Regadenoson is an A2A adenosine receptor agonist that acts as a coronary vasodilator and is used as a pharmacologic stress agent in radionuclide myocardial perfusion imaging. Regadenoson can be used as an alternative to adenosine for diagnosing coronary artery disease. Although similar in activity to adenosine, there is an increased ease of use with regadenoson as it is given as a rapid intravenous injection vs. the infusion used in adenosine-facilitated perfusion imaging studies. Initial studies have shown adverse events rates to be similar to adenosine; however, regadenoson has an increased selectivity for the A2A adenosine receptor and lower affinity for the A1, A2B, and A3 receptors as compared to adenosine. The activation of the non-A2A adenosine receptors are often implicated in high-degree AV block and bronchoconstriction. Additionally, studies comparing the images obtained with regadenoson to those obtained with adenosine demonstrate that they are similar in assessing the extent of reversible perfusion abnormalities (62% +/- 2% and 63% +/-3% vs. 61% +/- 3% and 64% +/-4%, respectively). Regadenoson was FDA-approved in April 2008.
General Administration Information
For storage information, see the specific product information within the How Supplied section.
NOTE: Prior to administration of the stress test, screen all candidates for their suitability to receive the drug and have ready access to cardiac resuscitation equipment and a trained medical staff.
Route-Specific Administration
Injectable Administration
-Visually inspect parenteral drug products for particulate matter and discoloration prior to administration, whenever solution and container permit. Regadenoson solution is clear and colorless. Do not administer if particulate matter or discoloration is present.
-Prefilled syringes are for single use only.
Intravenous Administration
-Administer as an IV injection within 10 seconds into a peripheral vein using a 22 gauge or larger catheter or needle.
-Administer a 5 mL saline flush immediately after the injection of regadenoson.
-Administer the radionuclide myocardial perfusion imaging agent 10 to 20 seconds after the saline flush. The radionuclide may be injected directly into the same catheter as regadenoson.
Adverse reactions associated with regadenoson administration are typically mild and short in duration. In 2 studies comparing regadenoson and adenosine, adverse reactions occurred at similar rates (80% and 83%, respectively). In addition, the most common adverse reactions to regadenoson were similar to adenosine, began soon after dosing, and generally resolved within approximately 15 minutes. Aminophylline may be used to attenuate severe or persistent adverse reactions of regadenoson. Aminophylline, at a dose of 50 to 250 mg administered by slow intravenous injection (50 to 100 mg over 30 to 60 seconds), injected 1 minute after regadenoson in subjects undergoing cardiac catheterization was shown to shorten the duration of the coronary blood flow response as measured by pulsed-wave Doppler ultrasonography. Aminophylline was used to treat the reactions in 3% of regadenoson patients and 2% of adenosine patients.
Fatal cardiac arrest and myocardial infarction (0.2%) may result from the ischemia induced by pharmacologic stress agents; therefore, cardiac resuscitation equipment and trained staff should be available when using regadenoson. Additionally, chest discomfort (13% vs. 18% for adenosine), angina pectoris or ST segment depression (12% vs. 18%), and chest pain (unspecified) (7% vs. 10%) were commonly reported in patients taking either regadenoson or adenosine. There were no statistically significant differences reported between the adverse events in patients receiving regadenoson vs. adenosine during clinical trials. Acute coronary syndromes has been observed in a clinical trial (0.2%) and during postmarketing experience.
Hypotension was generally experienced within 45 minutes after administration of regadenoson. The rates of a systolic blood pressure < 90 mmHg or a decrease of > 35 mmHg over baseline were similar in patients receiving regadenoson or adenosine (2% vs. 3% and 7% vs. 8%, respectively). Few patients had a diastolic blood pressure < 50 mm Hg (2% vs. 4%) or a decrease > 25 mmHg (4% vs.5%) over baseline. The risk of serious hypotension may be higher in patients with autonomic dysfunction, hypovolemia, left main coronary artery stenosis, stenotic valvular heart disease, pericarditis or pericardial effusions, or stenotic carotid artery disease with cerebrovascular insufficiency. In postmarketing experience, syncope and transient ischemic attacks have occurred with symptomatic hypotension and required intervention.
