ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : -24 مورد

Fosinopril: Drug information

Fosinopril: Drug information
2025© UpToDate, Inc. and its affiliates and/or licensors. All Rights Reserved.
For additional information see "Fosinopril: Patient drug information" and "Fosinopril: Pediatric drug information"

For abbreviations, symbols, and age group definitions show table
ALERT: US Boxed Warning
Fetal toxicity:

When pregnancy is detected, discontinue fosinopril as soon as possible. Drugs that act directly on the renin-angiotensin system can cause injury and death to the developing fetus.

Brand Names: Canada
  • APO-Fosinopril;
  • CO Fosinopril;
  • Fosinopril-10 [DSC];
  • Fosinopril-20 [DSC];
  • TEVA-Fosinopril
Pharmacologic Category
  • Angiotensin-Converting Enzyme (ACE) Inhibitor;
  • Antihypertensive
Dosing: Adult
Heart failure with reduced ejection fraction

Heart failure with reduced ejection fraction:

Note: If tolerated, an angiotensin II receptor-neprilysin inhibitor is generally preferred over an angiotensin-converting enzyme inhibitor (Ref).

Oral: Initial: 5 to 10 mg once daily; increase dose (eg, double) as tolerated every ≥1 to 2 weeks to a target dose of 40 mg once daily (Ref).

Hypertension, chronic

Hypertension, chronic:

Note: For patients who warrant combination therapy (BP >20/10 mm Hg above goal or suboptimal response to initial monotherapy), may use with another appropriate agent (eg, long-acting dihydropyridine calcium channel blocker or thiazide diuretic) (Ref).

Oral: Initial: 10 mg once daily; evaluate response after ~2 to 4 weeks and titrate dose as needed (eg, increase the daily dose by doubling); usual dose range: 10 to 40 mg once daily; if additional BP control is needed, consider combination therapy; maximum dose: 80 mg/day (Ref).

HIV-associated nephropathy

HIV-associated nephropathy (HIVAN) (off-label use): Oral: 10 mg once daily (Ref).

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Adult

Mild impairment: No dosage adjustment necessary.

Moderate-severe impairment: Initial dose reduction to 5 mg once daily recommended for heart failure patients. No other dose adjustments are required; hepatobiliary elimination partially compensates for diminished renal elimination.

Hemodialysis: Poorly dialyzed; supplemental dose not required (Ref).

Peritoneal dialysis: Poorly dialyzed; supplemental dose not required (Ref).

Dosing: Liver Impairment: Adult

The liver dosing recommendations are based upon the best available evidence and clinical expertise. Senior Editorial Team: Matt Harris, PharmD, MHS, BCPS, FAST, FCCP; Jeong Park, PharmD, MS, BCTXP, FCCP, FAST; Arun Jesudian, MD; Sasan Sakiani, MD.

Note: Use of angiotensin-converting enzyme inhibitors in patients with cirrhosis and ascites should be avoided as use can further diminish renal blood flow and precipitate hepatorenal syndrome (Ref). Due to the dual routes of elimination by the liver and kidneys, fosinoprilat (active metabolite of fosinopril) exposure is not significantly different in patients with Child-Turcotte-Pugh class A and B compared to healthy subjects (Ref).

Liver impairment prior to treatment initiation:

Initial or dose adjustment in patients with preexisting liver cirrhosis:

Child-Turcotte-Pugh class A to C: No dosage adjustment necessary (Ref); avoid use in patients with ascites (Ref).

Dosing: Older Adult

Refer to adult dosing.

Dosing: Pediatric

(For additional information see "Fosinopril: Pediatric drug information")

Hypertension

Hypertension: Children ≥6 years and Adolescents: Oral: Note: Dosage must be titrated according to patient's response; use lowest effective dose.

≤50 kg: Initial: 0.1 mg/kg/dose once daily; may titrate as needed up to maximum daily dose: 0.6 mg/kg/day, not to exceed 40 mg/day; some patients may require a lower initial dose (Ref)

>50 kg: Initial: 5 mg once daily, as monotherapy; maximum daily dose: 40 mg/day (Ref)

Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Dosing: Kidney Impairment: Pediatric

Children ≥6 years and Adolescents: No dosage adjustment needed since hepatobiliary elimination compensates adequately for diminished renal elimination. Poorly dialyzed (hemodialysis and peritoneal); supplemental dose not required (Ref).

Dosing: Liver Impairment: Pediatric

Children ≥6 years and Adolescents: There are no dosage adjustments provided in the manufacturer's labeling; fosinopril metabolic clearance may be reduced in hepatic impairment; consider decreased dose; use with caution and monitor closely.

Adverse Reactions (Significant): Considerations
Acute kidney injury

Use may be associated with increased blood urea nitrogen and increased serum creatinine, resulting in oliguria and acute kidney injury (AKI). Increases in serum creatinine are expected due to pharmacologic mechanism and generally stabilize within 20% to 30% of the baseline value. Higher increases may indicate high efferent tone (such as with hypovolemia, congestive heart failure, or renal artery stenosis) (Ref).

Mechanism: Related to pharmacologic action; inhibits efferent arteriolar vasoconstriction, which can lead to a reduction in the glomerular filtration rate (GFR). Kidney hypoperfusion from systemic hypotension may also occur (Ref).

Onset: Intermediate; increases in serum creatinine generally occur within 2 weeks of initiation and stabilize within 2 to 4 weeks (Ref). However, more immediate increases can occur in patients with other risk factors for AKI (Ref).

Risk factors:

• Patients with low renal blood flow whose GFR is dependent on efferent arteriolar vasoconstriction by angiotensin II including (Ref):

- Low effective circulating volume (sodium or volume depletion)

- Congestive heart failure

- Hypotension or shock

- Renal artery stenosis

• High dose at initiation (Ref).

• Older patients (Ref).

• Preexisting kidney impairment (Ref).

• Concurrent diuretic and/or nonsteroidal anti-inflammatory drug use (Ref)

Angioedema

Angioedema may occur rarely; edema may manifest in the head and neck (potentially compromising airway) or the intestine (presenting as abdominal pain). Use is contraindicated in patients with idiopathic or hereditary angioedema or previous angioedema associated with any angiotensin-converting enzyme inhibitors or neprilysin inhibitors (Ref).

Mechanism: Related to pharmacologic action (ie, increased bradykinin and substance P, vascular permeability, vasodilation) (Ref).

Onset: Varied; may occur at any time during treatment. Most cases occur within the first week of therapy but may also occur years after therapy (Ref).

Risk factors:

• Black patients (estimated 4- to 5-fold higher risk); the mechanism for this is not completely understood but may be related to genetic variants) (Ref)

• Females (Ref)

• Smoking history (Ref)

• Previous history of angioedema (Ref)

• Age >65 years (Ref)

• Seasonal allergies (Ref)

• Concurrent use of mechanistic target of rapamycin (mTOR) inhibitors (eg, everolimus) (Ref)

• Concurrent use of neprilysin inhibitor (contraindicated)

Cough

A dry, hacking, nonproductive cough that is typically associated with tickling or scratching in the throat may occur with angiotensin converting enzyme inhibitors (ACEI) in adult and pediatric patients (Ref). Recurrence is likely with rechallenge (Ref). Resolution of cough typically occurs 1 to 4 weeks after ACEI discontinuation but may persist for up to 3 months (Ref).

Mechanism: Various proposed mechanisms. May be related to pharmacologic action (increase in bradykinin and substance P, resulting in accumulation in the lungs and bronchoconstriction (Ref).

Onset: Varied; within hours to 4 weeks after initiation but can be delayed for up to 6 months (Ref).

Risk factors:

• Females (Ref)

• Possibly certain genetic variants (some of which may be independent of the bradykinin pathway) (Ref)

Hyperkalemia

Hyperkalemia (elevated serum potassium) may occur on therapy with angiotensin converting enzyme inhibitors (ACEI), including fosinopril (Ref).

Mechanism: Related to pharmacologic action; inhibits formation of circulating angiotensin II, which leads to efferent arteriole vasodilation and subsequent lowering of glomerular filtration rate, which lowers potassium elimination. Additionally, interferes with the generation and release of aldosterone from the adrenal cortex, leading to an impairment of potassium excretion from the kidney (Ref).

