2013 hypertension-1


Effect of fetal and child health on kidney development and long-term risk of hypertension and kidney disease.

Lancet. 2013 Jul 20;382(9888):273-83.

Luyckx VA, Bertram JF, Brenner BM, Fall C, Hoy WE, Ozanne SE, Vikse BE.

Division of Nephrology, University of Alberta, Edmonton, AB, Canada. vluyckx@ualberta.ca


Developmental programming of non-communicable diseases is now an established paradigm. With respect to hypertension and chronic kidney disease, adverse events experienced in utero can affect development of the fetal kidney and reduce final nephron number. Low birthweight and prematurity are the most consistent clinical surrogates for a low nephron number and are associated with increased risk of hypertension, proteinuria, and kidney disease in later life. Rapid weight gain in childhood or adolescence further compounds these risks. Low birthweight, prematurity, and rapid childhood weight gain should alert clinicians to an individual’s lifelong risk of hypertension and kidney disease, prompting education to minimise additional risk factors and ensuring follow-up. Birthweight and prematurity are affected substantially by maternal nutrition and health during pregnancy. Optimisation of maternal health and early childhood nutrition could, therefore, attenuate this programming cycle and reduce the global burden of hypertension and kidney disease in the future.

Copyright © 2013 Elsevier Ltd. All rights reserved.

PMID: 23727166

2013 hypertension-10


Systemic Hypertension in Low Gradient Severe Aortic Stenosis with Preserved Ejection Fraction.

Circulation. 2013 Aug 16.

Eleid MF, Nishimura RA, Sorajja P, Borlaug BA.

Mayo Clinic College of Medicine, Rochester, MN.



Low gradient (LG) severe aortic stenosis (AS) with preserved ejection fraction (EF) is an increasingly recognized entity, and symptomatic patients may benefit from aortic valve replacement. However, systemic hypertension frequently coexists with LG severe AS, which itself may cause elevated left ventricular (LV) filling pressures with resultant symptoms of dyspnea.


Symptomatic patients with hypertension (aortic systolic pressure>140 mmHg) and LG (mean gradient<40 mmHg) severe AS (aortic valve area<1 cm2) with preserved EF (EF>50%) who underwent invasive hemodynamic left and right heart catheterization received infusion of intravenous sodium nitroprusside to reduce blood pressure and arterial afterload. At baseline, patients had severe hypertension (aortic systolic pressure 176±26 mmHg), pulmonary hypertension (mean pressure 39±12 mmHg), elevated LV end diastolic pressure (19±5 mmHg) and reduced stroke volume (33±8 ml/m2). All measures of afterload were reduced with nitroprusside (p<0.001 for all). Nitroprusside reduced mean pulmonary artery pressure (25±10 mmHg) and LV end diastolic pressure (11±5 mmHg) (p<0.001 for both as compared to baseline). Aortic valve area (0.86±0.11 to 1.02±0.16 cm2, p=0.001) and mean gradient (27±5 to 29±6 mmHg, p=0.02) increased with nitroprusside.


Systemic hypertension in LG severe AS with preserved EF is associated with elevated LV filling pressures and pulmonary hypertension. Treatment of hypertension with vasodilator therapy results in a lowering of the total LV afterload, with a decrease in LV filling pressures and pulmonary artery pressures. These findings have important implications for the management of patients with LG severe AS with preserved EF and hypertension.


afterload, aortic stenosis, ejection fraction, hypertension, low gradient, vasodilator

PMID: 23956211


2013 hypertension-11


Renal tubular NEDD4-2 deficiency causes NCC-mediated salt-dependent hypertension.

J Clin Invest. 2013 Feb 1;123(2):657-65.

Ronzaud C, Loffing-Cueni D, Hausel P, Debonneville A, Malsure SR, Fowler-Jaeger N, Boase NA, Perrier R, Maillard M, Yang B, Stokes JB, Koesters R, Kumar S, Hummler E, Loffing J, Staub O.

Department of Pharmacology and Toxicology, University of Lausanne, Lausanne, Switzerland.


