Lisinopril is an angiotensin-converting enzyme (ACE) inhibitor.1, 2, 3, 4, 5
Lisinopril is used alone or in combination with other classes of antihypertensive agents in the management of hypertension.1, 2, 3, 4, 5 Lisinopril is FDA-labeled for use in adults and pediatric patients ≥6 years of age for the treatment of hypertension.1, 2, 5
The ALLHAT study, a large (33,357 patients), multicenter, randomized, active-control study in hypertensive patients 55 years of age or older with at least one other coronary heart disease risk factor, compared the cardiovascular benefit of therapy with an angiotensin-converting enzyme (ACE) inhibitor (lisinopril 10-40 mg daily) or a dihydropyridine-derivative calcium-channel blocker (amlodipine 2.5-10 mg daily) relative to therapy with a thiazide diuretic (chlorthalidone 12.5-25 mg daily).53, 54, 72 After a mean follow-up of 4.9 years, an intent-to-treat analysis revealed no difference in the primary outcome of combined fatal coronary heart disease or nonfatal myocardial infarction (MI) among the treatments.53, 54, 72
Compared with chlorthalidone, the relative risks for the primary outcome were 0.99 for lisinopril and 0.98 for amlodipine.53, 54 In addition, all-cause mortality, a secondary outcome, did not differ among the treatments.53, 54 Although each drug decreased blood pressure substantially, the extent of reduction was not equivalent.53, 54 Five-year systolic blood pressures were significantly higher in the lisinopril (2 mm Hg) and amlodipine (0.8 mm Hg) groups relative to that achieved with chlorthalidone, and 5-year diastolic blood pressure was significantly lower with amlodipine (0.8 mm Hg) relative to the thiazide.53, 54 Control of hypertension (systolic and diastolic blood pressures less than 140 and 90 mm Hg, respectively) was achieved in approximately two-thirds of patients by 5 years of follow-up (61, 66, or 68% of patients treated with lisinopril, amlodipine, or chlorthalidone, respectively).53, 54
Subgroup analysis of the ALLHAT study for race-related effects revealed no difference in the primary outcome of combined fatal coronary heart disease or nonfatal MI among the treatments in both Black and non-Black patients.70, 71 However, substantial race-related effects were observed in the incidence of secondary outcomes (e.g., stroke, combined cardiovascular disease events, heart failure).70, 71, 72 Compared with chlorthalidone, the relative risks for lisinopril were 1.4 and 1 for stroke and 1.19 and 1.06 for combined cardiovascular disease events in Black and non-Black patients, respectively.70, 71 When amlodipine was compared with chlorthalidone, the only race-related difference observed was in the incidence of heart failure; the relative risk was 1.46 and 1.32 in Black and non-Black patients, respectively.70, 71 The relative risk for heart failure was 1.19 in both Black and non-Black patients receiving lisinopril and was not considered to be statistically significant.70 In addition, after 4 years, in each treatment group, blood pressure reductions were greater in non-Black than in Black patients; about 68 or 60% of non-Black or Black patients, respectively, achieved a systolic/diastolic blood pressure <140/90 mm Hg.70, 71 In non-Black patients receiving chlorthalidone, amlodipine, or lisinopril 69, 69, or 67% achieved the mentioned blood pressure, respectively, while in Black patients receiving chlorthalidone, amlodipine, or lisinopril 63, 60, or 54% achieved such blood pressure, respectively.70, 71
Although the ALLHAT study provides strong evidence that these classes of antihypertensive agents (ACE inhibitors, dihydropyridine-derivative calcium-channel blockers, thiazide diuretics) are comparably effective in providing important cardiovascular benefit, apparent differences in certain secondary outcomes were observed.53, 54, 72 Thiazide diuretic therapy was superior to ACE inhibitor therapy in preventing aggregate cardiovascular events, principally stroke, heart failure, angina, and the need for coronary revascularization.53, 54, 72 Thiazide therapy also was better tolerated than ACE inhibitor therapy.53, 54 For example, angioedema was more likely in Black compared to non-Black patients). 53, 54
Post hoc analysis of the ALLHAT study directly comparing cardiovascular and other outcomes in patients receiving amlodipine or lisinopril revealed no difference in the primary outcome of combined fatal coronary heart disease or nonfatal MI between patients receiving an ACE inhibitor and those receiving a calcium-channel blocker.72, 73 However, patients receiving lisinopril were at higher risk for stroke, combined cardiovascular disease, GI bleeding, and angioedema, while those receiving amlodipine were at higher risk of developing heart failure.72, 73 ALLHAT investigators suggested the observed differences in cardiovascular outcome may be attributable, at least in part, to the greater antihypertensive effect of amlodipine compared with that of lisinopril, especially in women and Black patients.72, 73
The principal goal of preventing and treating hypertension is to reduce the risk of cardiovascular and renal morbidity and mortality, including target organ damage.1200, 1300 The relationship between blood pressure and cardiovascular disease is continuous, consistent, and independent of other risk factors.1200, 1300 The higher the blood pressure, the more likely the development of coronary artery disease, heart failure, stroke, and chronic kidney disease across all ages and ethnic groups.1200, 1300 Each 20-mm Hg increment in systolic blood pressure or 10-mm Hg increment in diastolic blood pressure has been shown to double the risk of death from stroke, heart disease, or other vascular disease.171, 1200, 1300
