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)

A 55-year-old Caucasian woman suddenly developed substernal chest pain at rest accompanied by pallor, diaphoresis, nausea, and vomiting. Physical examination was otherwise unremarkable. The resting ECG showed T-wave inversion in all anterior leads which returned to normal 24 h after the onset of the symptoms. The pain was eliminated promptly by sublingual isosorbide dinitrate. "Impending" acute myocardial infarction was diagnosed. Coronary arteriography, however, failed to reveal any change in any major coronary artery but an apical aneurysm of the left ventricle was detected. As the complement-fixation test for Chagas' disease was positive, the diagnosis of chronic Chagas' heart disease was then established. This unusual clinical manifestation of Chagas' disease is thought to be the consequence of a transient imbalance in the cardiac autonomic nervous system, which is considered to play a central role in the pathogenesis of chronic Chagas' heart disease. In addition, the present case may alert clinicians to the thus far neglected atypical chest pain, which is frequently seen in chagasic patients but whose etiology remains obscure.
Clin Cardiol 1987 Jun
PMID:Chronic Chagas' heart disease presenting as an impending myocardial infarction: a case favoring the neurogenic pathogenesis concept. 359 60

Nausea and vomiting occurring during myocardial ischemia is believed to be associated with inferior wall infarction. However, data supporting such an association are limited, and an alternative hypothesis that cardiac vomiting is related to infarct size has also been advanced. The 2 hypotheses were tested in a cross-sectional study of 265 patients consecutively admitted to the coronary care unit. Nausea or vomiting was a good predictor of myocardial infarction (p less than 0.0001). The odds of having an infarction was 3.14 times greater for patients with nausea or vomiting than for those without these symptoms. Nausea was not a good predictor for inferior wall infarction (p = 0.14): 51% of patients with inferior infarcts had nausea or vomiting and 66% with anterior infarcts had these symptoms. Using peak serum creatine kinase level as an index of infarct size, nausea or vomiting was a good predictor of larger infarction. While 55% of all patients with infarction had nausea or vomiting, for patients with infarctions that produced a peak creatine kinase level of more 1,000 IU/liters, 78% had nausea or vomiting. Sex was a marginally important variable. After adjusting for sex, the presence of nausea or vomiting still predicted infarct size (p less than 0.001). Thus, cardiogenic nausea and vomiting are associated with larger myocardial infarctions but do not suggest infarcts in a particular location.
Am J Cardiol 1987 Jul 01
PMID:Nausea and vomiting during acute myocardial infarction and its relation to infarct size and location. 360 39

Although the diagnostic utility of thallium-201 myocardial imaging after dipyridamole infusion is well established, the intravenous form of the drug is not yet commercially available in North America. Fifty patients referred for coronary angiography were prospectively studied. Within a 2 week period, each patient underwent cardiac catheterization and thallium-201 myocardial imaging after both oral and intravenous dipyridamole administration. For the oral protocol, patients were randomly assigned to treatment with either 200 or 400 mg of dipyridamole in tablet form. Coronary artery stenoses of 70% or greater were considered significant. For the 25 patients who received a 200 mg oral dose of dipyridamole, the scintigraphic study showed perfusion defects in 65% of patients with significant coronary artery disease after the oral dose and in 85% of patients after the intravenous dose. For the 25 patients who received a 400 mg oral dose, the sensitivity of the scintigram was 84% after the oral dose and 79% after the intravenous dose. Except for headache and nausea, side effects were less severe and less frequent with oral (either 200 or 400 mg) than with intravenous dipyridamole. Because of the delayed and variable absorption of dipyridamole tablets, the oral studies required a longer period of medical supervision (45 to 60 minutes), and aminophylline was empirically administered after completion of the first set of thallium-201 images. It is concluded from this study that thallium-201 myocardial imaging after coronary vasodilation with a 400 mg oral dose of dipyridamole is a safe, widely available and reliable alternative for the evaluation of coronary artery disease in patients unable to achieve an adequate exercise level on stress testing.
J Am Coll Cardiol 1986 Jul
PMID:Thallium-201 myocardial imaging during pharmacologic coronary vasodilation: comparison of oral and intravenous administration of dipyridamole. 371 34

