title: The vasopressor system in patients with heart failure due to idiopathic dilated cardiomyopathy--influence of the clinical stage of disease and of chronic drug treatment.
abstract: Alterations in the vasopressor system found in cardiac failure are part of compensatory measures that may modify pharmacologic-therapeutic response. Therefore, in 64 patients with dilated cardiomyopathy, we investigated its enhanced activity in different clinical stages of the disease as compared to normal controls. Patients in NYHA class II (n = 20) demonstrated increased activity of the sympathico-adrenal, renin-angiotensin-aldosterone, vasopressin, and atrial natriuretic factor systems, while maximum values were found in patients of NYHA class IV (n = 24). In these patients, noradrenaline was enhanced by a factor of 7, adrenaline by a factor of 2, plasma-renin-activity by a factor of 7, angiotensin II by a factor of 2.5, aldosterone by a factor of 5, vasopressin by a factor of 1.5, and ANF by a factor of 4 as compared to normal controls. Clinical NYHA classes correlated to a certain degree with the various plasma hormones. Patients treated with an aldosterone inhibitor in addition to digitalis and diuretics revealed significantly higher values for aldosterone, vasopressin, and angiotensin II as compared to those who received digitalis and diuretics alone. The addition of ACE-inhibitor therapy resulted in a decrease of angiotensin II, aldosterone, and vasopressin. Plasma catecholamines and ANF, however, did not change under the influence of cardiac medication. Diuretic treatment in NYHA class II patients reduced plasma volumes (p less than 0.01). Plasma volume in NYHA class IV patients only was found to be higher than in normal controls. Thus, analysis of the neurohumoral system can aid both in the identification of the clinical degree of dilated cardiomyopathy and in its optimal therapy.
authors.affiliation: Kerckhoff-Klinik, Bad Nauheim, FRG.
authors.forename: V
authors.initials: V
authors.lastname: Mitrovic
authors.forename: J
authors.initials: J
authors.lastname: Thormann
authors.forename: P
authors.initials: P
authors.lastname: Kornecki
authors.forename: M
authors.initials: M
authors.lastname: Volz
authors.forename: H
authors.initials: H
authors.lastname: Neuss
authors.forename: M
authors.initials: M
authors.lastname: Schlepper
mesh_terms: D000328:Adult; D000368:Aged; D009320:Atrial Natriuretic Factor / Q000097:blood; D002303:Cardiac Output, Low / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D002311:Cardiomyopathy, Dilated / Q000150:complications / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D002395:Catecholamines / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010953:Plasma Volume / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000097:blood*
chemical_list: D002395:Catecholamines; D014662:Vasoconstrictor Agents; D009320:Atrial Natriuretic Factor