Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • 1995-1999  (2)
  • Chest pain  (1)
  • Key words Chronic hypoxia  (1)
  • Organic Chemistry
  • 1
    ISSN: 1433-0474
    Keywords: Schlüsselwörter Herzerkrankung ; Thoraxschmerz ; Psychosomatische Störung ; Key words Heart disease ; Chest pain ; Psychosomatic disorder
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Aims: Chest pain in children is often suspected to originate from cardiac disease. Aim of this study was to characterise the symptomatology of supposed cardiac chest pain in children and to investigate whether cardiac disease indeed underlies the pain or not. Furthermore, indications for a psychosomatic origin of the pain were searched for. Methods: The study involved 456 children referred to a pediatric cardiology outpatient department for chest pain. The patients were evaluated by ECG and echocardiogram. In selected cases, a chest radiograph, exercise ECG, or a 24-hour ECG monitoring was performed. A subgroup of 52 children and parents was interviewed on the basis of a questionnaire to evaluate the symptomatology of the pain, the family history, and psychosocial factors. Results: 15% of the children had diverse structural anomalies or arrhythmias usually of a low grade. The frequency of these findings did not differ from that of a control group without chest pain. Independent of the presence of these findings cardiac function was normal during exercise. The characteristic symptomatology (short, sharp, no radiation) did not correspond to that of ischemic heart disease, and was largely identical in children with and without cardiac findings. Factors typical of psychosomatic disorders were observed: a positive family history of „functional cardiac complaints” and other psychosomatic disorders particularly with regard to the mother, other somatic complaints prior to or along with the chest pain, and the presence of stressful life events. Conclusions: These data suggest that the described chest pain in children is a psychosomatic condition rather than caused by organic cardiac disease.
    Notes: Zusammenfassung Fragestellung: Thoraxschmerzen bei Kindern werden häufig mit Erkrankungen des Herzens in Zusammenhang gebracht. Im Rahmen dieser Studie sollten der Symptomkomplex kindlicher „Herzschmerzen” charakterisiert und seine Genese aus kardiologischer Sicht untersucht werden. Ein weiteres Ziel bestand darin, Hinweise auf psychogene Faktoren in der Schmerzgenese zu erhalten. Methode: In die Studie waren 456 Kinder einbezogen, die unter dem Verdacht von „Herzschmerzen” an kinderkardiologische Ambulanzen überwiesen worden waren. Die Basisdiagnostik umfaßte EKG und Echokardiographie. In vielen Fällen erfolgten zusätzlich Langzeit-EKG, Thoraxröntgen oder Belastungs-EKG. Zur Beschreibung der Symptomatik und zur Evaluierung familiärer und psychosozialer Faktoren wurde ein Fragebogen ausgearbeitet und damit eine Untergruppe von 52 Kindern untersucht. Ergebnisse: Bei 15% der Kinder wurden verschiedenartige und meist geringfügige strukturelle und funktionelle Abweichungen vom Normalbefund des Herzens beobachtet. Ihre Prävalenz war nicht höher als in einer Kontrollpopulation. Unabhängig vom Vorhandensein dieser Befunde war die kardiale Leistungsfähigkeit normal. Die typische Symptomatik (kurz, stechend, ohne Ausstrahlung) entsprach nicht der des ischämischen Herzschmerzes und war bei Kindern mit und ohne kardiale Veränderungen weitgehend identisch. Es wurden Faktoren beobachtet, die typisch für psychosomatische Erkrankungen sind: eine positive Familienanamnese für „funktionelle Herzbeschwerden” und andere psychosomatische Erkrankungen insbesondere hinsichtlich der Mutter, das gleichzeitige oder zeitlich versetzte Auftreten anderer Schmerzsyndrome und potentielle psychosoziale Belastungen. Schlußfolgerungen: Vermutlich spielen nicht manifeste organische Veränderungen am Herzen, sondern psychosomatische Faktoren in der Pathogenese des hier charakterisierten kindlichen Thoraxschmerzes eine Rolle.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1432-2013
    Keywords: Key words Chronic hypoxia ; Atrial natriuretic peptide ; Right ventricular hypertrophy ; ANP gene expression ; β/α-Myosin gene expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  It is unclear whether the increase in plasma atrial natriuretic peptide (ANP) concentration during hypoxia is due to direct, hypoxia-induced upregulation of ANP secretion in the heart, or to pressure overload of the right ventricle (RV) following hypoxia-induced pulmonary hypertension. To test the hypothesis that hypoxia leads to an early upregulation of the ANP gene, we examined the influence of acute and prolonged inspiratory hypoxia (6 h, 1 or 3 weeks) on the expression of ANP messenger ribonucleic acid (mRNA) in rat heart and compared the results with the expression of the ANP gene after acute pressure overload induced by experimental coarctation of the main pulmonary artery. As a molecular marker for hypertrophy we determined the ratio of α- and β-myosin gene expression. Hypoxia increased systolic RV pressure from 20.0 ± 1.6 mmHg to 27.8 ± 1.6 mmHg (P 〈 0.01) and 41.6 ± 2.1 mmHg (P 〈 0.05) after 1 and 3 weeks hypoxia respectively. The ANP plasma concentration did not change significantly after 6 h or 1 week: 232 ± 21 pg/ml (control), 246 ± 25 pg/ml (6 h), 268 ± 25 pg/ml (1 week), but increased significantly after 3 weeks hypoxia (446.8 ± 99.56 pg/ml; P 〈 0.05). ANP mRNA levels in different regions of the heart did not change after 6 h or 1 week hypoxia. After 3 weeks hypoxia ANP mRNA had increased 2.7-fold in the RV (P 〈 0.05), 4.2-fold in the left ventricle (LV, P 〈 0.05), 3.5-fold in the septum (S, P 〈 0.05) and about 1.4-fold in the right (n.s.) and left atrium (n.s.). Relative ventricular masses increased significantly only for the RV (190%, P 〈 0.05) during hypoxia. The β/α-myosin mRNA ratio did not change after 6 h hypoxia but, contrary to ANP gene expression, increased after just 1 week (6.1-fold in RV, 7.8-fold in LV, 6-fold in S; P 〈 0.05) and was more pronounced in the RV after 3 weeks (9.4-fold in RV, 7.6-fold in LV, 9.1-fold in S; P 〈 0.05). The increase in the β/α-myosin mRNA ratio in the LV contrasts with a lack of increase in relative ventricular mass. Acute pressure overload in the RV after pulmonary arterial banding significantly increased ANP-mRNA and the β/α-myosin mRNA ratio after 1 day in the RV. In the LV ANP mRNA was unchanged. The delayed upregulation of the ANP gene suggests that hypoxia per se is not a significant stimulus for ANP gene expression in the heart and that hypoxia-induced ANP-gene expression in the heart is regulated predominantly by the increase in RV afterload due to hypoxia-induced increased pulmonary pressure. The upregulation of ANP and β-myosin mRNA in the LV during chronic hypoxia has yet to be elucidated.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...