Cardiac and noncardiac side effects were studied in 293 consecutive patients referred for nonexercise stress thallium imaging with intravenous dipyridamole. Six minutes after the initiation of infusion, there was a mean 9-beat/min increase in heart rate and a mean 12-mm Hg decrease in systolic blood pressure. The largest increase in heart rate exceeded 20 beats/min in only 13% of patients and the largest decrease in systolic blood pressure exceeded 20 mm Hg in 31%. Noncardiac side effects were headache (11%), lightheadedness or dizziness (5%) and nausea (4%). Only 9 patients required intravenous aminophylline for relief of noncardiac side effects: severe headache in 7 and nausea in 2. Cardiac side effects included chest pain in 76 patients (26%), of whom 70% were given aminophylline for relief of symptoms. Sixty patients (20%) had ischemic ST-segment depression and 56 (19%) had arrhythmias (ventricular in 50 and atrial in 6). There were no deaths, myocardial infarctions or sustained arrhythmias due to dipyridamole administration. Among 62 patients also undergoing cardiac catheterization, side effects except for arrhythmias were unrelated to the number of vessels with coronary artery disease. Intravenous dipyridamole is safe for nonexercise stress testing and has few serious side effects. However, the possibility of ischemia requires careful selection of patients and monitoring of vital signs and the electrocardiogram during the test.
Am J Cardiol 1987 Jan 01
PMID:Safety of intravenous dipyridamole for stress testing with thallium imaging. 381 27

Stress thallium imaging with intravenous dipyridamole permits assessment of coronary artery disease (CAD) without the need for exercise. However, intravenous dipyridamole is available in the United States only on an experimental basis. To study the use of oral dipyridamole as a clinically available alternative to intravenous dipyridamole for this purpose, 100 patients underwent thallium imaging with oral dipyridamole. Each patient received 300 mg of pulverized tablets in a 30-ml suspension. Maximal increase in mean heart rate and decrease in mean blood pressure occurred 30 minutes after ingestion. At 45 minutes, 2 mCi of thallium was given intravenously and serial imaging was begun within 7 minutes. The serum dipyridamole level (mean +/- standard deviation) 45 minutes after 300 mg was administered orally (3.7 +/- 2.2 micrograms/ml) was similar to that 5 minutes after 0.56 mg/kg was given intravenously (4.6 +/- 1.3 micrograms/ml). Fifty-five patients had some adverse effects between 15 and 75 minutes after oral ingestion, including nausea, headache, dizziness, chest pain (25 patients) and electrocardiographic changes (14 patients). Intravenous aminophylline was used to resolve these adverse effects in 21 patients. There were no severe arrhythmias, myocardial infarctions or deaths. Of the 43 patients with angiographically documented CAD, 39 had an initial perfusion defect that redistributed on the delayed images. When the results in patients who had undergone catheterization were analyzed by individual segment, the presence of thallium redistribution was associated with normal or hypokinetic contrast left ventriculographic wall motion of that segment, whereas the presence of a persistent defect was associated with akinesia or dyskinesia (Fisher's standardized Z = 9.14).(ABSTRACT TRUNCATED AT 250 WORDS)
Am J Cardiol 1986 Mar 01
PMID:Usefulness of oral dipyridamole suspension for stress thallium imaging without exercise in the detection of coronary artery disease. 395 32