Risk factors:

• Disease states associated with hyperkalemia (congestive heart failure, diabetes mellitus, chronic kidney disease) (Ref)

• Concurrent use of medications which cause hyperkalemia (ACEI, angiotensin II receptor blockers, spironolactone, nonsteroidal anti-inflammatory drugs, beta blockers, heparin, tacrolimus, cyclosporine) (Ref)

• Acute kidney injury (elevated BUN and/or serum creatinine) (Ref)

• High dietary intake of potassium or concomitant use of potassium supplements (including potassium-containing salt substitutes) (Ref)

• Baseline elevated potassium level (≥5 mmol/L) (Ref)

Adverse Reactions

The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Frequency ranges include data from hypertension and heart failure trials. Higher rates of adverse reactions have generally been noted in patients with heart failure. However, the frequency of adverse effects associated with placebo is also increased in this population.

>10%: Nervous system: Dizziness (2% to 12%)

1% to 10%:

Cardiovascular: Hypotension (4%), orthostatic hypotension (1% to 2%)

Endocrine & metabolic: Hyperkalemia (3%)

Gastrointestinal: Diarrhea (2%), nausea and vomiting (1%)

Neuromuscular & skeletal: Asthenia (1%)

Respiratory: Cough (2% to 10%) (table 1), upper respiratory infection (2%)

Fosinopril: Adverse Reaction: Cough

Drug (Fosinopril)

Placebo

Indication

Number of Patients (Fosinopril)

Number of Patients (Placebo)

10%

5%

Heart failure

361

373

2%

0%

Hypertension

688

184

<1%:

Cardiovascular: Acute myocardial infarction, angina pectoris, bradycardia, cardiac arrhythmia, cardiac conduction disorder, cerebral infarction, cerebrovascular accident, chest pain, claudication, edema, flushing, hypertension, hypertensive crisis, lower extremity edema, palpitations, shock, syncope, tachycardia, transient ischemic attacks

Dermatologic: Diaphoresis, hyperhidrosis, pruritus, skin photosensitivity, skin rash, urticaria

Endocrine & metabolic: Decreased libido, gout, weight changes, weight gain

Gastrointestinal: Abdominal distention, abdominal pain, change in appetite, constipation, dysgeusia, dysphagia, flatulence, heartburn, pancreatitis, xerostomia

Genitourinary: Sexual disorder, urinary frequency, urination disorder

Hematologic & oncologic: Eosinophilia, lymphadenopathy

Hepatic: Hepatitis, hepatomegaly

Hypersensitivity: Angioedema

Infection: Influenza

Nervous system: Behavioral changes, confusion, depression, drowsiness, falling, memory impairment, mood changes, noncardiac chest pain, numbness, pain, paresthesia, sensation of cold, sleep disorder, vertigo, voice disorder

Neuromuscular & skeletal: Arthralgia, muscle cramps, muscle weakness of the extremities, musculoskeletal pain, myalgia, swelling of extremities, tremor

Ophthalmic: Eye irritation, visual disturbance

Otic: Tinnitus

Renal: Renal insufficiency, renal pain

Respiratory: Bronchospasm, epistaxis, hoarseness, irregular breathing, laryngitis, paranasal sinus disease (abnormality), pharyngitis, pleuritic chest pain, rhinitis, sinusitis, tracheobronchitis

Miscellaneous: Fever

Frequency not defined:

Endocrine & metabolic: Hyponatremia

Hematologic & oncologic: Decreased hemoglobin

Nervous system: Fatigue, headache

Postmarketing:

Dermatologic: Psoriasis (Song 2021)

Endocrine & metabolic: Increased lactate dehydrogenase

Hepatic: Cholestatic jaundice (Chou 2008), increased serum alkaline phosphatase, increased serum bilirubin, increased serum transaminases

Contraindications

Hypersensitivity to fosinopril, any other ACE inhibitor, or any component of the formulation; angioedema related to previous treatment with an ACE inhibitor; concomitant use with aliskiren in patients with diabetes mellitus.

Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.

Warnings/Precautions

Concerns related to adverse effects:

• Hypersensitivity reactions: Anaphylaxis/nonimmune anaphylaxis can occur with ACE inhibitors. Severe nonimmune anaphylaxis may be seen during hemodialysis (eg, CVVHD) with high-flux dialysis membranes (eg, AN69), and rarely, during low density lipoprotein apheresis with dextran sulfate cellulose. Rare cases of nonimmune anaphylaxis have been reported in patients undergoing sensitization treatment with hymenoptera (bee, wasp) venom while receiving ACE inhibitors.

• Hypotension/syncope: Symptomatic hypotension with or without syncope can occur with ACE inhibitors (usually with the first several doses); effects are most often observed in volume-depleted patients; correct volume depletion prior to initiation; close monitoring of patient is required especially with initial dosing and dosing increases; blood pressure must be lowered at a rate appropriate for the patient's clinical condition. Although dose reduction may be necessary, hypotension is not a reason for discontinuation of future ACE inhibitor use especially in patients with heart failure where a reduction in systolic blood pressure is a desirable observation.

Disease-related concerns:

• Aortic stenosis: Use with caution in patients with severe aortic stenosis; may reduce coronary perfusion resulting in ischemia.

• Ascites: Generally, avoid use in patients with ascites due to cirrhosis or refractory ascites; if use cannot be avoided in patients with ascites due to cirrhosis, monitor BP and kidney function carefully to avoid rapid development of kidney failure (AASLD [Biggins 2021]; AASLD [Runyon 2013]).

• Cardiovascular disease: Initiation of therapy in patients with ischemic heart disease or cerebrovascular disease warrants close observation due to the potential consequences posed by falling blood pressure (eg, MI, stroke). Fluid replacement, if needed, may restore blood pressure; therapy may then be resumed. Discontinue therapy in patients whose hypotension recurs.

• Collagen vascular disease: Use with caution in patients with collagen vascular disease, especially with concomitant kidney impairment; may be at increased risk for hematologic toxicity.

• Hypertrophic cardiomyopathy with left ventricular outflow tract obstruction: Use with caution in patients with hypertrophic cardiomyopathy and left ventricular outflow tract obstruction since reduction in afterload may worsen symptoms associated with this condition (AHA/ACC [Ommen 2024]).

• Kidney impairment: Use with caution in preexisting kidney insufficiency; dosage adjustment may be needed. Avoid rapid dosage escalation which may lead to further kidney impairment.

Special populations:

• Race/Ethnicity: Some studies suggest that when used as monotherapy for hypertension, the BP-lowering effects of renin-angiotensin system (RAS) inhibitors (eg, ACE inhibitors) may be somewhat less pronounced in Black patients (ACC/AHA [Whelton 2018]). The mechanism is not known but may be related to social determinants of health rather than race, as pharmacogenetic differences have not been found to adequately predict BP response (Brewster 2013; Gardner 2022). These observed BP differences were not apparent when RAS inhibitors were used as part of combination therapy (eg, combined with a calcium channel blocker or thiazide diuretic) (Jamerson 2008). Drug selection should be individualized and based on multiple patient-specific factors and not purely race/ethnicity (Holt 2022).

• Surgical patients: In patients on chronic ACE inhibitor therapy, intraoperative hypotension may occur with induction and maintenance of general anesthesia; use with caution before, during, or immediately after major surgery. Cardiopulmonary bypass, intraoperative blood loss, or vasodilating anesthesia increases endogenous renin release. Use of ACE inhibitors perioperatively will blunt angiotensin II formation and may result in hypotension. However, discontinuation of therapy prior to surgery is controversial. If continued preoperatively, avoidance of hypotensive agents during surgery is prudent (Hillis 2011). Based on current research and clinical guidelines in patients undergoing non-cardiac surgery, continuing ACE inhibitors is reasonable in the perioperative period. If ACE inhibitors are held before surgery, it is reasonable to restart postoperatively as soon as clinically feasible (ACC/AHA [Fleisher 2014]).

Warnings: Additional Pediatric Considerations

Pediatric racial differences were identified in a multicentered, prospective, double-blind, placebo-controlled trial that investigated the dose-response of fosinopril in 253 children 6 to 16 years of age; this study found that black children required a higher dose of fosinopril (per kg body weight) in order to adequately control blood pressure (Menon 2006); the findings of this study are consistent with adult studies assessing ACE inhibitors; consider dosage adjustments in these patients.

