Ziac Drug Interactions

Combinations not recommended: Lithium: Bisoprolol + hydrochlorothiazide (Ziac) may intensify the cardiotoxic and neurotoxic effect of lithium through a reduction of lithium excretion.
Calcium antagonists of the verapamil type and to a lesser extent of the diltiazem type: Negative effect on contractility and atrio-ventricular conduction. Intravenous administration of verapamil in patients on s-blocker treatment may lead to profound hypotension and atrioventricular block.
Centrally-acting antihypertensive agents (e.g. clonidine, methyldopa, moxonidine, rilmenidine): Concomitant use of centrally-acting antihypertensive agents may lead to a further reduction in heart rate and cardiac output and to vasodilatation. Abrupt withdrawal, particularly if prior to beta-blocker discontinuation, may increase the risk of 'rebound hypertension'.
Combinations to be used with caution: Calcium antagonists of the dihydropyridine type (e.g. nifedipine, amlodipine): Concomitant use may increase the risk of hypotension, and an increase in the risk of a further deterioration of the ventricular pump function in patients with heart failure cannot be excluded.
Concomitant use with other antihypertensive agents or with other medicinal products with blood pressure lowering potential (e.g. tricyclic antidepressants, barbiturates, phenothiazines) may increase the risk of hypotension.
ACE inhibitors (e.g. captopril, enalapril), Angiotensin II antagonists: Risk of significant fall in blood pressure and/or acute renal failure during initiation of ACE inhibitor therapy in patients with preexisting sodium depletion (particularly in patients with renal artery stenosis).
If prior diuretic therapy has produced sodium depletion, either stop the diuretic 3 days before starting ACE inhibitor therapy, or initiate ACE inhibitor therapy at a low dose.
Class-I antiarrhythmic agents (e.g. quinidine, disopyramide, lidocaine, phenytoin; flecainide, propafenone): Effect on atrio-ventricular impulse conduction time may be potentiated and negative inotropic effect increased.
Class-III antiarrhythmic agents (e.g. amiodarone): Effect on atrio-ventricular conduction time may be potentiated.
Antiarrhythmic agents that may induce torsade de pointes (Class IA e.g. quinidine, hydroquinidine, disopyramide, and Class III e.g. amiodarone, sotalol, dofetilide, ibutilide): Hypokalemia may facilitate the occurrence of torsades de pointes.
Nonantiarrhythmic agents that may induce torsade de pointes (e.g. astemizole, i.v. erythromycin, halofantrine, pentamidine, sparfloxacin, terfenadine, vincamine): Hypokalemia may facilitate the occurrence of torsades de pointes.
Parasympathomimetic agents: Concomitant use may increase atrio-ventricular conduction time and the risk of bradycardia.
Topical beta-blockers (e.g. eye drops for glaucoma treatment) may add to the systemic effects of bisoprolol.
Insulin and oral antidiabetic agents: Increase of blood sugar lowering effect.
Blockade of beta-adrenoceptors may mask symptoms of hypoglycemia.
Anesthetic agents: Attenuation of the reflex tachycardia and increase of the risk of hypotension (see Precautions).
Digitalis glycosides: Increase of atrio-ventricular conduction time, reduction in heart rate. If hypokalemia and/or hypomagnesemia develop during treatment with bisoprolol + hydrochlorothiazide (Ziac), the myocardium may show increased sensitivity to cardiac glycosides, leading to an enhanced effect and adverse effects of the glycosides.
Non-steroidal anti-inflammatory drugs (NSAIDs): NSAIDs may reduce the hypotensive effect. In patients developing hypovolemia, the concomitant administration of NSAIDs can trigger acute renal failure.
Beta-sympathomimetics (e.g. isoprenaline, dobutamine): Combination with bisoprolol may reduce the effect of both agents.
Sympathomimetics that activate both beta- and alpha-adrenoceptors (e.g. norepinephrine, epinephrine): Combination with bisoprolol may lead to blood pressure increase and exacerbated intermittent claudication. Such interactions are considered to be more likely with nonselective beta-blockers.
Potassium-wasting medicinal products (e.g. corticosteroids, ACTH, carbenoxolone, amphotericin B, furosemide, or laxatives): Concomitant use may result in increased potassium losses.
Methyldopa: Hemolysis due to the formation of antibodies to hydrochlorothiazide has been described in isolated cases.
The effect of uric-acid-lowering agents may be attenuated in concomitant administration of bisoprolol + hydrochlorothiazide (Ziac).
Cholestyramine and colestipol: Reduces the absorption of the hydrochlorothiazide component of bisoprolol + hydrochlorothiazide (Ziac).
Combinations to be considered: Mefloquine: Increased risk of decelerating the heart rate (bradycardia).
Monoamine oxidase inhibitors (except MAO-B inhibitors): Enhanced hypotensive effect of the beta-blockers but also risk of hypertensive crisis.
Corticosteroids: Reduced antihypertensive effect due to corticosteroid-induced water and sodium retention.
Rifampicin: Slight reduction of the half-life of bisoprolol possible due to the induction of hepatic drug-metabolizing enzymes. Normally no dosage adjustment is necessary.
Ergotamine derivatives: Exacerbation of peripheral circulatory disturbances.
In high-dose salicylate administration the toxic effect of salicylates on the central nervous system may be enhanced.