The actions of acetylprocainamide, the major metabolite of procainamide in man, were studied in a placebo-controlled oral-dose-ranging trial in 16 persons with arrhythmias. The occurrences of arrhythmias decreased in 15 patients receiving acetylprocainamide and increased subsequently in 10 of 13 patients given placebo. The frequency of arrhythmias was reduced by more than 75 percent in nine patients. Antiarrhythmic effects were dependent on dose and serum drug concentrations, with levels of 10 to 24 microgram/ml observed in patients with a reduction of more than 70 percent in premature ventricular complexes. The ratio of preejection period to left ventricular ejection time decreased during therapy. Side effects of light-headedness, insomnia, nausea and diarrhea occurred in six patients at serum levels ranging from 11 to 22 microgram/ml. The serum half-life of acetylprocainamide lengthened from 7 to 21 hours as the creatinine clearance decreased from 105 to 35 ml/min. Acetylprocainamide has antiarrhythmic efficacy, but causes side effects in human beings. This compound appears to contribute to the effects of procainamide therapy and may be useful as an antiarrhythmic drug.
Am J Cardiol 1980 Jun
PMID:The clinical pharmacology and antiarrhythmic efficacy of acetylprocainamide in patients with arrhythmias. 615 64

The electrophysiologic properties of N-acetylprocainamide (NAPA) were studied in 10 patients undergoing cardiac catheterization. Each patient received two successive intravenous infusions: one loading infusion over 15 minutes and one maintenance infusion at a slower rate for 30 minutes. Eight patients received 10.5 mg/kg body weight and two received larger doses (16 and 21 mg/kg, respectively). NAPA plasma concentration was measured at 5 minute intervals from 0 to 25 minutes, and then at 15 and 30 minutes of the second infusion. Mean blood pressure and electrophysiologic data obtained by programmed stimulation were recorded before drug administration and at 15 and 30 minutes of the infusion when the concentration of NAPA was nearly constant in each patient (range 12 to 35 microgram/ml). NAPA decreased blood pressure (p less than 0.005), increased corrected Q-T interval (p less than 0.01) and increased the atrial and ventricular effective refractory periods from 267 +/- 40 to 307 +/- 41 ms (p less than 0.01) and from 278 +/- 37 to 301 +/- 32.8 ms (p less than 0.05), respectively. NAPA did not significantly change sinus cycle length or sinus nodal recovery time, conduction intervals (A-H, H-V, P-R, QRS), atrioventricular nodal functional refractory period or nodal Wenckebach cycle length. The patient receiving the largest dose experienced mild nausea when the plasma concentration was above 35 microgram/ml. These data show that the electrophysiology of NAPA in human beings is different from that reported for procainamide. At the plasma concentrations studied NAPA increases atrial and ventricular refractory periods without increasing cardiac conduction times
Am J Cardiol 1981 May
PMID:Electrophysiologic effects of N-acetylprocainamide in human beings. 616 85

To evaluate the potential benefit of MDL 17043, a new inotrope-vasodilator agent, in the short- and long-term management of severe heart failure, its hemodynamic effects were determined after both intravenous (cumulative average dose 3.7 mg/kg) and oral (average 18.4 mg/kg) administration in 38 patients with severe intractable heart failure. After both intravenous and oral therapy, cardiac index increased from a control value of 2.1 +/- 0.4 to 3.6 +/- 0.9 liters/min per m2, p less than 0.001 (intravenous) and from 2.2 +/- 0.5 to 3.4 +/- 0.6 liters/min per m2, p less than 0.001 (oral). Pulmonary capillary wedge pressure decreased from 26 +/- 6 to 14 +/- 7 mm Hg (p less than 0.001) and from 26 +/- 7 to 18 +/- 8 mm Hg (p less than 0.001) after intravenous and oral routes, respectively. Stroke volume index and stroke work index increased, and right atrial and pulmonary arterial pressures and systemic vascular resistance decreased by similar magnitude after both intravenous and oral MDL 17043 (all p less than 0.001). The hemodynamic effects persisted during 4 hours of observation. Thirty-seven patients were discharged while receiving MDL 17043 therapy and were followed up for a mean of 5.6 months (range 0.5 to 13). Thirty-three of the 37 patients had short-term improvement clinically by at least one New York Heart Association functional class. Undesirable effects, including nausea (35%), anorexia (27%), fluid retention (24%) and thrombocytopenia (less than 1%), necessitated discontinuation of therapy in 11 patients (30%) who were receiving multiple drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1984 Nov
PMID:Intravenous and oral MDL 17043 (a new inotrope-vasodilator agent) in congestive heart failure: hemodynamic and clinical evaluation in 38 patients. 623 76