Dosage Forms: US

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral, as sodium:

Generic: 10 mg, 20 mg, 40 mg

Generic Equivalent Available: US

Yes

Pricing: US

Tablets (Fosinopril Sodium Oral)

10 mg (per each): $0.41 - $4.32

20 mg (per each): $0.53 - $4.44

40 mg (per each): $0.82 - $4.56

Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.

Dosage Forms: Canada

Excipient information presented when available (limited, particularly for generics); consult specific product labeling.

Tablet, Oral, as sodium:

Generic: 10 mg, 20 mg

Administration: Pediatric

Oral: May be administered without regard to food.

Use: Labeled Indications

Heart failure with reduced ejection fraction: Adjunctive treatment of heart failure.

Hypertension, chronic: Management of hypertension.

Use: Off-Label: Adult

HIV-associated nephropathy

Medication Safety Issues
Sound-alike/look-alike issues:

Fosinopril may be confused with FLUoxetine, Fosamax, furosemide, lisinopril

Metabolism/Transport Effects

None known.

Drug Interactions

Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.

Alfuzosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Aliskiren: May increase hyperkalemic effects of Angiotensin-Converting Enzyme Inhibitors. Aliskiren may increase nephrotoxic effects of Angiotensin-Converting Enzyme Inhibitors. Aliskiren may increase hypotensive effects of Angiotensin-Converting Enzyme Inhibitors. Management: Aliskiren use with ACEIs or ARBs in patients with diabetes is contraindicated. Combined use in other patients should be avoided, particularly when CrCl is less than 60 mL/min. If combined, monitor potassium, creatinine, and blood pressure closely. Risk D: Consider Therapy Modification

Allopurinol: Angiotensin-Converting Enzyme Inhibitors may increase hypersensitivity effects of Allopurinol. Risk C: Monitor

Alteplase: Angiotensin-Converting Enzyme Inhibitors may increase adverse/toxic effects of Alteplase. Specifically, the risk for angioedema may be increased. Risk C: Monitor

Amifostine: Blood Pressure Lowering Agents may increase hypotensive effects of Amifostine. Management: When used at chemotherapy doses, hold blood pressure lowering medications for 24 hours before amifostine administration. If blood pressure lowering therapy cannot be held, do not administer amifostine. Use caution with radiotherapy doses of amifostine. Risk D: Consider Therapy Modification

Amphetamines: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor

Angiotensin II Receptor Blockers: May increase adverse/toxic effects of Angiotensin-Converting Enzyme Inhibitors. Angiotensin II Receptor Blockers may increase serum concentration of Angiotensin-Converting Enzyme Inhibitors. Management: Use of telmisartan and ramipril is not recommended. It is not clear if any other combination of an ACE inhibitor and an ARB would be any safer. Consider alternatives when possible. Monitor blood pressure, renal function, and potassium if combined. Risk D: Consider Therapy Modification

Angiotensin II: Angiotensin-Converting Enzyme Inhibitors may increase therapeutic effects of Angiotensin II. Risk C: Monitor

Antacids: May decrease serum concentration of Fosinopril. Management: Separate administration of antacids and fosinopril by 2 hours. Risk D: Consider Therapy Modification

Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may increase hypotensive effects of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor

Aprotinin: May decrease antihypertensive effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Arginine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

AzaTHIOprine: Angiotensin-Converting Enzyme Inhibitors may increase myelosuppressive effects of AzaTHIOprine. Risk C: Monitor

Barbiturates: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Benperidol: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Brigatinib: May decrease antihypertensive effects of Antihypertensive Agents. Brigatinib may increase bradycardic effects of Antihypertensive Agents. Risk C: Monitor

Brimonidine (Topical): May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Bromperidol: May decrease hypotensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase hypotensive effects of Bromperidol. Risk X: Avoid

Dapoxetine: May increase orthostatic hypotensive effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Dexmethylphenidate: May decrease therapeutic effects of Antihypertensive Agents. Risk C: Monitor

Diazoxide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Dipeptidyl Peptidase-IV Inhibitors: May increase adverse/toxic effects of Angiotensin-Converting Enzyme Inhibitors. Specifically, the risk of angioedema may be increased. Risk C: Monitor

Drospirenone-Containing Products: May increase hyperkalemic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

DULoxetine: Blood Pressure Lowering Agents may increase hypotensive effects of DULoxetine. Risk C: Monitor

Everolimus: May increase adverse/toxic effects of Angiotensin-Converting Enzyme Inhibitors. Specifically, the risk of angioedema may be increased. Risk C: Monitor

Ferric Gluconate: Angiotensin-Converting Enzyme Inhibitors may increase adverse/toxic effects of Ferric Gluconate. Risk C: Monitor

Ferric Hydroxide Polymaltose Complex: Angiotensin-Converting Enzyme Inhibitors may increase adverse/toxic effects of Ferric Hydroxide Polymaltose Complex. Specifically, the risk for angioedema or allergic reactions may be increased. Risk C: Monitor

Finerenone: Angiotensin-Converting Enzyme Inhibitors may increase hyperkalemic effects of Finerenone. Risk C: Monitor

Flunarizine: May increase therapeutic effects of Antihypertensive Agents. Risk C: Monitor

Gelatin (Succinylated): Angiotensin-Converting Enzyme Inhibitors may increase adverse/toxic effects of Gelatin (Succinylated). Specifically, the risk of a paradoxical hypotensive reaction may be increased. Risk C: Monitor

Grass Pollen Allergen Extract (5 Grass Extract): Angiotensin-Converting Enzyme Inhibitors may increase adverse/toxic effects of Grass Pollen Allergen Extract (5 Grass Extract). Specifically, ACE inhibitors may increase the risk of severe allergic reaction to Grass Pollen Allergen Extract (5 Grass Extract). Risk X: Avoid

Heparin: May increase hyperkalemic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Heparins (Low Molecular Weight): May increase hyperkalemic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Herbal Products with Blood Pressure Increasing Effects: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor

Herbal Products with Blood Pressure Lowering Effects: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Hypotension-Associated Agents: Blood Pressure Lowering Agents may increase hypotensive effects of Hypotension-Associated Agents. Risk C: Monitor

Icatibant: May decrease antihypertensive effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Iloperidone: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Indoramin: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor

Iron Dextran Complex: Angiotensin-Converting Enzyme Inhibitors may increase adverse/toxic effects of Iron Dextran Complex. Specifically, patients receiving an ACE inhibitor may be at an increased risk for anaphylactic-type reactions. Risk C: Monitor

Isocarboxazid: May increase antihypertensive effects of Antihypertensive Agents. Risk X: Avoid

Lanthanum: May decrease serum concentration of Angiotensin-Converting Enzyme Inhibitors. Management: Administer angiotensin-converting enzyme (ACE) inhibitors at least two hours before or after lanthanum. Risk D: Consider Therapy Modification

Levodopa-Foslevodopa: Blood Pressure Lowering Agents may increase hypotensive effects of Levodopa-Foslevodopa. Risk C: Monitor

Lithium: Angiotensin-Converting Enzyme Inhibitors may increase serum concentration of Lithium. Management: Lithium dosage reductions will likely be needed following the addition of an ACE inhibitor. Monitor for increased concentrations/toxic effects of lithium if an ACE inhibitor is initiated/dose increased, or if switching between ACE inhibitors. Risk D: Consider Therapy Modification

Loop Diuretics: May increase hypotensive effects of Angiotensin-Converting Enzyme Inhibitors. Loop Diuretics may increase nephrotoxic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Lormetazepam: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Metergoline: May decrease antihypertensive effects of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may increase orthostatic hypotensive effects of Metergoline. Risk C: Monitor

Methylphenidate: May decrease antihypertensive effects of Antihypertensive Agents. Risk C: Monitor

Molsidomine: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Naftopidil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Nicergoline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Nicorandil: May increase hyperkalemic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Nicorandil: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Nitroprusside: Blood Pressure Lowering Agents may increase hypotensive effects of Nitroprusside. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents (Topical): May decrease therapeutic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Nonsteroidal Anti-Inflammatory Agents: May decrease antihypertensive effects of Angiotensin-Converting Enzyme Inhibitors. Angiotensin-Converting Enzyme Inhibitors may increase adverse/toxic effects of Nonsteroidal Anti-Inflammatory Agents. Specifically, the combination may result in a significant decrease in renal function. Risk C: Monitor

