Thursday, February 22, 2007

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NORVASC
Generic Name: Amlodipine (am LOE di peen)
Brand Names: Norvasc



What is the most important information I should know about Norvasc(Amlodipine)?



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• Do not stop taking Norvasc(Amlodipine) without first talking to your doctor, even if you begin to feel better. If you stop taking the medication, your condition could become worse.

What is Norvasc(Amlodipine)?



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• Norvasc(Amlodipine) is in a class of drugs called calcium channel blockers. Norvasc(Amlodipine) relaxes (widens) the blood vessels (veins and arteries), making it easier for the heart to pump and reducing its workload.

• Norvasc(Amlodipine) is used to treat hypertension (high blood pressure) and to treat angina (chest pain).

• Norvasc(Amlodipine) may also be used for purposes other than those listed in this medication guide.

What should I discuss with my healthcare provider before taking Norvasc(Amlodipine)?



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• Before taking Norvasc(Amlodipine), tell your doctor if you have · liver disease; or · another disease of the heart or blood vessels such as sick sinus syndrome, aortic stenosis, heart failure, low blood pressure, or coronary artery disease.

• You may not be able to take Norvasc(Amlodipine), or you may require a dosage adjustment or special monitoring during treatment if you have any of the conditions listed above.

• Norvasc(Amlodipine) is in the FDA pregnancy category C. This means that it is not known whether Norvasc(Amlodipine) will be harmful to an unborn baby. Do not take this medication without first talking to your doctor if you are pregnant or could become pregnant during treatment.

• It is not known whether Norvasc(Amlodipine) passes into breast milk. Do not take this medication without first talking to your doctor if you are breast-feeding a baby.

• If you are over 65 years of age, you may be more likely to experience side effects from Norvasc(Amlodipine). Your doctor may prescribe a lower dose of this medication.

How should I take Norvasc(Amlodipine)?



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• Take Norvasc(Amlodipine) exactly as directed by your doctor. If you do not understand these directions, ask your pharmacist, nurse, or doctor to explain them to you.

• Take each dose with a full glass of water.

• Do not stop taking Norvasc(Amlodipine) without first talking to your doctor, even if you begin to feel better. If you stop taking the medication, your condition could become worse.

• Store Norvasc(Amlodipine) at room temperature away from moisture and heat.

What happens if I miss a dose?



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• Take the missed dose as soon as you remember. However, if it is almost time for the next dose, skip the missed dose and take only the next regularly scheduled dose. Do not take a double dose of this medication.

What happens if I overdose?



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• Seek emergency medical attention.

• Symptoms of an Norvasc(Amlodipine) overdose include dizziness, weakness, chest pain, shortness of breath, fainting, unusually fast or slow heartbeat, coma, slurred speech, and confusion.

What should I avoid while taking Norvasc(Amlodipine)?



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• Follow any recommendations your doctor makes about diet or exercise.

• Use caution when you stand or sit up from a lying position, especially if you wake up during the night. You may become dizzy when changing positions.

• Use alcohol cautiously. Alcohol may further lower blood pressure and increase drowsiness or dizziness while taking Norvasc(Amlodipine).

What are the possible side effects of Norvasc(Amlodipine)?



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• If you experience any of the following serious side effects, stop taking Norvasc(Amlodipine) and contact your doctor immediately or seek emergency medical treatment: · an allergic reaction (difficulty breathing; closing of the throat; swelling of the lips, tongue, or face; or hives); · unusually fast or slow heartbeat; · chest pain; · severe dizziness or fainting; · psychosis; · jaundice (yellowing of the skin or eyes); or · swelling of the legs or ankles.

• Other, less serious side effects may be more likely to occur. Continue to take Norvasc(Amlodipine) and talk to your doctor if you experience · fatigue or tiredness; · headache; · insomnia; · vivid or abnormal dreams; · flushing; · abdominal pain; · nausea, diarrhea, or constipation; or · increased or difficult urination.

• Side effects other than those listed here may also occur. Talk to your doctor about any side effect that seems unusual or that is especially bothersome.

