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  IN THIS Article
 ::  Abstract
 :: Introduction
 :: Chemistry
 :: Pharmacodynamics
 :: Pharmacokinetics
 ::  Metabolism and E...
 :: Special Population
 ::  Indications and ...
 ::  Dosage and Admin...
 :: Adverse Effects
 :: Precautions
 :: Drug Interactions
 :: Conclusions
 ::  References
 ::  Article Figures
 ::  Article Tables

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DRUG REVIEW
Year : 2012  |  Volume : 58  |  Issue : 2  |  Page : 140-146

Regadenoson


Department of Pharmacology, Sri Devaraj Urs Medical College, Tamaka, Kolar, Karnataka, India

Date of Submission30-May-2011
Date of Decision22-Nov-2011
Date of Acceptance04-May-2012
Date of Web Publication14-Jun-2012

Correspondence Address:
G M Bengalorkar
Department of Pharmacology, Sri Devaraj Urs Medical College, Tamaka, Kolar, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0022-3859.97177

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 :: Abstract 

Single-photon emission computerized tomography for myocardial perfusion imaging (MPI) is a non-invasive technique. MPI is performed by subjecting the patient to exercise or by using a pharmacological stress agent. Regadenoson is a selective A 2A adenosine receptor agonist used when MPI with exercise is contraindicated. It binds to the A 2A receptor and stimulates adenylate cyclase, resulting in increased cAMP, which phosphorylates protein kinase A thereby opening the ATP-dependant potassium channels leading to hyperpolarization in the coronary vascular smooth muscle. After a single bolus dose of regadenoson 400 μg, a peak plasma concentration (C max ) of 13.6 ng/mL is attained in 1-4 min, with a terminal half-life of 2 h. It has a quick onset, short duration sufficient enough for hyperemic response, with comparable efficacy to adenosine, but with fewer side-effects. The adverse effects of this drug are dyspnea, headache, flushing, chest pain and atrioventricular block. Regadenoson is used for MPI in patients with co-morbid conditions like mild-to-moderate reactive airway disease, obstructive lung disease and renal impairment.


Keywords: Regadenoson, A 2A adenosine receptor agonist, myocardial perfusion imaging


How to cite this article:
Bengalorkar G M, Bhuvana K, Sarala N, Kumar T N. Regadenoson. J Postgrad Med 2012;58:140-6

How to cite this URL:
Bengalorkar G M, Bhuvana K, Sarala N, Kumar T N. Regadenoson. J Postgrad Med [serial online] 2012 [cited 2019 Jun 16];58:140-6. Available from: http://www.jpgmonline.com/text.asp?2012/58/2/140/97177



 :: Introduction Top


Coronary artery disease (CAD) is the most common form of heart disease diagnosed by invasive and non-invasive techniques. One of the non-invasive techniques is myocardial perfusion imaging (MPI), using single-photon emission computerized tomography (SPECT), magnetic resonance imaging (MRI) and positron emission tomography (PET). [1],[2] MPI evaluates coronary perfusion at rest and during stress using radionuclide agents or perfusion tracers such as technetium-99m (Tc-99m) and, thus, identifies areas of reduced perfusion and restriction in coronary blood flow (CBF), which helps in diagnosis and prognosis. [3] Serial MPIs can monitor disease progression, detect post-revascularization restenosis and efficacy of therapy. [3] In CAD, the CBF is reduced to the regions of the myocardium supplied by diseased arteries, and hence MPI studies use either physical exercise or pharmacological stress agents (PSA) to induce maximum myocardial hyperemia. [4] Exercise MPI is contraindicated in patients with large abdominal aortic aneurysm, left bundle branch block, peripheral vascular disease and neurological and orthopedic problems. In such instances, stress MPI is done using PSAs like adenosine, dipyridamole and dobutamine. [3],[5]

Adenosine and dipyridamole are non-selective activators of adenosine A 1 , A 2A , A 2B and A 3 receptors that result in undesirable side-effects such as chest pain, flushing, dyspnea, bronchospasm, atrioventricular (AV) block and hypotension. [2],[3] Dobutamine produces chest pain and arrhythmias. The above drugs are to be administered by special infusion devices continuously based on body weight. [3] To overcome these adverse effects and practical problems, a new adenosine analog, regadenoson, a selective A 2A adenosine receptor agonist, has been approved by the FDA in April 2008 for use in MPI studies. [6] This article reviews the clinical pharmacology, therapeutic indications, adverse effects and clinical efficacy of regadenoson.


