Brand and Other Names:Mavik
- Classes: ACE Inhibitors
Dosing & Uses
Dosage Forms & Strengths
In patients not taking a diuretic
- 1 mg PO qDay in nonblack patients
- 2 mg PO qDay in black patients
- 2-4 mg PO qDay; may divide q12hr if BP response diminishes
Congestive Heart Failure or Left Ventricular Dysfunction Post-MI
Initial: 1 mg PO qDay
Maintenance: 4 mg PO qDay
Renal impairment (CrCl <30 mL/min): 0.5 mg PO qDay
Hepatic impairment (cirrhosis): 0.5 mg PO qDay
Monitor potassium levels
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 hypertension or CHF
May prolong survival in CHF, may preserve renal function in DM
May help to prevent migraine HA
No sexual dysfunction side effect
Good choice in hyperlipidemia patients
Requires weeks for full effect; to start, use low dose & titrate q1-2Weeks
Abrupt discontinuance not associated with rapid increase in BP
<18 years old: safety & efficacy not established
Serious - Use Alternative
Significant - Monitor Closely
Elevated Uric Acid (15%)
Frequency Not Defined
ARF if renal artery stenosis
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
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 (see Black Box Warnings)
Less effective in Blacks
Excessive hypotension if concomitant diuretics, hypovolemia, hyponatremia
Renal impairment may occur
Coadministration with mTOR inhibitors (eg, temsirolimus, sirolimus, everolimus) may increased risk for angioedema
Cough may occur within the first few months
Cholestatic jaundice may occur
Risk of hyperkalemia, especially in renal impairment, diabetes melliuts, or coadministration with potassium-elevating drugs
ACE inhibition also causes increased bradykinin levels which putatively mediates angioedema; higher incidence of angioedema in black than nonblack patients
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
Intestinal angioedema reported in patients treated with ACE inhibitors; it should be included in differential diagnosis of patients, taking ACE inhibitors and presenting with abdominal pain
Pregnancy & Lactation
Pregnancy Category: C (1st trimester); D (2nd/3rd trimesters)
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
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
Protein Bound: 80% (trandolapril); 65-94% (trandolaprilat)
Vd: 18 L
Onset: 1-2 hr
Duration: 72 hr after single dose
Peak Plasma Time: 1 hr
Half-Life: 6 hr trandolapril; 22.5 hr trandolaprilat
- CrCl <30 mL/min may result in accumulation of active metabolite
Metabolite: Trandolaprilat (active)
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