Accurate blood pressure measurement in the office or clinic is essential for proper diagnosis and management of hypertension.1200, 1300, 1302 Out-of-office blood pressure measurements are recommended to confirm the diagnosis of hypertension.1200, 1300, 1642 Blood pressure categories range from normal to different grades/stages of hypertension and are intended to align therapeutic approaches with blood pressure levels.1300, 1302 Guidelines published in 2025, written and developed by the American College of Cardiology (ACC), the American Heart Association (AHA), and several other US professional organizations, define stage 1 hypertension as a systolic blood pressure of 130-139 mm Hg or a diastolic blood pressure of 80-89 mm Hg.1200 Treatment recommendations generally include nonpharmacologic therapy with consideration of pharmacologic therapy based on cardiovascular risk.1200, 1300, 1302, 1642
Comprehensive guidelines for the management of hypertension have been published by various authoritative groups.501, 1200, 1300, 1301, 1302, 1642 The first such guideline was published by the National Heart Lung and Blood Institute (NHLBI) in 1977, followed by a series of Joint National Committee (JNC) guidelines with JNC8 being the last iteration of these guidelines in 2014.501, 1200 ACC, AHA, and other experts including the International Society of Hypertension (ISH) have published more recent clinical practice guidelines for the treatment of hypertension.1200, 1300, 1302, 1642 These guidelines all state that lifestyle/behavioral modifications (e.g., weight reduction in patients who are overweight or obese, dietary changes, sodium reduction, potassium supplementation, increased physical activity, moderation of alcohol intake, smoking cessation) are essential in the management of hypertension and should be implemented as first-line therapy to lower blood pressure and reduce total cardiovascular risk.1200, 1300, 1302, 1642 The decision whether to initiate antihypertensive drug therapy should be based on blood pressure levels while also considering cardiovascular risk factors.1200, 1219, 1300, 1302, 1642 The 2025 ACC/AHA guidelines recommend initiation of drug therapy in all patients with confirmed blood pressure ≥140/90 mm Hg.1200 These guidelines also recommend initiation of drug therapy in patients with blood pressure ≥130/80 mm Hg who have clinical cardiovascular disease, diabetes, or chronic kidney disease (CKD), or who are at increased short-term cardiovascular disease risk.1200 In patients with hypertension and low cardiovascular risk, the 2025 ACC/AHA guidelines recommend initiation of drug therapy if blood pressure remains ≥130/80 mm Hg after a 3- to 6-month trial of lifestyle interventions.1200
Current evidence-based practice guidelines for the management of hypertension in adults generally recommend the use of drugs from 4 classes of antihypertensive agents (angiotensin-converting enzyme [ACE] inhibitors, angiotensin II receptor antagonists, long-acting dihydropyridine calcium-channel blockers, and thiazide or thiazide-like diuretics); data from clinical outcome trials indicate that lowering blood pressure with any of these drug classes can reduce the complications of hypertension and provide similar cardiovascular risk reduction benefits. 501, 503, 1200, 1300, 1302, 1642 However, recommendations for initial drug selection and use in specific patient populations may vary across these guidelines.501, 503, 1200 Ultimately, choice of antihypertensive therapy should be individualized, considering the clinical characteristics of the patient (e.g., age, ethnicity/race, comorbid conditions, cardiovascular risk factors) as well as drug-related factors (e.g., ease of administration, availability, adverse effects, costs).501, 503, 510, 1200, 1300, 1302, 1642 Angiotensin II receptor antagonists or ACE inhibitors may be particularly useful in the management of hypertension in patients with certain coexisting conditions such as diabetes mellitus, chronic coronary artery disease, heart failure, peripheral artery disease, or CKD.1200 Other antihypertensive drugs such as nondihydropyridine calcium-channel blockers, beta-adrenergic blockers, direct vasodilators, alpha-1 blockers, loop diuretics, and aldosterone antagonists are available, but generally recommended as second-line agents or only in specific clinical situations.1200
Experts state that initiation of drug therapy with a single first-line antihypertensive drug is reasonable in adults with stage 1 hypertension (systolic BP 130-139 and diastolic BP 80-89 mm Hg), older adults (e.g., frail), or in those with a history of hypotension or multiple drug-related adverse events; this should be followed by dosage titration and sequential addition of other antihypertensive drugs as need to achieve the target blood pressure.1200 Because most patients with hypertension will require at least 2 antihypertensive drugs to achieve adequate blood pressure control, use of single pill combinations are generally recommended to improve adherence and blood pressure control when available.1302 Drug regimens with complementary activity, where a second antihypertensive agent is used to block compensatory responses to the first agent or affect a different pressor mechanism, can result in additive blood pressure lowering and are preferred.1200 Drug combinations that have similar mechanisms of action or clinical effects (e.g., the combination of an ACE inhibitor and an angiotensin II receptor antagonist) generally should be avoided.1200 Antihypertensive drug dosages should be adjusted and/or other agents substituted or added until goal blood pressure is achieved.1200 After initiation of antihypertensive drug therapy, a blood pressure goal of less than 130/80 mm Hg within 3 months is generally recommended if tolerated, but should be individualized.1200, 1301, 1302 While there is evidence from a randomized controlled study (SPRINT) demonstrating that intensive systolic blood pressure lowering (to <120 mm Hg) may be beneficial in patients with increased risk of cardiovascular disease, the study excluded patients with diabetes mellitus or prior stroke, and those younger than 50 years of age, which may decrease the generalizability of these findings.1210, 1219
