Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five male patients, aged between 31 and 58 years, presented with anginal chest pain with nausea and sweating after the interruption of exercise. Prinzmetal variant angina was observed during the recovery phase of exercise tolerance testing. Coronary arteriography and selective left ventricular angiography were normal in all cases. Ergonovine, used in one case, induced coronary artery spasm. The angina was eased by Nifedipine in three patients and passed off with time in the other two patients. In one case attack occurred with amiodarone therapy and in another with glyceril trinitrate, after normal exercise tolerance tests. Vagotonia, all the more pronounced when sympathetic tonus is increased, and hyperventilation seem to be the causative factors of what probably results from coronary artery spasm. Nifedipine, a calcium-blocking agent would appear to be the treatment of choice.
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PMID:[Prinzmetal's angina initiated by interruption of exercise. 5 cases with normal coronary radiograms]. 11 38

The potential antianginal effects of orally administered ethyl-adenosine-5-carboxylate hydrochloride (EACH) were assessed in 9 patients with stable angina pectoris who underwent two standardized exercise tests for 3 consecutive days. The first daily exercise performed after placebo revealed no daily variation. The second test was preceded by placebo, 26 mg EACH or 33 mg EACH administered in a double-blind fashion with the use of crossover design. After the completion of the study in the first 6 patients, the 33-mg dose of EACH had to be discontinued because 3 patients had severe angina and another one had nausea and diffuse numbness after this dose. In the remaining 3 patients a 6-mg dose of EACH was used instead of 33 mg, after which the study was terminated because no difference could be determined. EACH, 26-mg and 6-mg, had no significant effect on resting and exercise heart rate, on blood pressure, on onset or duration of angina and positive-exercise electrocardiogram, or on exercise duration. Our study revealed that EACH had no potential antianginal effect and that at a dosage of 33 mg it may induce angina.
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PMID:Trials with an adenosine analogue as antianginal medication. 33 39

Besides the vascular changes caused by arteriosclerosis the compression stenosis is the most frequent form of the isolated restriction of the arteria coeliaca. The compression of the arteria coeliaca, caused by the ligamentum arcuatum medianum or a fribromatous ganglion tissue, can cause complaints similar to the symptoms of angina abdominalis: pains in the epigastrium, postprandial pains, loss of weight, nausea/vomiting, diarrhea, 93% of the patients with severe vascular compression have an abdominal vascular murmur. Of 31 patients with angiographically proved compression stenosis, 11 patients suffering from occlusion or intense stenosis had to be operated because of heavy complaints. The angiographic and intraoperative findings allow the conclusion that there is a connection between the extent of the stenosis and the clinical appearance. The decompression of the arteria coeliaca, in other words the detachment of the compressing tissue leads to total complaintlessness in 83% of the patients. If the arteria coeliaca is hypoplastic a vessel widening or a bypass operation is necessary to establish normal blood circulation in the epigastric organs.
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PMID:[Compression of the celiac trunk (author's transl)]. 97 81

Amlodipine, a potent long-acting dihydropyridine calcium antagonist, was compared with placebo in a parallel, randomized, double-blind study in 134 patients with chronic stable angina pectoris maintained on beta-adrenergic blocking agents. After a single-blind, two-week placebo period, patients were randomized to receive either amlodipine (2.5, 5, and 10 mg) or placebo once daily for four weeks. The effects of amlodipine on maximal exercise time, work, time to angina onset, and subjective indices including angina frequency, nitroglycerin tablet consumption, and patient and investigator ratings were assessed. Each dose of amlodipine produced increases in exercise time and calculated total work accomplished compared to baseline. Improvements at 5 and 10 mg were significantly greater than placebo which produced no significant change (p less than 0.05). Qualitative improvements in the severity of angina were produced by amlodipine at 5 and 10 mg daily assessed by patient-rating questionnaires (p less than 0.05). Reductions in angina frequency attacks per week and weekly nitroglycerin tablet consumption occurred but were not statistically significant when compared with placebo. Adverse effects observed during amlodipine treatment prompted discontinuation of treatment in only 2 out of 100 patients. Three patients discontinued treatment for reported lack of efficacy. No laboratory abnormalities prompted treatment discontinuation and minor side effects of dizziness, nausea, headache, and fatigue were observed infrequently. The results of this controlled, large-scale multicenter trial suggest that amlodipine significantly increased exercise capacity and was well tolerated when added to the antianginal regimen of patients remaining symptomatic while receiving beta-blocking agents.
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PMID:Amlodipine combined with beta blockade for chronic angina: results of a multicenter, placebo-controlled, randomized double-blind study. 135 85

