Urinary retention in patients with bladder outlet obstruction (BOO) and in patients taking antimuscarinic medications for the treatment of OAB has been reported in postmarketing experience in patients taking mirabegron. A controlled clinical safety study in patients with BOO did not demonstrate increased urinary retention in Myrbetriq patients; however, Myrbetriq should be administered with caution to patients with clinically significant BOO. Myrbetriq should also be administered with caution to patients taking antimuscarinic medications for the treatment of OAB.
In addition to its effects on myocardial contractility, digoxin exerts autonomic effects through its binding to sodium pumps in the plasma membranes of neurons in the central and peripheral nervous systems. These effects include inhibition of sympathetic nervous outflow, sensitization of baroreceptors, and increased parasympathetic (vagal) tone. Digoxin also alters the electrophysiologic properties of the heart by a direct action on the cardiac conduction system. At therapeutic doses, digoxin decreases automaticity at the AV node, prolonging the effective refractory period of AV nodal tissue and slowing conduction velocity through the node. These combined vagotonic and electrophysiologic properties underlie the use of digoxin in the treatment of patients with atrial fibrillation and rapid ventricular response rates; both the decreased automaticity of AV nodal tissue and the decreased conduction velocity through the node increase the degree of AV block, and thereby decrease the ventricular response rate.