Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenosine (adenine riboside), administered either as the free base or as the 5'-triphosphate (ATP) by rapid intravenous bolus, depresses atrioventricular (AV) nodal conduction, resulting in transient AV block. Adenosine is the active agent and ATP is rapidly converted to adenosine after exogenous administration. By blocking the anterograde AV nodal limb of a re-entrant circuit, adenosine 6 to 12 mg (or ATP 10 to 20 mg) converts almost all episodes of paroxysmal supraventricular tachycardia (PSVT) involving the AV node within 30 seconds of administration. This is at least equivalent in efficacy to verapamil in adults, and superior to lanatoside C in children, with a considerably more rapid onset of action. Furthermore, if a dose of adenosine is ineffective, the exceptionally short plasma half-life of the adenyl nucleosides (less than 10 sec) allows rapid upward dosage titration until PSVT is terminated. Because the induced conduction block primarily affects the AV node, adenosine is a useful diagnostic tool in patients with broad or narrow QRS complex tachycardia; it terminates arrhythmias dependent on the AV node, unmasks other supraventricular mechanisms during transient AV block, but almost always has no effect on ventricular tachycardia. Noncardiac adverse effects, i.e. flushing, dyspnoea and chest pain, may occur during acute arrhythmia termination or diagnosis with adenosine, and arrhythmias may develop; however, these effects are usually transient (lasting less than 1 minute). Adenosine has also been used to induce coronary vasodilation in patients undergoing thallium-201 single photon emission computed tomography (201Tl SPECT), 2-dimensional echocardiography or positron emission tomography to evaluate suspected coronary artery disease. Intravenous infusion of adenosine 140 micrograms/kg/min for 6 minutes was generally associated with only mild adverse effects. These usually resolved within 1 to 2 minutes of discontinuing adenosine, although occasionally patients required aminophylline and/or nitroglycerin (glyceryl trinitrate). Diagnoses based on the results of scintigraphy were of a sensitivity, specificity and predictive accuracy comparable to those achieved with exercise- or dipyridamole-201Tl SPECT. Adenosine is therefore particularly suitable for the diagnosis of tachycardias and the acute management of PSVT involving the AV node in all age groups, without the risks of cardiac arrest and hypotension associated with verapamil. Furthermore, intravenous adenosine infusion may be used to induce coronary vasodilation in patients unable to perform exercise stress tests for 201Tl scintigraphy, and is well tolerated.
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PMID:Adenosine. An evaluation of its use in cardiac diagnostic procedures, and in the treatment of paroxysmal supraventricular tachycardia. 171 62

Adenosine thallium-201 myocardial scintigraphy is a promising test for coronary artery disease detection, but its safety has not been reported in large patient cohorts. Accordingly, the tolerance and safety profile of adenosine infusion were analyzed in 607 patients (351 men, 256 women, mean age 63 +/- 11 years) undergoing this test either because of suspected coronary artery disease (Group I, n = 482) or for risk stratification early (5.2 +/- 2.8 days) after myocardial infarction (Group II, n = 125). Adenosine increased the heart rate from 74.5 +/- 14.0 to 91.8 +/- 15.9 beats/min (p less than 0.001) and decreased systolic blood pressure from 137.8 +/- 26.8 to 120.7 +/- 26.1 mm Hg (p less than 0.001). Side effects were frequent and similar in both groups. Flushing occurred in 35%, chest pain in 34%, headache in 21% and dyspnea in 19% of patients. Only 35.6% of Group I patients with chest pain during adenosine infusion had concomitant transient perfusion abnormalities, compared with 60.7% of Group II patients (p less than 0.05). First- and second-degree AV block occurred in 9.6% and 3.6% of patients, respectively, and ischemic ST changes in 12.5% of cases. Concomitance of chest pain and ischemic ST depression was uncommon (6%) but, when present, predicted perfusion abnormalities in 73% of patients. Most side effects ceased rapidly after stopping the adenosine infusion. The side effects were severe in only 1.6% of patients and in only six patients (1%) was it necessary to discontinue the infusion. No serious adverse reactions such as acute myocardial infarction or death occurred.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance and safety of pharmacologic coronary vasodilation with adenosine in association with thallium-201 scintigraphy in patients with suspected coronary artery disease. 186 36

