Some selected abstracts:

1.  

STUDY OBJECTIVES: Asthma and gastro-oesophageal reflux (GER) are both characterized by airway inflammation. DESIGN: The purposes of this work were (i) to study airway inflammation in patients troubled by gastro-oesophageal reflux (GER) and GER associated with asthma, (ii) to ascertain whether GER can aggravate asthma by exacerbating the pre-existing airway inflammation and oxidative stress and (iii) to establish the validity of analysing breath condensate and induced sputum when studying the airways of subjects affected by GER. PATIENT S AND METHODS: We enrolled 14 patients affected by mild asthma associated with GER (40 +/-12 years), nine with mild but persistent asthma (39 +/- 13 years), eight with GER (35 +/- 11 years) and 17 healthy subjects (37 +/- 9 years). Sputum cell counts and concentrations of interleukin-4 (IL-4), IL-6 and 8-isoprostane were measured in breath condensate and supernatant. MEASUREMENTS AND RESULTS: GER-related asthma is characterized by an eosinophilic inflammation, as determined by elevated concentrations of IL-4 in breath condensate and sputum supernatant, and by sputum cell analysis. GER alone presents a neutrophilic pattern of inflammation when determined by elevated concentrations of IL-6 in sputum cell analysis. A concomitant increase has been found in 8-isoprostane in GER associated (or not associated) with asthma. CONCLUSIONS: We conclude that GER is characterized by a neutrophilic airway inflammation and by increased oxidative stress. GER does not however aggravate pre-existing airway inflammation in asthma patients. Determinations of inflammatory and oxidant markers in the breath condensate of subjects with GER reflect these measured in the induced sputum.

2.  

Recent studies suggest that cognitive and behavioral interventions have enduring effects that reduce risk for subsequent symptom return following treatment termination. These enduring effects have been most clearly demonstrated with respect to depression and the anxiety disorders. It remains unclear whether these effects are a consequence of the amelioration of the causal processes that generate risk or the introduction of compensatory strategies that offset them and whether these effects reflect the mobilization of cognitive or other mechanisms. No such enduring effects have been observed for the psychoactive medications, which appear to be largely palliative in nature. Other psychosocial interventions remain largely untested, although claims that they produce lasting change have long been made. Whether such enduring effects extend to other disorders remains to be seen, but the capacity to reduce risk following treatment termination is one of the major benefits provided by the cognitive and behavioral interventions with respect to the treatment of depression and the anxiety disorders.

3.

Lucas FL, DeLorenzo MA, Siewers AE, Wennberg DE. Temporal trends in the utilization of diagnostic testing and treatments for cardiovascular disease in the United States, 1993-2001. Circulation. 2006 Jan 24;113(3):374-9.

Center for Outcomes Research and Evaluation, Maine Medical Center, Portland, ME 04102, USA. lucasl@mmc.org

BACKGROUND: Rates of invasive testing and treatment for coronary artery disease have increased over time. Less is known about trends in the utilization of noninvasive cardiac testing for coronary artery disease. The objective of this study was 2-fold: to explore temporal trends in the utilization of noninvasive and invasive cardiac services in relation to changes in the prevalence of cardiac disease, and to examine whether temporal increases have been targeted to potentially underserved populations. METHODS AND RESULTS: We performed an annual cross-sectional population-based study of Medicare patients from 1993 to 2001. We identified stress testing, cardiac catheterization, and revascularization procedures, as well as hospitalizations for acute myocardial infarction, during each year and calculated population-based rates for each using the total fee-for-service Medicare population as the denominator and adjusting for age, gender, and race. We observed marked growth in the utilization rates of cardiac services over time, with relative rates nearly doubling for most services. Acute myocardial infarction hospitalization rates have remained stable over the study period. Although rates of all procedures except coronary artery bypass increased in all subgroups, differences in rates of cardiac testing and treatment between nonblack men and other subgroups persisted over time. CONCLUSIONS: Temporal increases in the use of noninvasive and invasive cardiac services are not explained by changes in disease prevalence and have not succeeded in narrowing preexisting treatment differences by gender and race. Such increases, although conferring benefit for some, may expose others to risk and cost without benefit.