What other drugs will affect Norvasc(Amlodipine)?



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• Tell your doctor if you are taking any other heart medicines. Norvasc(Amlodipine) may compound the effects of other heart medications.

• Other drugs may also interact with Norvasc(Amlodipine) or affect your condition. Talk to your doctor and pharmacist before taking any prescription or over-the-counter medicines, including herbal products.

Where can I get more information?



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• Your pharmacist has additional information about Norvasc(Amlodipine) written for health professionals that you may read.

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• Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.

• Every effort has been made to ensure that the information provided by Cerner Multum, Inc. ('Multum') is accurate, up-to-date, and complete, but no guarantee is made to that effect. Drug information contained herein may be time sensitive. Multum information has been compiled for use by healthcare practitioners and consumers in the United States and therefore Multum does not warrant that uses outside of the United States are appropriate, unless specifically indicated otherwise. Multum's drug information does not endorse drugs, diagnose patients or recommend therapy. Multum's drug information is an informational resource designed to assist licensed healthcare practitioners in caring for their patients and/ or to serve consumers viewing this service as a supplement to, and not a substitute for, the expertise, skill, knowledge and judgment of healthcare practitioners. The absence of a warning for a given drug or drug combination in no way should be construed to indicate that the drug or drug combination is safe, effective or appropriate for any given patient. Multum does not assume any responsibility for any aspect of healthcare administered with the aid of information Multum provides. The information contained herein is not intended to cover all possible uses, directions, precautions, warnings, drug interactions, allergic reactions, or adverse effects. If you have questions about the drugs you are taking, check with your doctor, nurse or pharmacist.

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CLINICAL PHARMACOLOGY NORVASC