The 2025 ACC/AHA hypertension guidelines make specific recommendations for patients with hypertension and certain comorbidities.1200 In patients with hypertension and CKD (i.e., estimated glomerular filtration rate [eGFR] <60 mL/minute per 1.73 m2) and albuminuria of ≥30 mg/g, with or without diabetes, use of either an angiotensin II receptor antagonist or an ACE inhibitor, but not both, is recommended.1200 Use of either an ACE inhibitor or an angiotensin II receptor antagonist should be considered in patients with hypertension and diabetes with mild albuminuria (<30 mg/g).1200 Thiazide-type diuretics, ACE inhibitors, or angiotensin II receptor antagonists are the recommended drug classes in patients with hypertension who have had an ischemic stroke, transient ischemic attack, or intracerebral hemorrhage.1200
The 2025 ACC/AHA guidelines also provide recommendations for the management of patients with reisistant hypertension (defined as blood pressure above goal despite treatment with 3 antihypertensive medications with complementary mechanisms of action, including a diuretic at maximally tolerated doses, or blood pressure at goal but requiring 4 or more medications).1200 Risk factors for resistant hypertension include older age, obesity, chronic kidney disease, and diabetes; such patients have a ≥50% higher risk of MI, stroke, end-stage kidney disease, and cardiovascular death than adults with hypertension without resistance to treatment.1200 In adults with uncontrolled resistant hypertension despite optimal treatment with first-line antihypertensive therapies, additional agents such as a mineralocorticoid receptor antagonist (e.g., spironolactone, eplerenone), beta-adrenergic blocker, alpha-adrenergic blocker, amiloride, central sympatholytic drugs (e.g., clonidine), dual endothelin receptor antagonists (e.g., aprocitentan), or direct vasodilators (e.g., hydralazine) may be considered for further blood pressure reduction.1200
Specific guidelines and recommendations for the management of hypertension in pregnancy have been published by experts such as AHA and the American College of Obstetricians and Gynecologists (ACOG).1200, 1300, 1305, 1306 First-line oral antihypertensive drugs generally recommended in pregnant patients include labetalol, nifedipine (extended-release), or methyldopa.1200, 1302, 1305 Renin-angiotensin system (RAS) blockers (e.g., ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors) are contraindicated during pregnancy due to adverse fetal and neonatal outcomes.1200, 1300, 1302, 1305
The American Academy of Pediatrics (AAP) has published a clinical practice guideline for the management of high blood pressure in children and adolescents.1150 The guideline recommends long-acting calcium-channel blockers (e.g., nifedipine, amlodipine), ACE inhibitors, angiotensin II receptor antagonists, and thiazide diuretics for the initial management of hypertension in children requiring drug therapy.1150
Lisinopril is used as adjunctive therapy in the management of heart failure in patients who do not respond adequately to diuretics and a cardiac glycoside.1, 2, 5
Many patients with heart failure respond to lisinopril with improvement in cardiac function indices, symptomatic (e.g., dyspnea, fatigue) relief, improved functional capacity, and increased exercise tolerance.1, 2, 14 In some studies, improvement in cardiac function indices and exercise tolerance were sustained for up to 3 months.14 Although additional studies are needed to determine the specific role of lisinopril in the management of heart failure and its long-term efficacy, the efficacy of lisinopril appears to be similar to that of captopril and enalapril.14, 19, 20 However, like enalapril, lisinopril has a relatively long duration of action compared with captopril;17, 18, 19 therefore, lisinopril may produce more prolonged hypotensive effects, particularly at high doses, which potentially could result in adverse cerebral and renal effects.17, 18 In addition, because the renin-angiotensin system appears to contribute substantially to preservation of glomerular filtration in patients with heart failure in whom renal function is severely compromised, therapy with an ACE inhibitor may adversely affect renal function.1, 17, 19
Results of several studies suggest that high dosages are associated with a lower risk of cardiovascular death and hospitalization for heart failure than lower dosages.44, 1000 Results of a large, randomized, double blind study (Assessment of Treatment with Lisinopril and Survival [ATLAS] study) in patients with heart failure (New York Heart Association [NYHA] class II-IV) indicate that high lisinopril dosages (32.5-35 mg daily) were associated with a 12% lower risk of death or hospitalization for any cause and 24% fewer hospitalizations for heart failure than low dosages (2.5-5 mg) of the drug.44
Current American Heart Association/American College of Cardiology/Heart Failure Society of America (AHA/ACC/HFSA) guidelines for the management of heart failure recommend guideline-directed medical therapy with a combination of drug therapies to reduce morbidity and mortality, including ACE inhibitors, sodium-glucose cotransporter 2 (SGLT2) inhibitors, angiotensin II receptor antagonists, angiotensin receptor-neprilysin inhibitors (ARNIs), β-adrenergic blockers, and mineralocorticoid receptor antagonists.1000 Diuretics are recommended on an as-needed basis to improve symptoms of congestion and prevent worsening of disease in patients with fluid retention.1000 Once guideline-directed medical therapy is optimized, additional therapies (e.g., ivabradine, vericiguat, digoxin, polyunsaturated fatty acids, potassium binders) may be considered based on patient-specific factors.1000
