ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Moexipril: Drug information

Moexipril: Drug information
(For additional information see "Moexipril: Patient drug information")

For abbreviations, symbols, and age group definitions used in Lexicomp (show table)
ALERT: US Boxed Warning
Fetal toxicity:

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

Pharmacologic Category
  • Angiotensin-Converting Enzyme (ACE) Inhibitor;
  • Antihypertensive
Dosing: Adult
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: 3.75 to 7.5 mg once daily; evaluate response after approximately 2 to 4 weeks and titrate dose in 1-step increments (eg, increase the daily dose by doubling) as needed, up to 30 mg/day in 1 or 2 divided doses. Patients with severe asymptomatic hypertension and no signs of acute end organ damage should be evaluated for medication titration within 1 week (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

CrCl >40 mL/minute/1.73 m2: There are no dosage adjustments provided in the manufacturer’s labeling; use with caution.

CrCl ≤40 mL/minute/1.73 m2: Initial: 3.75 mg once daily; maximum dose: 15 mg/day

Dosing: Hepatic Impairment: Adult

There are no dosage adjustments provided in the manufacturer's labeling. However, hepatic impairment increases systemic exposure; use with caution, particularly in patients with ascites due to cirrhosis (Ref).

Dosing: Older Adult

Refer to adult dosing.

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; 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 moexipril (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 antagonists, 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.

1% to 10%:

Cardiovascular: Chest pain (≥1%), flushing (2%), peripheral edema (≥1%)

Dermatologic: Skin rash (2%)

Endocrine & metabolic: Hyperkalemia (1%)

Gastrointestinal: Diarrhea (3%), dyspepsia (≥1%), nausea (≥1%)

Genitourinary: Urinary frequency (≥1%)

Nervous system: Dizziness (4%), headache (≥1%), pain (≥1%)

Neuromuscular & skeletal: Myalgia (1%)

Renal: Increased blood urea nitrogen (≤1%; reversible), increased serum creatinine (≤1%; reversible) (table 1)

Moexipril: Adverse Reaction: Increased Serum Creatinine

Drug (Moexipril)

Comparator (Moexipril with Hydrochlorothiazide)

Comments

1%

2%

Increase to at least 140% of baseline value

Respiratory: Cough (6%) (table 2), flu-like symptoms (3%), pharyngitis (2%), rhinitis (≥1%), sinusitis (≥1%), upper respiratory tract infection (≥1%)

Moexipril: Adverse Reaction: Cough

Drug (Moexipril)

Placebo

Number of Patients (Moexipril)

Number of Patients (Placebo)

6%

2%

674

226

<1%:

Cardiovascular: Acute myocardial infarction, angina pectoris, cardiac arrhythmia, cerebrovascular accident, facial edema, orthostatic hypotension, palpitations, symptomatic hypotension, syncope

Dermatologic: Alopecia, diaphoresis, pemphigus, pruritus, skin photosensitivity, urticaria

Endocrine & metabolic: Weight changes

Gastrointestinal: Abdominal pain, change in appetite, constipation, dysgeusia, pancreatitis, vomiting, xerostomia

Genitourinary: Oliguria

Hematologic & oncologic: Hemolytic anemia

Hepatic: Hepatitis

Hypersensitivity: Angioedema

Nervous system: Anxiety, drowsiness, malaise, mood changes, nervousness, sleep disturbance

Neuromuscular & skeletal: Arthralgia

Otic: Tinnitus

Renal: Renal insufficiency

Respiratory: Bronchospasm, dyspnea, eosinophilic pneumonitis

Frequency not defined: Endocrine & metabolic: Hyponatremia

Postmarketing:

Dermatologic: Psoriasis (Song 2021)

Endocrine & metabolic: Increased uric acid

Hepatic: Increased liver enzymes

Contraindications

Hypersensitivity to moexipril 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 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 renal function carefully to avoid rapid development of renal failure (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.

• 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 2020]).