CLINICAL PHARMACOLOGY NORVASC Mechanism of Action Amlodipine is a dihydropyridine calcium antagonist (calcium ion antagonist or slow-channel blocker) that inhibits the transmembrane influx of calcium ions into vascular smooth muscle and cardiac muscle. Experimental data suggest that amlodipine binds to both dihydropyridine and nondihydropyridine binding sites. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Amlodipine inhibits calcium ion influx across cell membranes selectively, with a greater effect on vascular smooth muscle cells than on cardiac muscle cells. Negative inotropic effects can be detected in vitro but such effects have not been seen in intact animals at therapeutic doses. Serum calcium concentration is not affected by amlodipine. Within the physiologic pH range, amlodipine is an ionized compound (pKa=8.6), and its kinetic interaction with the calcium channel receptor is characterized by a gradual rate of association and dissociation with the receptor binding site, resulting in a gradual onset of effect. Amlodipine is a peripheral arterial vasodilator that acts directly on vascular smooth muscle to cause a reduction in peripheral vascular resistance and reduction in blood pressure. The precise mechanisms by which amlodipine relieves angina have not been fully delineated, but are thought to include the following: Exertional Angina: In patients with exertional angina, NORVASC reduces the total peripheral resistance (afterload) against which the heart works and reduces the rate pressure product, and thus myocardial oxygen demand, at any given level of exercise. Vasospastic Angina: NORVASC has been demonstrated to block constriction and restore blood flow in coronary arteries and arterioles in response to calcium, potassium epinephrine, serotonin, and thromboxane A2 analog in experimental animal models and in human coronary vessels in vitro. This inhibition of coronary spasm is responsible for the effectiveness of NORVASC in vasospastic (Prinzmetal†s or variant) angina. Pharmacokinetics and Metabolism After oral administration of therapeutic doses of NORVASC, absorption produces peak plasma concentrations between 6 and 12 hours. Absolute bioavailability has been estimated to be between 64 and 90%. The bioavailability of NORVASC is not altered by the presence of food. Amlodipine is extensively (about 90%) converted to inactive metabolites via hepatic metabolism with 10% of the parent compound and 60% of the metabolites excreted in the urine. Ex vivo studies have shown that approximately 93% of the circulating drug is bound to plasma proteins in hypertensive patients. Elimination from the plasma is biphasic with a terminal elimination half-life of about 30-50 hours. Steady-state plasma levels of amlodipine are reached after 7 to 8 days of consecutive daily dosing. The pharmacokinetics of amlodipine are not significantly influenced by renal impairment. Patients with renal failure may therefore receive the usual initial dose. Elderly patients and patients with hepatic insufficiency have decreased clearance of amlodipine with a resulting increase in AUC of approximately 40-60%, and a lower initial dose may be required. A similar increase in AUC was observed in patients with moderate to severe heart failure. Pediatric Patients Sixty-two hypertensive patients aged 6 to 17 years received doses of NORVASC between 1.25 mg and 20 mg. Weight-adjusted clearance and volume of distribution were similar to values in adults. Pharmacodynamics Hemodynamics: Following administration of therapeutic doses to patients with hypertension, NORVASC produces vasodilation resulting in a reduction of supine and standing blood pressures. These decreases in blood pressure are not accompanied by a significant change in heart rate or plasma catecholamine levels with chronic dosing. Although the acute intravenous administration of amlodipine decreases arterial blood pressure and increases heart rate in hemodynamic studies of patients with chronic stable angina, chronic oral administration of amlodipine in clinical trials did not lead to clinically significant changes in heart rate or blood pressures in normotensive patients with angina. With chronic once daily oral administration, antihypertensive effectiveness is maintained for at least 24 hours. Plasma concentrations correlate with effect in both young and elderly patients. The magnitude of reduction in blood pressure with NORVASC is also correlated with the height of pretreatment elevation; thus, individuals with moderate hypertension (diastolic pressure 105-114 mmHg) had about a 50% greater response than patients with mild hypertension (diastolic pressure 90-104 mmHg). Normotensive subjects experienced no clinically significant change in blood pressures (+1/¾2 mmHg). In hypertensive patients with normal renal function, therapeutic doses of NORVASC resulted in a decrease in renal vascular resistance and an increase in glomerular filtration rate and effective renal plasma flow without change in filtration fraction or proteinuria. As with other calcium channel blockers, hemodynamic measurements of cardiac function at rest and during exercise (or pacing) in patients with normal ventricular function treated with NORVASC have generally demonstrated a small increase in cardiac index without significant influence on dP/dt or on left ventricular end diastolic pressure or volume. In hemodynamic studies, NORVASC has not been associated with a negative inotropic effect when administered in the therapeutic dose range to intact animals and man, even when co-administered with beta-blockers to man. Similar findings, however, have been observed in normals or well-compensated patients with heart failure with agents possessing significant negative inotropic effects. Electrophysiologic Effects: NORVASC does not change sinoatrial nodal function or atrioventricular conduction in intact animals or man. In patients with chronic stable angina, intravenous administration of 10 mg did not significantly alter A-H and H-V conduction and sinus node recovery time after pacing. Similar results were obtained in patients receiving NORVASC and concomitant beta blockers. In clinical studies in which NORVASC was administered in combination with beta-blockers to patients with either hypertension or angina, no adverse effects on electrocardiographic parameters were observed. In clinical trials with angina patients alone, NORVASC therapy did not alter electrocardiographic intervals or produce higher degrees of AV blocks. CLINICAL STUDIES Effects in Hypertension Adult Patients: The antihypertensive efficacy of NORVASC has been demonstrated in a total of 15 double-blind, placebo-controlled, randomized studies involving 800 patients on NORVASC and 538 on placebo. Once daily administration produced statistically significant placebo-corrected reductions in supine and standing blood pressures at 24 hours postdose, averaging about 12/6 mmHg in the standing position and 13/7 mmHg in the supine position in patients with mild to moderate hypertension. Maintenance of the blood pressure effect over the 24-hour dosing interval