Dosing and uses of Univasc (moexipril)
Adult dosage forms and strengths
tablet
- 7.5mg
- 15mg
Hypertension
Initial: 7.5mg PO qDay 1 hour prior to meal, OR 3.75mg PO qDay if on thiazide diuretc
Maintenance: 7.5-30 mg/day PO qDay or divided q12hr
Administer 1 hr before meals
Renal Impairment
CrCl <40 mL/min: Initial 3.75 mg PO qDay, no more than 15 mg/day
Dosing Considerations
Beneficial for many patients at risk for heart disease; reduces 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 HA
Good choice in hyperlipidemia patients
Requires weeks for full effect; to start, use low dose and titrate q1-2wk
Abrupt discontinuance not associated with rapid increase in Bp
Pediatric dosage forms and strengths
Safety and efficacy not established
Univasc (moexipril) adverse (side) effects
1-10%
Dizziness
Hypotension
Peripheral edema
Cough
Headache
Myalgia
Polyuria
Hyponatremia
Pharyngitis
Sinusitis
Rash
Nausea/vomiting
Hyperkalemia
Hyponatremia
Frequency not defined
Angioedema
Arrhythmia
Chest pain
Pneumonitis
Syncope
Proteinuria
Agranulocytosis (esp. if pt has CVD with or without renal impairment)
Hepatic failure (rare)
Renal failure
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 to moexipril/other ACE inhibitors
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): significant risk of fetal/neonatal morbidity and mortality
Cautions
Apheresis (LDL) with dextran sulfate, hypertrophic cardiomyopathy, collagen vascular dz, hemodialysis with high flux membrane, arotic stenosis
Less effective in African-Americans
Excessive hypotension if concomitant diuretics, hypovolemia, hyponatremia
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
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
Discontinue immediately if pregnant (see Contraindications and Black box warnings)
Renal impairment
Pregnancy and lactation
Pregnancy category: C (1st trimester); D (2nd & 3rd trimesters)
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: not known if excreted into breast milk; use caution
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 Univasc (moexipril)
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: 1 hr (moexepril); 2-9 hr (moexiprilat)
Duration: 24 hr
Onset: 1-2 hr (peak effect)
Total Body Clearance: 441 mL/min (Moexipril); 223 mL/min (moexiprilat)
Excretion: Feces (50%); urine (13%)
Peak Plasma Time: 1.5 hr
Bioavailability: 13-22%
Protein Bound: 90% (moexepril); 50-70% (moexeprilat)
Vd: 180 L
Metabolism: extensively metabolized in liver, minimally metabolized at intestinal walL
Metabolites: Moexiprilat (active)