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

Special populations:

• Race/Ethnicity: In Black patients, the BP-lowering effects of ACE inhibitors may be less pronounced. The exact mechanism is not known; differences in the renin-angiotensin-aldosterone system, low renin levels, and salt sensitivity more commonly found in Black patients may contribute (Brewster 2013; Helmer 2018).

• 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]).

Dosage Forms: US

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

Tablet, Oral, as hydrochloride:

Generic: 7.5 mg, 15 mg

Generic Equivalent Available: US

Yes

Pricing: US

Tablets (Moexipril HCl Oral)

7.5 mg (per each): $1.39

15 mg (per each): $1.46

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.

Administration: Adult

Oral: Administer on an empty stomach 1 hour prior to a meal.

Use: Labeled Indications

Hypertension, chronic: Management of hypertension.

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

Moexipril may be confused with Monopril

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 Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.

Alfuzosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Aliskiren: May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Aliskiren may enhance the hypotensive effect of Angiotensin-Converting Enzyme Inhibitors. Aliskiren may enhance the nephrotoxic effect 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 enhance the potential for allergic or hypersensitivity reactions to Allopurinol. Risk C: Monitor therapy

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

Amifostine: Blood Pressure Lowering Agents may enhance the hypotensive effect 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 diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy

Angiotensin II: Angiotensin-Converting Enzyme Inhibitors may enhance the therapeutic effect of Angiotensin II. Risk C: Monitor therapy

Angiotensin II Receptor Blockers: May enhance the adverse/toxic effect of Angiotensin-Converting Enzyme Inhibitors. Angiotensin II Receptor Blockers may increase the 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

Antipsychotic Agents (Second Generation [Atypical]): Blood Pressure Lowering Agents may enhance the hypotensive effect of Antipsychotic Agents (Second Generation [Atypical]). Risk C: Monitor therapy

Aprotinin: May diminish the antihypertensive effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Arginine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

AzaTHIOprine: Angiotensin-Converting Enzyme Inhibitors may enhance the myelosuppressive effect of AzaTHIOprine. Risk C: Monitor therapy

Barbiturates: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Benperidol: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Brigatinib: May diminish the antihypertensive effect of Antihypertensive Agents. Brigatinib may enhance the bradycardic effect of Antihypertensive Agents. Risk C: Monitor therapy

Brimonidine (Topical): May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Bromperidol: May diminish the hypotensive effect of Blood Pressure Lowering Agents. Blood Pressure Lowering Agents may enhance the hypotensive effect of Bromperidol. Risk X: Avoid combination

Dapoxetine: May enhance the orthostatic hypotensive effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Dexmethylphenidate: May diminish the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy

Diazoxide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

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

Drospirenone-Containing Products: May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

DULoxetine: Blood Pressure Lowering Agents may enhance the hypotensive effect of DULoxetine. Risk C: Monitor therapy

Eplerenone: May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

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

Ferric Gluconate: Angiotensin-Converting Enzyme Inhibitors may enhance the adverse/toxic effect of Ferric Gluconate. Risk C: Monitor therapy

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

Finerenone: Angiotensin-Converting Enzyme Inhibitors may enhance the hyperkalemic effect of Finerenone. Risk C: Monitor therapy

Flunarizine: May enhance the therapeutic effect of Antihypertensive Agents. Risk C: Monitor therapy

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

Grass Pollen Allergen Extract (5 Grass Extract): Angiotensin-Converting Enzyme Inhibitors may enhance the adverse/toxic effect 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 combination

Heparin: May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Heparins (Low Molecular Weight): May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Herbal Products with Blood Pressure Increasing Effects: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy

Herbal Products with Blood Pressure Lowering Effects: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Hypotension-Associated Agents: Blood Pressure Lowering Agents may enhance the hypotensive effect of Hypotension-Associated Agents. Risk C: Monitor therapy

Icatibant: May diminish the antihypertensive effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Indoramin: May enhance the hypotensive effect of Antihypertensive Agents. Risk C: Monitor therapy