was observed, with little difference in peak and trough effect. Tolerance was not demonstrated in patients studied for up to 1 year. The 3 parallel, fixed dose, dose response studies showed that the reduction in supine and standing blood pressures was dose-related within the recommended dosing range. Effects on diastolic pressure were similar in young and older patients. The effect on systolic pressure was greater in older patients, perhaps because of greater baseline systolic pressure. Effects were similar in black patients and in white patients. Pediatric Patients: Two-hundred sixty-eight hypertensive patients aged 6 to 17 years were randomized first to NORVASC 2.5 or 5 mg once daily for 4 weeks and then randomized again to the same dose or to placebo for another 4 weeks. Patients receiving 5 mg at the end of 8 weeks had lower blood pressure than those secondarily randomized to placebo. The magnitude of the treatment effect is difficult to interpret, but it is probably less than 5 mmHg systolic on the 5-mg dose. Adverse events were similar to those seen in adults. Effects in Chronic Stable Angina: The effectiveness of 5-10 mg/day of NORVASC in exercise-induced angina has been evaluated in 8 placebo-controlled, double-blind clinical trials of up to 6 weeks duration involving 1038 patients (684 NORVASC, 354 placebo) with chronic stable angina. In 5 of the 8 studies significant increases in exercise time (bicycle or treadmill) were seen with the 10 mg dose. Increases in symptom-limited exercise time averaged 12.8% (63 sec) for NORVASC 10 mg, and averaged 7.9% (38 sec) for NORVASC 5 mg. NORVASC 10 mg also increased time to 1 mm ST segment deviation in several studies and decreased angina attack rate. The sustained efficacy of NORVASC in angina patients has been demonstrated over long-term dosing. In patients with angina there were no clinically significant reductions in blood pressures (4/1 mmHg) or changes in heart rate (+0.3 bpm). Effects in Vasospastic Angina: In a double-blind, placebo-controlled clinical trial of 4 weeks duration in 50 patients, NORVASC therapy decreased attacks by approximately 4/week compared with a placebo decrease of approximately 1/week (p<0.01). Two of 23 NORVASC and 7 of 27 placebo patients discontinued from the study due to lack of clinical improvement. Effects in Documented Coronary Artery Disease: In PREVENT, 825 patients with angiographically documented coronary artery disease were randomized to NORVASC (5-10 mg once daily) or placebo and followed for 3 years. Although the study did not show significance on the primary objective of change in coronary luminal diameter as assessed by quantitative coronary angiography, the data suggested a favorable outcome with respect to fewer hospitalizations for angina and revascularization procedures in patients with CAD. CAMELOT enrolled 1318 patients with CAD recently documented by angiography, without left main coronary disease and without heart failure or an ejection fraction <40%. Patients (76% males, 89% Caucasian, 93% enrolled at US sites, 89% with a history of angina, 52% without PCI, 4% with PCI and no stent, and 44% with a stent) were randomized to double-blind treatment with either NORVASC (5 ¾ 10 mg once daily) or placebo in addition to standard care that included aspirin (89%), statins (83%), beta-blockers (74%), nitroglycerin (50%), anti-coagulants (40%), and diuretics (32%), but excluded other calcium channel blockers. The mean duration of follow-up was 19 months. The primary endpoint was the time to first occurrence of one of the following events: hospitalization for angina pectoris, coronary revascularization, myocardial infarction, cardiovascular death, resuscitated cardiac arrest, hospitalization for heart failure, stroke/TIA, or peripheral vascular disease. A total of 110 (16.6%) and 151 (23.1%) first events occurred in the NORVASC and placebo groups respectively for a hazard ratio of 0.691 (95% CI: 0.540-0.884, p= 0.003). The primary endpoint is summarized in Figure 1 below. The outcome of this study was largely derived from the prevention of hospitalizations for angina and the prevention of revascularization procedures (see Table 1). Effects in various subgroups are shown in Figure 2. In an angiographic substudy (n=274) conducted within CAMELOT, there was no significant difference between amlodipine and placebo on the change of atheroma volume in the coronary arteryas assessed by intravascular ultrasound. Figure 1: Kaplan-Meier analysis of composite clinical outcomes for NORVASC versus placebo Figure 2 ¾ Effects on primary endpoint of NORVASC versus placebo across sub-groups Table 1 below summarizes the significant clinical outcomes from the composites of the primary endpoint. The other components of the primary endpoint including cardiovascular death, resuscitated cardiac arrest, myocardial infarction, hospitalization for heart failure, stroke/TIA, or peripheral vascular disease did not demonstrate a significant difference between NORVASC and placebo. Table 1. Incidence of Significant Clinical Outcomes for CAMELOT Clinical OutcomesN (%) NORVASC(N=663) Placebo(N=655) RiskReduction(p-value) Composite CVEndpoint 110(16.6) 151(23.1) 31%(0.003) Hospitalization forAngina* 51(7.7) 84(12.8) 42%(0.002) CoronaryRevascularization* 78(11.8) 103(15.7) 27%(0.033) *Total patients with these events Studies in Patients with Congestive Heart Failure: NORVASC has been compared to placebo in four 8-12 week studies of patients with NYHA class II/III heart failure, involving a total of 697 patients. In these studies, there was no evidence of worsened heart failure based on measures of exercise tolerance, NYHA classification, symptoms, or left ventricular ejection fraction. In a long-term (follow-up at least 6 months, mean 13.8 months) placebo-controlled mortality/morbidity study of NORVASC 5-10 mg in 1153 patients with NYHA classes III (n=931) or IV (n=222) heart failure on stable doses of diuretics, digoxin, and ACE inhibitors, NORVASC had no effect on the primary endpoint of the study which was the combined endpoint of all-cause mortality and cardiac morbidity (as defined by life-threatening arrhythmia, acute myocardial infarction, or hospitalization for worsened heart failure), or on NYHA classification, or symptoms of heart failure. Total combined all-cause mortality and cardiac morbidity events were 222/571 (39%) for patients on NORVASC and 246/583 (42%) for patients on placebo; the cardiac morbid events represented about 25% of the endpoints in the study. Another study (PRAISE-2) randomized patients with NYHA class III (80%) or IV (20%) heart failure without clinical symptoms or objective evidence of underlying ischemic disease, on stable doses of ACE inhibitor (99%), digitalis (99%) and diuretics (99%), to placebo (n=827) or NORVASC (n=827) and followed them for a mean of 33 months. There was no statistically significant difference between NORVASC and placebo in the primary endpoint of all cause mortality (95% confidence limits from 8% reduction to 29% increase on NORVASC). With NORVASC there were more reports of pulmonary edema.