In clinical studies, the majority of patients experienced an increase in heart rate including sinus tachycardia within 45 minutes after administration of regadenoson. A heart rate > 100 beats per minute (bpm) was observed in 22% and 13% of patients receiving regadenoson and adenosine, respectively. Increases in heart rate > 40 bpm over baseline were observed in 5% vs. 3% of patients. In a study, regadenoson-treated patients experienced an increase in maximum heart rate that was significantly higher than adenosine-treated patients (25 +/- 11 bpm vs. 20 +/- 10 bpm, p < 0.001).
Life threatening ventricular arrhythmias may result from the ischemia induced by pharmacologic stress agents; therefore, cardiac resuscitation equipment and trained staff should be available when using regadenoson. Overall rates of rhythm or conduction abnormalities (PACs, PVCs, atrial fibrillation, atrial flutter, wandering atrial pacemaker, supraventricular or ventricular arrhythmia) following regadenoson vs. adenosine were 26% vs. 30%, respectively. Rhythm abnormalities occurred in 20% of both regadenoson and adenosine patients, including premature atrial contractions (PACs) (7% vs. 9%) and premature ventricular contractions (PVCs) (14% vs. 12%). Adenosine receptor agonists can depress the SA and AV nodes and may cause first-, second-, or third-degree AV block or sinus bradycardia requiring intervention. First-degree AV block occurred in 3% vs. 7% of regadenoson and adenosine patients, respectively. Second-degree AV block occurred in 0.1% of regadenoson patients vs. 1% of adenosine patients. AV conduction abnormalities (other than AV block) were rare in both groups (0.1% regadenoson patients). Ventricular conduction abnormalities occurred in 6% of regadenoson patients and 5% of adenosine patients. Third-degree heart block and asystole within minutes of regadenoson administration have been observed during postmarketing experience. Additionally, QT prolongation has been reported shortly after regadenoson administration.
Adenosine receptor agonists, including regadenoson, may cause dyspnea, bronchoconstriction or bronchospasm, and respiratory compromise. In clinical trials, dyspnea was reported in 28% of patients overall. In a clinical trial in 999 patients with asthma (n = 532) or stable chronic obstructive pulmonary disease (COPD, n = 467), the overall incidence of respiratory adverse events (i.e., dyspnea, wheezing, obstructive airway disorder, exertional dyspnea, tachypnea) was greater (p < 0.001) in the regadenoson group (12.9% asthma patients, 19% COPD patients) compared to the placebo group (2.3% asthma patients, 4% COPD patients). Dyspnea was reported in 10.7% of asthma patients (1.1% placebo) and in 18% of COPD patients (2.6% placebo), while wheezing was noted in 3.1% of asthma patients (1.1% placebo) and in 0.9% of COPD patients (0.7% placebo). Most pulmonary adverse events resolved without therapy, with a small number of patients requiring treatment. No differences were observed in FEV1 changes between the groups.
Patients commonly experienced headache after receiving regadenoson and adenosine (26% vs. 17%, respectively). Unlike other symptoms, headache often took longer to dissipate in studies, usually resolving within 30 minutes for most patients.
Commonly reported gastrointestinal symptoms for regadenoson, compared to adenosine, include abdominal pain or discomfort (5% vs. 2%), dysgeusia (5% vs. 7%), and nausea (6% for both agents). Abdominal pain, occasionally severe, has been reported within a few minutes of regadenoson administration and has been associated with nausea or vomiting. Diarrhea and fecal incontinence have also been noted in postmarketing reports.
Flushing (16%) and feeling hot (5%) were commonly reported with regadenoson, and at similar rates to adenosine (25% and 8%, respectively).
Administration of adenosine receptor agonists, including regadenoson, may result in clinically significant hypertension in some patients. In clinical trials, increased blood pressure was observed within minutes of regadenoson administration with most increases resolving within 10 to 15 minutes; however, in some cases, increases were observed up to 45 minutes after drug administration. Increases in systolic blood pressure >= 200 mmHg were reported in 1.9% of patients and increases >= 50 mmHg were reported in 0.7% of patients during clinical trials. Additionally, 4.6% of patients had a systolic blood pressure of >= 180 mmHg with increases of >= 20 mmHg from baseline. Increases in diastolic blood pressure to >= 115 mmHg were reported in 0.9% of patients and increases >= 30 mmHg were noted in 0.5% of patients in trials. Postmarketing cases of clinically significant hypertension have been reported, especially in patients with underlying hypertension or when low-level exercise was included during imagining.
