Chemical formula: C₁₃H₂₄N₄O₃S Molecular mass: 316.42 g/mol PubChem compound: 33624
Timolol interacts in the following cases:
Enhanced risk of ventricular arrhythmia, particularly torsades de pointes.
Clinical and ECG monitoring is recommended.
Enhancement of hypotensive effect. Increased risk of orthostatic hypotension.
Reduction in the antihypertensive effect (inhibition of vasodilator prostaglandins by non-steroidal anti-inflammatory drugs and of water and salt retention by phenylbutazone).
Potentiated systemic beta-blockade (e.g. decreased heart rate, depression) has been reported during combined treatment with CYP2D6 inhibitors (e.g. quinidine, fluoxetine, paroxetine) and timolol.
All beta-blockers may mask certain symptoms of hypoglycaemia: palpitations and tachycardia.
Warn the patient and, particularly at the beginning of treatment, self-monitoring of glycaemia by the patient should be increased.
Contractility, automatism and conduction disorders (suppression of compensatory sympathetic mechanisms).
Clinical and ECG monitoring is recommended.
Enhancement of hypotension risk, notably orthostatic.
Oral calcium-channel antagonists may be used in combination with beta-adrenergic blocking agents when heart function is normal, but should be avoided in patients with impaired cardiac function.
The potential exists for hypotension, AV conduction disturbances and left ventricular failure to occur in patients receiving a beta-blocking agent when an oral calcium-channel blocker is added to the treatment regimen. The nature of any cardiovascular adverse effects tends to depend on the type of calcium-channel blocker used. Dihydropyridine derivatives, such as nifedipine, may lead to hypotension, whereas verapamil or diltiazem have a greater propensity to lead to AV conduction disturbances or left ventricular failure when used with a beta-blocker.
Intravenous calcium channel blockers should be used with caution in patients receiving beta-adrenergic blocking agents.
Hypotension, cardiac failure in patients with latent or uncontrolled cardiac insufficiency (additional negative inotropic effects). Moreover, the beta-blocker can minimise the sympathetic reflex reaction, which comes into play in the event of excessive haemodynamic repercussion.
Reduction in compensatory cardiovascular mechanisms by beta-blockers. Beta-adrenergic inhibition may be counteracted during surgery by beta-mimetics.
As a general rule, do not discontinue beta-blocker therapy, and in any event, avoid a sudden discontinuation. The anaesthetist should be advised of this treatment.
Enhancement of hypotension risk, notably orthostatic. Vasodilatator effect and risk of hypotension, notably orthostatic (additional effect).
Enhancement of hypotension risk, notably orthostatic.
Automatism and conduction disorders (suppression of compensatory sympathetic mechanisms).
Clinical and ECG monitoring is recommended.
Enhancement of hypotension risk, notably orthostatic.
Blood pressure monitoring and, if necessary, dosage adjustment of the antihypertensive.
Automatism disorders (excessive bradycardia, sinus arrest), sinoatrial and atrioventricular conduction disorders and increased risk of ventricular rhythm disorders (torsades de pointes) as well as cardiac failure.
This combination should only take place under close clinical and ECG monitoring, particularly in elderly subjects or in those beginning treatment.
Oral beta-adrenergic blocking agents may exacerbate the rebound hypertension which can follow the withdrawal of clonidine.
Automatism disorders (excessive bradycardia, sinus arrest) sinoatrial and atrioventricular conduction disorders and cardiac failure.
This combination should only take place under close clinical and ECG monitoring, particularly in elderly subjects or those starting treatment.
With the dipyridamole by intravenous route: enhancement of the anti-hypertensive effect.
Potentiation of bradycardic effects can have fatal consequences. Beta-blockers are more at risk that they prevent adrenergic compensation mechanism.
Continuous clinical and ECG monitoring during 24 hours after the first dose.
With lidocaine used intravenously: increase in plasmatic concentrations of lidocaine with a possibility of adverse neurological and cardiac side effects (reduction in hepatic clearance of lidocaine).
Clinical and ECG monitoring and possibly testing of the plasmatic concentrations of lidocaine during the combined therapy and after the beta-blocker has been withdrawn. Adaptation if necessary of dosage regimen of lidocaine.
Risk of excessive bradycardia (additive bradycardial effects).
Contractility, automatism and conduction disorders (suppression of compensatory sympathetic mechanisms).
Clinical and ECG monitoring is recommended.
Close observation of the patient is recommended when a beta-blocker is administered to patients receiving catecholamine-depleting drugs such as reserpine, because of possible additive effects and the production of hypotension and/or marked bradycardia, which may produce vertigo, syncope, or postural hypotension.
Automatism disorders (excessive bradycardia, sinus arrest) sinoatrial and atrioventricular conduction disorders and cardiac failure.
This combination should only take place under close clinical and ECG monitoring, particularly in elderly subjects or those starting treatment.
Due to its negative effect on conduction time, beta-blockers should only be given with caution to patients with first degree heart block.
Choroidal detachment has been reported with administration of aqueous suppressant therapy (e.g. timolol, acetazolamide) after filtration procedures.
Patients with severe peripheral circulatory disturbance/disorders (i.e. severe forms of Raynaud’s disease or Raynaud’s syndrome) should be treated with caution.
It should be used with caution in patients with metabolic acidosis.
Beta-blockers have been reported to aggravate psoriasis and its use in this condition therefore deserves careful consideration.
There are no adequate data for the use of timolol in pregnant women. Timolol should not be used during pregnancy unless clearly necessary.
Epidemiological studies have not revealed malformative effects but show a risk for intra uterine growth retardation when beta-blockers are administered by the oral route. In addition, signs and symptoms of betablockade (e.g. bradycardia, hypotension, respiratory distress and hypoglycaemia) have been observed in the neonate when beta-blockers have been administered until delivery. If timolol is administered until delivery, the neonate should be carefully monitored during the first days of life.
Beta-blockers are excreted in breast milk. However, at therapeutic doses of timolol it is not likely that sufficient amounts would be present in breast milk to produce clinical symptoms of beta-blockade in the infant.
Timolol has not been found to have any effect on fertility in animal studies.
Timolol has minor influence on the ability to drive and use machines.
No studies on the effect of this medicinal product on the ability to drive have been conducted. While driving vehicles or operating different machines, it should be taken into account that occasionally visual disturbances may occur including refractive changes, diplopia, ptosis, frequent episodes of mild and transient blurred vision and occasional episodes of dizziness or fatigue.
© All content on this website, including data entry, data processing, decision support tools, "RxReasoner" logo and graphics, is the intellectual property of RxReasoner and is protected by copyright laws. Unauthorized reproduction or distribution of any part of this content without explicit written permission from RxReasoner is strictly prohibited. Any third-party content used on this site is acknowledged and utilized under fair use principles.