4.

Meng CQ. Atherosclerosis is an inflammatory disorder after all. Curr Top Med Chem. 2006;6(2):93-102. Review.

AtheroGenics, Inc., 8995 Westside Parkway, Alpharetta, Georgia 30004, USA. cmeng@atherogenics.com

Inflammation has been increasingly recognized as an important player in the pathophysiology of numerous human disorders. Accumulating evidence has led to the conclusion that atherosclerosis is an inflammatory disease, although it was believed to be a disorder of high cholesterol levels in the bloodstream for over a century. Cholesterol does contribute to the pathogenesis of atherosclerosis, but through inflammatory mechanisms. Statins lower cholesterol levels and hence reduce inflammation in the vasculature and prevent heart disease. Statins may also exert anti-inflammatory effects through mechanisms independent of cholesterol lowering. Adhesion molecules, cytokines, oxidative stress, etc. appear to contribute to the inflammatory state of atherosclerosis and therapeutic approaches directed toward these markers or targets have the potential to be effective in reducing inflammation and treating atherosclerosis.

5.

Ventricular remodelling describes structural changes in the left ventricle in response to chronic alterations in loading conditions, with three major patterns: concentric remodelling, when a pressure load leads to growth in cardiomyocyte thickness; eccentric hypertrophy, when a volume load produces myocyte lengthening; and myocardial infarction, an amalgam of patterns in which stretched and dilated infarcted tissue increases left-ventricular volume with a combined volume and pressure load on non-infarcted areas. Whether left-ventricular hypertrophy is adaptive or maladaptive is controversial, as suggested by patterns of signalling pathways, transgenic models, and clinical findings in aortic stenosis. The transition from apparently compensated hypertrophy to the failing heart indicates a changing balance between metalloproteinases and their inhibitors, effects of reactive oxygen species, and death-promoting and profibrotic neurohumoral responses. These processes are evasive therapeutic targets. Here, we discuss potential novel therapies for these disorders, including: sildenafil, an unexpected option for anti-transition therapy; surgery for increased sphericity caused by chronic volume overload of mitral regurgitation; an antifibrotic peptide to inhibit the fibrogenic effects of transforming growth factor beta; mechanical intervention in advanced heart failure; and stem-cell therapy.

6.

Obese patients have many physical limitations and much psychiatric burden to overcome. Several studies have shown that the prevalence of psychiatric morbidity in the obese is similar to those with normal weight. However, in obese patients seeking treatment there is an increased prevalence (40-60%) of psychiatric morbidity, most commonly depression. It is difficult to separate the effects of depression on obesity and, on the contrary, the neuroendocrine changes associated with stress and depression may cause metabolic changes that predispose and perpetuate obesity. The stigma associated with obesity causes bullying in school as well as childhood psychiatric morbidity. Prejudice is not limited to the general public but exists among health professionals too. This chapter discusses the treatment of depression in obesity and the psychiatric evaluation of the pre-bariatric surgery patient. Education of society, starting with schools and including healthcare professionals will reduce bias and stigma as well as assist this vulnerable group of patients to seek help for their obesity and the many problems that come with it. Given that by the year 2025 obesity will be the world's number one health problem with the US leading the way, it is very important that we pursue preventive measures as well as encourage research for treatments of obesity.

  Asthma:  

14498.  Sanadi RM, Vandana KL. Stress and its implications inperiodontics. J Indian Acad Oral Med Radiol 2005, 17(1), 8-10.

  Depression:

14508.   Hoge CW, Auchterlonie JL, Milliken CS. Mental health problems, use of mental health services, and attrition from military service after returning from deployment to Iraq or Afghanistan. JAMA. 2006 Mar 1;295(9):1023-32.