DRUG INTERACTIONS NORVASC

DRUG INTERACTIONS NORVASC In vitro data indicate that NORVASC has no effect on the human plasma protein binding of digoxin, phenytoin, warfarin, and indomethacin. Effect of other agents on NORVASC. CIMETIDINE: Co-administration of NORVASC with cimetidine did not alter the pharmacokinetics of NORVASC. GRAPEFRUIT JUICE: Co-administration of 240 mL of grapefruit juice with a single oral dose of amlodipine 10 mg in 20 healthy volunteers had no significant effect on the pharmacokinetics of amlodipine. MAALOX (antacid): Co-administration of the antacid Maalox with a single dose of NORVASC had no significant effect on the pharmacokinetics of NORVASC. SILDENAFIL: A single 100 mg dose of sildenafil (ViagraÒ) in subjects with essential hypertension had no effect on the pharmacokinetic parameters of NORVASC. When NORVASC and sildenafil were used in combination, each agent independently exerted its own blood pressure lowering effect. Effect of NORVASC on other agents. ATORVASTATIN: Co-administration of multiple 10 mg doses of NORVASC with 80 mg of atorvastatin resulted in no significant change in the steady state pharmacokinetic parameters of atorvastatin. DIGOXIN: Co-administration of NORVASC with digoxin did not change serum digoxin levels or digoxin renal clearance in normal volunteers. ETHANOL (alcohol): Single and multiple 10 mg doses of NORVASC had no significant effect on the pharmacokinetics of ethanol. WARFARIN: Co-administration of NORVASC with warfarin did not change the warfarin prothrombin response time. In clinical trials, NORVASC has been safely administered with thiazide diuretics, beta-blockers, angiotensin-converting enzyme inhibitors, long-acting nitrates, sublingual nitroglycerin, digoxin, warfarin, non-steroidal anti-inflammatory drugs, antibiotics, and oral hypoglycemic drugs.