Obinutuzumab: May increase hypotensive effects of Blood Pressure Lowering Agents. Management: Consider temporarily withholding blood pressure lowering medications beginning 12 hours prior to obinutuzumab infusion and continuing until 1 hour after the end of the infusion. Risk D: Consider Therapy Modification

Pentoxifylline: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Perazine: May increase hypotensive effects of Antihypertensive Agents. Risk C: Monitor

Pholcodine: Blood Pressure Lowering Agents may increase hypotensive effects of Pholcodine. Risk C: Monitor

Phosphodiesterase 5 Inhibitors: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Polyethylene Glycol-Electrolyte Solution: Angiotensin-Converting Enzyme Inhibitors may increase nephrotoxic effects of Polyethylene Glycol-Electrolyte Solution. Risk C: Monitor

Potassium Salts: May increase hyperkalemic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Potassium-Sparing Diuretics: May increase hyperkalemic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Prazosin: Antihypertensive Agents may increase hypotensive effects of Prazosin. Risk C: Monitor

Pregabalin: Angiotensin-Converting Enzyme Inhibitors may increase adverse/toxic effects of Pregabalin. Specifically, the risk of angioedema may be increased. Risk C: Monitor

Prostacyclin Analogues: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Quinagolide: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Racecadotril: May increase adverse/toxic effects of Angiotensin-Converting Enzyme Inhibitors. Specifically, the risk for angioedema may be increased with this combination. Risk C: Monitor

Ranolazine: May increase adverse/toxic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Sacubitril: Angiotensin-Converting Enzyme Inhibitors may increase adverse/toxic effects of Sacubitril. Specifically, the risk of angioedema may be increased with this combination. Risk X: Avoid

Salicylates: May decrease therapeutic effects of Angiotensin-Converting Enzyme Inhibitors. Salicylates may increase nephrotoxic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Silodosin: May increase hypotensive effects of Blood Pressure Lowering Agents. Risk C: Monitor

Sirolimus Products: May increase adverse/toxic effects of Angiotensin-Converting Enzyme Inhibitors. Specifically, the risk for angioedema may be increased. Risk C: Monitor

Sodium Phosphates: Angiotensin-Converting Enzyme Inhibitors may increase nephrotoxic effects of Sodium Phosphates. Specifically, the risk of acute phosphate nephropathy may be enhanced. Risk C: Monitor

Sparsentan: May increase adverse/toxic effects of Angiotensin-Converting Enzyme Inhibitors. Risk X: Avoid

Tacrolimus (Systemic): Angiotensin-Converting Enzyme Inhibitors may increase hyperkalemic effects of Tacrolimus (Systemic). Risk C: Monitor

Temsirolimus: May increase adverse/toxic effects of Angiotensin-Converting Enzyme Inhibitors. Specifically, the risk of angioedema may be increased. Risk C: Monitor

Terazosin: Antihypertensive Agents may increase hypotensive effects of Terazosin. Risk C: Monitor

Thiazide and Thiazide-Like Diuretics: May increase hypotensive effects of Angiotensin-Converting Enzyme Inhibitors. Thiazide and Thiazide-Like Diuretics may increase nephrotoxic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Tolvaptan: May increase hyperkalemic effects of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor

Trimethoprim: May increase hyperkalemic effects of Angiotensin-Converting Enzyme Inhibitors. Management: Consider avoiding coadministration if possible. If combined, monitor serum potassium closely, particularly for patients with other risk factors (eg, renal impairment, older age, and other medications that increase potassium. Risk X: Avoid

Urapidil: And Angiotensin-Converting Enzyme Inhibitors may interact via an unclear mechanism. Management: Avoid concomitant use of urapidil and angiotensin-converting enzyme (ACE) inhibitors. Risk D: Consider Therapy Modification

Urokinase: May increase adverse/toxic effects of Angiotensin-Converting Enzyme Inhibitors. Specifically, the risk of angioedema may be increased. Risk C: Monitor

Reproductive Considerations

Medications considered acceptable for the treatment of chronic hypertension during pregnancy may generally be used in patients trying to conceive. Angiotensin-converting enzyme (ACE) inhibitors are fetotoxic. Transition patients prior to conception to an agent preferred for use during pregnancy unless treatment with an ACE inhibitor is absolutely necessary (ACC/AHA [Whelton 2018]; ACOG 2019; NICE 2019).

ACE inhibitors are not recommended for the treatment of heart failure in patients planning to become pregnant (AHA/ACC/HFSA [Heidenreich 2022]).

Pregnancy Considerations

Fosinopril crosses the placenta.

Drugs that act on the renin-angiotensin system can cause injury and death to the developing fetus. Exposure to an angiotensin-converting enzyme (ACE) inhibitor during the first trimester of pregnancy may be associated with an increased risk of fetal malformations (ACOG 2019; ESC [Regitz-Zagrosek 2018]). Following exposure during the second or third trimesters, drugs that act on the renin-angiotensin system are associated with oligohydramnios. Oligohydramnios, due to decreased fetal renal function, may lead to fetal lung hypoplasia and skeletal malformations. Oligohydramnios may not appear until after an irreversible fetal injury has occurred. ACE inhibitor use during pregnancy is also associated with anuria, hypotension, renal failure, skull hypoplasia, and death in the fetus/neonate. Monitor infants exposed to an ACE inhibitor in utero for hyperkalemia, hypotension, and oliguria. Exchange transfusions or dialysis may be required to reverse hypotension or improve renal function.

Chronic maternal hypertension is also associated with adverse events in the fetus/infant. Chronic maternal hypertension may increase the risk of birth defects, low birth weight, premature delivery, stillbirth, and neonatal death. Actual fetal/neonatal risks may be related to the duration and severity of maternal hypertension. Untreated chronic hypertension may also increase the risks of adverse maternal outcomes, including gestational diabetes, preeclampsia, delivery complications, stroke, and myocardial infarction (ACOG 2019).

Discontinue ACE inhibitors as soon as possible once pregnancy is detected. Agents other than ACE inhibitors are recommended for the treatment of chronic hypertension during pregnancy (ACOG 2019; ESC [Cífková 2020]; SOGC [Magee 2022]). Consider the use of ACE inhibitors only for pregnant patients with hypertension refractory to other medications (ACOG 2019). Closely monitor pregnant patients on ACE inhibitors with serial ultrasounds.

ACE inhibitors are not recommended for the treatment of heart failure during pregnancy (AHA/ACC/HFSA [Heidenreich 2022]; ESC [Regitz-Zagrosek 2018]).

Breastfeeding Considerations

Fosinoprilat is present in breast milk.

According to product labeling, fosinoprilat was detected in breast milk following administration of fosinopril 20 mg for 3 days.

Breastfeeding is not recommended by the manufacturer. When postpartum treatment with an angiotensin-converting enzyme (ACE) inhibitor is needed, consider use of an agent other than fosinopril (AHA/ACC/HFSA [Heidenreich 2022]; ESC [Cífková 2020]). Avoid breastfeeding if high maternal doses of an ACE inhibitor are needed (ACOG 2019).

Dietary Considerations

Should not take a potassium salt supplement without the advice of healthcare provider.

Monitoring Parameters

BP; BUN, serum creatinine; electrolytes (eg, potassium [especially in patients on concomitant potassium-sparing diuretics, potassium supplements and/or potassium containing salts]); if patient has collagen vascular disease and/or kidney impairment, periodically monitor CBC with differential. If angioedema is suspected, assess risk of airway obstruction (eg, involvement of tongue, glottis, larynx, and/or history of airway surgery).

Mechanism of Action

Competitive inhibitor of angiotensin-converting enzyme (ACE); prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor; results in lower levels of angiotensin II which causes an increase in plasma renin activity and a reduction in aldosterone secretion; a CNS mechanism may also be involved in hypotensive effect as angiotensin II increases adrenergic outflow from CNS; vasoactive kallikreins may be decreased in conversion to active hormones by ACE inhibitors, thus reducing blood pressure

Pharmacokinetics (Adult Data Unless Noted)

Onset of action: 1 hour

Duration: 24 hours

Absorption: 36%

Protein binding: >99%

Metabolism: Prodrug, hydrolyzed to its active metabolite fosinoprilat by intestinal wall and hepatic esterases; fosinopril is also metabolized to a glucuronide conjugate and a p-hydroxy metabolite of fosinoprilat

Bioavailability: 36%

Half-life elimination, serum (fosinoprilat):

Children and Adolescents 6-16 years: 11-13 hours

Adults: 12 hours

Adults with CHF: 14 hours

Time to peak, serum: ~3 hours

Excretion: Urine and feces (as fosinoprilat and other metabolites in roughly equal proportions)

Pharmacokinetics: Additional Considerations (Adult Data Unless Noted)

Altered kidney function: In patients with end-stage kidney disease (CrCl <10 mL/minute/1.73 m2), fosinoprilat total body clearance is decreased ~50%.

