heart failure
6 interactions related to heart failure
digoxin + hawthorn
Hawthorn (Crataegus) has digoxin-like positive inotropic activity, may modulate P-glycoprotein efflux, and can interfere with serum digoxin immunoassays. Concurrent use raises the risk of additive cardiac effects and erroneous digoxin level readings even though formal pharmacokinetic studies show little change in digoxin AUC.
spironolactone + potassium
Spironolactone is a mineralocorticoid receptor antagonist that blocks aldosterone-driven potassium excretion in the collecting duct, causing the kidneys to retain potassium. Adding a potassium supplement, salt substitute, or potassium-rich diet on top of spironolactone can produce fatal hyperkalemia, especially in patients with chronic kidney disease, heart failure, diabetes, or who are also on an ACE inhibitor or ARB.
furosemide + potassium
Furosemide blocks the Na-K-2Cl cotransporter in the loop of Henle and is the most potent diuretic class for causing dose-dependent hypokalemia, affecting 25-36% of users. Supplementation or potassium-sparing co-therapy is frequently required, but uncontrolled dosing combined with ACE inhibitors or kidney disease can flip levels into hyperkalemia.
furosemide + magnesium
Furosemide inhibits the Na-K-2Cl cotransporter, which abolishes the lumen-positive voltage driving paracellular magnesium reabsorption in the thick ascending limb. Long-term loop diuretic use causes urinary magnesium wasting and hypomagnesemia, which worsens loop-diuretic hypokalemia and increases arrhythmia risk.
alcohol + digoxin
Alcohol can precipitate atrial fibrillation and other arrhythmias that overlap with digoxin's narrow therapeutic window; concurrent diuretic-induced hypokalemia and hypomagnesemia, common in this population, sharply increase the risk of digoxin toxicity. Alcohol may also alter digoxin absorption and worsen heart failure that the drug is meant to treat.
licorice tea + digoxin
Licorice (Glycyrrhiza glabra) contains glycyrrhizin, which inhibits renal 11-beta-hydroxysteroid dehydrogenase type 2 and causes potassium loss through mineralocorticoid-like activity. The resulting hypokalemia sharply increases digoxin's binding to cardiac Na/K-ATPase, raising the risk of life-threatening digoxin toxicity and arrhythmia.