Cordarone Disease Interactions

Amiodarone and its active metabolite are not removed by hemodialysis.

Pulmonary toxicities such as hypersensitivity pneumonitis or interstitial/alveolar pneumonitis are potentially fatal (approximately 10% of the time) and have occurred in as many as 10% to 17% of patients administered daily dosages of approximately 400 mg of amiodarone. More frequently, asymptomatic abnormal diffusion capacity has been observed. Patients with preexisting pulmonary dysfunction does not appear to have an increased risk of pulmonary toxicity; however, they have a poorer prognosis if toxicity does develop. Thus, the risks and benefits of amiodarone therapy should be weighed carefully. Clinical monitoring of pulmonary function, including chest X-ray (baseline and every 3 to 6 months) and pulmonary function tests (with diffusion capacity), is recommended in all patients receiving amiodarone therapy. Any new respiratory symptom during treatment should be evaluated promptly and thoroughly, since toxicity is more likely to be reversible if diagnosed and managed early. Patients who develop hypersensitivity pneumonitis should be withdrawn permanently from amiodarone therapy and treated with steroids. In the case of interstitial/alveolar pneumonitis, steroid therapy and dosage reduction or discontinuation of amiodarone, if possible, usually result in clinical improvement. Subsequent rechallenge with amiodarone at reduced dosages does not always lead to return of toxicity and may be considered in some patients. The use of a lower loading dose and maintenance doses may also decrease the incidence of amiodarone- induced pulmonary toxicity.

The use of amiodarone is contraindicated for use in patients with cardiogenic shock, severe sinus node dysfunction causing marked sinus bradycardia, second- or third-degree AV block, or symptomatic bradycardia in the absence of a functioning pacemaker.

Optic neuropathy and/or neuritis has occurred during administration of amiodarone and has resulted in visual impairment such as changes in visual acuity, decrease in peripheral vision, and blindness. Optic toxicity can occur at any time following initiation of amiodarone. Therapy with amiodarone should be administered cautiously in patients with visual defects. Regular ophthalmologic examinations including fundoscopy and slit- lamp examinations are recommended.

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.

The use of certain antimalarial agents is contraindicated in patients with known prolongation of QT interval as these patients can develop fatal arrhythmias. These drugs should also be avoided in patients with clinical conditions known to prolong the QT interval, such as uncorrected hypokalemia or hypomagnesemia, bradycardia, and certain other cardiac conditions. Caution is advised in patients taking other medications that can prolong the QT interval.

There have been rare reports of fatal hepatocellular necrosis after treatment with amiodarone. In patients with life-threatening arrhythmias, the potential risk of hepatic injury should be weighed against the potential benefit of amiodarone therapy. Patients with hepatic impairment should be monitored for evidence of progressive hepatic injury. Consideration should be given to reducing the rate of administration or withdrawing treatment if needed.

Reversible and dose-related nervous system toxicity such as dizziness, paresthesia, tremor and involuntary movements, lack of coordination, abnormal gait and ataxia is commonly noted in patients receiving amiodarone. Therapy with amiodarone should be administered cautiously and dosage modifications considered in patients with or predisposed to neurologic dysfunction.

Amiodarone inhibits peripheral conversion of thyroxine (T4) to triiodothyronine (T3) and also contributes inorganic iodine that can result in altered thyroid function tests, hypothyroidism, or hyperthyroidism. Therapy with amiodarone should be administered cautiously in patients with thyroid dysfunction. Clinical monitoring, including baseline and periodic evaluation of thyroid function is recommended. Modification of thyroid therapy may be necessary.

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.