The calcium antagonist, diltiazem is effective in the treatment of patients with various types of angina pectoris, as well as with essential and renovascular arterial hypertension. Sustained-release diltiazem in dose of 180 mg once daily is effective as sustained-release diltiazem in dose of 90 mg twice daily. Besides, in patients with stable angina pectoris and essential arterial hypertension the monotherapy with sustained-release diltiazem in dose of 180 mg is similarly effective as beta blockers and thiazide diuretics. However, monotherapy with sustained-release diltiazem is at least effective as monotherapy with sustained-release verapamil. Comparative clinical investigations showed that diltiazem is more effective than propranolol in decreasing ischemic attacks, whereas the risk of bradycardia is smaller. On the other hand, nifedipine (dihydropyridine calcium antagonist) is more effective than diltiazem in lowering ischemic electrocardiographic changes, incidence of attacks and improving working capability. The efficacy of diltiazem, nifedipine and verapamil is similar in the treatment of patients with spastic angina pectoris, whereas the least effective is propranolol. As far as the arterial hypertension is concerned, clinical investigations showed that the efficacy of diltiazem and nifedipine is similar. Side effects are relatively rare (1.8-9.6% patients) and depend on the dose (nausea, fatigue, dizziness, headache and itching).
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PMID:[Pharmacology--new therapy. Calcium channel blockers: new aspects of therapeutic use of diltiazem]. 146 75

The antianginal efficacy of bepridil, a calcium antagonist with an extended plasma elimination half-life, has been compared with placebo and the calcium antagonists nifedipine and diltiazem in patients refractory to diltiazem. The earliest observations in the United States of antianginal effects of bepridil were revealed in a single-blind, multicenter, placebo-controlled trial of 77 patients with chronic stable angina pectoris that demonstrated that bepridil (300 mg/day) improved exercise duration by 26%, from 6.9 +/- 0.4 (standard error of the mean) to 8.7 +/- 0.5 minutes (p less than 0.001), and exercise work by 52%, from 2.7 +/- 0.3 to 4.1 +/- 0.4 x 10(-3) KPM (p less than 0.001), on a standardized treadmill protocol, and it reduced angina frequency by 68%, from 8.5 +/- 1.1 to 2.7 +/- 0.7 attacks per week, and nitroglycerin use by 76% (p less than 0.001). Minor side effects such as nausea, epigastric discomfort, and tremor were infrequent and no major side effects occurred. Double-blind, parallel-design treatment evaluations confirmed beneficial effects of bepridil alone and in combination with beta blockade. Chronic efficacy was confirmed by evaluations up to 24 months in a controlled withdrawal study. Antianginal effects of nifedipine were compared with those of bepridil in a double-blind, parallel group study of 101 patients with chronic stable angina treated for 3 months. Bepridil (mean final dose 284 mg/day; range 200-400 mg/day) produced modest but statistically significantly (p less than 0.05) greater improvements in exercise work, time to angina, or 1 mm ST-segment change than nifedipine (mean final dose 59 mg/day; range 30-120 mg/day).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bepridil treatment of chronic stable angina: a review of comparative studies versus placebo, nifedipine, and diltiazem. 153 68

We conducted an intracardiac study of the electrophysiologic effects and kinetics of intravenous nicardipine (N) in 16 patients with or without impaired cardiac conduction, using a randomized, double-blind, crossover design versus placebo (P). N or P were infused intravenously over 5 min: the dose of N was 9.46 +/- 3.85 mg. Standard electrophysiologic parameters of atrioventricular (AV) conduction and sinus function were measured under basal conditions, between 10 and 25 min, and at 65 min, after beginning the first infusion of N or P, and between 10 and 25 min after beginning the second infusion of N or P. Treatment with N significantly reduced systolic (S) and diastolic (D) blood pressure (BP) at 10 min (35 +/- 19 and 25 +/- 17 mm Hg, respectively). N significantly shortened sinus cycle length (SCL), corrected sinus recovery time (CSNRT), AH interval, AV node (AVN) Wenckebach cycle length, and anterograde and retrograde effective (ERPs) and functional refractory periods (FRPs) of the AVN. Infranodal parameters were unaffected. Mean plasma N concentrations at 10 min were 18.5 +/- 7.7 ng/ml/kg and 5.3 +/- 3 ng/ml/kg at 60 min. Two patients experienced slight adverse effects (anginal pain and nausea); another with sick sinus syndrome developed a sinus pause. We conclude that intravenous N affects nodal, but not His conduction, and that it should be administered with care in the presence of SSS.
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PMID:Electrophysiologic effects of intravenous nicardipine on sinus node function and conduction in humans. 168 70