14514.   Pouwer F, Beekman AT, Lubach C, Snoek FJ. Nurses' recognition and registration of depression, anxiety and diabetes-specific emotional problems in outpatients with diabetes mellitus. Patient Educ Couns. 2006 Feb;60(2):235-40.

14515.  Wessa M, Rohleder N, Kirschbaum C, Flor H. Altered cortisol awakening response in posttraumatic stress disorder. Psychoneuroendocrinology. 2006 Feb;31(2):209-15.

  Hypertension:

14525. Vanderkaay MM, Patterson SM. Nicotine and acute stress: effects of nicotine versus nicotine withdrawal on stress-induced hemoconcentration and cardiovascular reactivity. Biol Psychol. 2006 Feb;71(2):191-201.

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October 2006

Some selected abstract:

Carvajal C, Dumont Y, Quirion R. Neuropeptide y: role in emotion and alcohol dependence. CNS Neurol Disord Drug Targets. 2006 Apr;5(2):181-95. Review.
Douglas Hospital Research Centre, Dept. of Psychiatry, McGill University, 6875 LaSalle Blvd., Montreal, QC, Canada, H4H 1R3.
Neuropeptide Y (NPY) is considered to be an important neuromodulator in the regulation of emotional behavior. For example, NPY is consistently involved in anxiety-related behaviors and there is increasing support for a role of this peptide in mood disorders such as depression. Furthermore, recent evidence suggests that NPY has a significant role in the neurobiological response to alcohol, including alcohol consumption, dependence, and withdrawal. In addition, NPY is beginning to emerge as an important modulator in the etiology of alcoholism that is independent from the addictive and reinforcing properties of the traditional system commonly associated with dopamine and instead, is strongly associated with innate emotionality. The recent developments elucidating the role of NPY in emotion and alcohol dependence are reviewed and the potential of the NPY system as a novel therapeutic strategy in the treatment of anxiety, depression and alcohol-related disorders is examined.
 

Holmes A, Picciotto MR. Galanin: a novel therapeutic target for depression, anxiety disorders and drug addiction? CNS Neurol Disord Drug Targets. 2006 Apr;5(2):225-32. Review.
Laboratory for Integrative Neuroscience, Section on Behavioral Science and Genetics, National Institute of Alcoholism and Alcohol Abuse, National Institutes of Health, Bethesda, Maryland 20892, USA. holmesan@mail.nih.gov
Galanin is a neuropeptide synthesized in many neuronal types including brainstem norepinephrine-producing cells of the locus coeruleus and the serotonin-producing neurons of the dorsal raphe nucleus. Galanin inhibits the firing of rodent norepinephrine, serotonin and dopamine neurons and reduces release of these neurotransmitters in forebrain target regions. The distribution of galanin and its receptors and its actions on monoamine signaling has fostered interest in this neuropeptide in the field of behavioral pharmacology and the potential role of galanin in the pathophysiology of neurological diseases such as Alzheimer's disease, epilepsy, stroke, and in psychiatric disorders such as anxiety, depression, and drug addiction, particularly withdrawal. In rodent models, expression of galanin in brain is altered by various stressors, while administration of galanin can modulate anxiety-like responses to stress. Emerging evidence further supports a role for galanin in the mediation of depression-related behaviors in rodents. Recently, galanin agonists have been shown to decrease behavioral signs of opiate withdrawal, which are thought to result from hyperactivation of brain stress pathways. Studies using genetically modified mice suggest that galanin normally plays a protective role against opiate reinforcement and withdrawal. The present article reviews current evidence on a potential role for galanin in modulating stress-related neural pathways and behaviors, and speculates on the therapeutic potential of targeting this galanin system for emotional disorders and opiate addiction.
 