Liver function impairment: In patients with alcoholic or biliary cirrhosis, the rate of fosinoprilat formation is slowed, its total body clearance decreased, and its AUC approximately doubled.

Brand Names: International
International Brand Names by Country
For country code abbreviations (show table)

  • (AE) United Arab Emirates: Apo-fosinopril | Staril;
  • (AT) Austria: Fosinopril actavis | Fosinopril Stada | Fositens;
  • (AU) Australia: Apo-fosinopril | Fosinopril Sandoz | Fosipril | Genrx Fosinopril | Monace | Monopril;
  • (BE) Belgium: Fosinil;
  • (BG) Bulgaria: Fosicard | Fosinopril teva | Monopril;
  • (BR) Brazil: Fosinopril Sodico | Monopril;
  • (CH) Switzerland: Fositen;
  • (CL) Chile: Monopril;
  • (CN) China: Meng nuo | Monopril;
  • (CO) Colombia: Monopril | Simipril;
  • (CZ) Czech Republic: Fosinogen | Fosinopril +Pharma | Fosinopril actavis | Fosinopril rivopharm | Monopril;
  • (DE) Germany: Dynacil | Fosino | Fosinopril Basics | Fosinorm;
  • (DO) Dominican Republic: Monopril;
  • (EC) Ecuador: Monopril;
  • (EE) Estonia: Monopril;
  • (EG) Egypt: Monopril;
  • (ES) Spain: Fosinopril actavis | Fosinopril aurobindo | Fosinopril ranbaxy | Fositens | Hiperlex | Tenso stop;
  • (FR) France: Fosinopril actavis | Fosinopril Arrow | Fosinopril Biogaran | Fosinopril Cristers | Fosinopril EG | Fosinopril mylan | Fosinopril qualimed | Fosinopril winthrop | Fozitec;
  • (GB) United Kingdom: Fosinopril | Fosinopril Arrow | Fosinopril Focus | Fosinopril Kent | Staril;
  • (GR) Greece: Monopril;
  • (HK) Hong Kong: Monopril;
  • (HR) Croatia: Monopril;
  • (HU) Hungary: Fosinogen | Monopril | Noviform;
  • (ID) Indonesia: Acenor-m;
  • (IE) Ireland: Fosinopril | Fosipres | Staril;
  • (IN) India: Fosinace | Fovas;
  • (IT) Italy: Eliten | Fosinopril | Fosinopril aurobindo | Fosinopril Doc | Fosinopril mylan | Fosinopril ranbaxy | Fosinopril Zentiva | Fosipres | Tensogard;
  • (JO) Jordan: Staril;
  • (KR) Korea, Republic of: Fosiril | Monopril;
  • (KW) Kuwait: Staril;
  • (LB) Lebanon: Staril;
  • (LT) Lithuania: Monopril | Oloko;
  • (LU) Luxembourg: Fosinil;
  • (LV) Latvia: Monopril;
  • (MX) Mexico: Monopril;
  • (MY) Malaysia: Monopril;
  • (NL) Netherlands: Fosinopril | Fosinoprilnatrium alpharma | Fosinoprilnatrium Aurobindo | Fosinoprilnatrium cf | Fosinoprilnatrium pch | Fosinoprilnatrium ratiopharm | Fosinoprilnatrium Sandoz | Fosinorm | Newace;
  • (NO) Norway: Monopril;
  • (PE) Peru: Monopril;
  • (PH) Philippines: Bpnorm | Sapril;
  • (PK) Pakistan: Fosvac | Monopril | Munil;
  • (PR) Puerto Rico: Fosinopril sdium | Monopril;
  • (PT) Portugal: Fosinopril | Fosinopril aurobindo | Fosinopril generis | Fosinopril mylan | Fosinopril ranbaxy | Fosinopril teva | Fosinopril winthrop | Fositen;
  • (RO) Romania: Fosinopril | Fosinopril aurobindo | Fosinopril terapia | Fosiran | Fosypril;
  • (RU) Russian Federation: Fosicard | Fosinap | Fosinopril | Fosinopril obl | Fosinopril teva | Fosinotec | Monopril;
  • (SA) Saudi Arabia: Apo-fosinopril | Staril;
  • (SE) Sweden: Fosinopril actavis;
  • (SG) Singapore: Monopril;
  • (SI) Slovenia: Fosicard | Fozinopril Arrow | Monopril;
  • (SK) Slovakia: Fosinopril teva | Fosinopril winthrop | Monopril;
  • (TH) Thailand: Monopril;
  • (TW) Taiwan: Fonosil | Forsine | Monopril | Mopopriol;
  • (UA) Ukraine: Fosicard | Monopril;
  • (VE) Venezuela, Bolivarian Republic of: Monopril;
  • (ZA) South Africa: Monopril
  1. Adelborg K, Nicolaisen SK, Hasvold P, Palaka E, Pedersen L, Thomsen RW. Predictors for repeated hyperkalemia and potassium trajectories in high-risk patients - a population-based cohort study. PLoS One. 2019;14(6):e0218739. doi:10.1371/journal.pone.0218739 [PubMed 31226134]
  2. Alharbi FF, Kholod AAV, Souverein PC, et al. The impact of age and sex on the reporting of cough and angioedema with renin-angiotensin system inhibitors: a case/noncase study in VigiBase. Fundam Clin Pharmacol. 2017;31(6):676-684. doi:10.1111/fcp.12313 [PubMed 28767167]
  3. ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group, “Major Outcomes in High-Risk Hypertensive Patients Randomized to Angiotensin-Converting Enzyme Inhibitor or Calcium Channel Blocker vs Diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT),” JAMA, 2002, 288(23):2981-97. [PubMed 12479763]
  4. American College of Obstetricians and Gynecologists (ACOG). ACOG practice bulletin no. 203: chronic hypertension in pregnancy. Obstet Gynecol. 2019;133(1):e26-e50. [PubMed 30575676]
  5. Amsterdam EA, Wenger NK, Brindis RG, et al; American College of Cardiology; American Heart Association Task Force on Practice Guidelines; Society for Cardiovascular Angiography and Interventions; Society of Thoracic Surgeons; American Association for Clinical Chemistry. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines [published correction appears in J Am Coll Cardiol. 2014;64(24):2713-2714]. J Am Coll Cardiol. 2014;64(24):e139-e228. doi: 10.1016/j.jacc.2014.09.017. [PubMed 25260718]
  6. Antman EM, Anbe SC, Alpert JS, et al, “ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction - Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction),” Circulation, 2004, 110(5):588-636. [PubMed 15289388]
  7. Antman EM, Hand M, Armstrong PW, et al, “2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines,” J Am Coll Cardiol, 2008, 51(2):210-49. [PubMed 18191746]
  8. Baker-Smith CM, Benjamin DK Jr, Califf RM, et al, "Cough in Pediatric Patients Receiving Angiotensin-Converting Enzyme Inhibitor Therapy or Angiotensin Receptor Blocker Therapy in Randomized Controlled Trials," Clin Pharmacol Ther, 2010, 87(6):668-71. [PubMed 20130570]
  9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: is this a cause for concern? Arch Intern Med. 2000;160(5):685-693. doi:10.1001/archinte.160.5.685 [PubMed 10724055]
  10. Banerji A, Blumenthal KG, Lai KH, Zhou L. Epidemiology of ACE inhibitor angioedema utilizing a large electronic health record. J Allergy Clin Immunol Pract. 2017;5(3):744-749. doi:10.1016/j.jaip.2017.02.018 [PubMed 28377081]
  11. Bezalel S, Mahlab-Guri K, Asher I, Werner B, Sthoeger ZM. Angiotensin-converting enzyme inhibitor-induced angioedema. Am J Med. 2015;128(2):120-125. doi:10.1016/j.amjmed.2014.07.011 [PubMed 25058867]
  12. Bianchi S, Aucella F, De Nicola L, Genovesi S, Paoletti E, Regolisti G. Management of hyperkalemia in patients with kidney disease: a position paper endorsed by the Italian Society of Nephrology. J Nephrol. 2019;32(4):499-516. doi:10.1007/s40620-019-00617-y [PubMed 31119681]
  13. Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021;74(2):1014-1048. doi:10.1002/hep.31884 [PubMed 33942342]
  14. Brewster LM, Seedat YK. Why do hypertensive patients of African ancestry respond better to calcium blockers and diuretics than to ACE inhibitors and β-adrenergic blockers? A systematic review. BMC Med. 2013;11:141. doi:10.1186/1741-7015-11-141 [PubMed 23721258]