AHA/ACC/HFSA recommends that asymptomatic patients with stage B pre-heart failure and reduced left ventricular ejection fraction (LVEF) ≤40% receive treatment with an ACE inhibitor and a β-adrenergic blocker to reduce mortality and prevent symptomatic heart failure.1000 In patients with symptomatic heart failure with reduced ejection fraction (HFrEF; LVEF ≤40%, stage C symptomatic HF), AHA/ACC/HFSA recommends inhibition of the renin-angiotensin-aldosterone (RAA) system with an ARNI in conjunction with an evidence-based beta-adrenergic blocker, SGLT2 inhibitor, and a mineralocorticoid antagonist.1000, 1001 These 4 key medication classes should be initiated and titrated to target doses as soon as possible in newly diagnosed patients with stage C HFrEF.1001 Although ACE inhibitors have shown clear benefits in patients with HFrEF, ARNIs are preferred because of improved morbidity and mortality.1000, 1001 ACE inhibitors and angiotensin II receptor antagonists should only be considered for the treatment of HFrEF stage C heart failure when an ARNI is contraindicated, inaccessible, or poorly tolerated.1001 Existing data do not indicate a difference in symptoms or survival among the available ACE inhibitors for the treatment of heart failure.1000
Mortality Reduction After Acute Myocardial Infarction
Lisinopril is used in conjunction with standard therapies (e.g., thrombolytic agents, aspirin, β-blockers) to improve survival in hemodynamically stable patients with acute MI.1, 2, 5
Results of a multicenter, randomized, controlled, clinical study indicate that patients who received lisinopril or lisinopril concomitantly with nitrates within 24 hours of MI in addition to conventional therapy (thrombolytic agents, aspirin, β-adrenergic blockers) had an 11% lower risk of death (6 weeks after infarction) compared with patients receiving conventional therapy only; mortality rates were 6.4 or 7.2% in patients receiving lisinopril and conventional therapy or conventional therapy alone, respectively.1, 2, 5, 27
Studies with various ACE inhibitors have shown that these drugs reduce fatal and nonfatal cardiovascular events in patients with recent MI.527, 1100 The magnitude of benefit appears to be greatest in certain high-risk patients (e.g., those with an anterior infarction, ejection fraction of ≤40%, heart failure, prior infarction, or tachycardia).527, 1100
Current expert guidelines recommend an ACE inhibitor within the first 24 hours of acute MI in patients with an anterior infarction, heart failure, or ejection fraction ≤40% who do not have any contraindications (e.g., hypotension, shock, renal dysfunction).527 While early treatment within the first 24 hours of MI has been shown to be beneficial, ACE inhibitors should be used with caution (and with gradual upward titration) during the initial postinfarction period because of the possibility of hypotension or renal dysfunction.527, 1100 ACE inhibitor therapy generally should be continued indefinitely in all patients with left ventricular dysfunction or other compelling indications for use (e.g., hypertension, diabetes mellitus, CKD).1100 The benefits of long-term ACE inhibitor therapy are less certain in low-risk patients who have undergone revascularization and are receiving aggressive antilipemic therapy.527
Both ACE inhibitors and angiotensin II receptor antagonists have been shown to slow the rate of progression of renal disease in patients with diabetes mellitus and persistent albuminuria†, and use of a medication from either class is recommended in such patients with modestly elevated (30-300 mg/24 hours) or higher (exceeding 300 mg/24 hours) levels of urinary albumin excretion.1200, 1600, 1601
Lisinopril has been used for the prevention of migraine headaches.74, 1800, 1801 Based on a review of the currently available evidence, the American Headache Society and other experts suggest the use of lisinopril for the prevention of episodic migraines†.74, 1800, 1801
Dispensing and Administration Precautions
Lisinopril is administered orally as tablets or an oral solution.1, 2, 5 Lisinopril is also commercially available in fixed-combination tablets containing lisinopril and hydrochlorothiazide (Zestoretic®); see the full prescribing information for administration of this combination product.3, 4
Food does not alter the bioavailability of lisinopril tablets.1, 2
Store lisinopril tablets at controlled room temperature at 20—25°C.1, 2 Protect from moisture, freezing, and excessive heat.1, 2 Dispense in a tight container.1, 2
Store lisinopril oral solution at controlled room temperature at 20—25°C in a tight container.5 Protect from freezing and excessive heat.5
For the management of hypertension in adults not receiving a diuretic, the usual initial dosage of lisinopril is 10 mg orally once daily.1, 2, 5 Adjust the dosage of lisinopril according to blood pressure response.1, 2, 5 The usual maintenance dosage of lisinopril in adults is 20-40 mg daily, given as a single dose.1, 2, 5 Dosages up to 80 mg daily have been used, but do not appear to have a greater effect.1, 2, 5
Experts recommend a usual lisinopril dosage of 10—40 mg once daily.1200
If blood pressure is not adequately controlled with lisinopril alone, a low dosage of a diuretic (e.g., hydrochlorothiazide 12.5 mg) may be added.1, 2, 5 After the addition of a diuretic, it may be possible to reduce the dosage of lisinopril.1, 2, 5
In adults with hypertension taking diuretics, the recommended initial dosage of lisinopril is 5 mg once daily.5