The E3 ubiquitin ligase NEDD4-2 (encoded by the Nedd4L gene) regulates the amiloride-sensitive epithelial Na+ channel (ENaC/SCNN1) to mediate Na+ homeostasis. Mutations in the human β/γENaC subunits that block NEDD4-2 binding or constitutive ablation of exons 6-8 of Nedd4L in mice both result in salt-sensitive hypertension and elevated ENaC activity (Liddle syndrome). To determine the role of renal tubular NEDD4-2 in adult mice, we generated tetracycline-inducible, nephron-specific Nedd4L KO mice. Under standard and high-Na+ diets, conditional KO mice displayed decreased plasma aldosterone but normal Na+/K+ balance. Under a high-Na+ diet, KO mice exhibited hypercalciuria and increased blood pressure, which were reversed by thiazide treatment. Protein expression of βENaC, γENaC, the renal outer medullary K+ channel (ROMK), and total and phosphorylated thiazide-sensitive Na+Cl- cotransporter (NCC) levels were increased in KO kidneys. Unexpectedly, Scnn1a mRNA, which encodes the αENaC subunit, was reduced and proteolytic cleavage of αENaC decreased. Taken together, these results demonstrate that loss of NEDD4-2 in adult renal tubules causes a new form of mild, salt-sensitive hypertension without hyperkalemia that is characterized by upregulation of NCC, elevation of β/γENaC, but not αENaC, and a normal Na+/K+ balance maintained by downregulation of ENaC activity and upregulation of ROMK.

PMID: 23348737

2013 hypertension-2


Selective Inactivation of PTEN in Smooth Muscle Cells Synergizes With Hypoxia to Induce Severe Pulmonary Hypertension.

J Am Heart Assoc. 2013 May 31;2(3):e000188.

Horita H, Furgeson SB, Ostriker A, Olszewski KA, Sullivan T, Villegas LR, Levine M, Parr JE, Cool CD, Nemenoff RA, Weiser-Evans MC.

Division of Renal Diseases and Hypertension, Department of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO.



Pulmonary vascular remodeling in pulmonary hypertension (PH) is characterized by increased vascular smooth muscle cell (SMC) and adventitial fibroblast proliferation, small vessel occlusion, and inflammatory cell accumulation. The underlying molecular mechanisms driving progression remain poorly defined. We have focused on loss of the phosphatase PTEN in SMCs as a major driver of pathological vascular remodeling. Our goal was to define the role of PTEN in human PH and in hypoxia-induced PH using a mouse model with inducible deletion of PTEN in SMCs.


Staining of human biopsies demonstrated enhanced inactive PTEN selectively in the media from hypertensive patients compared to controls. Mice with induced deletion of PTEN in SMCs were exposed to normoxia or hypoxia for up to 4 weeks. Under normoxia, SMC PTEN depletion was sufficient to induce features of PH similar to those observed in wild-type mice exposed to chronic hypoxia. Under hypoxia, PTEN depletion promoted an irreversible progression of PH characterized by increased pressure, extensive pulmonary vascular remodeling, formation of complex vascular lesions, and increased macrophage accumulation associated with synergistic increases in proinflammatory cytokines and proliferation of both SMCs and nonSMCs.


Chronic inactivation of PTEN selectively in SMC represents a critical mediator of PH progression, leading to cell autonomous events and increased production of factors correlated to proliferation and recruitment of adventitial and inflammatory cells, resulting in irreversible progression of the disease.


hypoxia, inflammation, pulmonary hypertension, remodeling, smooth muscle

PMID: 23727701



hyper dis-2

2013 hypertension-3


Blood pressure variability and multiple organ damage in primary hypertension.

J Hum Hypertens. 2013 Jun 6.

Leoncini G, Viazzi F, Storace G, Deferrari G, Pontremoli R.

Department of Internal Medicine, University of Genoa, IRCCS Azienda Ospedaliera Universitaria San Martino – IST, Genoa, Italy.


