Indicated for the treatment of hypertension in patients not adequately controlled on monotherapy with either agent.

Begin therapy with Lotrel only after a patient has either (a) failed to achieve the desired antihypertensive effect with amlodipine or benazepril monotherapy, or (b) demonstrated inability to achieve adequate antihypertensive effect with amlodipine therapy without developing edema.

Do not co-administer aliskiren with angiotensin receptor blockers (ARBs), ACE inhibitors, including Lotrel in patients with diabetes.

Lotrel is contraindicated in patients with a history of angioedema, with or without previous ACE inhibitor treatment, or patients who are hypersensitive to benazepril, to any other ACE inhibitor, to amlodipine, or to any of the excipients of Lotrel.

Lotrel is contraindicated in combination with a neprilysin inhibitor (e.g., sacubitril). Do not administer Lotrel within 36 hours of switching to or from a neprilysin inhibitor, e.g., sacubitril/valsartan.

Lotrel is not recommended in patients with creatinine clearance (CrCl) less than or equal to 30 mL/min. No dose adjustment of Lotrel is required in patients with CrCl greater than 30 mL/min/1.73m² (serum creatinine roughly less than or equal to 3 mg/dL or 265 micromol/L).

Avoid use of aliskiren with Lotrel in patients with renal impairment [glomerular filtration rate (GFR) < 60 mL/min].

Worsening angina and acute myocardial infarction can develop after starting or increasing the dose of amlodipine, particularly in patients with severe obstructive coronary artery disease.

Special caution is required when using amlodipine in patients suffering from aortic or mitral stenosis, or obstructive hypertrophic cardiomyopathy.

Lotrel can cause symptomatic hypotension and in patients with congestive heart failure, with or without associated renal insufficiency, ACE inhibitor therapy may cause excessive hypotension, which may be associated with oliguria, azotemia, and (rarely) with acute renal failure and death. Symptomatic hypotension is most likely to occur in patients who have been volume or salt depleted as a result of diuretic therapy, dietary salt restriction, dialysis, diarrhea, or vomiting.

As with all other vasodilators, special caution is required when using amlodipine in patients suffering from aortic or mitral stenosis, or obstructive hypertrophic cardiomyopathy.

Angioedema of the face, extremities, lips, tongue, glottis, and larynx has been reported in patients treated with ACE inhibitors.

Intestinal angioedema has been reported in patients treated with ACE inhibitors.

There have been rare reports of predominantly cholestatic hepatitis and isolated cases of acute liver failure, some of them fatal, in patients on ACE inhibitors.

Monitor serum potassium periodically in patients receiving Lotrel. Drugs that affect the RAS can cause hyperkalemia.

Presumably due to the inhibition of the degradation of endogenous bradykinin, persistent nonproductive cough has been reported with all ACE inhibitors, generally resolving after discontinuation of therapy.

Patients receiving co-administration of ACE inhibitor and mTOR (mammalian target of rapamycin) inhibitor (e.g.,temsirolimus, sirolimus, everolimus) therapy may be at increased risk for angioedema.

In general, avoid combined use of RAS inhibitors. Dual blockade of the RAS with angiotensin receptor blockers, ACE inhibitors, or aliskiren is associated with increased risks of hypotension, hyperkalemia, and changes in renal function (including acute renal failure) compared to monotherapy.

In rare cases, diabetic patients receiving an ACE inhibitor (including benazepril) concomitantly with insulin or oral antidiabetics may develop hypoglycemia.

In patients undergoing surgery or during anesthesia with agents that produce hypotension, benazepril will block the angiotensin II formation that could otherwise occur secondary to compensatory renin release.

Co-administration of simvastatin with amlodipine increases the systemic exposure of simvastatin. Limit the dose of simvastatin in patients on amlodipine to 20 mg daily.

Co-administration with CYP3A inhibitors (moderate and strong) results in increased systemic exposure to amlodipine and may require dose reduction.

Blood pressure should be monitored when amlodipine is coadministered with CYP3A4 inducers (e.g. rifampicin, St. John’s Wort).

Benazepril can attenuate potassium loss caused by thiazide diuretics. Potassium-sparing diuretics (spironolactone, amiloride, triamterene, and others) or potassium supplements can increase the risk of hyperkalemia. 

Increased serum lithium levels and symptoms of lithium toxicity have been reported in patients receiving ACE inhibitors during therapy with lithium.

In patients who are elderly, volume-depleted (including those on diuretic therapy), or with compromised renal function, co-administration of NSAIDs, including selective COX-2 inhibitors, with ACE inhibitors, including benazepril, may result in deterioration of renal function, including possible acute renal failure.

Anaphylactoid reactions during desensitization treatment with hymenoptera  (wasp sting) venom while receiving ACE inhibitors and anaphylactoid reactions during membrane exposure in patients dialyzed with high-flux membranes and treated concomitantly with an ACE inhibitor and in patients undergoing low-density lipoprotein apheresis with dextran sulfate absorption.

Nitritoid reactions (symptoms include facial flushing, nausea, vomiting and hypotension) have been reported rarely in patients on therapy with injectable gold (sodium aurothiomalate) and concomitant ACE inhibitor therapy.

Use of drugs that act on the RAS during the second and third trimesters of pregnancy reduces fetal renal function and increases fetal and neonatal morbidity and death. Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations. Potential neonatal adverse effects include skull hypoplasia, anuria, hypotension, renal failure, and death. When pregnancy is detected, discontinue Lotrel as soon as possible.

It is not known whether amlodipine is excreted in human milk. Nursing or drug should be discontinued.Minimal amounts of unchanged benazepril and of benazeprilat are excreted into the breast milk of lactating women treated with benazepril, so that a newborn child ingesting nothing but breast milk would receive less than 0.1% of the maternal doses of benazepril and benazeprilat.

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• Dosage greater than 10 mg of amlodipine and 40 mg of benazepril per day. GoToSource

• Initial therapy for hypertension. GoToSource

• Use in patients under the age of 18. GoToSource

Fetal injury and death. GoToSource

Kidney toxicity and elevated levels of potassium. GoToSource

Angioedema of the stomach and small intestine. GoToSource

Cholestatic hepatitis and liver injury. GoToSource

Constipation. GoToSource

Petechial rash and toxic epidermal necrolysis (severe drug reaction). GoToSource

Peripheral edema (accumulation of fluid under skin). GoToSource

Cough, upper respiratory tract infection and nasopharyngitis (inflammation of nose and back of throat). GoToSource

Tachycardia (rapid heart rate), gastroesophageal reflux, leukocytoclastic vasculitis (inflammation of blood vessels) and cutaneous hyperpigmentation (skin discoloration). GoToSource

Dysgeusia (taste disturbance) and erectile dysfunction. GoToSource

Pruritus (severe itching). GoToSource

Arthralgia (joint pain) and myalgia (muscle pain). GoToSource

Increased blood urea nitrogen and increased serum creatinine. GoToSource

Hypotension (low blood pressure). GoToSource

Agranulocytosis (decreased number of granulocytes, type of white blood cell). GoToSource

Lawsuits filed for birth defects.