For the management of heart failure, the usual initial dosage of lisinopril, when used with diuretics and (usually) digitalis as adjunctive therapy for systolic heart failure, is 5 mg orally once daily.1, 2, 5 The recommended initial dosage in patients with hyponatremia (serum sodium <130 mEq/L) is 2.5 mg once daily.1, 2, 5 Increase the dosage as tolerated to a maximum of 40 mg once daily.1, 2, 5
For the management of heart failure with reduced ejection fraction, experts recommend an initial lisinopril dosage of 2.5—5 mg once daily, with a target dosage of 20—40 mg once daily, as part of guideline-directed medical therapy.1000, 1001
Diuretic dosage may need to be adjusted to minimize hypovolemia, which may contribute to hypotension.1, 2, 5 Hypotension occurring after the initial dose of lisinopril does not preclude subsequent dosage titration, provided hypotension has been managed effectively.1, 2, 5
Mortality Reduction After Acute Myocardial Infarction
To improve survival after acute myocardial infarction (MI) in hemodynamically stable patients, administer a 5-mg dose of lisinopril orally within 24 hours of onset of symptoms of MI followed by a 5- and 10-mg dose 24 and 48 hours later, respectively.1, 2, 5 Thereafter, administer a maintenance dosage of 10 mg daily and continue for 6 weeks.1, 2, 5
In patients who have low blood pressure during the first 3 days after MI, initiate lisinopril at a lower dose (i.e., 2.5 mg).1, 2, 5
If hypotension (i.e., systolic blood pressure ≤100 mm Hg) occurs, reduce the maintenance dosage to 5 mg daily, which may be temporarily reduced further to 2.5 mg daily if needed.1, 2, 5 If prolonged hypotension occurs (i.e., systolic pressure <90 mm Hg lasting for >1 hour), discontinue lisinopril.1, 2, 5
For the management of hypertension in children ≥6 years of age with glomerular filtration rate (GFR) >30 mL/minute per 1.73 m2, the usual initial dosage of lisinopril is 0.07 mg/kg (up to 5 mg) orally once daily.1, 2, 5 Adjust the dosage according to blood pressure response up to a maximum of 0.61 mg/kg (up to 40 mg) once daily.1, 2, 5 The safety and efficacy of doses exceeding 0.61 mg/kg (or in excess of 40 mg) have not been established.1, 2, 5
The manufacturer makes no specific dosage recommendations for patients with hepatic impairment.1, 2, 5
No dosage adjustment is necessary in patients with creatinine clearance >30 mL/minute.1, 2, 5
In adult patients with creatinine clearance 10-30 mL/minute, reduce the initial dosage of lisinopril to half of the usual recommended dosage (i.e., 5 mg once daily in patients with hypertension, and 2.5 mg once daily in patients with systolic heart failure or acute MI).1, 2, 5 Uptitrate as tolerated to a maximum of 40 mg daily.1, 2
For adult patients with creatinine clearance <10 mL/minute or on hemodialysis, the recommended initial dosage is 2.5 mg once daily.1, 2, 5
In pediatric patients, lisinopril is not recommended in those with GFR <30 mL/minute per 1.73 m2.5
The manufacturer makes no specific dosage recommendations for geriatric patients.1, 2, 5
Fetal/Neonatal Morbidity and Mortality
A boxed warning about the risk of fetal toxicity is included in the prescribing information for lisinopril.1, 2, 5 Use of lisinopril during pregnancy can cause fetal harm.1, 2, 5 Use of medications that impact the renin-angiotensin system during the second and third trimesters of pregnancy decreases fetal renal function and increases fetal/neonatal morbidity and mortality.1, 2, 5 Oligohydramnios caused by medications that act on the system can result in fetal lung hypoplasia, skeletal deformations (including skull hypoplasia), anuria, hypotension, renal failure, and death.1, 2, 5 Discontinue lisinopril as soon as possible when pregnancy is detected.1, 2, 5 In the rare case that there is no appropriate alternative therapy, apprise the mother of the potential risk to the fetus.1, 2, 5 If lisinopril is taken during pregnancy, perform serial ultrasound examinations to assess the intra-amniotic environment.1, 2, 5 However, oligohydramnios may not appear until after the fetus has sustained irreversible injury.1, 2, 5 Closely observe neonates who have been exposed to lisinopril in utero for signs of hypotension, oliguria, and hyperkalemia.1, 2, 5 If oliguria or hypotension occurs, support blood pressure and renal perfusion.1, 2, 5 Exchange transfusions or dialysis may be required.1, 2, 5
Other Warnings and Precautions
Angioedema and Anaphylactoid Reactions
Angioedema of the face, extremities, lips, tongue, glottis, and/or larynx, including some fatal reactions, have occurred in patients treated with ACE inhibitors, including lisinopril, at any time during treatment.1, 2, 5
Patients with head and neck angioedema involving the tongue, glottis, or larynx are likely to experience airway obstruction, especially those with a history of airway surgery.1, 2, 5 If angioedema occurs, discontinue lisinopril immediately and provide appropriate therapy and monitoring until complete and sustained resolution of signs and symptoms.1, 2, 5
Lisinopril use is contraindicated in patients with a history of angioedema or hypersensitivity related to previous treatment with an ACE inhibitor.1, 2, 5 Patients with a history of angioedema unrelated to ACE inhibitor therapy may be at increased risk of angioedema while receiving an ACE inhibitor.1, 2, 5 Additionally, patients taking a concomitant mammalian target of rapamycin (mTOR) inhibitor (e.g., temsirolimus, sirolimus, everolimus) or a neprilysin inhibitor (e.g., sacubitril) with lisinopril may be at increased risk for angioedema.1, 2, 5
Intestinal angioedema (occasionally without a prior history of facial angioedema or elevated serum levels of complement 1 [C1] esterase inhibitor) has been reported in patients receiving ACE inhibitors.1, 2, 5 These patients frequently presented with abdominal pain (with or without nausea or vomiting), and intestinal angioedema was sometimes diagnosed by abdominal CT scan, ultrasound, or at surgery; manifestations resolved after discontinuance of the ACE inhibitor.1, 2, 5