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of adenosine in the treatment of episodes of paroxysmal supraventricular trachycardia (PSVT) are reviewed. Adenosine is an endogenous adenine nucleoside that markedly decreases heart rate and prolongs atrioventricular (AV)-nodal conduction. Adenosine is rapidly cleared from plasma by the cellular elements of the blood and by vascular endothelial cells and subjected to enzymatic metabolism. The drug has a half-life of 0.6 to 10 seconds. In noncomparative clinical trials, adenosine terminated 85% to 100% of induced or spontaneous episodes of PSVT involving the AV node in the reentrant circuit. In patients with arrhythmias that do not involve the AV node in the reentrant circuit, adenosine produces AV block and does not restore sinus rhythm. Prospective, randomized trials comparing adenosine with verapamil in adults have not yet been performed. The adverse effects of adenosine include flushing, dyspnea, headache, cough, chest pain, sinus bradycardia, atrial fibrillation, ventricular arrhythmias, and various degrees of AV block. Because of the short half-life of adenosine, these effects are transient and well tolerated. The initial dose of adenosine in treating acute PSVT is 6 mg given by rapid i.v. bolus injection, followed in one to two minutes by up to two additional 12-mg boluses if necessary. Adenosine has been found to be effective in terminating PSVT and thus offers an alternative to verapamil. Prospective, randomized trials comparing adenosine with verapamil are needed to definitively establish adenosine's role in the therapy of PSVT.
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PMID:Adenosine in the episodic treatment of paroxysmal supraventricular tachycardia. 218 71

The diagnostic and therapeutic potential of intravenous adenosine was studied in 64 patients during 92 episodes of regular sustained tachycardia. In 40 patients who had narrow complex tachycardias (QRS less than 0.12 s) adenosine (2.5-25 mg) restored sinus rhythm in 25 with junctional tachycardias (46 of 48 episodes) and produced atrioventricular block to reveal atrial or sinus tachycardia in 15. In 24 patients with broad complex tachycardias (QRS greater than or equal to 0.12 s) adenosine terminated the tachycardias in six patients and revealed atrial or sinus arrhythmias in four. The tachycardias persisted in 14 patients despite doses up to 20 mg, but adenosine allowed the diagnosis of ventricular tachycardia with retrograde atrial activation in two patients by producing transient ventriculoatrial dissociation. Diagnosis based on adenosine induced atrioventricular nodal block was correct in all patients with narrow complex tachycardias and in 92% of those with broad complex tachycardias, compared with correct electrocardiographic diagnoses in 90% and 75% respectively. Adenosine gave diagnostic information additional to the electrocardiogram in 25%. The response to adenosine in broad complex tachycardias identified those of supraventricular origin with 90% sensitivity, 93% specificity, and 92% predictive accuracy. Adenosine restored sinus rhythm in all patients with junctional reentrant tachycardias, but in 10 (35%) the arrhythmias recurred within two minutes. Symptomatic side effects (dyspnoea, chest pain, flushing, headache) were reported by 40 (63%) patients and, although transient, were severe in 23 (36%). There were ventricular pauses of over 2 s in 16% of patients, the longest pause being 6.1 s. Adenosine is of value in the diagnosis and treatment of narrow and broad complex tachycardias, but its use is limited by symptomatic side effects, a tenfold range in minimal effective dosage, occasional action at sites other than the atrioventricular node, and early recurrence or arrhythmia.
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PMID:Value and limitations of adenosine in the diagnosis and treatment of narrow and broad complex tachycardias. 278 11

