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Adenosine has recently become widely available for the treatment of paroxysmal supraventricular tachycardia. In order to evaluate its role in the management of arrhythmias, we have reviewed the literature on the cellular mechanisms, metabolism, potential for adverse effects, and clinical experience of the efficacy and safety of intravenous adenosine. Adenosine produces transient atrioventricular nodal block when injected as an intravenous bolus. This is of therapeutic value in the conversion to sinus rhythm of the majority of paroxysmal supraventricular tachycardias, which involve the atrioventricular node in a re-entrant circuit. The mean success rate was 93% from over 600 reported episodes. Compared with other antiarrhythmic agents, adenosine is remarkable for its rapid metabolism and brevity of action, with a half-life of a few seconds. It commonly produces subjective symptoms, particularly chest discomfort, dyspnea, and flushing, which are of short duration only. No serious adverse effect has been reported. Arrhythmias may recur within minutes in a minority of patients. Comparative studies have shown that adenosine is as effective as verapamil in the treatment of supraventricular tachycardia, and has less potential for adverse effects. Patients with supraventricular tachycardia should initially be treated using vagotonic physical maneuvers. Immediate electrical cardioversion is indicated if the arrhythmia is associated with hemodynamic collapse. Adenosine is the preferred drug in those patients in whom verapamil has failed or may cause adverse effects, such as those with heart failure or wide-complex tachycardia. The safety profile of adenosine suggests that it should be the drug of first choice for the treatment of supraventricular tachycardia, but only limited comparative data to support this view are available at present.
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PMID:Adenosine and the treatment of supraventricular tachycardia. 160 47

In this pilot study some cardiac effects of exogenous adenosine on the denervated heart were studied in a patient with transplanted heart since 3 years. He was instrumented with catheters into the left coronary artery, the coronary sinus and the right ventricle. Adenosine was given in increasing doses intracoronarily, into the aorta at the diaphragmal level and into a peripheral vein. When given into the aorta pain was provoked dose-dependently and not different from a reference group. When given intracoronarily no pain was provoked except at the highest dose when a slight discomfort of the chest was provoked. After intravenous injection no pain was provoked in the chest or in adjacent structures. Coronary sinus flow increased dose-dependently and not different from the reference group. No increased heart rate response occurred after intravenous or intracoronary injections. Extensive degrees of sinus and AV nodal blockade occurred. In conclusion, the results are in keeping with a role for adenosine as a messenger between myocardial ischaemia and angina pectoris and cardiac sympathetic pressure response. The importance of innervation for proper sinus and AV nodal function was also illustrated.
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PMID:Effects of exogenous adenosine in a patient with transplanted heart. Evidence for adenosine as a messenger in angina pectoris. 207 41

The acute haemodynamic effects of intravenous infusion of adenosine, a dilator of most vascular beds, were studied in 16 patients (seven with coronary artery disease, nine with normal coronary arteries) undergoing cardiac catheterization for investigation of chest pain. At the lowest dose used (4.3 mg min-1) adenosine increased minute ventilation by 44% (P less than 0.01, n = 11) and reduced pulmonary vascular resistance by 20% (P less than 0.05) without causing other significant haemodynamic changes. Symptoms, including chest discomfort in 14 patients and dyspnoea in 11, limited the maximum dose to 8.5 +/- 2.3 mg min-1 (mean +/- SD, 108 +/- 24 micrograms kg-1 min-1). At this dose, adenosine reduced pulmonary and systemic vascular resistance (by 38% and 34%, respectively) and increased heart rate (by 34%), stroke index (by 12%) and cardiac index (by 52%). Systemic blood pressure and right atrial pressure did not change. Unexpectedly, adenosine increased left ventricular end-diastolic pressure (LVEDP) (from 5 +/- 6 to 14 +/- 10 mmHg, n = 8), pulmonary capillary wedge pressure (from 3 +/- 2 to 10 +/- 5 mmHg, n = 16) and consequently mean pulmonary artery pressure (from 10 +/- 2 to 16 +/- 5 mmHg). Minute ventilation increased by 84% (n = 11), resulting in hypocapnia (PCO2: 31 +/- 3 mmHg, n = 8) and alkalosis (pH: 7.46 +/- 0.02, n = 8). Oxygen consumption was unchanged during the infusion, but increased by 21% 5 min post infusion. All effects were similar in patients with and without coronary artery disease. Adenosine therefore causes pulmonary and systemic vasodilation and respiratory stimulation. Symptoms and an increase in LVEDP of uncertain cause, which occur with high doses, may limit the use of adenosine as a systemic vasodilator in conscious subjects. However at lower doses adenosine causes selective pulmonary vasodilation which merits further study.
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PMID:Acute haemodynamic effects of intravenous infusion of adenosine in conscious man. 228 21