  15. Brown NJ, Ray WA, Snowden M, Griffin MR. Black Americans have an increased rate of angiotensin converting enzyme inhibitor-associated angioedema. Clin Pharmacol Ther. 1996;60(1):8-13. doi:10.1016/S0009-9236(96)90161-7 [PubMed 8689816]
  16. Brown NJ, Snowden M, Griffin MR. Recurrent angiotensin-converting enzyme inhibitor--associated angioedema. JAMA. 1997;278(3):232-233. doi:10.1001/jama.278.3.232 [PubMed 9218671]
  17. Brown T, Gonzalez J, Monteleone C. Angiotensin-converting enzyme inhibitor-induced angioedema: a review of the literature. J Clin Hypertens (Greenwich). 2017;19(12):1377-1382. doi:10.1111/jch.13097 [PubMed 28994183]
  18. Chase MP, Fiarman GS, Scholz FJ, et al, “Angioedema of the Small Bowel Due to an Angiotensin-Converting Enzyme Inhibitor,” J Clin Gastroenterol, 2000, 31(3):254-7. [PubMed 11034011]
  19. Chobanian AV, Bakris GL, Black HR, et al, “The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report,” JAMA, 2003, 289(19):2560-72. [PubMed 12748199]
  20. Chou JW, Yu CJ, Chuang PH, et al. Successful treatment of fosinopril-induced severe cholestatic jaundice with plasma exchange. Ann Pharmacother. 2008;42(12):1887-1892. doi:10.1345/aph.1L229 [PubMed 19017832]
  21. Cífková R, Johnson MR, Kahan T, et al. Peripartum management of hypertension: a position paper of the ESC Council on Hypertension and the European Society of Hypertension. Eur Heart J Cardiovasc Pharmacother. 2020;6(6):384-393. doi:10.1093/ehjcvp/pvz082 [PubMed 31841131]
  22. “Consensus Recommendations for the Management of Chronic Heart Failure. On Behalf of the Membership of the Advisory Council to Improve Outcomes Nationwide in Heart Failure,” Am J Cardiol, 1999, 83(2A):1A-38A. [PubMed 10072251]
  23. David D, Jallad N, Germino FW, et al. A comparison of the cough profile of fosinopril and enalapril in hypertensive patients with a history of ACE inhibitor-associated cough. Am J Ther. 1995;2(10):806-813. doi:10.1097/00045391-199510000-00013 [PubMed 11854791]
  24. Dicpinigaitis PV. Angiotensin-converting enzyme inhibitor-induced cough: ACCP evidence-based clinical practice guidelines. Chest. 2006;129(1 Suppl):169S-173S. doi:10.1378/chest.129.1_suppl.169S [PubMed 16428706]
  25. Duerr M, Glander P, Diekmann F, Dragun D, Neumayer HH, Budde K. Increased incidence of angioedema with ACE inhibitors in combination with mTOR inhibitors in kidney transplant recipients. Clin J Am Soc Nephrol. 2010;5(4):703-708. doi:10.2215/CJN.07371009 [PubMed 20093343]
  26. Expert opinion. Senior Hepatic Editorial Team: Matt Harris, PharmD, MHS, BCPS, FAST, FCCP; Jeong Park, PharmD, MS, BCPS, FCCP, FAST; Arun Jesudian, MD; Sasan Sakiani, MD.
  27. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular evaluation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;130(24):e278-e333. [PubMed 25085961]
  28. Flynn JT, Kaelber DC, Baker-Smith CM, et al. Clinical practice guideline for screening and management of high blood pressure in children and adolescents. Pediatrics. 2017;140(3). pii: e20171904. Erratum in: Pediatrics. 2017;140(6). pii: e20173035. [PubMed 28827377]
  29. Ford NF, Lasseter KC, Van Harken DR, Hammett JL, Raymond R, Manning J. Single-dose and steady-state pharmacokinetics of fosinopril and fosinoprilat in patients with hepatic impairment. J Clin Pharmacol. 1995;35(2):145-150. doi:10.1002/j.1552-4604.1995.tb05003.x [PubMed 7751424]
  30. Fosinopril [prescribing information]. Burbank, CA: Bryant Ranch Prepack; October 2020.
  31. Fox KM and EURopean Trial on Reduction of Cardiac Events With Perindopril in Stable Coronary Artery Disease Investigators, “Efficacy of Perindopril in Reduction of Cardiovascular Events Among Patients With Stable Coronary Artery Disease: Randomised, Double-Blind, Placebo-Controlled, Multicentre Trial (The EUROPA Study),” Lancet, 2003, 362(9386):782-8. [PubMed 13678872]
  32. Funder JW, Carey RM, Mantero F, et al. The management of primary aldosteronism: case detection, diagnosis, and treatment: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2016;101(5):1889-1916. doi: 10.1210/jc.2015-4061. [PubMed 26934393]
  33. Gardner NJ. Treating hypertension in Black patients. JAAPA. 2022;35(2):15-18. doi:10.1097/01.JAA.0000791512.37549.64 [PubMed 35076435]
  34. Gehr TW, Sica DA, Grasela DM, et al. Fosinopril pharmacokinetics and pharmacodynamics in chronic ambulatory peritoneal dialysis patients. Fosinopril pharmacokinetics and pharmacodynamics in chronic ambulatory peritoneal dialysis patients. Eur J Clin Pharmacol. 1991;41(2):165-169. [PubMed 1835932]
  35. Gehr TW, Sica DA, Grasela DM, et al. The pharmacokinetics and pharmacodynamics of fosinopril in haemodialysis patients. Eur J Clin Pharmacol. 1993;45(5):431-436. [PubMed 8112372]
  36. Go AS, Bauman M, King SM, et al. An effective approach to high blood pressure control: a science advisory from the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention [published online November 15, 2013]. Hypertension. [PubMed 24243703]
  37. “Guidelines for the Evaluation and Management of Heart Failure. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Evaluation and Management of Heart Failure),” Circulation, 1995, 92(9):2764-84. [PubMed 7594057]
  38. Hallberg P, Persson M, Axelsson T, et al. Genetic variants associated with angiotensin-converting enzyme inhibitor-induced cough: a genome-wide association study in a Swedish population. Pharmacogenomics. 2017;18(3):201-213. doi:10.2217/pgs-2016-0184 [PubMed 28084903]
  39. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Joint Committee on clinical practice guidelines. Circulation. 2022;145(18):e895-e1032. doi:10.1161/CIR.0000000000001063 [PubMed 35363499]
  40. Helmer A, Slater N, Smithgall S. A review of ACE inhibitors and ARBs in black patients with hypertension. Ann Pharmacother. 2018;52(11):1143-1151. doi:10.1177/1060028018779082 [PubMed 29808707]
  41. Henriksen JH, Moller S. Liver cirrhosis and arterial hypertension. World J Gastroenterol. 2006;12(5):678-685. doi:10.3748/wjg.v12.i5.678 [PubMed 16521178]
  42. Hillis LD, Smith PK, Anderson JL, et al, “2011 ACCF/AHA Guideline for Coronary Artery Bypass Graft Surgery: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines,” Circulation, 2011, 124(23):2610-42. [PubMed 22064600]
  43. Holt HK, Gildengorin G, Karliner L, Fontil V, Pramanik R, Potter MB. Differences in hypertension medication prescribing for Black Americans and their association with hypertension outcomes. J Am Board Fam Med. 2022;35(1):26-34. doi:10.3122/jabfm.2022.01.210276 [PubMed 35039409]
  44. Hunt SA, Abraham WT, Chin MH, et al, “2009 Focused Update Incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Developed in Collaboration With the International Society for Heart and Lung Transplantation,” CIrculation, 2009, 119(14):e391-479. [PubMed 19324966]
  45. Israili ZH, Hall WD. Cough and angioneurotic edema associated with angiotensin-converting enzyme inhibitor therapy. A review of the literature and pathophysiology. Ann Intern Med. 1992;117(3):234-242. doi:10.7326/0003-4819-117-3-234 [PubMed 1616218]
