title: ACE inhibition improves vagal reactivity in patients with heart failure.
abstract: The deranged autonomic control of heart rate was studied in 34 patients with heart failure (New York Heart Association [NYHA] functional class II to III) by examining the carotid sinus baroreflex. The carotid sinus baroreceptors were stimulated by graded suction. The slope of the regression line between increases in cycle length and the degree of neck suction was taken as an index of baroreflex sensitivity. The reflex response is mediated by a selective increase of vagal efferent activity. Baroreflex sensitivity therefore represents a measure of vagal reactivity. Using multiple regression analysis, baroreflex sensitivity (BS) correlated positively to stroke volume index (SVI) and inversely to plasma renin activity (PRA) and to age: BS = 0.47 SVI - 0.38 PRA - 0.23 age + constant (r = 0.74; p less than 0.0005). In addition to digitalis and diuretics, angiotensin-converting enzyme (ACE) inhibitors (captopril or enalapril) were given to 16 patients for a mean of 17 +/- 3 days. The patients with hemodynamic improvement (group A) exhibited improved baroreflex sensitivity (1.4 +/- 0.4 to 3.6 +/- 1.2 msec/mm Hg; p less than 0.01). Baroreflex sensitivity remained unchanged (3.1 +/- 0.8 to 2.4 +/- 1.0 msec/mm Hg; n.s.) in the patients without hemodynamic improvement (group B). The increase in reflex sensitivity did not correlate with hemodynamic alterations. Baroreflex sensitivity during ACE inhibition (BSD) was only related to the baseline baroreflex sensitivity (BSB): BSD = 2.8 BSB - 0.46 (r = 0.84; p less than 0.005). In patients with heart failure, reflex bradycardia decreases with age and with PRA and increases with stroke volume. Chronic therapy with ACE inhibitors enhances vagal reactivity in patients with hemodynamic improvement.
authors.affiliation: Department of Internal Medicine, Ruprecht-Karls-University, Heidleberg, W. Germany.
authors.forename: K J
authors.initials: KJ
authors.lastname: Osterziel
authors.forename: R
authors.initials: R
authors.lastname: Dietz
authors.forename: W
authors.initials: W
authors.lastname: Schmid
authors.forename: K
authors.initials: K
authors.lastname: Mikulaschek
authors.forename: J
authors.initials: J
authors.lastname: Manthey
authors.forename: W
authors.initials: W
authors.lastname: Kübler
mesh_terms: D000328:Adult; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002216:Captopril / Q000627:therapeutic use; D002311:Cardiomyopathy, Dilated / Q000188:drug therapy / Q000503:physiopathology*; D002346:Carotid Sinus / Q000187:drug effects / Q000503:physiopathology; D003327:Coronary Disease / Q000188:drug therapy / Q000503:physiopathology*; D004656:Enalapril / Q000627:therapeutic use; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011311:Pressoreceptors / Q000187:drug effects / Q000503:physiopathology; D012018:Reflex / Q000187:drug effects / Q000502:physiology; D014630:Vagus Nerve / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D004656:Enalapril; D002216:Captopril