Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute effects on exercise tolerance and electrocardiographic ischaemia of felodipine and diltiazem, alone or in combination, were investigated in 12 patients with documented stable effort-induced angina pectoris. After being withdrawn from their previous antianginal treatments, patients received a single oral dose of felodipine 10 mg, diltiazem 60 mg, their combination or placebo on four different days, according to a double-blind, 4 x 4 latin-square design. Exercise time to ischaemic threshold (ST-segment depression = 1 mm) and to peak exercise was significantly prolonged by the felodipine-diltiazem combination (492 and 504 s, respectively) against placebo (301 and 370 s, both P less than 0.01), felodipine alone (381 and 428 s, both P less than 0.01) and diltiazem alone (367 and 422 s, both P less than 0.01). The effects on total work followed a similar pattern. In comparison with placebo, the administration of felodipine and diltiazem alone significantly increased exercise duration as well as total work to ischaemic threshold and to peak exercise, with no differences between the two drugs. Systolic blood pressure during exercise was not affected by any of the treatments. However, in comparison with both placebo and diltiazem, the combination induced an increase (P less than 0.01) in heart rate during exercise. One patient suffered from symptomatic hypotension with the combination, and another had sinus tachycardia after felodipine. In conclusion, the acute concomitant administration of felodipine and diltiazem in patients with stable effort angina induces a marked improvement in exercise tolerance in comparison with placebo, felodipine alone and diltiazem alone. However, the benefit/risk profile of such a combination requires further, long-term investigation.
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PMID:Acute effects on exercise tolerance of felodipine and diltiazem, alone and in combination, in stable effort angina. 200 94

We compared electrocardiographic abnormalities and plasma norepinephrine concentrations in 40 patients with subarachnoid hemorrhage within the first 24 hours, at 72 hours, and after 1 week. In 20 patients with high plasma norepinephrine concentrations within the first 24 hours, sinus tachycardia (p less than 0.02) and negative T waves (p less than 0.01) were more frequent than in the 20 patients with normal plasma norepinephrine concentrations. After 72 hours, only sinus tachycardia (p less than 0.03) was found with increased frequency in the 26 patients with high plasma norepinephrine concentrations. Although 24 patients had high plasma norepinephrine concentrations after 1 week, we found no differences in the frequency of electrocardiographic abnormalities compared to patients with normal plasma norepinephrine. However, QTc prolongation, U waves, ST depression, and arrhythmias were found with similar frequency in patients with both high and normal plasma norepinephrine concentrations. We conclude that, with the exception of sinus tachycardia and negative T waves, electrocardiographic changes in patients with subarachnoid hemorrhage do not depend on elevated plasma norepinephrine concentrations.
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PMID:Effect of elevated plasma norepinephrine on electrocardiographic changes in subarachnoid hemorrhage. 175 60

A cooperative prospective study of consecutive cases of carbamazepine overdose was conducted to determine if serum levels were predictive of toxicity and if risk factors such as age, chronic exposure, or previous disorder or cardiovascular disease could be used as prognostic indicators. Seventy-three consecutive cases were collected from two regional certified poison control centers from January 1989 to August 1989. There were 25 exposures in children less than 6 yrs., 11 exposures in adolescents, and 37 exposures in adults. Ten adult cases and one adolescent case were excluded from the study due to the presence of coingestants or inadequate information. Peak measured serum levels ranged from 0.3 to 56 mcg/ml. Using the presence of coma, seizure activity or respiratory depression requiring mechanical ventilation as measures of toxicity, we found poor correlation between rising serum levels of carbamazepine and toxicity. Increased serum levels of carbamazepine did appear to correlate with increased hospital stay, but not with ICU stay. History of a seizure disorder appears to pose increased risk of a seizure in carbamazepine overdose. In this series chronic exposure to carbamazepine did not appear to increase the risk of coma or respiratory depression for a given toxic serum level and may add some protective effect. Serum levels below 40 mcg/ml do not appear to accurately predict the severity of toxicity. Cardiac conduction defects were rare (one child). Anticholinergic findings, as evidence by decreased bowel motility and sinus tachycardia were common. Previous cardiovascular disease and age did not appear to be important prognostic indicators.
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PMID:Carbamazepine overdose: a prospective study of serum levels and toxicity. 226 99