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

Lanthanum: May decrease the 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 enhance the hypotensive effect of Levodopa-Foslevodopa. Risk C: Monitor therapy

Lithium: Angiotensin-Converting Enzyme Inhibitors may increase the 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 enhance the hypotensive effect of Angiotensin-Converting Enzyme Inhibitors. Loop Diuretics may enhance the nephrotoxic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Lormetazepam: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Methylphenidate: May diminish the antihypertensive effect of Antihypertensive Agents. Risk C: Monitor therapy

Molsidomine: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Naftopidil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Nicergoline: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Nicorandil: May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Nicorandil: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Nitroprusside: Blood Pressure Lowering Agents may enhance the hypotensive effect of Nitroprusside. Risk C: Monitor therapy

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

Nonsteroidal Anti-Inflammatory Agents (Topical): May diminish the therapeutic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Obinutuzumab: May enhance the hypotensive effect 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 enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Pholcodine: Blood Pressure Lowering Agents may enhance the hypotensive effect of Pholcodine. Risk C: Monitor therapy

Phosphodiesterase 5 Inhibitors: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Polyethylene Glycol-Electrolyte Solution: Angiotensin-Converting Enzyme Inhibitors may enhance the nephrotoxic effect of Polyethylene Glycol-Electrolyte Solution. Risk C: Monitor therapy

Potassium Salts: May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Potassium-Sparing Diuretics: May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Prazosin: Antihypertensive Agents may enhance the hypotensive effect of Prazosin. Risk C: Monitor therapy

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

Prostacyclin Analogues: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

Quinagolide: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

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

Ranolazine: May enhance the adverse/toxic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

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

Salicylates: May enhance the nephrotoxic effect of Angiotensin-Converting Enzyme Inhibitors. Salicylates may diminish the therapeutic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Silodosin: May enhance the hypotensive effect of Blood Pressure Lowering Agents. Risk C: Monitor therapy

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

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

Sparsentan: May enhance the adverse/toxic effect of Angiotensin-Converting Enzyme Inhibitors. Risk X: Avoid combination

Tacrolimus (Systemic): Angiotensin-Converting Enzyme Inhibitors may enhance the hyperkalemic effect of Tacrolimus (Systemic). Risk C: Monitor therapy

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

Terazosin: Antihypertensive Agents may enhance the hypotensive effect of Terazosin. Risk C: Monitor therapy

Thiazide and Thiazide-Like Diuretics: May enhance the hypotensive effect of Angiotensin-Converting Enzyme Inhibitors. Thiazide and Thiazide-Like Diuretics may enhance the nephrotoxic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Tolvaptan: May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Trimethoprim: May enhance the hyperkalemic effect of Angiotensin-Converting Enzyme Inhibitors. Risk C: Monitor therapy

Urapidil: May interact via an unknown mechanism with Angiotensin-Converting Enzyme Inhibitors. Management: Avoid concomitant use of urapidil and angiotensin-converting enzyme (ACE) inhibitors. Risk D: Consider therapy modification

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

Food Interactions

Food reduces moexiprilat's Cmax and AUC by 70% to 80% and 40% to 50%, respectively. Management: Take on an empty stomach 1 hour before a meal.

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).

Pregnancy Considerations

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, pre-eclampsia, 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.

Breastfeeding Considerations

It is not known if moexipril is present in breast milk.

The manufacturer recommends that caution be exercised when administering moexipril to breastfeeding patients. When postpartum treatment with an angiotensin-converting enzyme (ACE) inhibitor is needed, consider use of an agent other than moexipril (ESC [Cífková 2020]). Avoid breastfeeding if high maternal doses of an ACE inhibitor are needed (ACOG 2019).

Dietary Considerations

Take on an empty stomach.