Bepridil, a new calcium-channel blocking agent with an extended plasma elimination half-life of greater than 50 hours, was compared to placebo in 77 patients with confirmed coronary artery disease and chronic stable angina pectoris. The effects of bepridil were compared with those of placebo on angina frequency, nitroglycerin tablet use, the resting ECG and hemodynamics at rest and maximal exercise using a study design comprising 5 sequential 2-week single-blind treatment phases. After 2 weeks of placebo (phase 1), bepridil was given for 3 phases (2, 3 and 4) at total daily dosages of 200, 300 and 400 mg, respectively; the study was completed after a final reintroduction of placebo (phase 5). Within each phase once- and twice-daily regimens of bepridil were randomly compared. Bepridil (300 mg/day) reduced anginal frequency 68%, from 8.5 +/- 1.1 (standard error of the mean) to 2.7 +/- 0.7 attacks/week and nitroglycerin tablet use 76% (p less than 0.001). Bepridil improved exercise duration 26%, from 6.9 +/- 0.4 to 8.7 +/- 0.5 minutes (p less than 0.001) and exercise work 52%, from 2.7 +/- 0.3 to 4.1 +/- 0.4 kpm X 10(-3) (p less than 0.001) on a standardized treadmill protocol. Resting and peak exercise heart rate and blood pressure were unaffected by bepridil. The antianginal effects were similar with either once- or twice-daily treatment schedules. Minor side effects of nausea, epigastric discomfort and tremor were infrequent and there were no major side effects. The results of this large but preliminary, single-blind and short-term study suggest that bepridil is an effective and well tolerated antianginal agent when administered once daily.
Am J Cardiol 1984 Jan 01
PMID:Bepridil for chronic stable angina pectoris: results of a prospective multicenter, placebo-controlled, dose-ranging study in 77 patients. 636 86

The majority of sudden cardiac deaths in children occur in patients with prior arrhythmias and an abnormal heart. Amiodarone was given to 39 young patients (35 with an abnormal heart) with arrhythmias unresponsive to conventional treatment. Their age ranged from 6 weeks to 30 years with nine patients younger than 2 years of age. Atrial flutter was present in 16 patients, ventricular tachycardia in 14 patients and supraventricular tachycardia in 9 patients. The most common diagnosis (14 patients) was postoperative repair of congenital heart disease. The dose ranged from 2.5 to 21.6 mg/kg per day (mean 8.2). Elimination of arrhythmia (on 24 hour electrocardiography) occurred in 15 of 16 patients with atrial flutter, 11 of 14 with ventricular tachycardia and 5 of 9 with supraventricular tachycardia. Symptomatic side effects were: rash (three patients), headache (two patients), nausea (one patient) and peripheral neuropathy (one patient); seven patients had asymptomatic corneal microdeposits which normalized in all after the drug was discontinued. No side effects occurred in patients younger than 10 years of age. The following changed with treatment (p less than 0.05): heart rate decreased (three patients with atrial flutter and sick sinus syndrome required pacemaker implantation for bradycardia) and QTc increased; thyroxine (T4) and serum reverse triiodothyronine (T3) increased. During follow-up study (range 6 months to 3 years), 21 of the 39 patients continued to take amiodarone with complete control of arrhythmias, 9 were no longer taking the drug and 9 died (7 nonsudden and 2 sudden deaths). Amiodarone is an extremely effective treatment for infants and children with tachyarrhythmias resistant to conventional treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1984 Oct
PMID:Amiodarone treatment of critical arrhythmias in children and young adults. 638 28


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