PDE inhibitors are typically used for short-term management ofheart failure or long-term management in patients awaiting heart transplant surgery. Specific PDE inhibitors are inamrinone and milrinone.
Administered I.V., inamrinone is distributed rapidly, metabolized by the liver, and excreted by the kidneys. It’s rarely used because secondary thrombocytopenia may occur as an adverse reaction.
Milrinone is also administered I.V. It’s distributed rapidly and ex-creted by the kidneys, primarily as unchanged drug.
PDE inhibitors improve cardiac output by strengthening contrac-tions. These drugs are thought to help move calcium into the car-diac cell or to increase calcium storage in the sarcoplasmic reticu-lum. By directly relaxing vascular smooth muscle, they also de-crease peripheral vascular resistance (afterload) and the amount of blood returning to the heart (preload).
Inamrinone and milrinone are used to manage heart failure in pa-tients who haven’t responded adequately to treatment with car-diac glycosides, diuretics, or vasodilators. Prolonged use of these drugs may increase the patient’s risk of complications and death. (See Adverse reactions to PDE inhibitors.)
· PDE inhibitors may interact with disopyramide, causing hy-potension.
· Because PDE inhibitors reduce serum potassium levels, taking them with a potassium-wasting diuretic may lead to hypokalemia.