Monitoring Parameters

Blood pressure; 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

Pharmacokinetics (Adult Data Unless Noted)

Onset of action: Within 2 hours; Peak effect: 3 to 6 hours

Duration: 24 hours

Absorption: Incomplete

Distribution: Vd: Moexiprilat: ~183 L

Protein binding, plasma: Moexiprilat: ~50%

Metabolism: Prodrug, rapidly converted to moexiprilat; Moexiprilat ~1,000 times more potent

Bioavailability: Moexiprilat: ~13%; reduced with food (Cmax and AUC decreased by 70% to 80% and 40% to 50%, respectively)

Half-life elimination: Moexipril: 1.3 hours; Moexiprilat: 2 to 9.8 hours

Time to peak: Moexiprilat: ~1.5 hours

Excretion: Moexiprilat: Feces (52%); urine (~7%)

Pharmacokinetics: Additional Considerations (Adult Data Unless Noted)

Altered kidney function: Effective elimination half-life and AUC of moexipril and moexiprilat are increased with decreasing renal function.

Hepatic function impairment: In patients with mild to moderate cirrhosis, the Cmax of moexipril was increased ~50% and the AUC increased ~120%, while the Cmax for moexiprilat was decreased ~50% and the AUC increased by almost 300%.

Older adult: AUC and Cmax of moexiprilat is increased ~30%.

