Dosing and uses of Monopril (fosinopril)
Adult dosage forms and strengths
tablets
- 10mg
- 20mg
- 40mg
Hypertension
10 mg PO qDay initially, no more than 40 mg/day
Congestive Heart Failure
Adjunctive to diuretics &/or digitalis
5-10 mg PO qDay initially, no more than 40 mg/day
Dosing Considerations
Beneficial for many patients at risk for heart disease; reduce risk of MI, stroke, diabetic nephropathy , microalbuminuria, new onset Dm
Consider starting an ACE inhibitor in high-risk patients, even if no HTN or CHF
May prolong survival in CHF, may preserve renal function in Dm
May help to prevent migraine headache
No sexual dysfunction side effect
Good choice in hyperlipidemia patients
Requires weeks for full effect; to start, use low dose and titrate every 1-2 weeks
Abrupt discontinuance not associated with rapid increase in Bp
Pediatric dosage forms and strengths
tablets
- 10mg
- 20mg
- 40mg
Hypertension
<50 kg: Limited data suggests 0.1-0.6 mg/kg PO qDay
>50 kg: As adults; 5-10 mg PO qDay initially, not to exceed 40 mg/day
Monopril (fosinopril) adverse (side) effects
>10%
Dizziness (1.6-11.9%)
1-10%
Cough (2.2-9.7%)
Headache (3.2%)
Hyperkalemia (2.6%)
Diarrhea (2.2%)
Orthostatic hypotension (1.4-1.9%)
Fatigue (1-2%)
Frequency not defined
Angioedema
ARF if renal artery stenosis
Aplastic anemia
Neutropenia
Arthralgia
Interstitial nephritis
Vasculitis
Rash
Warnings
Black box warnings
Discontinue as soon as possible when pregnancy is detected; affects renin-angiotensin system causing oligohydramnios, which may result in fetal injury and/or death
Contraindications
Hypersensitivity
History of hereditary or angioedema associated with previous ACE inhibitor treatment
Bilateral renal artery stenosis
Do not coadminister with aliskiren in patients with diabetes mellitus or with renal impairment (ie, GFR <60 mL/min/1.73 m²)
Pregnancy (2nd and 3rd trimesters)
Cautions
Renal impairment, hepatic impairment, volume depletion, electrolyte abnormalities
Risk of hyperkalemia, especially with renal impairment, DM, or those taking concomitant K+-elevating drugs
Dual blockade of the renin angiotensin system with ARBs, ACE inhibitors, or aliskiren associated with increased risk for hypotension, hyperkalemia, and renal function changes (including acute renal failure) compared to monotherapy
ACE inhibition also causes increased bradykinin levels which putatively mediates angioedema
Coadministration with mTOR inhibitors (eg, temsirolimus) may increased risk for angioedema
Discontinue STAT if pregnant (see Contraindications and Black box warnings)
Less effective in blacks
Renal impairment may occur
Neutropenia/agranulocytosis reported
Cough may occur within the first few months
Cholestatic jaundice may occur
Use caution in severe aortic stenosis
Excessive hypotension if concomitant diuretics, hypovolemia, hyponatremia
Pregnancy and lactation
Pregnancy category: d
Discontinue as soon as pregnancy detected; during the second and third trimesters of pregnancy, drugs that act directly on the renin-angiotensin have been associated with fetal injury that includes hypotension, neonatal skull hypoplasia, anuria, reversible or irreversible renal failure, and death
Lactation: excreted in breast milk; not recommended
Pregnancy categories
A: Generally acceptable. Controlled studies in pregnant women show no evidence of fetal risk.
B: May be acceptable. Either animal studies show no risk but human studies not available or animal studies showed minor risks and human studies done and showed no risk.
C: Use with caution if benefits outweigh risks. Animal studies show risk and human studies not available or neither animal nor human studies done.
D: Use in LIFE-THREATENING emergencies when no safer drug available. Positive evidence of human fetal risk.
X: Do not use in pregnancy. Risks involved outweigh potential benefits. Safer alternatives exist.
NA: Information not available.
Pharmacology of Monopril (fosinopril)
Mechanism of action
Angiotensin converting enzyme (ACE) inhibitors dilate arteries and veins by competively inhibiting the conversion of angiotensin I to angiotensin II (a potent endogenous vasoconstrictor) and by inhibiting bradykinin metabolism; these actions result in preload and afterload reductions on the heart
ACE inhibitors also promote sodium and water excretion by inhibiting angiotensin-II induced aldosterone secretion; elevation in potassium may also be observed
ACE inhibitors also elicit renoprotective effects through vasodilation of renal arterioles
ACE inhibitors reduce cardiac and vascular remodeling associated with chronic hypertension, heart failure, and myocardial infarction
Pharmacokinetics
Half-Life: 12 hr
Onset: 1 hr
Peak Plasma Time: 3 hr
Bioavailability: 36%
Protein Bound: 95%
Total Body Clearance: 26-39 mL/min
Metabolite: Fosinoprilat (active)
Absorption: (36%)
Metabolism: Liver
Excretion: Urine (45-50%); feces (45-50%)
Dialyzable: Minimally
