digoksiinin

Digoksiinin, the Finnish form of digoxin, is a cardiac glycoside derived from Digitalis species. It has a positive inotropic effect, increasing the force of heart muscle contractions, and a parasympathomimetic effect that slows atrioventricular conduction. By inhibiting the Na+/K+-ATPase pump in cardiac myocytes, it raises intracellular calcium, enhancing cardiac contractility and, through increased vagal tone, reducing heart rate.

Indications for digoksiinin include symptomatic heart failure with reduced ejection fraction, where it may improve exercise tolerance and symptoms, as well as rate control in atrial fibrillation or atrial flutter when rapid ventricular response needs management. It is typically considered when other treatments are insufficient or unsuitable.

Pharmacokinetics and dosing considerations: digoksiinin is administered orally or intravenously and is renally cleared. It has a relatively narrow therapeutic index, requiring careful dosing and monitoring. Plasma concentrations are influenced by renal function, age, body weight, and drug interactions. The recommended dose is individualized, and ongoing monitoring of kidney function and electrolytes, especially potassium and calcium, is essential.

Adverse effects and toxicity: common non-cardiac symptoms include nausea, vomiting, and anorexia. Cardiac toxicity can cause bradycardia, various arrhythmias, or AV-blocks. Visual disturbances (such as blurred vision or xanthopsia) and confusion are possible. Toxicity risk increases with hypokalemia, kidney impairment, advanced age, and interactions with other medications.

Interactions and monitoring: many drugs interact with digoksiinin, including amiodarone, verapamil, quinidine, macrolide antibiotics, and loop diuretics. Regular monitoring of electrolytes, renal function, and digoxin serum levels is recommended to maintain safety and efficacy. Digiksiinin remains a well-established, though carefully managed, option in specific cardiovascular conditions.