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

  • (BG) Bulgaria: Moex;
  • (CZ) Czech Republic: Moex;
  • (DE) Germany: Fempress;
  • (EG) Egypt: Minotensol | Primox;
  • (FI) Finland: Perdix;
  • (FR) France: Moex;
  • (GB) United Kingdom: Perdix;
  • (IL) Israel: Perdix;
  • (IT) Italy: Femipres | Primoxil;
  • (JO) Jordan: Perdix;
  • (KR) Korea, Republic of: Univasc;
  • (LB) Lebanon: Perdix;
  • (LT) Lithuania: Moex;
  • (MX) Mexico: Renoprotec;
  • (PE) Peru: Fempres;
  • (PH) Philippines: Univasc;
  • (PL) Poland: Cardiotensin;
  • (PR) Puerto Rico: Moexipril HCL | Univasc;
  • (RU) Russian Federation: Moex;
  • (SK) Slovakia: Moex;
  • (TR) Turkey: Univasc;
  • (UA) Ukraine: Moex;
  • (ZA) South Africa: Perdix
  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. Available at: http://www.circulationaha.org/cgi/content/full/110/5/588. Last accessed October 26, 2004. [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, Murphy MD, Li JS, Smith PB. 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):668-671. doi:10.1038/clpt.2009.231 [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. Bateman BT, Patorno E, Desai RJ, et al. Angiotensin-converting enzyme inhibitors and the risk of congenital malformations. Obstet Gynecol. 2017;129(1):174-184. [PubMed 27926639]
  12. 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]
  13. 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]
  14. 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]
  15. 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]
  16. 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]
  17. 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]
  18. 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]
  19. 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]
  20. Chrysant SG, Chrysant GS. Pharmacological and clinical profile of moexipril: a concise review. J Clin Pharmacol. 2004;44(8):827-836. doi:10.1177/0091270004267194 [PubMed 15286086]
  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. Conlin P, Moore T, Swartz S, et al, “Effect of Indomethacin on Blood Pressure Lowering by Captopril and Losartan in Hypertensive Patients,” Hypertension, 2000, 36(3):461-5. [PubMed 10988282]
  23. 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]
  24. 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]
  25. Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2014;130(19):1749-1767. doi: 10.1161/CIR.0000000000000095. [PubMed 25070666]
  26. Fihn SD, Gardin JM, Abrams J, et al, “2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons,” Circulation, 2012, 126(25):3097-137. [PubMed 23166211]
  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. 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]
  29. 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]
  30. 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]
  31. 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]
  32. 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]
  33. 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]
  34. 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]
  35. 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]
  36. 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]
  37. 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]
  38. 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]
  39. 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.
  40. 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):337-414.
  41. 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]
  42. 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]
  43. Lewis EJ, Hunsicker LG, Bain RP, et al, “The Effect of Angiotensin-Converting Enzyme Inhibition on Diabetic Nephropathy,” N Engl J Med, 1993, 329(20):1456-62. [PubMed 8413456]
  44. 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]
  45. Mann JFE, Flack JM. Choice of drug therapy in primary (essential) hypertension. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com. Accessed March 7, 2023.
  46. Maroteau C, Siddiqui MK, Veluchamy A, et al. 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]
  47. 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]
  48. Moexipril HCl [prescribing information]. Sellersville, PA: Teva; September 2012.
  49. Moexipril [prescribing information]. North Wales PA: Teva Pharmaceuticals USA Inc; August 2015.
  50. Montinaro V, Cicardi M. ACE inhibitor-mediated angioedema. Int Immunopharmacol. 2020;78:106081. doi:10.1016/j.intimp.2019.106081 [PubMed 31835086]
  51. 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]
  52. Mu G, Xiang Q, Zhang Z, et al. 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]
  53. 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]
  54. Nadeem S, Hashmat S, Defreitas MJ, et al. Renin angiotensin system blocker fetopathy: a Midwest Pediatric Nephrology Consortium report. J Pediatr. 2015;167(4):881-885. [PubMed 26130112]
  55. 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.
  56. 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]
  57. O'Gara PT, Kushner FG, Ascheim DD, et al; American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines [published correction appears in Circulation. 2013;128(25):e481]. Circulation. 2013;127(4):e362-e425. doi: 10.1161/CIR.0b013e3182742cf6. [PubMed 23247304]
  58. Oktaviono YH, Kusumawardhani N. Hyperkalemia associated with angiotensin converting enzyme inhibitor or angiotensin receptor blockers in chronic kidney disease. Acta Med Indones. 2020;52(1):74-79. [PubMed 32291375]
  59. Ommen SR, Mital S, Burke MA, et al. 2020 AHA/ACC guideline for the diagnosis and treatment of patients with hypertrophic cardiomyopathy: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2020;76(25):e159-e240. doi:10.1016/j.jacc.2020.08.045 [PubMed 33229116]
  60. 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]
  61. 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]
  62. 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]
  63. 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]
  64. 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]
  65. 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):1893-906. [PubMed 14610160]
  66. 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]
  67. Raebel MA. Hyperkalemia associated with use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Cardiovasc Ther. 2012;30(3):e156-166. doi:10.1111/j.1755-5922.2010.00258.x [PubMed 21883995]
  68. 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]
  69. 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]
  70. 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]
  71. Rosendorff C, Lackland DT, Allison M, et al; American Heart Association, American College of Cardiology, and American Society of Hypertension. Treatment of hypertension in patients with coronary artery disease: A scientific statement from the American Heart Association, American College of Cardiology, and American Society of Hypertension. J Am Soc Hypertens. 2015;9(6):453-498. doi: 10.1016/j.jash.2015.03.002. [PubMed 25840695]
  72. 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]
  73. 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]
  74. 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]
  75. 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]
  76. 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]
  77. 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]
  78. Smoger SH and Sayed MA, “Simultaneous Mucosal and Small Bowel Angioedema Due to Captopril,” South Med J, 1998, 91(11):1060-3. [PubMed 9824192]
  79. 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]
  80. von Vigier RO, Mozzettini S, Truttmann AC, Meregalli P, Ramelli GP, Bianchetti MG. Cough is common in children prescribed converting enzyme inhibitors. Nephron. 2000;84(1):98. doi:10.1159/000045552 [PubMed 10644922]
  81. 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]
  82. 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]
  83. 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. doi:10.1161/HYP.0000000000000065 [PubMed 29133356]
  84. White WB, Stimpel M. Long-term safety and efficacy of moexipril alone and in combination with hydrochlorothiazide in elderly patients with hypertension. J Hum Hypertens. 1995;9(11):879-884. [PubMed 8583466]
  85. 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]
  86. 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]
  87. 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 9661 Version 297.0

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