Khan NA, McAlister FA, Rabkin SW, Padwal R, Feldman RD, Campbell NR, Leiter LA, Lewanczuk RZ, Schiffrin EL, Hill MD, Arnold M, Moe G, Campbell TS, Herbert C, Milot A, Stone JA, Burgess E, Hemmelgarn B, Jones C, Larochelle P, Ogilvie RI, Houlden R, Herman RJ, Hamet P, Fodor G, Carruthers G, Culleton B, Dechamplain J, Pylypchuk G, Logan AG, Gledhill N, Petrella R, Tobe S, Touyz RM; Canadian Hypertension Education Program. The 2006 Canadian Hypertension Education Program recommendations for the management of hypertension: Part II - Therapy. Can J Cardiol. 2006 May 15;22(7):583-93.
Division of General Internal Medicine, University of British Columbia, Vancouver, BC, Canada.
OBJECTIVE: To provide updated, evidence-based recommendations for the management of hypertension in adults. OPTIONS AND OUTCOMES: For lifestyle and pharmacological interventions, evidence from randomized, controlled trials and systematic reviews of trials was preferentially reviewed. Changes in cardiovascular morbidity and mortality were the primary outcomes of interest. For lifestyle interventions, blood pressure (BP) lowering was accepted as a primary outcome given the lack of long-term morbidity/mortality data in this field. For treatment of patients with kidney disease, the development of proteinuria or worsening of kidney function was also accepted as a clinically relevant primary outcome. EVIDENCE: MEDLINE searches were conducted from November 2004 to October 2005 to update the 2005 recommendations. In addition, reference lists were scanned and experts were contacted to identify additional published studies. All relevant articles were reviewed and appraised independently by content and methodological experts using prespecified levels of evidence. RECOMMENDATIONS: Lifestyle modifications to prevent and/or treat hypertension include the following: perform 30 min to 60 min of aerobic exercise four to seven days per week; maintain a healthy body weight (body mass index of 18.5 kg/m2 to 24.9 kg/m2) and waist circumference (less than 102 cm for men and less than 88 cm for women); limit alcohol consumption to no more than 14 standard drinks per week in men or nine standard drinks per week in women; follow a diet that is reduced in saturated fat and cholesterol and that emphasizes fruits, vegetables and low-fat dairy products; restrict salt intake; and consider stress management in selected individuals. Treatment thresholds and targets should take into account each individual's global atherosclerotic risk, target organ damage and comorbid conditions. BP should be lowered to less than 140/90 mmHg in all patients, and to less than 130/80 mmHg in those with diabetes mellitus or chronic kidney disease (regardless of the degree of proteinuria). Most adults with hypertension require more than one agent to achieve these target BPs. For adults without compelling indications for other agents, initial therapy should include thiazide diuretics. Other agents appropriate for first-line therapy for diastolic hypertension with or without systolic hypertension include beta-blockers (in those younger than 60 years), angiotensin-converting enzyme (ACE) inhibitors (in nonblack patients), long-acting calcium channel blockers or angiotensin receptor antagonists. Other agents for first-line therapy for isolated systolic hypertension include long-acting dihydropyridine calcium channel blockers or angiotensin receptor antagonists. Certain comorbid conditions provide compelling indications for first-line use of other agents: in patients with angina, recent myocardial infarction or heart failure, beta-blockers and ACE inhibitors are recommended as first-line therapy; in patients with diabetes mellitus, ACE inhibitors or angiotensin receptor antagonists (or in patients without albuminuria, thiazides or dihydropyridine calcium channel blockers) are appropriate first-line therapies; and in patients with nondiabetic chronic kidney disease, ACE inhibitors are recommended. All hypertensive patients should have their fasting lipids screened, and those with dyslipidemia should be treated using the thresholds, targets and agents recommended by the Canadian Hypertension Education Program Working Group on the management of dyslipidemia and the prevention of cardiovascular disease. Selected patients with hypertension, but without dyslipidemia, should also receive statin therapy and/or acetylsalicylic acid therapy. VALIDATION: All recommendations were graded according to strength of the evidence and voted on by the 45 members of the Canadian Hypertension Education Program Evidence-Based Recommendations Task Force. All recommendations reported here achieved at least 95% consensus. These guidelines will continue to be updated annually.
 