Organ damage (OD) is an indicator of increased cardiovascular risk. Blood pressure variability (BPV) is related to greater incidence of events, regardless of the severity of hypertension. We investigated the relationship between ambulatory blood pressure monitoring (ABPM)-derived indices of BPV and the presence of multiple OD in primary hypertension (PH). One hundred and sixty-nine untreated patients with PH were evaluated. Systolic (SBP) and diastolic blood pressure (DBP) variability were assessed as the crude and weighted (w.) standard deviation (s.d.), and average real variability (ARV) of the mean value of 24-h, awake and asleep ABPM recordings. Left ventricular mass index, intima-media thickness, estimated-glomerular filtration rate and urinary albumin excretion were assessed as indices of cardiac, vascular and renal damage, respectively. Risk profile progressively increased starting from patients without OD to patients with only one sign of OD, and then to those with multiple OD. In addition to greater severity of the organ involvement, the only variables that were found to significantly differ between subjects with multiple and single OD were office SBP (160±14 vs 154±11 mm Hg, P=0.0423) and DBP (101±7 vs 97±8 mm Hg, P=0.0291), ambulatory arterial stiffness index (AASI) (0.60±0.10 vs 0.50±0.17, P=0.0158) and indices of BPV (24-h SBP s.d., 23±5 vs 20±6 mm Hg, P=0.0300; awake SBP s.d., 22±6 vs 19±6 mm Hg, P=0.0366; 24-h SBP w.s.d., 20±5 vs 17±5 mm Hg, P=0.0385; and 24-h SBP ARV, 18±4 vs 15±5 mm Hg, P=0.0420). All the above mentioned BPV parameters turned out to be determinants of multiple OD, regardless of several confounding variables, including BP levels. Therefore, in hypertensive patients increased SBP variability is associated with multiple signs of OD, regardless of BP values.Journal of Human Hypertension advance online publication, 6 June 2013; doi:10.1038/jhh.2013.45.

PMID: 23739158

2013 hypertension-4


TRPV4 Channel Contributes to Serotonin-Induced Pulmonary vasoconstriction and the Enhanced Vascular Reactivity in Chronic Hypoxic Pulmonary Hypertension.

Am J Physiol Cell Physiol. 2013 Jun 5.

Xia Y, Fu Z, Hu J, Huang C, Paudel O, Cai S, Liedtke W, Sham JS.

Southern Medical University.


Transient receptor potential vanilloid 4 (TRPV4) is a mechanosensitive channel in pulmonary arterial smooth muscle cells (PASMCs). Its upregulation by chronic hypoxia is associated with enhanced myogenic tone and genetic deletion of trpv4 suppresses the development of chronic hypoxic pulmonary hypertension (CHPH). Here we further examine the roles of TRPV4 in agonist-induced pulmonary vasoconstriction and in the enhanced vasoreactivity in CHPH. Initial evaluation of TRPV4-selective antagonists HC-067047 and RN-1734 in KCl-contracted PAs of trpv4-/- mice found that submicromolar HC-067047 was devoid of off-target effect on pulmonary vasoconstriction. Inhibition of TRPV4 with 0.5 µM HC-067047 significant reduced the sensitivity of serotonin (5-HT) induced contraction in WT PAs, but had no effect on endothelin-1 or phenylephrine-activated response. Similar shift in the concentration-response curve of 5-HT was observed in trpv4-/- PAs, confirming specific TRPV4 contribution to 5-HT-induced vasoconstriction. 5-HT-induced Ca2+ response was attenuated by HC-067047 in WT PASMCs but not in trpv4-/- PASMCs, suggesting TRPV4 is a major Ca2+ pathway for 5-HT-induced Ca2+ mobilization. Chronic exposure (3-4 weeks) of WT mice to 10% O2 caused significant increase in 5-HT-induced maximal contraction, which was partially reversed by HC-067047. In concordance, the enhancement of 5-HT-induced contraction was significantly reduced in PAs of CH trpv4-/- mice. These results suggest unequivocally that TRPV4 contributes to 5-HT-dependent pharmco-mechanical coupling, and plays a major role in the enhanced pulmonary vasoreactivity to 5-HT in CHPH. Since TRPV4 participates in multiple pathological changes in CHPH, it can be considered as a potential target for the treatment of pulmonary hypertension.


TRPV4, chronic hypoxia, pulmonary arteries, pulmonary hypertension, serotonin

PMID: 23739180


2013 hypertension-5


Survival and prognostic factors in systemic sclerosis-associated pulmonary hypertension: A systematic review and meta-analysis.

Arthritis Rheum. 2013 Jun 5.

Lefèvre G, Dauchet L, Hachulla E, Montani D, Sobanski V, Lambert M, Hatron PY, Humbert M, Launay D.

Université Lille Nord de France, Service de Médecine Interne, Centre National de Référence de la Sclérodermie Systémique, Hôpital Claude-Huriez, CHRU Lille, Lille, France; Université Lille Nord de France, Laboratoire d’Immunologie EA2686, IMPRT IFR 114, Faculté de Médecine, Lille, France.