Six normal male subjects, ages 28-40 years, were studied on separate days during increasing infusions with adenosine, 40-120 micrograms kg-1 min-1, before and during infusions of two xanthine derivatives, theophylline (mean plasma concentration 9 mg l-1) and enprofylline (mean plasma concentration 3 mg l-1). The study was double-blind, randomized, placebo controlled. Cardio-respiratory variables were measured non-invasively. Adenosine by itself increased heart rate (P less than 0.05), skin temperature (P less than 0.05), resting minute ventilation (P less than 0.01) and decreased estimated Pa, CO2 (P less than 0.01). Compared with placebo enprofylline increased heart rate (P less than 0.05) and shifted the heart rate and ventilation dose-response curves of adenosine upwards (P less than 0.05 and P less than 0.02, respectively). Theophylline did not by itself affect heart rate but significantly (P less than 0.05) reduced the heart rate response to adenosine. Compared with placebo theophylline caused a small increase in minute ventilation (P less than 0.05) and flattened the dose-response curves of the effects of adenosine on ventilation (P less than 0.01) and Pa, CO2 (P less than 0.01). Theophylline also reduced abdominal and chest discomfort caused by adenosine permitting significantly (P less than 0.05) higher infusion rates of adenosine. These findings suggest that, with equipotent bronchodilating plasma concentrations, theophylline can inhibit while enprofylline augments some cardio-respiratory stimulant effects of infused adenosine in man.
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PMID:Contrasting effects of two xanthines, theophylline and enprofylline, on the cardio-respiratory stimulation of infused adenosine in man. 342 50

Adenosine infusion (100 micrograms X kg-1 X min-1) in humans stimulates ventilation but also causes abdominal and chest discomfort. To exclude the effects of symptoms and to differentiate between a central and peripheral site of action, we measured the effect of adenosine infused at a level (70-80 micrograms X kg-1 X min-1) below the threshold for symptoms. Resting ventilation (VE) and progressive ventilatory responses to isocapnic hypoxia and hyperoxic hypercapnia were measured in six normal men. Compared with a control saline infusion given single blind on the same day, adenosine stimulated VE [mean increase: 1.3 +/- 0.8 (SD) l/min; P less than 0.02], lowered resting end-tidal PCO2 (PETCO2) (mean fall: -3.9 +/- 0.9 Torr), and increased heart rate (mean increase: 16.1 +/- 8.1 beats/min) without changing systemic blood pressure. Adenosine increased the hypoxic ventilatory response (control: -0.68 +/- 0.4 l X min-1 X %SaO2-1, where %SaO2 is percent of arterial O2 saturation; adenosine: -2.40 +/- 1.2 l X min-1 X %SaO2-1; P less than 0.01) measured at a mean PETCO2 of 38.3 +/- 0.6 Torr but did not alter the hypercapnic response. This differential effect suggests that adenosine may stimulate ventilation by a peripheral rather than a central action and therefore may be involved in the mechanism of peripheral chemoreception.
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PMID:Effects of adenosine on ventilatory responses to hypoxia and hypercapnia in humans. 378 85

Isometric exercise increases sympathetic nerve activity and blood pressure. This exercise pressor reflex is partly mediated by metabolic products activating muscle afferents (metaboreceptors). Whereas adenosine is a known inhibitory neuromodulator, there is increasing evidence that it activates afferent nerves. We, therefore, examined the hypothesis that adenosine stimulates muscle afferents and participates in the exercise pressor reflex in healthy volunteers. Intraarterial administration of adenosine into the forearm, during venous occlusion to prevent systemic effects, mimicked the response to exercise, increasing muscle sympathetic nerve activity (MSNA, lower limb microneurography) and mean arterial blood pressure (MABP) at all doses studied (2, 3, and 4 mg). Heart rate increased only with the highest dose. Intrabrachial adenosine (4 mg) increased MSNA by 96 +/- 25% (n = 6, P < 0.01) and MABP by 12 +/- 3 mmHg (P < 0.01). Adenosine produced forearm discomfort, but equivalent painful stimuli (forearm ischemia and cold exposure) increased MSNA significantly less than adenosine. Furthermore, adenosine receptor antagonism with intrabrachial theophylline (1 microgram/ml forearm per min) blocked the increase in MSNA (92 +/- 15% vs. 28 +/- 6%, n = 7, P < 0.01) and MABP (38 +/- 6 vs. 27 +/- 4 mmHg, P = 0.01) produced by isometric handgrip (30% of maximal voluntary contraction) in the infused arm, but not the contralateral arm. Theophylline did not prevent the increase in heart rate produced by handgrip, a response mediated more by central command than muscle afferent activation. We propose that endogenous adenosine contributes to the activation of muscle afferents involved in the exercise pressor reflex in humans.
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PMID:Role of adenosine in the sympathetic activation produced by isometric exercise in humans. 816 67