Dizziness has been reported after regadenoson administration and at a similar frequency as adenosine (8% vs. 7%). Tremor, seizures, transient ischemic attack, stroke, and intracranial bleeding have been noted in postmarketing reports. Seizures may be more common in patients with a history of seizure or may be associated with symptomatic hypotension. Aminophylline may increase the risk of seizure and should be avoided in any patient who experiences a regadenoson-associated seizure. Regadenoson-induced hypotension or hypertension may be associated with ischemic or hemorrhagic stroke events.
Hypersensitivity reactions have been reported in < 1% of patients during regadenoson clinical trials and include anaphylaxis (anaphylactoid reactions, anaphylactic shock), angioedema, cardiac or respiratory arrest, respiratory distress, decreased oxygen saturation, hypotension, throat tightness, urticaria, and rash (unspecified).
Musculoskeletal pain has been noted in postmarketing reports with regadenoson and typically occurs within 10 to 20 minutes of drug administration. The pain was occasionally severe and localized in the arms and lower back (back pain) and extended to the buttocks and lower leg bilaterally. Myalgia has been associated with abdominal pain that has been reported with the use of regadenoson.
Prior to administration of regadenoson as part of a cardiac nuclear stress test, screen all candidates for their suitability to receive the drug; rare cases of fatal and nonfatal myocardial infarction (MI), ventricular arrhythmias, and cardiac arrest have occurred. Avoid regadenoson use in patients with signs or symptoms of unstable angina or cardiovascular instability because they may be at increased risk for cardiovascular adverse events. Cardiac resuscitation equipment and a trained medical staff must be readily available. Adhere to the recommended duration of injection as longer injection times may increase the duration and magnitude of increase in coronary blood flow. If a serious reaction occurs, consider use of aminophylline (an adenosine antagonist) to shorten the duration of increased coronary blood flow. Regadenoson induces arterial vasodilation, resulting in increased blood flow to unblocked or unobstructed arteries and decreased blood flow to obstructed arteries. In some patients, reduced blood flow within obstructed arteries can result in MI, which may be fatal. An analysis of the FDA Adverse Event Reporting System (FAERS) has associated the use of regadenoson with 26 cases of MI and 29 cases of death; the majority occurred within 6 hours of drug administration. Of the 29 deaths, the most commonly reported adverse events were cardiac arrest, MI, loss of consciousness, respiratory arrest, ST segment depression, pulmonary edema, and ventricular fibrillation. In addition to MI, drug-induced arterial vasodilation can result in low blood pressure. The risk of serious hypotension may be higher in patients with autonomic neuropathy, hypovolemia, stenotic valvular heart disease, pericarditis or pericardial effusion, pre-existing hypotension, or other cardiac disease including stenosis of the left main coronary artery or carotid artery. Cerebrovascular accidents have been reported with regadenoson; these adverse reactions may be associated with the hemodynamic effects of the drug. Additionally, geriatric patients (75 years and older) may be at increased risk of hypotension. During clinical trials, elderly patients experienced a higher incidence of hypotension (2% vs. 1% or less). All other adverse events were similar between elderly and younger patients.
Regadenoson is contraindicated in patients with sinus node dysfunction, such as sick sinus syndrome or symptomatic bradycardia, and in patients with second- or third-degree AV block, except in patients with a functioning artificial pacemaker in place. Adenosine receptor agonists including regadenoson can depress the SA and AV nodes although regadenoson has a lower affinity for the adenosine A1 receptors. Regadenoson should be given cautiously to patients with pre-existing first-degree AV block or bundle-branch block.
Adenosine receptor agonists may cause dyspnea, bronchoconstriction, and respiratory compromise. Appropriate bronchodilator therapy and resuscitative measures should be available prior to and after regadenoson administration. Advise patients with chronic obstructive pulmonary disease (COPD) or asthma about the need for bronchodilator therapy pre- and post-study, and to seek medical attention if they experience any shortness of breath or difficulty breathing after a regadenoson study.
There are no data describing regadenoson use in human pregnancy to inform a drug-associated risk. Adverse developmental outcomes were observed in animal reproductive studies. Regadenoson doses at 10- to 20-times the maximum recommended human dose (MRHD) caused reduced fetal body weights, ossification delays in limb phalanges and metatarsals, and maternal toxicity. Maternal toxicity occurred in rabbits at doses 4-times the MRHD; maternal toxicity, increased embryo-fetal loss, and fetal malformations were noted with regadenoson doses 12- and 20-times the MRHD.