 :: Chemistry Top


The structural modification of adenosine has yielded several new molecules that are more stable in plasma, are lipophilic and have selective A 2A agonistic activity. [4] The chemical nature of regadenoson is adenosine, 2-[4-(methylamino)carbonyl]-1H-pyrazol-1-yl]-monohydrate. The 4-substituted pyrazole (regadenoson) confers high selectivity to the A 2A receptor. N-pyrazole class provides more affinity for the A 2A receptor than the C-pyrazole class. [7] Its structure is as shown in [Figure 1].
Figure 1: Structure of regadenoson

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 :: Pharmacodynamics Top


Exercise-induced increase in CBF is dependent on endothelium-mediated vasodilatation, whereas the vasodilator stress agents act directly and increase the coronary microcirculation. [8]

Regadenoson has a low affinity for the A 2A adenosine receptor, with less than 10-fold lower affinity for the A 1 adenosine receptor and weak affinity for the A 2B and A 3 adenosine receptors. [1] A 2A receptors are stimulatory G protein (Gs); binding of regadenoson to A 2A activates adenyl cyclase thus increasing cyclic adenosine 5Ͳ-monophosphate (cAMP) with subsequent phosphorylation of protein kinase A (PKA), which opens K ATP channels (ATP-dependant potassium current) producing membrane hyperpolarization. [9],[10],[11]

A 2A adenosine receptors are located on the surface of arterial vascular smooth muscle cells, activation of which dilates the coronary vessels resulting in increased CBF.

A maximum of 3.4 fold increase in CBF occurs in a dose-dependant manner due to a large A 2A receptor reserve, despite having a lower affinity for the receptor. When only 25% of the A 2A receptors are bound by regadenoson, maximal vasodilatation up to 90% is seen. [1],[2],[12],[13],[14],[15] Regadenoson-produced dilatation in the arteries is in the order of coronary >> brain > forelimb > pulmonary artery. [16]

Increase in CBF occurs within 0.5-2.3 min, with a two-fold increase at 8.5 min (range: 0.1-31 min), which is ample time for the administration and distribution of radiopharmaceutical. [1] This increase in blood flow has been observed in normal coronary arteries, with little or no increase in stenotic arteries. Myocardial uptake of the radionuclide agent [Technetium-99m (Tc-99m)] is directly proportional to CBF, and its uptake is lower in myocardial regions supplied by stenotic arteries. But, MPI studies have greater intensity in areas perfused by normal arteries, which helps in identifying the ischemic area.

Regadenoson is feasible with low-level exercise, well tolerated with improved quality of images in MPI. Low-level exercise for 4 min will induce a sympathetic response that can reduce the occurrence of hypotension and enhance the quality of image by greater distribution of blood (radiotracer) to the heart as compared with the gut and liver, thereby alienating the inferior wall of the myocardium from the intestines. [17],[18]

Hemodynamic actions

In clinical studies, the majority of patients had an increased heart rate up to 21 beats/min and a decrease in blood pressure of 24 (systolic) and 15 (diastolic) mmHg, respectively, within 45 min of regadenoson administration, but had returned to normal within 150 min. [13],[19] Aminophylline blocks adenosine receptors; therefore, 100 mg of the drug attenuated the increase in CBF, but not tachycardia caused by 400 μg of regadenoson. [13] The mechanism of regadenoson-mediated tachycardia was investigated in a rat heart model, wherein pre-treatment with a β-blocker, selective A 2A antagonist and ganglion blockers reduced the tachycardia. Further, it was observed that regadenoson caused more than two-fold increase in serum norepinephrine and epinephrine levels. These results suggest that sinus tachycardia is mainly due to the direct sympathetic stimulation rather than being baroreceptor mediated. [20] This increase in heart rate by regadenoson was significantly blunted in diabetic compared with non-diabetic patients, possibly due to sympathetic denervation in diabetic patients, supporting the above sympathoexcitation mechanism. [21]


 :: Pharmacokinetics Top


Regadenoson is administered as an intravenous bolus dose of 400 μg. The maximum plasma concentration (C max ) of 13.6 ng/mL was attained in 1-4 min in the dose range of 0.3-20 μg/kg in healthy subjects; age, gender, clearance, half-life and volume of distribution were independent of the dose given, and hence it was administered as a fixed bolus dose. [1],[6],[22] The comparison between regadenoson and adenosine is shown in [Table 1].
Table 1: Comparison between regadenoson and adenosine[1,4– 6,23,33]