Lehoux S, Castier Y, Tedgui A. Molecular mechanisms of the vascular responses to haemodynamic forces. J Intern Med. 2006 Apr;259(4):381-92. Review.
From the INSERM U589, Hopital Lariboisiere, Paris, France.
Blood vessels are permanently subjected to mechanical forces in the form of stretch, encompassing cyclic mechanical strain due to the pulsatile nature of blood flow and shear stress. Significant variations in mechanical forces, of physiological or physiopathological nature, occur in vivo. These are accompanied by phenotypical modulation of smooth muscle cells and endothelial cells, producing structural modifications of the arterial wall. In all the cases, vascular remodelling can be allotted to a modification of the tensional strain or shear, and underlie a trend to reestablish baseline mechanical conditions. Vascular cells are equipped with numerous receptors that allow them to detect and respond to the mechanical forces generated by pressure and shear stress. The cytoskeleton and other structural components have an established role in mechanotransduction, being able to transmit and modulate tension within the cell via focal adhesion sites, integrins, cellular junctions and the extracellular matrix. Mechanical forces also initiate complex signal transduction cascades, including nuclear factor-kappaB and mitogen-activated protein kinase pathways, leading to functional changes within the cell.
 

Ricciardolo FL, Nijkamp FP, Folkerts G. Nitric oxide synthase (NOS) as therapeutic target for asthma and chronic obstructive pulmonary disease. Curr Drug Targets. 2006 Jun;7(6):721-35. Review.
Unit of Pneumology, IRCCS Gaslini Institute, Genoa, Italy.
In the respiratory tract, NO is produced by residential and inflammatory cells. NO is generated via oxidation of L-arginine that is catalysed by the enzyme NO synthase (NOS). NOS exists in three distinct isoforms: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). NO derived from the constitutive isoforms of NOS (nNOS and eNOS) and other NO-adduct molecules (nitrosothiols) are able to modulate bronchomotor tone. NO derived from the inducible isoform of NO synthase, up-regulated by different cytokines via NF-kappaB-dependent pathway, seems to be a pro-inflammatory mediator with immunomodulatory effects. The production of NO under oxidative stress conditions secondarily generates strong oxidising agents (reactive nitrogen species) that may amplify the inflammatory response in asthma and COPD. Moreover, NO can be exhaled and levels are abnormal in stable atopic asthma and during exacerbations in both asthma and COPD. Exhaled NO might therefore be a non-invasive tool to monitor the underlying inflammatory process. It is suggested that NOS regulation provides a novel target in the prevention and treatment of chronic inflammatory diseases of the airways such as asthma and COPD.
 

Asthma:

14847.  Casalino-Matsuda SM, Monzon ME, Forteza RM. Epidermal growth factor receptor activation by epidermal growth factor mediates oxidant-induced goblet cell metaplasia in human airway epithelium. Am J Respir Cell Mol Biol. 2006 May;34(5):581-91.

14848.  Chen E, Hanson MD, Paterson LQ, Griffin MJ, Walker HA, Miller GE. Socioeconomic status and inflammatory processes in childhood asthma: the role of psychological stress. J Allergy Clin Immunol. 2006 May;117(5):1014-20.

14849.  Ghosh S, Janocha AJ, Aronica MA, Swaidani S, Comhair SA, Xu W, Zheng L, Kaveti S, Kinter M, Hazen SL, Erzurum SC. Nitrotyrosine proteome survey in asthma identifies oxidative mechanism of catalase inactivation. J Immunol. 2006 May 1;176(9):5587-97.

14850.  Li YF, Gauderman WJ, Avol E, Dubeau L, Gilliland FD. Associations of tumor necrosis factor G-308A with childhood asthma and wheezing. Am J Respir Crit Care Med. 2006 May 1;173(9):970-6.

