ramipril (Altace)
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Introduction
Tradename: Altace. C23H32N2O5
Indications
- hypertension
- chronic heart failure
- diabetic nephropathy
- nephroprotective agent in patients with diabetes mellitus
- nondiabetic proteinuric nephropathy
- atherosclerosis
- recovery from myocardial infarction
- reduces risk of fatal stroke* by 60%[4]
- scleroderma renal crisis[7]
* even in patients without high blood pressure
Dosage
HTN. Start 2.5 mg PO QD, max 20 mg/day
Tabs: 1.25, 2.5, 5, 10 mg.
Pharmacokinetics
- 28% oral bioavailability, not significantly affected by food
- peak plasma levels reached 1 hour after oral dose
- metabolized in the liver by ester hydrolysis to diacid ramiprilat (active metabolite)
- two other inactive metabolites
- peak ramiprilat obtained 2-4 hours after oral dose of ramipril
- ramiprilat has 6 times ACE inhibitory activity as ramipril
- protein binding of ramipril is 73%; that of ramiprilat is 56%
- 60% of drug eliminated in the urine, 40% in the feces
- < 2% of drug recovered unchanged in the urine
- elimination is triphasic
elimination via liver
elimination via kidney
protein binding = 73 %
1/2life = 13-17 hours ramiprilat
Adverse effects
- cough
- increased risk of angioedema
- hypotension
- dizziness
- syncope
- vertigo
- hepatic failure (rare)
- neutropenia/agranulocytosis (rare)
- hyperkalemia
- worsening renal function
- nausea/vomiting
- diarrhea
- chest pain
- drug adverse effects of renin-angiotensin-aldosterone system inhibitors (RAAS inhibitors)
- drug adverse effects of ACE inhibitors
- drug adverse effects of antihypertensive agents
Drug interactions
- NSAIDs may interfere with action of ACE inhibitors
- prostaglandins act on afferent glomerular arterioles
- increased risk of hyperkalemia
- phenothiazines may increase effect of ACE inhibitors
- K+ & K+ sparing diuretics increase the risk of hyperkalemia
- drug interaction(s) of fluticasone with HIV1 protease inhibitors
- drug interaction(s) of calcineurin inhibitors with ACE inhibitors
- drug interaction(s) of calcium channel blockers with ACE inhibitors
- drug interaction(s) of renin-angiotensin-aldosterone inhibitors with trimethoprim-sulfamethoxazole
- drug interaction(s) of lithium carbonate with ACE inhibitors
- drug interaction(s) of ACE inhibitor with trimethoprim
- drug interaction(s) of ACE inhibitors with potassium-sparing diuretics
- drug interaction(s) of ACE inhibitors with aliskiren
- drug interaction(s) of ACE inhibitors with angiotensin II receptor antagonists
- drug interaction(s) of potassium chloride with ACE inhibitors
- drug interaction(s) of spironolactone with ACE inhibitors
- drug interaction(s) of diuretics with ACE inhibitors
- drug interaction(s) of beta blockers with ACE inhibitors
- drug interaction(s) of NSAIDs, diuretics & ACE inhibitors
- drug interaction(s) of NSAIDs with ACE inhibitors
- drug interaction(s) of NSAIDs & antihypertensives
Mechanism of action
- see ACE inhibitor
- may prevent progression of atherosclerosis (10 mg/day)[4][5]
- treating 50 patients for 4 years seems to prevent 1 major cardiovascular event[5]
- see HOPE trial
More general terms
Additional terms
References
- ↑ The Pharmacological Basis of Therapeutics, 9th ed. Gilman et al, eds. Permagon Press/McGraw Hill, 1996
- ↑ Prescriber's Letter 7(11):62 2000
- ↑ Physician's Desk Reference (PDR), 56th ed, Medical Economics, 2002
- ↑ 4.0 4.1 4.2 Prescriber's Letter 9(4):19 2002
- ↑ 5.0 5.1 5.2 Prescriber's Letter 10(10):59 2003
- ↑ Journal Watch 24(8):62, 2004 Marre M et al, BMJ 328:495,2004 <PubMed> PMID: https://www.ncbi.nlm.nih.gov/pubmed/14960504 <Internet> http://bmj.bmjjournals.com/cgi/content/full/328/7438/495
- ↑ 7.0 7.1 Deprecated Reference