Brand and Other Names:Altace
- Classes: ACE Inhibitors
Dosing & Uses
Dosage Forms & Strengths
Initial (not on diuretic): 2.5 mg PO qDay
Initial (with diuretic): 1.25 mg PO qDay
Maintenance: 2.5-20 mg/day PO qDay or divided q12hr
Heart Failure (Post-Myocardial Infarction)
Stable patients with CHF signs within a few days of acute MI
Initial: 2.5 mg PO q12hr; may titrate to 5 mg PO q12hr; decrease to 1.25 mg q12hr if hypotension occurs; monitor for >2 hr after initial dose and reduce concomitant diuretic if hypotension occurs
Maintenance: After 1 week, increase dose (if tolerated) to target dose of 5 mg q12hr
Myocardial Infarction/Stroke Prevention
Reduce risk of MI, stroke, or death from cardiovascular causes in patients ≥55 years
Initial: 2.5 mg PO qDay for 1 week, THEN 5 mg qDay for 3 weeks
Maintenance: Increase as tolerated to 10 mg qDay; for hypertensive or recently post-MI patients, give 5 mg PO BID
- Reduce risk of MI, stroke, or death from cardiovascular causes in patients ≥55 years at high risk of developing a major cardiovascular event because of a history of coronary artery disease, stroke, or peripheral vascular disease, or of diabetes that is accompanied by at least 1 other cardiovascular risk factor (hypertension, elevated total cholesterol levels, low HDL levels, cigarette smoking, or documented microalbuminuria)
Diabetic Nephropathy (Off-label)
Initial (not on diuretic): 2.5 mg PO qDay
Initial (with diuretic): 1.25 mg PO qDay
Maintenance: 2.5-20 mg PO qDay; daily dose may be either increased or divided BID if antihypertensive effect is diminished toward the end of the dosing interval
- CrCl <40 mL/min and concomitant diuretic therapy: Not to exceed 5 mg/day (25% of normal dose)
- Renal/heart failure: 1.25 mg PO qDay; may increase to 1.25 mg q12hr and to a maximum dose of 2.5 mg q12hr depending on clinical response and tolerability
- Renal failure and hypertension: 1.25 mg PO qDay initially; may titrate upward, not to exceed 5 mg/day
- Geriatric patients: At increased risk for renal dysfunction; adjust dose to renal clearance and monitor closely
Requires weeks for full effect; to start, use low dose and titrate every 1-2 weeks
qDay dosing may result in diminished antihypertensive effect at end of day in some patients; consider increase in dosage or dosing interval (q12hr)
If BP is not adequately treated, consider adding diuretic
Consider ACE inhibitor in high-risk patients, even if no hypertension or CHF
Abrupt discontinuance not associated with rapid increase in BP
Swallow capsule whole; can also open capsule and sprinkle contents on small amount of applesauce or mixed in 120 mL of water or apple juice; mixture can be stored for <24 hours at room temperature or <48 hours under refrigeration
Safety and efficacy not established
Serious - Use Alternative
Significant - Monitor Closely
Angina pectoris (3%)
Postural hypotension (2%)
Abnormal kidney function (1%)
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
Hypersensitivity to drug or other ACE inhibitors
Do not coadminister with aliskiren in patients with diabetes mellitus or with renal impairment (ie, GFR <60 mL/min/1.73 m²)
Anaphylactoid and related reactions (head and neck/intestinal angioedema, anaphylaxis during desensitizing treatment with Hymenoptera venom, anaphylaxis during membrane exposure with high-flux membrane dialysis, and low-density lipoprotein apheresis with dextran sulfate absorption)
(Rare) risk of hepatic failure, which starts as cholestatic jaundice and progresses to sometimes fatal fulminant hepatic necrosis; discontinue if patient develops jaundice or marked elevations of hepatic enzymes
Excessive hypotension if on concomitant diuretics, hypovolemia, hyponatremia; increased risk in CHF patients; treat by placing patient in supine position and treating with IV infusion of physiologic saline if necessary
Increased hypotension risk in patients undergoing surgery or during anesthesia with agents that produce hypotension; correct by volume expansion in such situations
Coadministration with mTOR inhibitors (eg, temsirolimus) may increased risk for angioedema
African American patients may have a smaller average reduction in BP than other populations
Changes in renal function due to blockage of renin-angiotensin-aldosterone system; severe CHF patients are at increased risk for oliguria or progressive azotemia and (rarely) for acute renal failure or death; increase in BUN/SCr may occur in patients with unilateral or bilateral renal artery stenosis; monitor closely
Reduction in RBC and hemoglobin content with rare cases of agranulocytosis, pancytopenia and bone marrow depression reported; collagen-vascular disease (SLE, scleroderma) patients with impaired renal function are at increased risk; monitor closely
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
Risk of hyperkalemia, especially in patients with renal impairment, DM, concomitant use of K+-elevating drugs
Reversible, persistent, nonproductive cough thought to be due to inhibition of degradation of endogenous bradykinin
Pregnancy & Lactation
Pregnancy category: D
Discontinue as soon as pregnancy detected; during the second and third trimesters of pregnancy, therapy can result in fetal injury (eg, hypotension, neonatal skull hypoplasia, anuria, reversible and irreversible renal failure) and death
Lactation: Possibly excreted in breast milk; nursing not recommended
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.
Mechanism of Action
Competitively inhibits angiotensin-converting enzymes, resulting in decreased plasma angiotensin II concentrations; BP may be reduced in part through decreased vasoconstriction, increased renin activity, and decreased aldosterone secretion; increases renal blood flow
Bioavailability: 50-60%; not affected by food
Peak plasma time: 1 hr (ramipril); 2-4 hr (ramiprilat)
Protein bound: 73% (ramipril), 56% (ramiprilat)
Metabolized by liver through cleavage of ester group
Metabolite: Ramiprilat (active metabolite)
Half-life: 13-17 hr (ramiprilat)
Excretion: Urine (60%), feces (40%)
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