The effects of bromocriptine in patients with congestive heart failure

The sympathetic nervous system and the renin-angiotensin system are activated in patients with congestive heart fallure (CHF) and could be contributing to excessive peripheral vasoconstriction and impaired myocardial performance. Bromocriptine, an orally active ergot alkaloid with dopaminergic receptor agonist actions, is known to lower plasma norepinephrine in humans. It could also possess direct vasodilator activity through vascular dopaminergic receptors. To assess the effects of bromocriptine on hemodynamic measurements, sympathetic nervous system activity, and the renin-angiotensin system in patients with heart failure, we measured standard hemodynamic parameters and plasma norepinephrine and plasma renin activity before and following a single oral dose of 2.5 mg of bromocriptine in 10 patients with chronic stable heart failure. The following statistically significant (p < 0.01) peak responses were noted: plasma norepinephrine decreased from a mean ± 1 SD of 581 ± 194 to 366 ± 181 pg/ml; mean heart rate declined from 87 ± 16 to 78 ± 17 bpm; mean blood pressure was reduced from 87 ± 9 to 73 ± 9 mm Hg; systemic vascular resistance decreased from 1494 ± 361 to 1249 ± 289 dynes · sec · cm^-5; stroke volume index increased from 27 ± 7 to 33 ± 10 ml/beat/M²; left ventricular filling pressure decreased from 28 ± 8 to 21 ± 8 mm Hg; and mean right atrial pressure fell from 10 ± 4 to 7 ± 4 mm Hg. Plasma renin activity did not change significantly. All patients tolerated the drug well. Although the effects of bromocriptine on plasma norepinephrine may contribute to an improved hemodynamic state, other mechanisms of action are likely. A direct vasodilator effect via vascular dopaminergic receptor stimulation is possible. We conclude that bromocriptine improves the hemodynamic profile in heart failure acutely and that long-term studies are appropriate to better characterize the role of this agent.