Life-threatening anaphylactoid reactions have been reported in 2 patients receiving ACE inhibitors while undergoing desensitization with hymenoptera venom.1, 2, 5
Sudden and potentially life-threatening anaphylactoid reactions also have been reported in patients receiving ACE inhibitors while undergoing hemodialysis using high-flux membranes.1, 2, 5 In such patients, discontinue dialysis immediately, and initiate aggressive therapy for anaphylactic reactions.1, 2, 5 Antihistamines have not been effective for relieving symptoms in these patients; consider the use of a different type of dialysis membrane or a different class of antihypertensive agent.1, 2, 5 In addition, anaphylactoid reactions have been reported in patients undergoing low-density lipoprotein (LDL) apheresis with dextran sulfate absorption.1, 2, 5
Inhibition of the RAS may cause changes in renal function, including acute renal failure.1, 2, 5 Patients whose renal function may depend in part on the activity of the RAS (e.g., patients with renal artery stenosis, chronic kidney disease, severe congestive heart failure, post-myocardial infarction [MI], or volume depletion) may be at increased risk of developing acute renal failure during treatment with lisinopril.1, 2, 5
Consider withholding or discontinuing lisinopril in patients who develop a clinically important decrease in renal function during treatment.1, 2, 5
Monitor renal function periodically in patients treated with lisinopril.1, 2, 5
Symptomatic hypotension may occur, sometimes associated with oliguria, progressive azotemia, acute renal failure, or death.1, 2, 5 Patients at particular risk include those with heart failure with systolic blood pressure <100 mm Hg, hyponatremia, high-dose or recent intensive diuretic therapy, recent increase in diuretic dose, dialysis, or severe volume and/or salt depletion of any etiology.1, 2, 5 In such patients, initiate lisinopril therapy under very close medical supervision; follow the patient closely for the first 2 weeks of treatment and whenever the dosage of lisinopril and/or any concomitant diuretic is increased.1, 2, 5
Avoid use of lisinopril in patients who are hemodynamically unstable after acute MI.1, 2, 5 Symptomatic hypotension can also occur in patients with severe aortic stenosis or hypertrophic cardiomyopathy.1, 2, 5
In patients undergoing major surgery or undergoing anesthesia with drugs that produce hypotension, lisinopril may inhibit angiotensin II formation secondary to compensatory renin release.1, 2, 5 If hypotension occurs and is considered to be due to this mechanism, hypotension can be corrected by volume expansion.1, 2, 5
Drugs that inhibit the RAS can cause hyperkalemia.1, 2, 5 Hyperkalemia can develop especially in patients with renal insufficiency or diabetes mellitus or in those receiving drugs that can increase serum potassium concentration (e.g., potassium-sparing diuretics, potassium supplements, potassium-containing salt substitutes).1, 2, 5
Monitor serum potassium periodically in patients treated with lisinopril.1, 2, 5
There are reports of an ACE inhibitor-associated clinical syndrome that manifests initially by cholestatic jaundice or hepatitis, and progresses to fulminant hepatic necrosis and sometimes death.1, 2, 5 The mechanism of this syndrome is not understood.1, 2, 5
Patients receiving an ACE inhibitor, including lisinopril, who develop jaundice or marked elevations in hepatic enzymes should discontinue lisinopril and receive appropriate monitoring.1, 2, 5
When the fixed combination of lisinopril and hydrochlorothiazide is used, the cautions, precautions, contraindications, and drug interactions associated with both medications must be considered.3, 4 Consult the full prescribing information for the fixed combination preparation for specific information.3, 4
Lisinopril can cause fetal harm when administered to pregnant females.1, 2, 5
Use of medications that impact the RAS, such as lisinopril, during the second and third trimesters of pregnancy decreases fetal renal function and increases fetal/neonatal morbidity and mortality.1, 2, 5 Oligohydramnios caused by medications that act on the RAS can result in fetal lung hypoplasia, skeletal deformations (including skull hypoplasia), anuria, hypotension, renal failure, and death.1, 2, 5
Discontinue lisinopril as soon as possible when pregnancy is detected.1, 2, 5 In the rare case that there is no appropriate alternative to therapy with drugs affecting the RAS, apprise the mother of the potential hazard to the fetus.1, 2, 5
Perform serial ultrasound examinations to assess the intra-amniotic environment.1, 2, 5 Based on the week of pregnancy, fetal testing may be appropriate.1, 2, 5 However, patients and clinicians should be aware that oligohydramnios may not manifest until after the fetus has sustained irreversible injury.1, 2, 5 Closely observe neonates with a history of in utero exposure to lisinopril for hypotension, oliguria, and hyperkalemia.1, 2, 5 If oliguria or hypotension occurs, support blood pressure and renal perfusion.1, 2, 5 To reverse hypotension and substitute for disordered renal function, exchange transfusions or dialysis may be required.1, 2, 5
There are maternal and embryofetal risks associated with untreated hypertension during pregnancy.1, 2, 5 Hypertension in pregnancy increases the mother's risk for pre-eclampsia, gestational diabetes, premature delivery, and delivery complications; hypertension also increases the fetal risk for intrauterine growth restriction and intrauterine death.1, 2, 5 Monitor pregnant females with hypertension carefully and manage accordingly.1, 2, 5
Lisinopril is distributed into milk in rats; it is not known whether the drug is distributed into milk in humans.1, 2, 5 The effects of lisinopril on the breast-fed infant or on milk production are also unknown.1, 2, 5