Adenosine is a purine nucleoside with a rapid onset and brief duration of action after intravenous bolus administration. Its most prominent cardiac effect is impairment or blockade of atrioventricular nodal conduction, but other effects are depression of automaticity of the sinus node and attenuation of catecholamine-related ventricular after-depolarizations. The cardiac cell surface receptor is the A1 purinoceptor. The therapeutic value of adenosine is predominantly in those arrhythmias in which the atrioventricular node forms part of a reentry circuit, as clearly demonstrated by the high success rate for termination of atrioventricular nodal reentry tachycardia and of atrioventricular reentry tachycardia involving an accessory pathway in the Wolff-Parkinson-White syndrome. Ventricular tachycardias are generally unresponsive, with the exception of right ventricular outflow tract tachycardia. A diagnostic role has emerged for adenosine. The transient blockade of the atrioventricular node that it causes can reveal important electrocardiographic features in arrhythmias, such as atrial flutter, or can unmask latent preexcitation. In wide-QRS tachycardias, adenosine can help to distinguish ventricular tachycardia from supraventricular tachycardia with QRS aberration. Unlike verapamil, adenosine is safe in ventricular tachycardia. A suggested dosing scheme is to give incremental doses at 1-minute intervals, starting at 0.05 mg/kg and continuing until complete atrioventricular block is induced or a maximum of 0.25 mg/kg is reached. Side effects are transient, sometimes uncomfortable, and not hazardous; dyspnea and chest discomfort are most frequent. A history of asthma is a relative contraindication. Aminophylline antagonizes and dipyridamole potentiates the effects of adenosine.
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PMID:The therapeutic and diagnostic cardiac electrophysiological uses of adenosine. 848 69

The objective of this study was to evaluate the safety of myocardial perfusion scintigraphy with Tc-99 m sestamibi during adenosine stress in patients with recent thrombolytically treated myocardial infarction. Eighty-four patients with thrombolytically treated myocardial infarction, 59 males and 25 females, aged 62.9 +/- 8.4, were eligible for myocardial perfusion scintigraphy during adenosine provocation. Exclusion criteria for adenosine stress were hypotension, unstable angina pectoris, cardiac failure, pericarditis and atrioventricular block (AV block) II-III. Adenosine-stress and resting myocardial perfusion scintigraphy was performed 2-5 days after thrombolysis. Scintigraphy at rest was done 24 h after the stress study. Sixty patients (71%) experienced some kind of side-effects during adenosine infusion. The most frequent side-effects were dyspnoea in 43/84 patients (51%) and unspecific chest discomfort in 26/84 patients (31%). During infusion, ST depressions or elevations on ECG were seen in 9 patients (11%), 5 of whom experienced atypical chest discomfort. Five patients (6%) described typical angina but none of them showed electrographic signs of myocardial ischaemia during infusion. Six patients (7%) developed transient AV block I-II. Reversible scintigraphic perfusion defects were seen in 67 patients (79%). No serious complications, such as death, reinfarction or severe arrhythmias, occurred during adenosine infusion or during a 3-day clinical follow-up period. In conclusion, MIBI-SPECT during adenosine stress is a safe diagnostic method that can be performed in most patients early on after thrombolytically treated acute myocardial infarction. Side-effects are common but benign, and not different from those seen in patients with chronic coronary artery disease.
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PMID:Myocardial perfusion scintigraphy (SPECT) during adenosine stress can be performed safely early on after thrombolytic therapy in acute myocardial infarction. 956 47