There is no information on the presence of regadenoson in human milk or the effects of regadenoson on the breast-fed infant or milk production. Because of the potential risk of serious cardiac reactions in the breast-fed infant, advise the breast-feeding mother to pump and discard breast milk for 10 hours after regadenoson administration.
Regadenoson may lower the seizure threshold; obtain any patient history of seizures. During postmarketing use, regadenoson has been associated with the development of new-onset and recurrent convulsive type seizures. In some cases, the seizures were prolonged and required emergent anticonvulsive treatment. Advise patients who experience a regadenoson-associated seizure to avoid use of methylxanthines (i.e., caffeine, aminophylline, theophylline), as these drugs may increase the seizure risk.
For use in radionuclide myocardial perfusion imaging for coronary artery disease diagnosis in patients unable to undergo adequate exercise stress:
Intravenous dosage:
Adults: 0.4 mg IV once.
Maximum Dosage Limits:
-Adults
0.4 mg IV single dose.
-Geriatric
0.4 mg IV single dose.
-Adolescents
Safety and efficacy have not been established.
-Children
Safety and efficacy have not been established.
-Infants
Safety and efficacy have not been established.
-Neonates
Safety and efficacy have not been established.
Patients with Hepatic Impairment Dosing
Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.
Patients with Renal Impairment Dosing
Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.
*non-FDA-approved indication
Acetaminophen; Aspirin, ASA; Caffeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Acetaminophen; Caffeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Acetaminophen; Caffeine; Dihydrocodeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Acetaminophen; Caffeine; Pyrilamine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Aspirin, ASA; Butalbital; Caffeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Aspirin, ASA; Caffeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Aspirin, ASA; Caffeine; Orphenadrine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Aspirin, ASA; Dipyridamole: (Major) Dipyridamole may change the effects of regadenoson. Although the effects are not specified, this may be due to dipyridamole's coronary vasodilatory action. When possible, withhold dipyridamole for at least two days prior to the administration of regadenoson.
Butalbital; Acetaminophen; Caffeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Butalbital; Acetaminophen; Caffeine; Codeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Butalbital; Aspirin; Caffeine; Codeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Caffeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration. (Major) Regadenoson may cause an increased coronary blood flow without regard to prior caffeine ingestion. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Caffeine; Sodium Benzoate: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Digoxin: (Major) Because of the potential for additive or synergistic depressant effects on SA and AV nodes, regadenoson should be used with caution in the presence of agents that slow cardiac conduction, such as digoxin.
Dipyridamole: (Major) Dipyridamole may change the effects of regadenoson. Although the effects are not specified, this may be due to dipyridamole's coronary vasodilatory action. When possible, withhold dipyridamole for at least two days prior to the administration of regadenoson.
Ergotamine; Caffeine: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Green Tea: (Major) Caffeine is a non-specific adenosine receptor antagonist and can interfere with the efficacy of regadenoson. Patients should avoid consumption of any products containing caffeine (including caffeine from foods and beverages such as coffee, green tea, other teas, colas, and chocolate) for at least 12 hours before regadenoson administration.
Nicotine: (Major) Nicotine has been reported to enhance the cardiovascular effects of adenosine receptor agonists; an increase in angina-like chest pain, heart rate, or a decrease in blood pressure may be noted. While no special cautions are recommended for regadenoson, it may be advisable for patients to avoid nicotine products or tobacco prior to electrophysiologic studies or stress testing where adenosine receptor agonists will be administered.
Theophylline, Aminophylline: (Major) Methylxanthines, such as theophylline or aminophylline, are non-specific adenosine receptor antagonists and may interfere with the vasodilation activity of adenosine receptor agonists, such as regadenoson. Patients should avoid any drugs containing theophylline, aminophylline for at least 12 hours before regadenoson administration. Methylxanthines attenuate the duration, but not the peak increase of coronary blood flow produced by regadenoson; aminophylline may be used to attenuate severe or persistent adverse reactions of regadenoson. Aminophylline injected 1 minute after regadenoson in subjects undergoing cardiac catheterization was shown to shorten the duration of the coronary blood flow response as measured by pulsed-wave Doppler ultrasonography. In addition, theophylline, aminophylline may increase the risk of seizures associated with regadenoson; avoid methylxanthine use in patients who have experienced a regadenoson-associated seizure.
Trandolapril; Verapamil: (Major) Because of the potential for additive or synergistic depressant effects on SA and AV nodes, regadenoson should be used with caution in the presence of agents that slow cardiac conduction, such as verapamil.