Because of the potential for serious adverse reactions in breastfeeding infants, advise women not to breast-feed during treatment with lisinopril.1, 2, 5
Safety and efficacy of lisinopril have been established in pediatric patients 6—16 years of age for treatment of hypertension.1, 2, 5 No important differences were observed in the adverse reaction profile between pediatric and adult patients.1, 2, 5
Safety and efficacy of lisinopril have not been established in children <6 years of age or in pediatric patients with glomerular filtration rate <30 mL/minute per 1.73 m2.1, 2, 5
If oliguria or hypotension occurs in neonates with a history of in utero exposure to lisinopril, support blood pressure and renal perfusion.1, 2, 5 Exchange transfusions or dialysis may be necessary in order to reverse hypotension and/or substitute for disordered renal function.1, 2, 5
In a clinical study of lisinopril in patients with MI, 47% of patients were ≥65 years of age, and 18% were ≥75 years of age.1, 2, 5 In this study, 4.8% of patients ≥75 years of age discontinued lisinopril because of renal dysfunction compared to 1.3% of patients <75 years of age.1, 2, 5 No other differences in safety or effectiveness were observed between geriatric and younger patients; however, greater sensitivity of some older individuals cannot be excluded.1, 2, 5
The manufacturer makes no specific dosage recommendations for patients with hepatic impairment.1, 2, 5 Cholestatic jaundice and hepatic failure may occur during treatment with lisinopril.1, 2, 5
Changes in renal function can be caused by drugs that inhibit the RAS, such as lisinopril.1, 2, 5
Dosage adjustment of lisinopril is required in patients undergoing hemodialysis or whose creatinine clearance is ≤30 mL/minute.1, 2, 5 No dosage adjustment of lisinopril is required in patients with creatinine clearance >30 mL/minute.1, 2, 5
Lisinopril is excreted principally through the kidneys.1, 2, 5 Impaired renal function decreases lisinopril elimination, but this decrease becomes clinically important only when the glomerular filtration rate (GFR) is <30 mL/minute.1, 2, 5 Above this GFR, the elimination half-life is minimally altered.1, 2, 5 With greater impairment, however, peak and trough lisinopril levels increase, the time to peak plasma concentration increases, and the time to attain steady state is prolonged.1, 2, 5 Lisinopril can be removed by hemodialysis.1, 2, 5
Lisinopril was less effective in decreasing blood pressure in Black patients compared to non-Black patients.1, 2, 5 Increased incidence of angioedema has also been observed in Black patients treated with ACE inhibitors compared to non-Black patients.1, 2, 5
Adverse effects reported in >2% of patients receiving lisinopril for the management of hypertension and more frequently than with placebo include headache, dizziness, and cough.1, 2, 5
Adverse effects reported in >2% of patients receiving lisinopril for the management of heart failure and more frequently than with placebo include hypotension and chest pain.1, 2, 5
Adverse effects reported in >2% of patients receiving lisinopril for the management of acute MI and more frequently than with placebo include hypotension.1, 2, 5
Drugs that Increase Serum Potassium
Additive hyperkalemic effect may occur with concomitant use of lisinopril and potassium-sparing diuretics, potassium supplements, or other medications that can increase serum potassium.1, 2, 5
Do not use lisinopril with potassium supplements or salt substitutes containing potassium without consulting a clinician.1, 2, 5
Monitor potassium levels frequently if concomitant use of lisinopril and potassium sparing diuretics is indicated.1, 2, 5
Drugs Inhibiting the Renin-Angiotensin System
There is an increased risk of hypotension, hyperkalemia, and changes in renal function (e.g., acute renal failure) with concomitant use of other medications that block the renin-angiotensin system (RAS) (e.g., aliskiren, angiotensin II receptor antagonists).1, 2, 5
In general, avoid concomitant use of medications that block the RAS.1, 2, 5 If lisinopril is used concomitantly with medications that block the RAS, closely monitor blood pressure, renal function, and serum electrolyte concentrations.1, 2, 5
Concomitant use of lisinopril and aliskiren is contraindicated in patients with diabetes mellitus; in addition, avoid concomitant use in patients with renal impairment (glomerular filtration rate [GFR] less than <60 mL/minute per 1.73 m2).1, 2, 5
Concomitant administration of lisinopril and antidiabetic agents (insulins or oral hypoglycemic agents) can cause an increased hypoglycemic effect, especially during the first month of combined treatment.1, 2, 5
Initiation of lisinopril in patients on diuretics may cause significant reductions in blood pressure.1, 2, 5 The possibility of hypotensive effects can be minimized by decreasing the dosage of the diuretic, discontinuing the diuretic, or increasing the salt intake prior to initiating lisinopril.1, 2, 5 If this is not possible, reduce the starting dosage of lisinopril.1, 2, 5
Lisinopril decreases potassium loss caused by thiazide-type diuretics.1, 2, 5 Concomitant use of lisinopril and potassium-sparing diuretics (e.g., spironolactone, amiloride, triamterene) can increase the risk of hyperkalemia.1, 2, 5 Monitor potassium levels frequently if concomitant use is indicated.1, 2, 5
There are rare reports of nitritoid reactions (manifested by facial flushing, nausea, vomiting, and hypotension) in patients receiving injectable gold (sodium aurothioglucose) concomitantly with angiotensin-converting enzyme (ACE) inhibitors, including lisinopril.1, 2, 5
Increased lithium concentrations (lithium toxicity) has occurred in patients receiving lithium concomitantly with drugs that cause elimination of sodium, including ACE inhibitors.1, 2, 5 Lithium toxicity was typically reversible upon discontinuation of lithium and the ACE inhibitor.1, 2, 5