14851.  Tsoumakidou M, Papadopouli E, Tzanakis N, Siafakas NM. Airway inflammation and cellular stress in noneosinophilic atopic asthma. Chest. 2006 May;129(5):1194-202.

Depression:

14852.  Adelman EM. Mind-body intelligence: a new perspective integrating Eastern and Western healing traditions. Holist Nurs Pract. 2006 May-Jun;20(3):147-51. Review.

14853.  Balaban V. Psychological assessment of children in disasters and emergencies. Disasters. 2006 Jun;30(2):178-98. Review.

14854.  Britton JR. Global satisfaction with perinatal hospital care: stability and relationship to anxiety, depression, and stressful medical events. Am J Med Qual. 2006 May-Jun;21(3):200-5.

14855.  Broad RD, Wheeler K. An adult with childhood medical trauma treated with psychoanalytic psychotherapy and EMDR: a case study. Perspect Psychiatr Care. 2006 May;42(2):95-105.

14856.  Croghan IT, Bronars C, Patten CA, Schroeder DR, Nirelli LM, Thomas JL, Clark MM, Vickers KS, Foraker R, Lane K, Houlihan D, Offord KP, Hurt RD. Is smoking related to body image satisfaction, stress, and self-esteem in young adults? Am J Health Behav. 2006 May-Jun;30(3):322-33.

14857.  Delahanty LM, Conroy MB, Nathan DM; Diabetes Prevention Program Research Group.  Psychological predictors of physical activity in the diabetes prevention program. J Am Diet Assoc. 2006 May;106(5):698-705.

14858.  Fekkes M, Pijpers FI, Fredriks AM, Vogels T, Verloove-Vanhorick SP. Do bullied children get ill, or do ill children get bullied? A prospective cohort study on the relationship between bullying and health-related symptoms. Pediatrics. 2006 May;117(5):1568-74.

14859.  Geracioti TD Jr, Carpenter LL, Owens MJ, Baker DG, Ekhator NN, Horn PS, Strawn JR, Sanacora G, Kinkead B, Price LH, Nemeroff CB. Elevated cerebrospinal fluid substance p concentrations in posttraumatic stress disorder and major depression. Am J Psychiatry. 2006 Apr;163(4):637-43.

14860.  Landgraf R. The involvement of the vasopressin system in stress-related disorders. CNS Neurol Disord Drug Targets. 2006 Apr;5(2):167-79. Review.

14861.  Meiser-Stedman RA, Yule W, Dalgleish T, Smith P, Glucksman E. The role of the family in child and adolescent posttraumatic stress following attendance at an emergency department. J Pediatr Psychol. 2006 May;31(4):397-402.

14862.  Merali Z, Kent P, Du L, Hrdina P, Palkovits M, Faludi G, Poulter MO, Bedard T, Anisman H. Corticotropin-releasing hormone, arginine vasopressin, gastrin-releasing peptide, and neuromedin B alterations in stress-relevant brain regions of suicides and control subjects. Biol Psychiatry. 2006 Apr 1;59(7):594-602.

14863.  Mitani H, Shirayama Y, Yamada T, Kawahara R. Plasma levels of homovanillic acid, 5-hydroxyindoleacetic acid and cortisol, and serotonin turnover in depressed patients. Prog Neuropsychopharmacol Biol Psychiatry. 2006 May;30(3):531-4.

14864.  Moreno A, Piwowarczyk L, LaMorte WW, Grodin MA. Characteristics and utilization of primary care services in a torture rehabilitation center. J Immigr Minor Health. 2006 Apr;8(2):163-71.

14865.  Nakao M, Yano E. A comparative study of behavioural, physical and mental health status between term-limited and tenure-tracking employees in a population of Japanese male researchers. Public Health. 2006 Apr;120(4):373-9.

14866.  Rapkin AJ, Morgan M, Sogliano C, Biggio G, Concas A. Decreased neuroactive steroids induced by combined oral contraceptive pills are not associated with mood changes. Fertil Steril. 2006 May;85(5):1371-8.    