One hundred and seventeen episodes of supraventricular tachycardia in 50 children, including 28 infants, were treated with intravenous adenosine. Adenosine was prepared in a sterile solution of 0.9% saline (1 mg/ml) and given in incremental doses of 0.05 mg/kg every two minutes to a maximum of 0.25 mg/kg. Ninety of the 117 episodes were terminated. This included 88 of the 102 episodes of junctional tachycardia (79 of the 92 episodes of atrioventricular reentry tachycardia, seven of the eight episodes of atrioventricular nodal reentry tachycardia, and both of the episodes of long R-P' tachycardia). Only one of four episodes of His bundle tachycardia and one of the eight episodes of ectopic atrial tachycardia were terminated. None of the three episodes of atrial flutter were terminated. Side effects were frequent but mild and included transient complete atrioventricular block (less than 6 s), sinus bradycardia (less than 40 s), ventricular extrasystoles, flushing, nausea, headache, and respiratory disturbance. Reinitiation (within 5 s) of supraventricular tachycardia occurred in 13 of the terminated episodes. Although reinitiation limited its clinical efficacy in some patients, intravenous adenosine offered a safe and efficient method of rapid termination of most episodes of supraventricular tachycardia and in some cases facilitated diagnosis of the mechanism.
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PMID:Efficacy and safety of adenosine in the treatment of supraventricular tachycardia in infants and children. 278 12

Aqueous diltiazem was given to ten healthy male volunteers in a single oral dose of 2.5 mg/kg body weight. Serum diltiazem levels were measured at various intervals up to 24 hours after administration of the drug as were blood pressure, heart rate, and PR interval. The pharmacokinetics followed a one-compartment model in six and two-compartment model in four subjects. The mean distribution half-life in the latter four subjects was 15.8 +/- 3.7 minutes (range, 10.4-18.8 min). In the ten subjects, the peak serum diltiazem level was attained in 20 to 45 minutes (mean, 32.5 +/- 9.5 min) and ranged from 136 to 701 ng/mL (mean, 332 +/- 180 ng/mL). The elimination half-life ranged from 2.8 to 4.8 hours (mean, 3.8 +/- 0.6 hr). The area under the concentration-time curve varied from 508 to 2,245 ng-hr/mL, indicating differing bioavailability. Slight but significant blood pressure reduction was seen only at one to three hours. Changes in heart rate were not significant at any measurement. Transient facial flushing, beginning at ten to 20 minutes after administration, was noted in nine subjects, reflecting the vasodilatory effect of the drug. Significant prolongation (greater than 10%) of PR intervals began at ten minutes in three, at 20 minutes in six, and at 30 minutes in one participant, and progressed to second-degree Wenckebach atrioventricular (AV) block in six subjects 20 to 60 minutes after administration and third-degree AV block in one person 45 minutes after dosing. These AV blocks resolved by the third hour without treatment, and PR prolongation resolved by the fifth to seventh hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacokinetics and pharmacodynamic effects of aqueous diltiazem in healthy humans. 368 May 61

The diagnostic accuracy, safety and tolerance of adenosine thallium scintigraphy have been reported using a 2-site intravenous infusion with either a titrated or fixed-dose protocol. A single-site infusion would considerably simplify the test procedure, but its safety must be established before it can be recommended. Accordingly, 400 consecutive patients who had adenosine and thallium-201 administered through the same intravenous line were classified into 2 groups. Group I (n = 201) patients received a 7-minute titrated intravenous infusion of adenosine, with an initial dose of 50 micrograms/kg/min that increased at 1-minute intervals to a maximum of 140 micrograms/kg/min. Group II (n = 199) patients received a fixed dose of adenosine at 140 micrograms/kg/min for 6 minutes. Adenosine significantly (p < 0.001) increased heart rate and decreased systolic blood pressure by similar amounts in both groups. Adverse effects occurred more often (88 vs 71%, p < 0.001) and started earlier (2.8 vs 3.6 minutes, p < 0.001) in group II. There was no significant difference in the occurrence of second- and third-degree atrioventricular block between the 2 groups (4.0 vs 5.0%); however, chest pain, flushing and nausea were all more frequent in group II. Severe side effects were seldom seen in either group and occurred in 9 group I and 8 group II patients. Scintigraphic findings were similar in both groups. Transient perfusion defects were seen more often in patients with than without second- or third-degree atrioventricular block (42 vs 21%, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety of single-site adenosine thallium-201 scintigraphy. 829 44

