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)

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

We report a case of nearly fatal cardiovascular collapse attributable to an idiopathic anaphylactic reaction in a 76-year-old man. The event began with gastrointestinal symptoms of abdominal cramps, diarrhea, nausea, and vomiting as manifestations of IA. The patient subsequently progressed to develop urticaria, flushing, cardiovascular symptoms of chest pain, hypotension, and eventually cardiovascular collapse and myocardial infarction over a five-hour interval. This case emphasizes that the potential for life-threatening cardiovascular events from IA exists in patients without previously defined cardiac risk factors.
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PMID:Nearly fatal idiopathic anaphylactic reaction resulting in cardiovascular collapse and myocardial infarction. 237 90

Vasodilators of resistive vessels may induce ischemia in patients with coronary artery disease. To evaluate this possibility during prostacyclin (PGI2; scalar doses up to 10 ng/kg/min) and prostacyclin analog (iloprost; scalar doses up to 6 ng/kg/min) infusions, we studied 33 patients with angina pectoris and proved coronary artery disease. Patients were also submitted to dipyridamole (0.15 mg/kg/min for 4 minutes) and exercise stress testing (starting at 25 W and increasing 25 W every 2 minutes). In a preliminary study the hemodynamic and side effects of iloprost were studied in seven healthy subjects. At an iloprost dose of 4 to 6 ng/kg/min, these subjects had a significant decrease in mean arterial pressure and total peripheral and pulmonary vascular resistances. Side effects were limited to facial flushing and slight headache and were readily reversible. PGI2 induced typical chest pain and significant ST segment depression in six patients with severe coronary artery disease (three with left main and three with triple vessel disease) and poor exercise tolerance (means +/- SD = 362 +/- 99 seconds). All six patients had had angina during the dipyridamole infusion. Similar findings were observed after iloprost infusion in four of these. Aminophylline (125 mg iv) completely relieved chest pain. Although the rate-pressure products occasionally rose during PGI2 and iloprost infusions, there were no significant changes between ischemic (11.3 +/- 2.3 and 10.6 +/- 1.4 X 10(-3) U) and preischemic (10.8 +/- 1.5 and 10.7 +/- 1.4 X 10(-3) U) rates of infusion. Our data indicate that PGI2 and iloprost may induce ischemia independently of changes in oxygen demand, and suggest that these drugs dilate small coronary vessels. This may result in decreased subendocardial perfusion pressure and/or "coronary steal."
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PMID:Myocardial ischemia induced by prostacyclin and iloprost. 240 9

Lisinopril, a long-acting angiotensin converting enzyme inhibitor, and the calcium channel blocker nifedipine in its retard formulation, were compared as monotherapy in a group of 45 patients with essential hypertension. Lisinopril in single daily doses (range 20-80 mg, median dose 40 mg) and nifedipine retard in twice daily doses (total daily dose range 40-80 mg, median dose 60 mg) were equally effective in controlling hypertension. The lisinopril group (n = 30), at baseline supine blood pressure 178/109 +/- 23/9 mm Hg (mean +/- 1 SD), after 12 weeks' therapy measured 148/88 +/- 27/14 mm Hg; the nifedipine group (n = 15), at baseline 185/110 +/- 23/11 mm Hg, after 12 weeks' therapy measured 151/89 +/- 14/10 mm Hg. The number of patients who experienced clinical adverse effects was significantly greater in the nifedipine group: 8 of 15 (53%) compared to 4 of 30 (13%) in the lisinopril group. The commonest adverse effects of patients on nifedipine were swollen ankles, flushing, and headache. Two patients on nifedipine were withdrawn from the study because of their adverse experiences. Of the patients on lisinopril there were single reports of flushing, ankle swelling, tiredness, and chest pain. No patient withdrew from lisinopril because of an adverse experience. No adverse laboratory experiences were recorded in either group. In conclusion, lisinopril and nifedipine retard were equally effective in controlling essential hypertension. Lisinopril was, however, better tolerated during this study.
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PMID:Comparative efficacy of lisinopril and nifedipine retard in essential hypertension: a double-blind, placebo-controlled trial. 245 54

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

Treatment with metoprolol (100 mg twice daily), nifedipine (10 mg 3 times daily) and both drugs combined were compared for effect on clinical variables, bicycle ergometer exercise tolerance and adverse effects in a randomized double-blind, crossover study in patients with stable effort angina (n = 62). Nitroglycerin consumption and anginal attack rate as recorded in patient diaries indicated a higher antianginal efficacy (p less than or equal to 0.001) with metoprolol and combination therapy than with nifedipine monotherapy. All exercise test variables showed a significantly higher antianginal efficacy with combination therapy than with nifedipine monotherapy (15 to 26%). The combination therapy was also better than metoprolol in all exercise variables (9 to 14%), except for onset and duration of chest pain. Furthermore, metoprolol showed a higher efficacy than nifedipine in all exercise variables (7 to 23%) except total exercise time. More adverse symptoms of peripheral vasodilation were reported for nifedipine than for metoprolol (tachycardia, flushing, headache, p less than or equal to 0.05). It is concluded that combined treatment with metoprolol and nifedipine increased antianginal efficacy compared with the monotherapies, without increasing adverse effects. In effort angina, metoprolol in these doses was more effective and better tolerated than nifedipine.
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PMID:Metoprolol, nifedipine, and the combination in stable effort angina pectoris. 308 64