14867.  Roth G, Ekblad S. A longitudinal perspective on depression and sense of coherence in a sample of mass-evacuated adults from Kosovo. J Nerv Ment Dis. 2006 May;194(5):378-81.

14868.  Schwartz L, Drotar D. Posttraumatic stress and related impairment in survivors of childhood cancer in early adulthood compared to healthy peers. J Pediatr Psychol. 2006 May;31(4):356-66.

14869.  Smith MV, Poschman K, Cavaleri MA, Howell HB, Yonkers KA. Symptoms of posttraumatic stress disorder in a community sample of low-income pregnant women. Am J Psychiatry. 2006 May;163(5):881-4.

14870.  Taylor FB, Lowe K, Thompson C, McFall MM, Peskind ER, Kanter ED, Allison N, Williams J, Martin P, Raskind MA. Daytime prazosin reduces psychological distress to trauma specific cues in civilian trauma posttraumatic stress disorder. Biol Psychiatry. 2006 Apr 1;59(7):577-81.

14871.  Vieweg WV, Julius DA, Fernandez A, Beatty-Brooks M, Hettema JM, Pandurangi AK.  Posttraumatic stress disorder: clinical features, pathophysiology, and treatment. Am J Med. 2006 May;119(5):383-90. Review.

14872.  Vollmer-Conna U, Aslakson E, White PD. An empirical delineation of the heterogeneity of chronic unexplained fatigue in women. Pharmacogenomics. 2006 Apr;7(3):355-64.

Hypertension:                                  

14873.  Bigi R, Bestetti A, Strinchini A, Conte A, Gregori D, Brusoni B, Fiorentini C. Combined assessment of left ventricular perfusion and function by gated single-photon emission computed tomography for the risk stratification of high-risk hypertensive patients. J Hypertens. 2006 Apr;24(4):767-73.

14874.  Harmsen P, Lappas G, Rosengren A, Wilhelmsen L. Long-term risk factors for stroke: twenty-eight years of follow-up of 7457 middle-aged men in Goteborg, Sweden. Stroke. 2006 Jul;37(7):1663-7.    

14875.  Heistad DD. Oxidative stress and vascular disease: 2005 Duff lecture. Arterioscler Thromb Vasc Biol. 2006 Apr;26(4):689-95.    

14876.  Karalliedde J, Viberti G. Evidence for renoprotection by blockade of the renin-angiotensin-aldosterone system in hypertension and diabetes. J Hum Hypertens. 2006 Apr;20(4):239-53. Review.

14877.  Paridon SM, Alpert BS, Boas SR, Cabrera ME, Caldarera LL, Daniels SR, Kimball TR, Knilans TK, Nixon PA, Rhodes J, Yetman AT; American Heart Association Council on Cardiovascular Disease in the Young, Committee on Atherosclerosis, Hypertension, and Obesity in Youth. Clinical stress testing in the pediatric age group: a statement from the American Heart Association Council on Cardiovascular Disease in the Young, Committee on Atherosclerosis, Hypertension, and Obesity in Youth. Circulation. 2006 Apr 18;113(15):1905-20.    

14878.  Seasholtz TM, Wessel J, Rao F, Rana BK, Khandrika S, Kennedy BP, Lillie EO, Ziegler MG, Smith DW, Schork NJ, Brown JH, O'Connor DT. Rho kinase polymorphism influences blood pressure and systemic vascular resistance in human twins: role of heredity. Hypertension. 2006 May;47(5):937-47.    

14879.  Webb MS, Gonzalez LO. The burden of hypertension: mental representations of African American women. Issues Ment Health Nurs. 2006 Apr;27(3):249-71. 