Objective: Pulmonary hypertension (PH) is a frequent and life-limiting complication of systemic sclerosis (SSc). However, there are still conflicting data on the survival rates, their evolution over time as well as on prognostic factors in this complication. Methods: We performed a systematic review and meta-analysis of literature in MEDLINE and Embase from January 1960 to January 2012. All cohort studies reporting survival and/or prognostic factors of SSc-associated PH were analyzed. We calculated pooled survival rates, analyzed their evolution over time and determined the prognostic factors. Results: Twenty-two studies were included corresponding to a total of 2244 patients. Pooled 1, 2 and 3-yr survival rates were 81% (95% CI: 79-84), 64% (59-69) and 52% (47-58) respectively. Meta-regression did not reveal a significant change over time while baseline hemodynamic severity of PH was significantly correlated with survival. In SSc patients with pulmonary arterial hypertension (PAH), age, male gender, DLCO, pericardial effusion and the parameters classically associated with idiopathic PAH severity, including six-minute walk test, mean pulmonary arterial pressure, cardiac index and right atrial pressure were significant prognostic factors. DLCO and pericardial effusion were the sole prognostic factors in patients with PH associated with interstitial lung disease. Conclusions: Our meta-analysis confirms a poor pooled 3-yr survival rate of 52% (47-58) in SSc-associated PH. PAH hemodynamic baseline severity but not period of inclusion correlated significantly with survival in SSc-associated PAH. All the usual prognostic factors found in idiopathic PAH, including six-minute walk test and right atrial pressure, were also prognostic factors in SSc-associated PAH. © 2013 American College of Rheumatology.

Copyright © 2013 American College of Rheumatology.

PMID: 23740572

2013 hypertension-6


Single nucleotide polymorphisms of the angiotensin-converting enzyme (ACE) gene are associated with essential hypertension and increased ACE enzyme levels in Mexican individuals.

PLoS One. 2013 May 31;8(5):e65700.

Martínez-Rodríguez N, Posadas-Romero C, Villarreal-Molina T, Vallejo M, Del-Valle-Mondragón L, Ramírez-Bello J, Valladares A, Cruz-López M, Vargas-Alarcón G.

Molecular Biology Department, Instituto Nacional de Cardiología Ignacio Chávez (INCICH), Mexico City, Mexico.



To explore the role of the ACE gene polymorphisms in the risk of essential hypertension in Mexican Mestizo individuals and evaluate the correlation between these polymorphisms and the serum ACE levels.


Nine ACE gene polymorphisms were genotyped by 5′ exonuclease TaqMan genotyping assays and polymerase chain reaction (PCR) in 239 hypertensive and 371 non- hypertensive Mexican individuals. Haplotypes were constructed after linkage disequilibrium analysis. ACE serum levels were determined in selected individuals according to different haplotypes.


Under a dominant model, rs4291 rs4335, rs4344, rs4353, rs4362, and rs4363 polymorphisms were associated with an increased risk of hypertension after adjusting for age, gender, BMI, triglycerides, alcohol consumption, and smoking. Five polymorphisms (rs4335, rs4344, rs4353, rs4362 and rs4363) were in strong linkage disequilibrium and were included in four haplotypes: H1 (AAGCA), H2 (GGATG), H3 (AGATG), and H4 (AGACA). Haplotype H1 was associated with decreased risk of hypertension, while haplotype H2 was associated with an increased risk of hypertension (OR = 0.77, P = 0.023 and OR = 1.41, P = 0.004 respectively). According to the codominant model, the H2/H2 and H1/H2 haplotype combinations were significantly associated with risk of hypertension after adjusted by age, gender, BMI, triglycerides, alcohol consumption, and smoking (OR = 2.0; P = 0.002 and OR = 2.09; P = 0.011, respectively). Significant elevations in serum ACE concentrations were found in individuals with the H2 haplotype (H2/H2 and H2/H1) as compared to H1/H1 individuals (P = 0.0048).


The results suggest that single nucleotide polymorphisms and the “GGATG” haplotype of the ACE gene are associated with the development of hypertension and with increased ACE enzyme levels.

PMID: 23741507

2013 hypertension-7


Hyperoxia Synergizes with Mutant BMPR2 to Cause Metabolic Stress, Oxidant Injury, and Pulmonary Hypertension.