Click here to view


It has been shown to have quick distribution, with a volume of distribution (Vd) of 78.7 L. [1],[6] Nearly 20-30% of regadenoson is protein bound. [16] The maximal tolerated dose (MTD) was 20 μg/kg while the C max at this dose ranged from 69 to 134 ng/mL. [16]


 :: Metabolism and Excretion Top


In vitro studies with human and animal liver microsomes have not detected any metabolites of regadenoson, indicating that the drug was not metabolized in the liver. [1],[6],[22] It follows triphasic elimination; the initial phase t½ was 2-4 min, which coincided with pharmacodynamic action, followed by an intermediate phase with a mean t΍ of 30 min that coincided with the loss of pharmacodynamic effect. The terminal elimination phase (t½) was ≈ 2 hrs. [1],[6] Regadenoson is not a substrate for either adenosine deaminase or cell nucleoside transporter; therefore, it is not rapidly metabolized in plasma like adenosine. [13] About 57% (range 19-77%) of the regadenoson is excreted unchanged in the urine, and the remaining in bile. [1],[5],[16],[23],[24] The average plasma renal clearance was 450 mL/min, indicating the role of renal tubular secretion in its elimination. [1],[23] Clearance increases with body weight. [6]

In renal impairment (CrCl < 30 mL/min), regadenoson renal clearance was decreased and elimination half-life increased as compared with healthy subjects (CrCl ≥ 80 mL/min), but no adverse consequences were reported. [4],[19] Hence, no dose adjustment is needed in these patients.


 :: Special Population Top


Pharmacokinetic parameters remained unchanged with advancing age, gender and race. [5] Regadenoson should be used in pregnant women only if the potential benefit to the patient justifies the risk to the fetus (category C). Breast feeding should be stopped for 10 hrs following drug administration as the drug gets cleared in 10 h. In a study, 56% of the study population was ≥65 years, and adverse events were same as in patients <65 years, but a higher incidence of hypotension was observed in patients ≥75 years of age. Safety and effectiveness in neonates, infants, children and adolescents <18 years of age has not been established. [5]


 :: Indications and Usage Top


  1. Regadenoson is a pharmacologic stress agent (PSA) indicated for radionuclide MPI in patients unable to undergo adequate exercise stress for diagnosing CAD [1],[5]
  2. It is also used as PSA in MPI studies indicated in post-cardiac transplantation, chronic kidney disease, non-dialysis patients and PET imaging [25],[26],[27]
  3. Real-time myocardial contrast echocardiography (RTCME)is a non-invasive method for the detection of CAD where regadenoson can be used without radionuclide, thereby obviating radiation exposure. [28]



 :: Dosage and Administration Top


The hyperemic response to regadenoson doses of 400 μg and 500 μg were similar in magnitude and duration, with mean peak CBF velocity maintained at >2.5-times that of baseline for 2.3 and 2.4 min, respectively. More patients in the 500 μg group reported flushing, dyspnea and dizziness, although the differences were not statistically significant. [13],[29] Hence, the recommended intravenous dose of 400 μg (5 mL) is administered as a rapid injection within 10 s into a peripheral vein and immediately flushed with 5 mL saline. Then, radionuclide MPI agent (technetium-99m sestamibi) * is injected directly into the same catheter within 10-20 s after the saline flush. [5] The dose of regadenoson need not be adjusted based on the weight and renal functions; therefore, it can be supplied in prefilled syringes (strength 0.4 mg/5 mL). [30]

*The other radionuclides' used are technetium-99m ( 99m Tc) compounds (tetrofosmin, teboroxime), thallium-201 ( 201 TI), iodine-123 ( 123 I)-labeled fatty acids, gallium citrate-67 ( 67 Ga), 123 I metaiodobenzylguanidine and Rubidium-82 (Rb-82 for PET MPI). [27],[31]


 :: Adverse Effects Top


Most adverse reactions have been mild and self-limiting. [5] The majority occur soon after administration and resolve within 15 min, except headache, which subsided within 30 min. [1] The most common reactions were dyspnea, headache and flushing. Less-common reactions were chest discomfort, dizziness, chest pain, nausea, abdominal discomfort, dysgeusia and flushing. [32] Rhythm or conduction abnormalities were seen in 26% versus 30% of the subjects receiving regadenoson versus adenosine. First-degree and second-degree AV blocks were 3% versus 7% and 0.1% versus 1%. [30] During post-marketing surveillance, the most frequently reported reactions were nausea, vomiting and diarrhea. [32] The other adverse effects reported include tremors, syncope, seizures, transient ischemic attacks, worsening of migraine, complete heart block with asystole (in persons with normal sinus rhythm), QTc prolongation, ST segment depression, hypersensitivity reactions and musculoskeletal pain. [17],[18],[28],[33],[34],[35],[36] Clinically significant increase in blood pressure was seen in hypertensives undergoing MPI with low-level exercise, which could have been due to sympathetic stimulation. [35],[17]