Adenosine is a purine nucleoside that impairs conduction through the AV node and is thus effective in terminating tachycardias involving the AV node. Gaining acceptance as the drug of choice for neonatal supraventricular tachycardia (SVT), it is given IV as a rapid bolus with an initial dose of 0.05 mg/kg and can be increased in increments of 0.05 mg/kg every one to two minutes until termination of SVT (to a maximum of 0.25 mg/kg). Because of its half-life of 0.6 to 10 seconds, adenosine will not prevent reinitiation of SVT, therefore other medications should be considered if prophylaxis is required. An advantage of the short half-life is the transient nature of adverse effects, which can include flushing, nondistressing alterations in respiratory pattern, irritability, sinus bradycardia, and varying degrees of AV block. Administration to critically ill infants, including those requiring mechanical ventilation, has been reported. The infant's blood pressure, electrocardiogram, respiratory status, and capillary refill should be monitored before, during, and after adenosine administration.
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PMID:Adenosine administration for neonatal SVT. 835 Aug 44

Diltiazem is a benzothiazepine derivative calcium antagonist available in several formulations, some of which enable once daily administration. The drug as monotherapy has demonstrated similar efficacy to diuretics in older patients with hypertension. Data comparing diltiazem with beta-blockers and angiotensin converting enzyme inhibitors are more limited, but available studies suggest at least comparable antihypertensive efficacy. Diltiazem as monotherapy or in combination with a beta-adrenoceptor-antagonist, isosorbide dinitrate, or another calcium antagonist, has demonstrated efficacy in patients with effort angina. The drug has also been used intravenously to terminate supraventricular tachycardias and to control the ventricular response to atrial fibrillation or flutter; it also appears to reduce the rate of early reinfarction in patients with non-Q-wave myocardial infarction. The most common adverse events during diltiazem therapy include headache, flushing, peripheral oedema and hypotension. Atrioventricular block although rare, is the most frequent serious adverse event related to diltiazem therapy and may be exacerbated by coadministration of beta-adrenoceptor antagonists, especially in the elderly. Thus, diltiazem appears to be an effective and well tolerated treatment for hypertension and angina in older patients and has shown promise as therapy for supraventricular tachycardias and as prophylaxis against early reinfarction in patients with non-Q-wave myocardial infarction.
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PMID:Diltiazem. A review of its pharmacology and therapeutic use in older patients. 836 96

An 81-year-old man with broad cerebral infarction presented with coronary air embolism secondary to bowel infarction and developed cardiogenic shock. Electrocardiography revealed ST elevation in the inferior leads and complete atrioventricular block with atrial fibrillation. Emergent angiography showed total occlusion of the right coronary artery without apparent thrombi. A multifunctional probe catheter was inserted into the right coronary artery for selective angiography. A moderate amount of air was aspirated from the catheter. The diagnosis was coronary air embolism. Coronary flow was restored after aspiration and normal saline flushing. Computed tomography showed massive portal venous gas. Emergent laparotomy disclosed broad bowel necrosis. The coronary air emboli may have originated from the portal vein and passed through the intrahepatic (portal to hepatic) shunt and patent foramen ovale(paradoxical embolization).
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PMID:[Right coronary air embolism secondary to bowel infarction: a case report]. 1506 2


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