Am J Respir Cell Mol Biol. 2013 Jun 6.

Fessel JP, Flynn CR, Robinson LJ, Penner NL, Gladson S, Kang C, Wasserman DH, Hemnes AR, West JD.

Vanderbilt University Medical Center, Department of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine, Nashville, Tennessee, United States ; joshua.p.fessel@vanderbilt.edu.


Pulmonary arterial hypertension (PAH) has been associated with a number of different but interrelated pathogenic mechanisms. Metabolic and oxidative stresses have been shown to play important pathogenic roles in a variety of model systems. However, many of these relationships remain at the level of association. We sought to establish a direct role for metabolic stress and oxidant injury in the pathogenesis of PAH. Mice that universally express a disease-causing Bmpr2 mutation were exposed to room air or to brief daily hyperoxia (95% oxygen for 3 hours) for 6 weeks and compared to wild-type animals with identical exposures. In both murine tissues and cultured endothelial cells, expression of mutant Bmpr2 was sufficient to cause oxidant injury that was particularly pronounced in mitochondrial membranes. With enhancement of mitochondrial generation of reactive oxygen species by hyperoxia, oxidant injury was substantially enhanced in mitochondrial membranes, even in tissues distant from the lung. Hyperoxia, despite its vasodilatory actions in the pulmonary circulation, significantly worsened the PAH phenotype (elevated RVSP, decreased cardiac output, increased pulmonary vascular occlusion) in Bmpr2 mutant animals. These studies demonstrate that oxidant injury and metabolic stress contribute directly to disease development and provide further evidence for PAH as a systemic disease with life-limiting cardiopulmonary manifestations.

PMID: 23742019

2013 hypertension-8


Echocardiographic parameters in patients with pulmonary arterial hypertension: correlations with right ventricular ejection fraction derived from cardiac magnetic resonance and hemodynamics.

PLoS One. 2013 Aug 14;8(8):e71276.

Yang T, Liang Y, Zhang Y, Gu Q, Chen G, Ni XH, Lv XZ, Liu ZH, Xiong CM, He JG.

State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.



Echocardiography is the most convenient method used to evaluate right ventricular function, and several echocardiographic parameters were studied in previous studies. But the value of these parameters to assess the right ventricular function in patients with pulmonary arterial hypertension (PAH) has not been well defined.


Patients with PAH were observed prospectively. Right heart catheterization, echocardiography and cardiac magnetic resonance (CMR) were performed within 1 week interval. The correlations between echocardiographic parameters and right ventricular ejection fraction (RVEF) derived from CMR as well as hemodynamics were analyzed.


Thirty patients were enrolled including 24 with idiopathic PAH, 5 with PAH associated with connective tissue diseases and 1 with hereditary PAH. All echocardiographic parameters except right ventricular myocardial performance index (RVMPI) correlated significantly with RVEF (tricuspid annual plane systolic excursion [TAPSE], r = 0.440, P = 0.015; tricuspid annular systolic excursion velocity [S’], r = 0.444, P = 0.016; isovolumic acceleration [IVA], r = 0.600, P = 0.001; right ventricular fraction area change [RVFAC], r = 0.416, P = 0.022; ratio of right ventricular transverse diameter to left ventricular transverse diameter [RVETD/LVETD], r = -0.649, P<0.001; RVMPI, r = -0.027, P = 0.888). After adjusted for mean right atrial pressure, mean pulmonary arterial pressure and pulmonary vascular resistance (PVR), only IVA and RVETD/LVETD could independently predict RVEF. Four echocardiographic parameters displayed significant correlations with PVR (TAPSE, r = -0.615, P<0.001; S’, r = -0.557, P = 0.002; RVFAC, r = -0.454, P = 0.012; RVETD/LVETD, r = 0.543, P = 0.002).


The echocardiographic parameters IVA and RVETD/LVETD can reflect RVEF independently regardless of hemodynamics in patients with PAH. In addition, TAPSE, S’, RVFAC and RVETD/LVETD can also reflect PVR in PAH patients.

PMID: 23967181



hyper dis-3

Data of Echocardiography and Cardiac Magnetic Resonance.