Seizures have been reported within 2-5 min of regadenoson administration in patients on treatment or without prior history of seizures. [33] Stimulation of A 2A receptors in striatum, nucleus accumbens, cortex and tuberculum olfactorium can lead to increased glutaminergic excitotoxicity, as well as inhibition of A 1 -mediated neuroprotection, which can exacerbate seizures from the cortex and limbic systems. [33],[37] Regadenoson-induced seizures can be controlled with benzodiazepines. [33]

Treatment of overdose

For regadenoson overdose or severe persistent adverse effects like systolic blood pressure <80 mmHg, second degree or complete heart block, wheezing, severe chest pain associated with ST depression, intravenous aminophylline is effective at a dose of 50-250 mg over 30-60 s. [17],[24]


 :: Precautions Top


Regadenoson can depress the SA and AV nodes (A 1 receptor) and hence it should not be used in patients with sinus bradycardia and sick sinus syndrome. [6]

  • The risk of serious hypotension may be higher in patients with autonomic neuropathy and pre-existing hypotension [1]
  • Regadenoson may cause bronchoconstriction and respiratory compromise in chronic obstructive pulmonary disease (COPD) or asthma because of its affinity to A 2B and A 3 receptor, and appropriate bronchodilator therapy should be kept on standby [6]
  • Anti-ischemic cardiac medications (including β-blockers, nitrates and calcium antagonists) should be withheld for
  • at least 48 h prior to performing a diagnostic imaging test. [24]



 :: Drug Interactions Top


  • Methylxanthines (caffeine and theophylline) are non-specific adenosine receptor antagonists and may interfere with the vasodilatory activity of regadenoson. [10],[12] They attenuate the duration but not the peak increase in CBF. Xanthines (coffee, green tea, colas and chocolate) should be avoided for at least 12 h prior to regadenoson administration [5],[22]
  • Dipyridamole may potentiate the vasodilatory effects of regadenoson, and should be withheld for at least 2 days prior to regadenoson administration [6]
  • n-acetyl cysteine, an inhibitor of adenosine deaminase, restores the oxidant-antioxidant balance in idiopathic pulmonary fibrosis, longterm enzyme inhibition and upregulation of adenosine receptors (including A 2A ). Thus, when regadenoson is administered to these patients, it can lead to complete heart block with asystole in patients with previous sinus rhythm. [34]


Clinical studies

The aim of the Adenoscan (adenosine) Versus Regadenoson Comparative Evaluation for Myocardial Perfusion Imaging (ADVANCE MPI) 1 and 2 trials was to demonstrate the non-inferiority of regadenoson in comparison with adenosine by examining the concordance of images detecting myocardial perfusion defects. ADVANCE MPI 1 and 2 were methodologically identical, double-blind, randomized, active-comparator, multicentric, phase III trials. [24],[25] The findings of the study are shown in [Table 2] under efficacy studies.
Table 2: Clinical studies

Click here to view



 :: Conclusions Top


The clinical efficacy of regadenoson during pharmacologic stress testing for MPI was similar to adenosine and produced sufficient hyperemic response but with fewer side-effects. It can be administered as a single bolus dose of 400 μg, having quick onset and short duration of action. Dose adjustment based on body weight or renal functions is not necessary. It simplifies drug delivery as specific infusion equipment is not required. It offers patients a quicker and easier procedure with mild side-effects. The drug can be safely used in patients with mild-to-moderate reactive airway disease and obstructive lung disease. Thus, it is a safe alternative to adenosine for SPECT MPI. The other A 2A agonists in phase III clinical trials are binodenoson and apadenoson. [3] Regadenoson can also be used to measure coronary hemodynamics in the cardiac catheterization with the flow-Doppler catheter. Stress MPI may also be performed with cardiac resonance and contrast echocardiography.[41]

 
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[PUBMED]  [FULLTEXT]  


    Figures

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    Tables

  [Table 1], [Table 2]

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Online since 12th February '04
© 2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
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