  46. Jamerson KA, Basile J. Prompt, aggressive BP lowering in high-risk patients. J Clin Hypertens (Greenwich). 2008;10(1 suppl 1):S40-S48. doi:10.1111/j.1524-6175.2007.08145.x [PubMed 18174783]
  47. James PA, Oparil S, Carter BL, et al. 2014 Evidence-Based Guideline for the Management of High Blood Pressure in Adults: Report From the Panel Members Appointed to the Eighth Joint National Committee (JNC 8) [published online December 18, 2013]. JAMA. [PubMed 24352797]
  48. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society [published online March 28, 2014]. Circulation. [PubMed 24682347]
  49. Kahegeshe NL, Pestiaux A, Henry JP, van Cauter J. Transient recurrent ascites. Acta Gastroenterol Belg. 2006;69(4):381-383. [PubMed 17343080]
  50. “K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, Classification, and Stratification. Kidney Disease Outcome Quality Initiative,” Am J Kidney Dis, 2002, 39(2 Suppl 2):1-246. [PubMed 11904577]
  51. Kernan WN, Ovbiagele B, Black HR, et al; American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, Council on Clinical Cardiology, and Council on Peripheral Vascular Disease. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association [published correction appears in Stroke. 2015;46(2):e54]. Stroke. 2014;45(7):2160-2236. doi: 10.1161/STR.0000000000000024. [PubMed 24788967]
  52. Kidney Disease: Improving Global Outcomes (KDIGO) Blood Pressure Work Group. KDIGO 2021 clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney Int. 2021;99(3S):S1-S87. doi:10.1016/j.kint.2020.11.003 [PubMed 33637192]
  53. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group, "KDIGO 2012 Clinical Practice Guidelines for the Evaluation and Management of Chronic Kidney Disease,"Kidney Inter, Suppl, 2013, 3:1-150.
  54. Kidney Disease: Improving Global Outcomes (KDIGO). KDIGO 2012 clinical practice guideline for the management of blood pressure in chronic kidney disease. Kidney Inter, Suppl . 2012; 2(5). [PubMed KDIGO.1]
  55. Kliegman RM, Stanton BMD, St. Geme J, Schor NF, eds. Nelson Textbook of Pediatrics. 20th ed. Philadelphia, PA: Saunders Elsevier; 2016.
  56. Konstam MA, Dracup K, Baker DW, et al, “Heart Failure Evaluation and Care of Patients With Left Ventricular Systolic Dysfunction,” J Card Fail, 1995, 1(2):183-7. [PubMed 9420649]
  57. Kostis JB, Kim HJ, Rusnak J, et al. Incidence and characteristics of angioedema associated with enalapril. Arch Intern Med. 2005;165(14):1637-1642. doi:10.1001/archinte.165.14.1637 [PubMed 16043683]
  58. Kostis WJ, Shetty M, Chowdhury YS, Kostis JB. ACE inhibitor-induced angioedema: a review. Curr Hypertens Rep. 2018;20(7):55. doi:10.1007/s11906-018-0859-x [PubMed 29884969]
  59. Li JS, Berezny K, Kilaru R, et al, "Is the Extrapolated Adult Dose of Fosinopril Safe and Effective in Treating Hypertensive Children?" Hypertension, 2004, 44(3):289-93. [PubMed 15262902]
  60. Lucas GM, Ross MJ, Stock PG, et al; HIV Medicine Association of the Infectious Diseases Society of America. Clinical practice guideline for the management of chronic kidney disease in patients infected with HIV: 2014 update by the HIV Medicine Association of the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(9):e96-e138. [PubMed 25234519]
  61. Magee LA, Smith GN, Bloch C, et al. Guideline no. 426: hypertensive disorders of pregnancy: diagnosis, prediction, prevention, and management. J Obstet Gynaecol Can. 2022;44(5):547-571.e1. doi:10.1016/j.jogc.2022.03.002 [PubMed 35577426]
  62. Maroteau C, Siddiqui MK, Veluchamy A, et al; PREDICTION-ADR. Exome sequencing reveals common and rare variants in F5 associated with ACE inhibitor and angiotensin receptor blocker-induced angioedema. Clin Pharmacol Ther. 2020;108(6):1195-1202. doi:10.1002/cpt.1927 [PubMed 32496628]
  63. Menon S, Berezny KY, Kilaru R, et al, “Racial Differences are Seen in Blood Pressure Response to Fosinopril in Hypertensive Children,” Am Heart J, 2006,152(2):394-9. [PubMed 16875928]
  64. Miller DR, Oliveria SA, Berlowitz DR, Fincke BG, Stang P, Lillienfeld DE. Angioedema incidence in US veterans initiating angiotensin-converting enzyme inhibitors. Hypertension. 2008;51(6):1624-1630. doi:10.1161/HYPERTENSIONAHA.108.110270. [PubMed 18413488]
  65. Montinaro V, Cicardi M. ACE inhibitor-mediated angioedema. Int Immunopharmacol. 2020;78:106081. doi:10.1016/j.intimp.2019.106081 [PubMed 31835086]
  66. Morimoto T, Gandhi TK, Fiskio JM, et al. An evaluation of risk factors for adverse drug events associated with angiotensin-converting enzyme inhibitors. J Eval Clin Pract. 2004;10(4):499-509. doi:10.1111/j.1365-2753.2003.00484.x [PubMed 15482412]
  67. Mu G, Xiang Q, Zhang Z, Liu C, Zhang H, Liu Z, Pang X, Jiang J, Xie Q, Zhou S, Wang Z, Hu K, Wang Z, Jiang S, Qin X, Cui Y. PNPT1 and PCGF3 variants associated with angiotensin-converting enzyme inhibitor-induced cough: a nested case-control genome-wide study. Pharmacogenomics. 2020;21(9):601-614. doi:10.2217/pgs-2019-0167 [PubMed 32397904]
  68. Mu G, Xiang Q, Zhou S, et al. Association between genetic polymorphisms and angiotensin-converting enzyme inhibitor-induced cough: a systematic review and meta-analysis. Pharmacogenomics. 2019;20(3):189-212. doi:10.2217/pgs-2018-0157 [PubMed 30672376]
  69. National Heart, Lung, and Blood Institute, “Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents,” Clinical Practice Guidelines, 2011, National Institutes of Health. Available at http://www.nhlbi.nih.gov/guidelines/cvd_ped/peds_guidelines_full.pdf. Last accessed: October 24 , 2012.
  70. National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents, “The Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and Adolescents,” Pediatrics, 2004, 114 (2 Suppl):555-76. [PubMed 15286277]
  71. National Institute for Health and Care Excellence (NICE). Hypertension in pregnancy: diagnosis and management. http://www.nice.org.uk/guidance/ng133. Published June 25, 2019. Accessed December 1, 2022.
  72. Nishimura RA, Otto CM, Bonow RO, et al, 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(23):2440-92. doi: 10.1161/CIR.0000000000000029. [PubMed 24589852]
  73. Oktaviono YH, Kusumawardhani N. Hyperkalemia associated with angiotensin converting enzyme inhibitor or angiotensin receptor blockers in chronic kidney disease. Acta Med Indones. 202;52(1):74-79. [PubMed 32291375]
  74. Ommen SR, Ho CY, Asif IM, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline for the management of hypertrophic cardiomyopathy: a report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines. Circulation. 2024;149(23):e1239-e1311. doi:10.1161/CIR.0000000000001250 [PubMed 38718139]
  75. Os I, Bratland B, Dahlöf B, Gisholt K, Syvertsen JO, Tretli S. Female preponderance for lisinopril-induced cough in hypertension. Am J Hypertens. 1994;7(11):1012-1015. doi:10.1093/ajh/7.11.1012 [PubMed 7848615]
  76. Oudit G, Girgrah N, Allard J. ACE inhibitor-induced angioedema of the intestine: case report, incidence, pathophysiology, diagnosis and management. Can J Gastroenterol. 2001;15(12):827-832. doi:10.1155/2001/247816 [PubMed 11773949]
