Index of drugs

Congestive heart failure (NYHA class II-IV). Control of fast ventricular function in patients with rapid flutter and atrial fibrillation. Treatment and prevention of recurrent supraventricular tachycardia. β-methyldigoxin increases the cardiac output (which is reflected in increased diuresis), thus relieving the symptoms of right ventricular failure caused by systemic venous congestion and the symptoms of left ventricular heart failure. The drug is usually used in combination therapy with ACE inhibitors or with diuretics.

1 tabl contains 100 μg of β-methyldigoxine. The preparation contains lactose.

Methyldigoxin is a derivative of digoxin. The mechanism of action is based on inhibition (Na⁺, K⁺) ATP-azy. Methyldigoxin produces a positive inotropic effect, acting directly on the myocardium, both in patients with normal cardiac function as well as in patients with cardiac dysfunction. As the contractility increases, cardiac output increases, venous pressure decreases, heart size decreases and compensatory reflex tachycardia decreases. Diuresis increases with the improvement of hemodynamic renal function. Cardiac glycosides reduce the rate of AV conduction and prolong the effective refractory period (ERP): vagal nerve activity is increased, they act directly on the AV node and have sympatholytic activity. The effect of glycosides on the AV node is not revealed clinically when the atrial rate is small enough to allow the AV node to return to its initial state during each cardiac contraction (however, in patients with supraventricular arrhythmias, e.g. flutter and atrial fibrillation, the number of depolarization waves arriving the chambers are reduced). Cardiac glycosides reduce the supraventricular effective refractory period, may prolong the PR interval, shorten the QT interval and lower the ST segment. The effects recorded in the ECG record are not sufficient to determine the degree of glycoside saturation. Metyldigoxin is rapidly and almost completely absorbed from the gastrointestinal tract. It is characterized by a better absorption profile than Digoxin due to the higher solubility in fats. Bioavailability is 70-100%. The rate of absorption and the highest blood concentrations were significantly reduced in patients given methyldigoxin 30 min after a meal. Maximum concentration in blood occurs 30 min after methyldigoxin administration. Possible fluctuations in glycoside concentration after methyldigoxin administration may be clinically relevant. A clinically significant positive inotropic effect was found 30-60 min after methyliodigoxin. The maximum therapeutic effect occurred after 4 hours. Methyldigoxin is bound to plasma proteins in 10-22%. It is metabolized to digoxin and excreted in the urine. T_0,5 is 36-47.5 hours.

Hypersensitivity to methyl Digoxin, digoxin, other cardiac glycosides or any of the excipients. Ventricular fibrillation and ventricular tachycardia. IIST. or IIIst. atrioventricular block in patients without a pacemaker. Wolff-Parkinson-White syndrome. Hyperkalemia. Hypokalemia. Hypercalcemia. Thoracic aortic aneurysm. Cardiomyopathy with narrowing of the outflow path from the left ventricle. Carotid sinus syndrome. Poisoning with cardiac glycoside.

Methyldigoxin should be discontinued 1-2 days before the patient is scheduled for cardioversion (risk of arrhythmias). Special precautions are required when using methyldigoxin in patients with severe lung disease, hypoxia, hypothyroidism, acute myocardial infarction, conduction abnormalities, severe bradycardia or ventricular arrhythmias, myocarditis and in elderly patients. Due to the risk of increased toxicity, hypokalaemia, hypercalcaemia, acidosis and alkalosis should be prevented. Caution should be exercised in patients with liver or kidney disease.The product contains lactose, therefore it should not be used in patients with rare hereditary problems of galactose intolerance, lactase intolerance (type Lapp) or malabsorption of glucose-galactose.

Cardiac glycosides penetrate the placenta and are secreted in breast milk. It may be used during pregnancy and breast-feeding only when necessary, when the expected benefit of treatment in the mother outweighs the potential risk to the fetus or child.

Premature ventricular contractions, bradycardia, twin cardiac rhythm and atrio-ventricular block (characteristic of digitalis poisoning); nausea, lack of appetite, diarrhea, vomiting (characteristic of digitalis poisoning), very rarely abdominal pain, myocardial infarction; fatigue, headache and dizziness, depression, drowsiness, insomnia, confusion, hallucinations, delirium, general muscle weakness, disorder of color recognition (toxicity equivalent to digoxin toxicity); hypersensitivity reactions (erythema, lupus-like syndrome, thrombocytopenia); rarely gynecomastia.

Orally. Adults. The dose of methyldigoxin must be strictly defined. Methyldigoxin is usually used in combination therapy with ACE inhibitors or diuretics. The initial dose is 150-600 μg - depending on whether the saturation state of the glycoside is to be achieved quickly or slowly. Higher doses of methyldigoxin are used in divided doses. In atrial fibrillation: 200-300 μg per day, in one or two doses. In rapid saturation in acute left ventricular failure 200 μg 3 times a day for 1-5 days. In the majority of patients, saturation is achieved within 2-3 days. Effective doses of methyldigoxin in maintenance therapy are in the range of 50-400 μg per day, in most patients 150-200 μg per day, in one or two doses.
In patients with renal impairment, the dose is determined based on creatinine clearance. The initial dose in dialysis patients is 30-50% of the usual recommended dose. In patients with anuria, 50 μg should be administered to ensure that the serum concentration of methylenedigine is 1 ng / ml, while in patients with a creatinine clearance in the range 0.8-1.25 ml / sec the dose is 150-200 μg per day. In patients with impaired hepatic function, the dose of methyldigoxin should be reduced. Caution should be exercised when using methyldigoxin in elderly patients.