Side-effects and complications from 2,600 intravenous digital-subtraction-angiographies (IV-DSA) are reported. All studies were performed in a standardized technique using a non-ionic contrast agent (Iopromid 370 mg J/ml). Side-effects or complications were noted in 2.5% of all IV-DSA. Most often nausea (0.92%), urticaria (0.5%), angina pectoris (0.5%) and symptomatic alterations of blood-pressure (0.27%) were recorded. 8.4% of all reactions occurred with a delay of at least one hour. All side-effects and complications resolved, partly under symptomatic therapy. In one (0.04%) out of 2,600 studies a severe allergoid reaction occurred, affording intensive-care therapy. With proper patient selection and a suitable technique, IV-DSA may be regarded--within the angiographic methods--as a procedure of relatively low risk.
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PMID:[Acute adverse effects and complications of central venous digital subtraction angiography (DSA). Results of 2,600 studies]. 177 Aug 95

Histamine, the main amine released during allergic reactions, can provoke coronary arterial spasm manifested as angina pectoris. This has been shown during clinical and laboratory studies. The effects of histamine on cardiac function are mediated via H1- and H2- receptors situated on the four cardiac chambers and coronary arteries. Coronary arteries of cardiac patients are hyperactive and contain stores of histamine which can initiate coronary artery spasm. Clinical observations indicate that angina pectoris or acute myocardial infarction can be provoked by acute allergic reaction. The coincidental occurrence of chest pain and allergic reaction accompanied by clinical and laboratory findings of classical angina pectoris seems to constitute the syndrome of allergic angina. The clinical symptoms of allergic angina include chest discomfort, dyspnoea, faintness, nausea, pruritus and urticaria. They are accompanied by signs such as hypotension, diaphoresis, pallor and bradycardia. There are also electrocardiographic findings indicating myocardial ischaemia, arrhythmias and conduction defects. Thus, in patients undergoing acute allergic reaction, the development of chest pain could be explained by the mechanism of coronary arterial spasm provoked by the release of histamine, which constitutes the syndrome of allergic angina.
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PMID:Histamine-induced coronary artery spasm: the concept of allergic angina. 179 97

A paired-comparison, multicenter study examined differences in patient and physician preferences for two transdermal nitroglycerin delivery systems, Nitro-Dur Transdermal Infusion System and Transderm-Nitro Transdermal Therapeutic System. For two weeks, 72 patients with angina pectoris wore both transdermal nitroglycerin patches simultaneously, each patch delivering half of each patient's need for nitroglycerin. (Each patch delivers nitroglycerin to the skin at a rate of about 0.02 mg/cm2 of patch per hour.) The patients and their physicians were then asked to rate the patches and to express their preferences with respect to eight patch characteristics: size, color, comfort, ease of application, adhesiveness, ease of removal, appearance, and associated redness/irritation. On each of the patch characteristics, significantly more of the patients expressed a preference for Nitro-Dur. Of the 67 patients who rated the patches overall, significantly more preferred Nitro-Dur (47 patients) than Transderm-Nitro (17 patients). Physician evaluations were also significantly biased in favor of Nitro-Dur. Treatment side effects included headache in 17 patients, application-site reactions in seven, nausea in four, dizziness in three, and fatigue in two. It is concluded that Nitro-Dur has greater patient acceptance than Transderm-Nitro and thus treatment compliance may be higher with Nitro-Dur than with Transderm-Nitro.
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PMID:A comparative evaluation of two transdermal nitroglycerin delivery systems: Nitro-Dur versus Transderm-Nitro. The Collaborative Investigation Group. 179 11


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