis, PAC (but not PVR) remains an independent predictor (Hazard ratio=0.92 [95percent CI: 0.84-1.0, P=0.037]). Treatment of heart failure resulted in a decrease in PVR (270±165 to 211±88 dynes.s-1.cm-5, P=0.002), a larger increase in PAC (1.65±0.64 to 2.61±1.42 mL-mm Hg, P0.0001), leading to an increase in pulmonary arterial time constant (PVR×PAC) (0.29±0.12 to 0.37±0.15 second, P0.0001). Conclusions-PAC bundles the effects of PVR and left-sided filling pressures on RV afterload, explaining its strong relation with RV dysfunction, poor long-term prognosis, and response to therapy. © 2012 American Heart Association, Inc.Aronson D, 2011, CIRC-HEART FAIL, V4, P644, DOI 10.1161-CIRCHEARTFAILURE.110.960864; BAKER BJ, 1984, AM J CARDIOL, V54, P596, DOI 10.1016-0002-9149(84)90256-X; Bonderman D, 2011, CHEST, V139, P122, DOI 10.1378-chest.10-0348; Butler J, 1999, J AM COLL CARDIOL, V34, P1802, DOI 10.1016-S0735-1097(99)00408-8; de Groote P, 1998, J AM COLL CARDIOL, V32, P948, DOI 10.1016-S0735-1097(98)00337-4; de Perrot M, 2011, CHEST, V140, P34, DOI 10.1378-chest.10-1263; DISALVO TG, 1995, J AM COLL CARDIOL, V25, P1143, DOI 10.1016-0735-1097(94)00511-N; Ghio S, 2001, J AM COLL CARDIOL, V37, P183, DOI 10.1016-S0735-1097(00)01102-5; HARRIS P, 1965, BRIT HEART J, V27, P651; Juilliere Y, 1997, EUR HEART J, V18, P276; Karatasakis GT, 1998, AM J CARDIOL, V82, P329, DOI 10.1016-S0002-9149(98)00344-0; Lankhaar JW, 2006, AM J PHYSIOL-HEART C, V291, pH1731, DOI 10.1152-ajpheart.00336.2006; Lankhaar JW, 2008, EUR HEART J, V29, P1688, DOI 10.1093-eurheartj-ehn103; MACKAY EH, 1978, THORAX, V33, P335, DOI 10.1136-thx.33.3.335; Mahapatra S, 2006, J AM COLL CARDIOL, V47, P799, DOI 10.1016-j.jacc.2005.09.054; Mahapatra S, 2006, J AM SOC ECHOCARDIOG, V19, P1045, DOI 10.1016-j.echo.2006.03.008; POLAK JF, 1983, J AM COLL CARDIOL, V2, P217; Saouti N, 2009, AM J PHYSIOL-HEART C, V297, pH2154, DOI 10.1152-ajpheart.00694.2009; Tedford RJ, 2012, CIRCULATION, V125, P289, DOI 10.1161-CIRCULATIONAHA.111.051540; Voelkel NF, 2006, CIRCULATION, V114, P1883, DOI 10.1161-CIRCULATIONAHA.106.632208; WESTERHO.N, 1971, J APPL PHYSIOL, V31, P776; Westerhof N, 2009, MED BIOL ENG COMPUT, V47, P131, DOI 10.1007-s11517-008-0359-212