Verapamil: (Major) Because of the potential for additive or synergistic depressant effects on SA and AV nodes, regadenoson should be used with caution in the presence of agents that slow cardiac conduction, such as verapamil.
Regadenoson is a low affinity agonist for the A2A adenosine receptors on arteriolar vascular smooth muscle. Activation of the A2A adenosine receptors by regadenoson produces coronary vasodilation and increases coronary blood flow.
Although the exact mechanism by which adenosine receptor activation relaxes vascular smooth muscle is not known, there is evidence to support both inhibition of the slow inward calcium current reducing calcium uptake, and activation of adenylate cyclase through A2 receptors in smooth muscle cells. Activation of these receptors may also lessen vascular tone by modulating sympathetic neurotransmission.
Regadenoson causes a rapid increase in coronary blood flow, which is sustained for a short duration due to its low affinity for the A2A adenosine receptors. In a study, increases in blood flow velocity peaked within 0.5 to 2.3 minutes, while the average duration of an increase in blood flow of at least 2-fold was 8.5 minutes (ranging from 0.1 to 31 minutes). Myocardial uptake of the radiopharmaceutical is directly proportional to coronary blood flow. Because regadenoson increases blood flow in normal coronary arteries with little or no increase in stenotic arteries, there is relatively less uptake of the radiopharmaceutical in vascular territories supplied by stenotic arteries as compared to normal arteries.
Coronary vasodilation is primarily generated by the activation of the A2A and A2B adenosine receptors. Stimulation of the A1 and A3 adenosine receptors is generally associated with side effects of adenosine vasodilator stress including chest pain, dyspnea, bronchoconstriction, and conduction abnormalities. Regadenoson has increased selectivity for the A2A adenosine receptors with at least 10-fold lower affinity for the A1 adenosine receptors, and weak, if any, affinity for the A2B and A3 adenosine receptors. However, in a phase III trial, patients reported chest pain and dyspnea with regadenoson, suggesting that these side effects may be due to regadenoson-induced sympathetic stimulation rather than solely mediated by A1 adenosine receptor activation.
Regadenoson is administered as a rapid intravenous injection. Terminal half-life and volume of distribution do not appear dependent upon the dose. The metabolism is unknown in humans; incubation with rat, dog, and human liver microsomes as well as human hepatocytes produced no detectable metabolites of regadenoson. In healthy volunteers, 57% (range 19% to 77%) of the dose is excreted unchanged in the urine, with an average plasma renal clearance around 450 mL/minute in excess of the glomerular filtration rate. This indicates that renal tubular secretion plays a role in regadenoson elimination.
Affected cytochrome P450 isoenzymes and drug transporters: none
Regadenoson is not known to be a substrate, inhibitor, or inducer of CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, or CYP3A4 in human liver microsomes; additionally, renal tubular secretion may be involved in regadenoson elimination, although whether regadenoson interacts with other drugs that also undergo renal tubular secretion is not known.
-Route-Specific Pharmacokinetics
Intravenous Route
Following intravenous administration, the plasma concentration-time profile is best characterized by a 3-compartment model. Initially, maximal plasma concentrations are achieved within 1 to 4 minutes. The half-life of this initial phase is approximately 2 to 4 minutes. An intermediate phase follows, with a half-life on average of 30 minutes that coincides with loss of the pharmacodynamic effect. The terminal phase consists of a decline in plasma concentration with a half-life of approximately 2 hours. Terminal half-life and volume of distribution do not appear dependent upon the dose.
-Special Populations
Renal Impairment
With increasing renal impairment, from mild (CrCl 50 to 79 mL/minute) to moderate (CrCl 30 to 49 mL/minute) to severe (CrCl < 30 mL/minute), the fraction of regadenoson excreted unchanged in the urine and the renal clearance is decreased, resulting in increased elimination half-life and AUC values compared to healthy subjects (CrCl >= 80 mL/minute). However, the maximum observed plasma concentrations as well as volume of distribution estimates were similar across the groups. The plasma concentration-time profiles were not significantly altered in the early stages after dosing when most pharmacologic effects are observed. The pharmacokinetics of regadenoson in patients on dialysis has not been assessed; however, an in vitro study suggests regadenoson is dialyzable. No dose adjustment is needed in patients with renal impairment.
Obesity
Clearance increases with increased body weight, although recommendations for dosage adjustments in obese patients are not available.