Landiolol Disease Interactions

Landiolol is contraindicated in patients with severe sinus bradycardia, sick sinus syndrome, or heart block greater than first degree. Patients with first-degree atrioventricular block, sinus node dysfunction, or conduction disorders are at increased risk of bradycardia (including sinus pause, heart block, severe bradycardia, and cardiac arrest). Heart rate and rhythm should be monitored in patients receiving landiolol. If bradyarrhythmia occurs, landiolol should be reduced or stopped.

Landiolol is contraindicated in patients with cardiogenic shock as it may precipitate further cardiovascular collapse and cause cardiac arrest.

Landiolol is contraindicated in patients with decompensated heart failure. Beta-blockers (like landiolol) can depress myocardial contractility and may precipitate heart failure and cardiogenic shock. At first sign/symptom of impending cardiac failure, landiolol should be stopped and supportive therapy should be started.

Landiolol is contraindicated in patients with pulmonary hypertension as it may precipitate cardiorespiratory decompensation.

Administration of beta-blockers alone in the setting of pheochromocytoma has been associated with a paradoxical increase in blood pressure due to the attenuation of beta receptor-mediated vasodilatation in skeletal muscle. In patients with pheochromocytoma, an alpha-blocking agent should be initiated prior to the use of any beta-blocking agent. Caution should be taken in the administration of these agents to patients suspected of having pheochromocytoma.

Hyperkalemic renal tubular acidosis may occur in patients with metabolic acidosis receiving landiolol; beta-blockers have been reported to cause this condition. Acidosis in general may be associated with reduced cardiac contractility.

Landiolol may prevent early warning signs of hypoglycemia (e.g., tachycardia) and increase the risk for severe/prolonged hypoglycemia at any time during treatment, especially in patients with diabetes mellitus or patients who are fasting (e.g., surgery, not eating regularly, or are vomiting). Patients receiving landiolol should be monitored for signs/symptoms of hypoglycemia.

When using beta-blockers (like landiolol), patients at risk of anaphylactic reactions may be more reactive to allergen exposure (accidental, diagnostic, or therapeutic). Patients using beta-blockers may be unresponsive to the usual doses of epinephrine used to treat anaphylactic or anaphylactoid reactions.

When landiolol is used in patients with hyperthyroidism, certain clinical signs (e.g., tachycardia) of hyperthyroidism may be masked by beta-adrenergic blockade. Abrupt withdrawal of beta-blockers may precipitate a thyroid storm. Patients should be monitored for signs of thyrotoxicosis when withdrawing landiolol therapy.

Patients with hemodynamic compromise, hypovolemia, or on interacting medications are at increased risk of hypotension while taking landiolol. Blood pressure should be monitored closely, especially if pretreatment blood pressure was low. Landiolol should be reduced or stopped for hypotension; the blood pressure effect should wane within 30 minutes.

Patients should be observed for signs of myocardial ischemia when discontinuing landiolol. Severe exacerbations of angina, myocardial infarction, and ventricular arrhythmias have been reported in patients with coronary artery disease following abrupt discontinuation of beta-blocker therapy.

The effect of moderate or severe liver dysfunction (Child-Pugh B or C) on landiolol pharmacokinetics is unknown; use of landiolol should be avoided in patients with moderate or severe liver dysfunction. In patients with mild liver dysfunction (Child-Pugh A), more conservative dose titration is recommended.

Landiolol may exacerbate anginal attacks in patients with Prinzmetal angina due to unopposed alpha receptor-mediated coronary artery vasoconstriction.

Landiolol may exacerbate peripheral circulatory disorders (e.g., Raynaud's disease/syndrome) and peripheral occlusive vascular disease.

Patients with reactive airways disease should generally not receive beta-blockers (like landiolol). Because of the relative beta-1 selectivity and titratability, landiolol may be titrated to the lowest possible effective dose. If bronchospasm occurs, the infusion should be stopped immediately; a beta-2 stimulating agent may be administered with appropriate monitoring of ventricular rates.

Landiolol can cause increases in serum potassium and hyperkalemia; the risk is increased in patients with risk factors such as renal dysfunction. Potentially life-threatening hyperkalemia has been reported in hemodialysis patients administered IV beta-blockers. Serum electrolytes should be monitored during landiolol therapy. The effect of renal dysfunction on landiolol pharmacokinetics is unknown.