Heart Disease:

14880.  Beeres SL, Bax JJ, Kaandorp TA, Zeppenfeld K, Lamb HJ, Dibbets-Schneider P, Stokkel MP, Fibbe WE, de Roos A, van der Wall EE, Schalij MJ, Atsma DE. Usefulness of intramyocardial injection of autologous bone marrow-derived mononuclear cells in patients with severe angina pectoris and stress-induced myocardial ischemia. Am J Cardiol. 2006 May 1;97(9):1326-31.  

14881.  Beeres SL, Bax JJ, Dibbets P, Stokkel MP, Zeppenfeld K, Fibbe WE, van der Wall EE, Schalij MJ, Atsma DE. Effect of intramyocardial injection of autologous bone marrow-derived mononuclear cells on perfusion, function, and viability in patients with drug-refractory chronic ischemia. J Nucl Med. 2006 Apr;47(4):574-80.

14882.  Denollet J, Pedersen SS, Vrints CJ, Conraads VM. Usefulness of type D personality in predicting five-year cardiac events above and beyond concurrent symptoms of stress in patients with coronary heart disease. Am J Cardiol. 2006 Apr 1;97(7):970-3.  

14883.  Guttormsen B, Nee L, Makielski JC, Keevil JG. Transient left ventricular apical ballooning: a review of the literature. WMJ. 2006 May;105(3):49-54. Review.

14884.  Koenig W, Twardella D, Brenner H, Rothenbacher D. Lipoprotein-associated phospholipase A2 predicts future cardiovascular events in patients with coronary heart disease independently of traditional risk factors, markers of inflammation, renal function, and hemodynamic stress. Arterioscler Thromb Vasc Biol. 2006 Jul;26(7):1586-93.  

14885.  Maeder M, Fehr T, Rickli H, Ammann P. Sepsis-associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides. Chest. 2006 May;129(5):1349-66. Review.

14886.  Meyer MC, Mooney RP, Sekera AK. A critical pathway for patients with acute chest pain and low risk for short-term adverse cardiac events: role of outpatient stress testing. Ann Emerg Med. 2006 May;47(5):435.e1-3.  

14887.  Mukherjee S, Belbin TJ, Spray DC, Mukhopadhyay A, Nagajyothi F, Weiss LM, Tanowitz HB. Microarray technology in the investigation of diseases of myocardium with special reference to infection. Front Biosci. 2006 May 1;11:1802-13. Review.

14888.  Owen PJ, Rajiv C, Vinereanu D, Mathew T, Fraser AG, Lazarus JH. Subclinical hypothyroidism, arterial stiffness, and myocardial reserve. J Clin Endocrinol Metab. 2006 Jun;91(6):2126-32.  

14889.  Quere JP, Monin JL, Levy F, Petit H, Baleynaud S, Chauvel C, Pop C, Ohlmann P, Lelguen C, Dehant P, Gueret P, Tribouilloy C. Influence of preoperative left ventricular contractile reserve on postoperative ejection fraction in low-gradient aortic stenosis. Circulation. 2006 Apr 11;113(14):1738-44.  

14890.  Sharma R, Gaze DC, Pellerin D, Mehta RL, Gregson H, Streather CP, Collinson PO, Brecker SJ. Cardiac structural and functional abnormalities in end stage renal disease patients with elevated cardiac troponin T. Heart. 2006 Jun;92(6):804-9.  

14891.  Skulstad H, Urheim S, Edvardsen T, Andersen K, Lyseggen E, Vartdal T, Ihlen H, Smiseth OA. Grading of myocardial dysfunction by tissue Doppler echocardiography: a comparison between velocity, displacement, and strain imaging in acute ischemia. J Am Coll Cardiol. 2006 Apr 18;47(8):1672-82.  

14892.  White M, Ducharme A, Ibrahim R, Whittom L, Lavoie J, Guertin MC, Racine N, He Y, Yao G, Rouleau JL, Schiffrin EL, Touyz RM. Increased systemic inflammation and oxidative stress in patients with worsening congestive heart failure: improvement after short-term inotropic support. Clin Sci (Lond). 2006 Apr;110(4):483-9.

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