The authors present a retrospective study of 46 consecutive patients aged from 70 to 79 years (mean 73.3 +/- 2.5 years) with suspected coronary artery disease who, being unfit for exercise tests, were explored by myocardial scintigraphy with thallium 201 after coronary dilatation with intravenous dipyridamole. The examination was well tolerated by 30 patients. Such classical side-effects as chest pain, malaise, dizziness, headache, flushing, vomiting and transient arrhythmia or repolarization disorders were recorded, but they were not more frequent than in younger subjects. However, the occurrence of severe hypotensive malaise relieved by theophylline in two cases and of angina in about one third of patients with myocardial ischaemia means that the procedure must be performed under close supervision. A fall in blood pressure (-11 mmHg on average) and a rise in heart rate (+8 beats/min on average) were usual. Post-scintigraphy follow-up of patients over a mean period of 11.1 +/- 6.2 months showed that a reversible defect of thallium 201 uptake, due to redistribution, is a highly selective indicator of patients who are particularly exposed to a cardiac accident in the short--or mid-term. Only one out of 26 patients without reversible ischaemia (4 p. 100) subsequently presented with a major coronary event (unstable angina). In contrast, in the group of 20 patients with reversible ischaemia three required early myocardial revascularization; furthermore, five serious accidents (29 p. 100) occurred among the 17 patients who were left under medical treatment, including two sudden deaths, two cases of unstable angina and one case of myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Tolerance and prognostic value of Thallium 201 myocardial tomoscintigraphy with dipyridamole in the aged subject]. 314 28

Two hundred patients clinically certified as suffering from anxiety state were investigated with a view to understanding the clinical manifestation of the condition in Nigeria. We found that 67 symptoms were manifested by those patients, but only 15 symptoms were presented by about 10% of the sample. These common symptoms were: frequent headaches, difficulty in falling asleep, flushing, difficulty in concentrating, rapid or irregular heart beating, weakness, hot flashes, dizziness, feeling of something crawling in the head, heaviness of the head, nervousness, poor appetite, poor sight, nightmares, and chest pain. The five major precipitating factors were physical ailments, studying and examinations, use of drugs, psychological phenomona, pregnancy and childbirth, in decreasing order of magnitude. The most vulnerable age group was between 18 and 23 years old. The first born children account for the highest number of anxiety patients, but as the number of siblings increases, the vulnerability of the last-born increases. Anxiety neurosis as seen here is predominantly a problem of single males and females with secondary school education.
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PMID:Clinical anxiety in Nigeria. 340 42

Epoprostenol (prostacyclin) is a potent inhibitor of platelet aggregation and causes relaxation of vascular smooth muscle. These effects may be beneficial in patients with acute myocardial infarction. The effect of epoprostenol infusion in patients with acute myocardial infarction was evaluated in a randomised double blind study of 45 patients with evidence of myocardial infarction of less than 16 hours' duration. The patients were given a 72 hour infusion of epoprostenol (23) or placebo (22). The maximum dose was 5 ng/kg/min. The mean time to treatment was 8.3 hours (range 3.8-15.9 hours). The mean dose was 4.9 ng/kg/min. The patients were followed until day 30. No significant differences were found between the groups in mortality, development of congestive heart failure, cardiogenic shock, arrhythmias, recurrent chest pain, reinfarction, peak creatine kinase concentration, or the time taken to attain peak creatine kinase concentration. No significant difference in baseline ejection fraction was noted between groups, and no significant change in ejection fraction occurred within each group or between groups. The only significant side effect was the development of facial flushing in the epoprostenol group. In this pilot study epoprostenol was well tolerated by patients with acute myocardial infarction. No benefit from epoprostenol could be demonstrated at the dose range used when the drug was administered within 16 hours of the onset of symptoms.
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PMID:Epoprostenol sodium (prostacyclin) infusion in acute myocardial infarction. 353 63

Although the exposure of human subjects to prostacyclin (PGI2) infusion has been broad, no systematic approaches have been made in order to investigate the dose-related side effects in patients with angina pectoris and coronary artery disease (CAD). We studied 25 patients with typical chest pain and overt CAD. All patients underwent a cycloergometer stress testing (25 W increments at 2-min intervals). PGI2 was infused in scalar doses up to 10 ng/kg/min. During the infusion 25 patients (100%) had facial flushing, 7 (28%) moderate headache and one (4%) had nausea. In addition, 4 patients experienced the typical chest pain and had significant (greater than or equal to 0.1 mV) ST segment depression at 8.10 ng/kg/min infusion rates. These patients had lower tolerance to exercise (6.7 +/- 1.7 vs. 8.8 +/- 1.9 min; p less than 0.05) and coronary artery lesions more severe than those observed in patients without drug-induced angina pectoris. Our data therefore indicate that PGI2 at therapeutic doses may induce myocardial ischemia in patients with angina pectoris, low tolerance to exercise and severe CAD. In patients with mild to moderate degree of CAD, PGI2 was found to be well tolerated. These findings suggest that patients with angina pectoris and low tolerance to exercise should be excluded from clinical studies directed at elucidating the effectiveness of PGI2 in cardiovascular disorders.
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PMID:Side effects of prostacyclin in patients with angina pectoris and coronary artery disease. 390 57


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