  77. Overlack A. ACE inhibitor-induced cough and bronchospasm. Incidence, mechanisms and management. Drug Saf. 1996;15(1):72-78. doi:10.2165/00002018-199615010-00006 [PubMed 8862965]
  78. Packer M, Poole-Wilson PA, Armstrong PW, et al, “Comparative Effects of Low and High Doses of the Angiotensin-Converting Enzyme Inhibitor, Lisinopril, on Morbidity and Mortality in Chronic Heart Failure,” Circulation, 1999, 100(23):2312-8. [PubMed 10587334]
  79. Palmer BF. Managing hyperkalemia caused by inhibitors of the renin-angiotensin-aldosterone system. N Engl J Med. 2004;351(6):585-592. doi:10.1056/NEJMra035279 [PubMed 15295051]
  80. Pfeffer MA, Greaves SC, Arnold JM, et al, “Early Versus Delayed Angiotensin-Converting Enzyme Inhibition Therapy in Acute Myocardial Infarction. The Healing and Early Afterload Reducing Therapy Trial,” Circulation, 1997, 95(12):2643-51. [PubMed 9193433]
  81. Pfeffer MA, McMurray JJ, Velazquez EJ, et al, “Valsartan, Captopril, or Both in Myocardial Infarction Complicated by Heart Failure, Left Ventricular Dysfunction, or Both,” N Engl J Med, 2003, 349(20):1893-1906. [PubMed 14610160]
  82. Prieto-García L, Pericacho M, Sancho-Martínez SM, et al. Mechanisms of triple whammy acute kidney injury. Pharmacol Ther. 2016;167:132-145. doi:10.1016/j.pharmthera.2016.07.011 [PubMed 27490717]
  83. Punzi HA. Safety update: focus on cough. Am J Cardiol. 1993;72(20):45H-48H. doi:10.1016/0002-9149(93)91054-l [PubMed 8285182]
  84. Quan A , “Fetopathy Associated With Exposure to Angiotensin Converting Enzyme Inhibitors and Angiotensin Receptor Antagonists,” Early Hum Dev, 2006, 82(1):23-8. [PubMed 16427219]
  85. Raebel MA. Hyperkalemia associated with use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Cardiovasc Ther. 2012;30(3):e156-66. doi:10.1111/j.1755-5922.2010.00258.x [PubMed 21883995]
  86. Reardon LC, Macpherson DS. Hyperkalemia in outpatients using angiotensin-converting enzyme inhibitors. How much should we worry? Arch Intern Med. 1998;158(1):26-32. doi:10.1001/archinte.158.1.26 [PubMed 9437375]
  87. Refer to manufacturer’s labeling.
  88. Regitz-Zagrosek V, Roos-Hesselink JW, Bauersachs J, et al. 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy. Eur Heart J. 2018;39(34):3165-3241. [PubMed 30165544]
  89. Rosenbaum AJ, Luciano JA, Marburger R, Hume E. Acute kidney injury in the setting of knee arthroplasty: a case report and discussion investigating angiotensin-converting enzyme inhibitors as the culprit. HSS J. 2011;7(2):183-186. doi:10.1007/s11420-010-9189-5 [PubMed 22754420]
  90. Runyon BA; AASLD. Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology. 2013;57(4):1651-1653. doi:10.1002/hep.26359 [PubMed 23463403]
  91. Sangole NV, Dadkar VN. Adverse drug reaction monitoring with angiotensin converting enzyme inhibitors: a prospective, randomized, open-label, comparative study. Indian J Pharmacol. 2010;42(1):27-31. doi:10.4103/0253-7613.62408 [PubMed 20606833]
  92. Sato A, Fukuda S. A prospective study of frequency and characteristics of cough during ACE inhibitor treatment. Clin Exp Hypertens. 2015;37(7):563-568. doi:10.3109/10641963.2015.1026040 [PubMed 25992489]
  93. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS; Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991. doi:10.1161/hc4101.096153 [PubMed 11602506]
  94. Scott J, Jones T, Redaniel MT, May MT, Ben-Shlomo Y, Caskey F. Estimating the risk of acute kidney injury associated with use of diuretics and renin angiotensin aldosterone system inhibitors: a population based cohort study using the clinical practice research datalink. BMC Nephrol. 2019;20(1):481. doi:10.1186/s12882-019-1633-2 [PubMed 31888533]
  95. Sharif MN, Evans BL, Pylypchuk GB. Cough induced by quinapril with resolution after changing to fosinopril. Ann Pharmacother. 1994;28(6):720-722. doi:10.1177/106002809402800606 [PubMed 7919557]
  96. Slater EE, Merrill DD, Guess HA, et al. Clinical profile of angioedema associated with angiotensin converting-enzyme inhibition. JAMA. 1988;260(7):967-970. [PubMed 2840522]
  97. Smith SC Jr, Benjamin EJ, Bonow RO, et al, “AHA/ACCF Secondary Prevention and Risk Reduction Therapy for Patients With Coronary and Other Atherosclerotic Vascular Disease: 2011 Update: A Guideline From the American Heart Association and American College of Cardiology Foundation,” Circulation, 2011, 124(22):2458-73. [PubMed 22052934]
  98. Smoger SH and Sayed MA, “Simultaneous Mucosal and Small Bowel Angioedema Due to Captopril,” South Med J, 1998, 91(11):1060-3. [PubMed 9824192]
  99. Song G, Yoon HY, Yee J, Kim MG, Gwak HS. Antihypertensive drug use and psoriasis: a systematic review, meta- and network meta-analysis. Br J Clin Pharmacol. Published online October 5, 2021. doi:10.1111/bcp.15060 [PubMed 34611920]
  100. von Vigier RO, Mozzettini S, Truttmann AC, et al. Cough is common in children prescribed converting enzyme inhibitors. Nephron. 2000;84(1):98. [PubMed 10644922]
  101. Wei A, Burns GC, Williams BA, Mohammed NB, Visintainer P, Sivak SL. Long-term renal survival in HIV-associated nephropathy with angiotensin-converting enzyme inhibition. Kidney Int. 2003;64(4):1462-1471. [PubMed 12969167]
  102. Weir MR. Are drugs that block the renin-angiotensin system effective and safe in patients with renal insufficiency? Am J Hypertens. 1999;12(12 Pt 3):195S-203S. doi:10.1016/s0895-7061(99)00104-1 [PubMed 10619572]
  103. Weir MR, Rolfe M. Potassium homeostasis and renin-angiotensin-aldosterone system inhibitors. Clin J Am Soc Nephrol. 2010;5(3):531-548. doi:10.2215/CJN.07821109 [PubMed 20150448]
  104. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Hypertension. 2018;71(6):e13-e115. [PubMed 29133356]
  105. White CM. Pharmacologic, pharmacokinetic, and therapeutic differences among ACE inhibitors. Pharmacotherapy. 1998;18(3):588-599. [PubMed 9620109]
  106. Woodard-Grice AV, Lucisano AC, Byrd JB, Stone ER, Simmons WH, Brown NJ. Sex-dependent and race-dependent association of XPNPEP2 C-2399A polymorphism with angiotensin-converting enzyme inhibitor-associated angioedema. Pharmacogenet Genomics. 2010;20(9):532-536. doi:10.1097/FPC.0b013e32833d3acb [PubMed 20625347]
  107. Yeo WW, Chadwick IG, Kraskiewicz M, Jackson PR, Ramsay LE. Resolution of ACE inhibitor cough: changes in subjective cough and responses to inhaled capsaicin, intradermal bradykinin and substance-P. Br J Clin Pharmacol. 1995;40(5):423-429. [PubMed 8703645]
  108. Yi Z, Li Z, Wu XC, et al, "Effect of Fosinopril in Children With Steroid-Resistant Idiopathic Nephrotic Syndrome," Pediatr Nephrol, 2006, 21(7):967-72. [PubMed 16773409]
  109. Yusuf S, Sleight P, Pogue J, et al, “Effects of an Angiotensin-Converting-Enzyme Inhibitor, Ramipril, on Cardiovascular Events in High-Risk Patients. The Heart Outcomes Prevention Evaluation Study Investigators,” N Engl J Med, 2000, 342(3):145-53. [PubMed 10639539]
Topic 8479 Version 415.0