Interactions between Mirabegron and Tambocor

The flecainide in Tambocor has a major potential interaction with Heart Block.

Flecainide is contraindicated in patients with pre-existing second- or third-degree AV block, or with right bundle branch block when associated with a left hemiblock (bifascicular block), unless a pacemaker is present to sustain the cardiac rhythm should complete heart block occur. Flecainide is also contraindicated in the presence of cardiogenic shock

The flecainide in Tambocor has a major potential interaction with Heart Failure.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

Mirabegron has a moderate potential interaction with High Blood Pressure.

Mirabegron can increase blood pressure. In clinical studies, the use of mirabegron was associated with dose-related increases in supine blood pressure. At the maximum recommended dose of 50 mg, the mean maximum increase in systolic/diastolic blood pressure was approximately 3.5/1.5 mmHg greater than placebo in healthy volunteers and approximately 0.5 to 1 mmHg greater than placebo in patients with overactive bladder. Worsening of preexisting hypertension was reported infrequently in patients receiving mirabegron. Therapy with mirabegron should be administered cautiously in patients with hypertension. Periodic blood pressure determinations are recommended. Mirabegron is not recommended for use in patients with severe, uncontrolled hypertension, defined as systolic blood pressure >=180 mm Hg and/or diastolic blood pressure >=110 mm Hg.

The flecainide in Tambocor has a moderate potential interaction with Hyperkalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

The flecainide in Tambocor has a moderate potential interaction with Hypokalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

The flecainide in Tambocor has a major potential interaction with Hypotension.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

Mirabegron has a moderate potential interaction with Liver Disease.

Mirebegron is partially metabolized by the liver through multiple pathways. Following administration of a single 100 mg dose, mean mirabegron peak plasma concentration (Cmax) and systemic exposure (AUC) increased by 9% and 19%, respectively, in volunteers with mild hepatic impairment (Child-Pugh Class A) and 175% and 65%, respectively, in volunteers with moderate hepatic impairment (Child-Pugh Class B) compared to volunteers with normal hepatic function. No dosage adjustment is necessary in patients with mild hepatic impairment. In patients with moderate hepatic impairment, the daily dosage of mirabegron should not exceed 25 mg. Mirabegron has not been studied in patients with severe hepatic impairment (Child-Pugh Class C). Mirabegron is not recommended for use in these patients.

The flecainide in Tambocor has a moderate potential interaction with Liver Disease.

Since flecainide elimination from plasma can be markedly slower in patients with significant hepatic impairment, flecainide should not be used in such patients unless the potential benefits clearly outweigh the risks. If used, frequent and early plasma level monitoring is required to guide dosage. Additionally, dosage increases should be made very cautiously when plasma levels have plateaued (after more than four days).

The flecainide in Tambocor has a moderate potential interaction with Magnesium Imbalance.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

Mirabegron has a moderate potential interaction with Renal Dysfunction.

Mirebegron is partially eliminated by the kidney through active tubular secretion and glomerular filtration, with renal clearance accounting for approximately 25% of the total clearance. Following administration of a single 100 mg dose, mean mirabegron peak plasma concentration (Cmax) and systemic exposure (AUC) increased by 6% and 31%, respectively, in volunteers with mild renal impairment (estimated GFR 60 to 89 mL/min/1.73 m2), 23% and 66%, respectively, in volunteers with moderate renal impairment (estimated GFR 30 to 59 mL/min/1.73 m2), and 92% and 118%, respectively, in patients with severe renal impairment (estimated GFR 15 to 29 mL/min/1.73 m2) compared to volunteers with normal renal function. No dosage adjustment is necessary in patients with mild or moderate renal impairment. In patients with severe renal impairment, the daily dosage of mirabegron should not exceed 25 mg. Mirabegron has not been studied in patients with end stage renal disease (CrCl <15 mL/min or estimated GFR <15 mL/min/1.73 m2 or requirement for hemodialysis). Mirabegron is not recommended for use in these patients.

The flecainide in Tambocor has a moderate potential interaction with Renal Dysfunction.

Flecainide is primarily eliminated by the kidney. Approximately 30% (10% to 50%) of flecainide is excreted in the urine unchanged. The serum concentration of flecainide is increased and the half-life prolonged in patients with renal impairment. Rare conditions such as a strict vegetarian diet or renal tubular acidosis that significantly increase the urinary pH slow the urinary elimination of flecainide. Adjustment of dosage is necessary and modification should be based on the degree of renal impairment. Clinical monitoring of cardiac function (ECG) and renal function is recommended.

Mirabegron has a moderate potential interaction with Urinary Retention.

Although an increased risk of urinary retention was not observed in a controlled clinical safety study in patients with bladder outlet obstruction, urinary retention has been reported in this population during postmarketing use. Therapy with mirabegron should be administered cautiously in patients with clinically significant bladder outlet obstruction and conditions predisposing to urinary retention.