Patients who have an accessory pathway (AP) of atrioventricular (AV) conduction may develop circus movement tachycardia otherwise known as atrioventricular re-entrant tachycardia (AVRT). Orthodromic AVRT is the most common form. It occurs as a result of antegrade conduction through the normal AV conduction system and retrograde conduction to the atria via the AP. Less commonly, conduction occurs in the opposite direction resulting in antidromic AVRT. Tachycardia may also involve multiple APs which may provide both antegrade and retrograde conduction and may alternate antegradely or retrogradely. Tachycardia may occur in which the AP simply acts as a bystander, and does not participate in the tachycardia mechanism. When atrial fibrillation is conducted to the ventricles via and AP, the resultant ventricular rate may be extremely rapid, placing the patient at risk of developing ventricular fibrillation and cardiac arrest. This paper reviews the anatomical and physiological substrates involved in the pathogenesis of AVRT. The acute and long-term management of patients who suffer from these arrhythmias will then be discussed. The normal AV annulus is composed exclusively of electrically inert fibrous tissue. The AV node and His bundle normally act as the sole route of electrical conduction. Accessory pathways occur at all points along the AV ring, and usually occur as isolated abnormalities, although a proportion of patients have associated congenital abnormalities. This is particularly true of right-sided APs. Most APs exhibit non-decremental conduction properties, and conduct faster than normal AV conduction tissue. In many patients with APs the surface ECG reveals clear evidence of pre-excitation, and a good idea of pathway localization is possible using one or more of several algorithms which have been developed. Patients with latent pre-excitation, intermittent pre-excitation, and patients with concealed APs have not evidence of pre-excitation on a proportion or all of Their surface ECGs. Patients present with a history of paroxysmal palpitations, often with associated symptoms such as chest discomfort Syncope is a rare presenting symptom. Unless bundle branch block is present, patients with orthodromic AVRT exhibit a narrow complex tachycardia on the surface ECG. Patients with pre-excited tachycardia including antidromic AVRT, and other forms of SVT in which the AP conducts to the ventricles as a bystander but does not participate in the tachycardias mechanism, present as broad complex tachycardias on the surface ECG which may be difficult to distinguish from ventricular tachycardia. Adenosine is increasingly used for this purpose since it is highly efficacious and has an extremely short half-life. Adenosine is also very useful in the diagnosis of broad-complex tachycardia, and in unmasking latent pre-excitation during sinus rhythm. Electrophysiology study in these patients is frequently performed at the same time as an attempt at catheter ablation; it aims to diagnose, localize and determine the functional characteristics of an AP, and to characterize the role of the pathway in tachycardia. AVRT can be reliably terminated by effective AV nodal blockade. Drug therapy for the prevention of AVRT is useful for temporary control whilst awaiting more definitive measures and in certain cases as long-term management. No class of drug stands out as 'therapy of choice', and physician preference, pro-arrhythmic effects and associated conditions need to be taken into account such that an individual choice can be made in each patient. The management of patients with AVRT has been revolutionized in recent years with the advent of catheter-based techniques for their cure. Whilst this method of treatment is highly effective and has low complication rates, pathways in particular locations such as the septal region remain challenging.
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PMID:Accessory pathway reciprocating tachycardia. 971 20

The efficacy, safety and diagnostic usefulness of adenosine in the treatment of supraventricular tachycardia in children were prospectively studied over a 2-year period. Only patients who were stable and without hypotension were included. Adenosine was given at a dose of 0.1 mg/kg and increased to 0.2 mg/kg for the second and third doses if there was no response. Adenosine was used on 5 occasions in 5 patients. Adenosine was found to be effective in terminating supraventricular tachycardia in all 5 patients; 4 responded to a dose of 0.2 mg/kg while 1 responded to 0.1 mg/kg. Wolff-Parkinson White Syndrome was detected in 2 patients after termination of supraventricular tachycardia. Transient hypotension was noted in 1 patient lasting 45 seconds with no haemodynamic consequences. Two patients had transient ventricular ectopics lasting 3 to 5 seconds. One out of 3 patients who were old enough to report side-effects, experienced chest discomfort and dizziness lasting 5 seconds. All side-effects were transient and mild. We concluded that adenosine is effective and safe in terminating supraventricular tachycardia in children after vagal manoeuvres have failed.
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PMID:Five paediatric case reports of the use of adenosine in supraventricular tachycardia. 977 81


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