In a study of 28 subjects, beta-adrenergic stimulation with dobutamine caused significant and comparable acceleration of left ventricular isovolumic relaxation in both normal and severe CHF patients.
Observational (n=28)
Does dobutamine infusion improve left ventricular isovolumic relaxation in patients with severe congestive heart failure compared to normal subjects?
Beta-adrenergic stimulation with dobutamine preserves its positive lusitropic effect (acceleration of left ventricular relaxation) in patients with severe heart failure, despite an attenuated positive inotropic response.
BACKGROUND: We tested the hypothesis that beta-adrenergic receptor-stimulated acceleration of left ventricular (LV) isovolumic relaxation (i.e., positive lusitropic response) is attenuated in patients with severe congestive heart failure (CHF) compared with patients without LV dysfunction or CHF. METHODS AND RESULTS: The beta-adrenergic agonist dobutamine was infused by the intracoronary route in 14 subjects (normal group, six; CHF patients, eight) and by the intravenous route in a second group of 14 subjects (normal group, four; CHF patients, 10). The positive inotropic response to intracoronary or intravenous dobutamine was substantially and significantly reduced in the patients with CHF. LV isovolumic relaxation rate was determined by the methods of Weiss (TL), Mirsky (T1/2), and by a nonlinear regression technique (TNL). LV isovolumic relaxation assessed by all three methods was significantly prolonged in CHF patients compared with normal subjects. Intracoronary and intravenous infusions of dobutamine caused significant acceleration of LV isovolumic relaxation in both normal subjects and patients with CHF. The magnitude of the dobutamine-stimulated acceleration of isovolumic relaxation in patients with CHF was comparable with that in normal subjects. CONCLUSIONS: These data demonstrate that beta-adrenergic receptor stimulation causes significant acceleration of LV isovolumic relaxation in both normal subjects and patients with severe CHF. Coronary to our hypothesis, the lusitropic response to beta-adrenergic stimulation is well preserved in patients with severe CHF despite substantial attenuation of the beta-adrenergic positive inotropic response. These findings have potentially important implications regarding the physiology and pharmacology of adrenergically mediated LV relaxation in humans.
Parker et al. (1991) conducted an observational in Severe congestive heart failure (CHF) (n=28). Dobutamine vs. Normal subjects was evaluated on Left ventricular (LV) isovolumic relaxation rate. In a study of 28 subjects, beta-adrenergic stimulation with dobutamine caused significant and comparable acceleration of left ventricular isovolumic relaxation in both normal and severe CHF patients.