Monitor serum lithium levels during concurrent use of lisinopril and lithium.1, 2, 5
Mammalian Target of Rapamycin (mTOR) Inhibitors
Patients using lisinopril concomitantly with an mTOR inhibitor (e.g. temsirolimus, sirolimus, everolimus) may be at increased risk for angioedema.1, 2, 5
Patients using lisinopril concomitantly with a neprilysin inhibitor (e.g., sacubitril) may be at increased risk for angioedema.1, 2, 5 Concomitant use of lisinopril with a neprilysin inhibitor is contraindicated: do not administer lisinopril within 36 hours of switching to or from sacubitril/valsartan.1, 2, 5
Nonsteroidal Anti-inflammatory Agents
Decreased antihypertensive effect may occur when lisinopril is used concomitantly with nonsteroidal anti-inflammatory agents (NSAIAs).1, 2, 5
Concomitant use of lisinopril and NSAIAs may result in deterioration of renal function, including possible acute renal failure, in patients who are elderly, volume-depleted (including those on diuretic therapy), or with compromised renal function; these effects are typically reversible.1, 2, 5
Monitor renal function periodically in patients receiving lisinopril and NSAIA therapy.1, 2, 5
Lisinopril is an inhibitor of angiotensin-converting enzyme (ACE, bradykinase, kininase II), the peptidyl dipeptidase that catalyzes the conversion of angiotensin I to angiotensin II.1, 2, 5 Angiotensin II is a vasoconstrictor that also stimulates aldosterone secretion; inhibition of ACE results in decreased plasma angiotensin II, leading to reduced vasopressor activity and aldosterone secretion.1, 2, 5 ACE also degrades bradykinin, a potent vasodepressor, although it is unknown whether increased levels of bradykinin play a role in the therapeutic effects of lisinopril.1, 2, 5 The beneficial effects of lisinopril in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin-aldosterone system.1, 2, 5 However, lisinopril is antihypertensive even in patients with low-renin hypertension.1, 2, 5
The onset of antihypertensive activity was observed at 1 hour following oral administration of a single dose of lisinopril, with peak reduction of blood pressure achieved by 6 hours.1, 2, 5 Although an antihypertensive effect was observed 24 hours after dosing with recommended single daily doses, the effect was more consistent and the mean effect was considerably larger in some studies with doses of ≥20 mg than with lower doses.1, 2, 5 However, at all doses studied, the mean antihypertensive effect was substantially smaller 24 hours after dosing than at 6 hours after dosing.1, 2, 5
In adults, peak serum concentrations occur within about 7 hours of oral administration of lisinopril tablets; there was a trend toward a small delay in time taken to reach peak serum concentrations in patients with acute myocardial infarction (MI).1, 2, 5 Based on urinary recovery, the mean extent of absorption of lisinopril is approximately 25%, with considerable intersubject variability (6—60%) at all doses tested (5—80 mg).1, 2, 5 In patients with stable New York Heart Association Class II—IV congestive heart failure, the absolute bioavailability of lisinopril is reduced to 16%.1, 2, 5 In patients with acute MI, the oral bioavailability of lisinopril is similar to that in healthy volunteers.1, 2, 5 Food does not alter the bioavailability of lisinopril tablets.1, 2, 5 Lisinopril oral solution is bioequivalent to lisinopril tablets under fasted and fed conditions.5
Declining serum concentrations of lisinopril exhibit a prolonged terminal phase, which likely represents saturable binding to ACE and is not proportional to dose.1, 2, 5 This terminal phase does not contribute to drug accumulation.1, 2, 5 Lisinopril does not appear to bind to serum proteins.1, 2, 5 Studies in rats indicate that lisinopril crosses the blood brain barrier poorly.1, 2, 5 Lisinopril does not undergo metabolism; it is excreted unchanged entirely in the urine.1, 2, 5 The effective half-life of lisinopril after multiple dosing is 12 hours.1, 2, 5
Additional Information
The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer's labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care.
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Solution | 1 mg/mL | Qbrelis® | |
Tablets | 2.5 mg* | TWI Pharmaceuticals | ||
Lisinopril Tablets | ||||
5 mg* | Zestril® | TWI Pharmaceuticals | ||
Lisinopril Tablets | ||||
10 mg* | Zestril® | TWI Pharmaceuticals | ||
Lisinopril Tablets | ||||
20 mg* | Zestril® | TWI Pharmaceuticals | ||
Lisinopril Tablets | ||||
30 mg* | Zestril® | TWI Pharmaceuticals | ||
Lisinopril Tablets | ||||
40 mg* | Zestril® | TWI Pharmaceuticals | ||
Lisinopril Tablets |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets | 10 mg with Hydrochlorothiazide 12.5 mg* | Almatica Pharma | |
Lisinopril and Hydrochlorothiazide Tablets | ||||
20 mg with Hydrochlorothiazide 12.5 mg* | Zestoretic® | Almatica Pharma | ||
Lisinopril and Hydrochlorothiazide Tablets | ||||
20 mg with Hydrochlorothiazide 25 mg* | Zestoretic® | Almatica Pharma | ||
Lisinopril and Hydrochlorothiazide Tablets |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
1. Camber Pharmaceuticals, Inc. Lisinopril tablets prescribing information. Piscataway, NJ; 2024 Aug. [Web]
2. TWi Pharmaceuticals. Zestril® (lisinopril) tablets prescribing information. Paramus, NJ; 2024 Jan. [Web]
3. Lupin Pharmaceuticals, Inc. Lisinopril and hydrochlorothiazide tablets prescribing information. Baltimore, MD; 2023 Oct. [Web]
4. Almatica Pharma LLC. Zestoretic® (lisinopril and hydrochlorothiazide) tablets prescribing information. Morristown, NJ: 2021 Jul. [Web]
5. Azurity Pharmaceuticals, Inc. Qbrelis® (lisinopril) oral solution prescribing information. Woburn, MA; 2024 Jun.
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