TAPSE, tricuspid annual plane systolic excursion; S’, tricuspid annular systolic excursion velocity; IVA, right ventricular isovolumic acceleration; RVFAC, right ventricular fraction area change; RVMPI, right ventricular myocardial performance index; RVETD/LVETD, ratio of right ventricular transverse diameter to left ventricular transverse diameter; RVEDV, right ventricular end-diastolic volume; RVESV, right ventricular end-systolic volume; RVEF, right ventricular ejection fraction; LVEDV, left ventricular end-diastolic volume; LVESV, left ventricular end-systolic volume; LVEF, left ventricular ejection fraction. (doi:10.1371/journal.pone.0071276.t002)

2013 hypertension-9


Substance P acting via the neurokinin-1 receptor regulates adverse myocardial remodeling in a rat model of hypertension.

Int J Cardiol. 2013 Jul 29. pii: S0167-5273(13)01415-0.

Dehlin HM, Manteufel EJ, Monroe AL, Reimer MH Jr, Levick SP.

Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, United States; Cardiovascular Research Center, Medical College of Wisconsin, Milwaukee, WI 53226, United States.



Substance P is a sensory nerve neuropeptide located near coronary vessels in the heart. Therefore, substance P may be one of the first mediators released in the heart in response to hypertension, and can contribute to adverse myocardial remodeling via interactions with the neurokinin-1 receptor. We asked: 1) whether substance P promoted cardiac hypertrophy, including the expression of fetal genes known to be re-expressed during pathological hypertrophy; and 2) the extent to which substance P regulated collagen production and fibrosis.


Spontaneously hypertensive rats (SHR) were treated with the neurokinin-1 receptor antagonist L732138 (5mg/kg/d) from 8 to 24weeks of age. Age-matched WKY served as controls. The gene encoding substance P, TAC1, was up-regulated as blood pressure increased in SHR. Fetal gene expression by cardiomyocytes was increased in SHR and was prevented by L732138. Cardiac fibrosis also occurred in the SHR and was prevented by L732138. Endothelin-1 was up-regulated in the SHR and this was prevented by L732138. In isolated cardiac fibroblasts, substance P transiently up-regulated several genes related to cell-cell adhesion, cell-matrix adhesion, and extracellular matrix regulation, however, no changes in fibroblast function were observed.


Substance P activation of the neurokinin-1 receptor induced expression of fetal genes related to pathological hypertrophy in the hypertensive heart. Additionally, activation of the neurokinin-1 receptor was critical to the development of cardiac fibrosis. Since no functional changes were induced in isolated cardiac fibroblasts by substance P, we conclude that substance P mediates fibrosis via up-regulation of endothelin-1.


Cardiac fibroblast, Fetal genes, Fibrosis, Hypertrophy, Substance P

PMID: 23962787


Allergy 1-10

Stress and Quality of Life in Caregivers of Inner-City Minority Children With Poorly Controlled Asthma

M. H. Bellin, J. Kub, K. D. Frick, M. E. Bollinger, M. Tsoukleris, J. Walker, C. Land and A. M. Butz

J Pediatr Health Care.2013 Mar-Apr;27(2):127-134.

Abstract: Introduction: Caregiver quality of life (QOL) is known to influence asthma management behaviors. Risk factors for low caregiver QOL in families of inner-city children with asthma remain unclear. This study evaluated the interrelationships of asthma control, stress, and caregiver QOL. Method: Data were analyzed from a home-based behavioral intervention for children with persistent asthma after treatment for asthma in the emergency department. Caregivers reported on baseline demographics, asthma control, asthma management stress, life stress, and QOL. Hierarchical regression analysis examined the contributions of sociodemographic factors, asthma control, asthma management stress, and life stress in explaining caregiver QOL. Results: Children (N = 300) were primarily African American (96%) and young (mean age, 5.5 years). Caregivers were predominantly the biological mother (92%), single (70%), and unemployed (54%). Poor QOL was associated with higher caregiver education and number of children in the home, low asthma control, and increased asthma management stress and life stress. The model accounted for 28% of variance in caregiver QOL. Discussion: Findings underscore the need for multifaceted interventions to provide tools to caregivers of children with asthma to help them cope with asthma management demands and contemporary life stressors. J Pediatr Health Care. (2013) 27, 127-134.

*Times cited: 1

Keywords: Asthma, caregiver, stress, quality of life, pediatric asthma, social support, health, impact, intervention, disparities, community, events, urban, validation

Link: http://www.ncbi.nlm.nih.gov/pubmed/23414978

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