The efficacy of beta adrenergic blocking agents has been observed in the treatment of a variety of cardiac arrhythmias. Electrophysiological experiments demonstrated that beta receptor blocking drugs prevent catecholamine-induced alterations of the transmembrane action potential. Clinically used beta blocking agents are effective in preventing arrhythmias provoked by sympathetic stimulation such as sinus tachycardia, paroxysmal junctional tachycardia, atrial, nodal, and ventricular premature contractions. Beta receptor blocking drugs are especially useful in tachycardias based on hyperkinetic heart syndrome and in exercise-induced premature beats in patients suffering from coronary heart disease. Beta blocking agents are--at least in our hands--most useful in combination with class I antiarrhythmic drugs with the intention to reduce the dosage--i.e. the side effects--of various antiarrhythmic drugs. In hyperthyroidism beta adrenergic blocking agents are effective complementary to the specific treatment. In cases of intoxication with beta blocking drugs complicated by myocardial depression and severe bradycardia glucagon must be regarded as a very useful compound.
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PMID:[Spectrum of effects of beta receptor blockade in cardiac arrhythmias]. 243 70

In this report, abnormal changes of 1266 ECG were assessed during antipsyhotic drugs medication. It was founded that cardiac dysrhythmia (sinus tachycardia) in the first place, T wave changes and depression of S-T segment in the next. The rate of abnormal ECG with chlorpromazine seemed to be higher than other drugs. Factors of dosage and time of treatment were non-significant.
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PMID:[Cardiotoxicity of antipsychotic drugs: abnormal ECG in 1266 cases]. 257 66

The antihypertensive efficacy and safety of IV labetalol were evaluated and compared with the efficacy and safety of IV hydralazine in the treatment of postoperative hypertension. Twenty patients undergoing major noncardiac surgery were entered into the study. Patients were randomized and treated for postoperative hypertension with either labetalol (n = 10) or hydralazine (n = 10). Labetalol and hydralazine both produced significant reductions in arterial blood pressure (p less than 0.001) within 10 minutes, which lasted at least 2 hours. In addition, labetalol produced a significant reduction in the heart rate and rate-pressure product without creating any adverse effects. In contrast, hydralazine produced significant sinus tachycardia requiring IV propranolol in three patients, two of whom developed transient ST segment depression. These results indicate that labetalol is safe and effective for the control of postoperative hypertension, especially in those patients who are least able to tolerate tachycardia.
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PMID:Comparative hemodynamic effects of labetalol and hydralazine in the treatment of postoperative hypertension. 262 88

To investigate the potential myocardial ischemic effects of ritodrine, we studied 36 singleton and four twin preterm pregnancies during ritodrine therapy. We serially determined serum creatinine phosphokinase (CPK-MB fraction) and lactic dehydrogenase isoenzymes and performed electrocardiography before and during ritodrine infusion and again within the first 24 hours of oral drug therapy. We observed that serum CPK-MB and lactic dehydrogenase isoenzymes remained within the normal range during therapy periods. The incidence of sinus tachycardia and non-specific T wave changes were 100% and 25%, respectively. In three of four twin pregnancies, ST-T segment depression in leads I, V4, V5, and V6 of the electrocardiogram was noted. Our study suggests that (1) the recommended ritodrine regimen does not produce direct myocardial damage, and (2) ritodrine may cause cardiac ischemia as determined by electrocardiography, which theoretically would progress to myocardial damage if not treated properly.
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PMID:Cardiac isoenzymes and electrocardiographic changes during ritodrine tocolysis. 224 70

A patient with resting heart rate over 100 beats per minute (bpm) displayed 1.5-2 mm ST segment depression in her ECG during daily activities. She had unprovoked further increase in her heart rate up to 145 bpm, and during these episodes, her ECG displayed further ST segment depression up to 3 mm and of 0.12 second duration. An organic cause could not be found to explain her sinus tachycardia. Results of all laboratory investigations, including coronary angiography, were normal. It was observed that during an episode of reflex vagotonia, when her heart rate was below 95 bpm, her previously depressed ST segments became isoelectric. With the thought that this patient's ST segment depression was rate-dependent, carotid sinus massage was performed, and when the heart rate slowed to 95 bpm her depressed ST segments became isoelectric. The same response was accomplished with beta blockers. Sympathetic hyperactivity was thought to be the most likely mechanism of ST segment depression in this patient. A critical increase in heart rate caused these ECG abnormalities.
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PMID:Rate-dependent ST segment depression--a case report. 276 12

Electrocardiographic (ECG) changes in nine patients under continuous ECG monitoring before, during and after balloon dilatation for achalasia were followed; of these, three had ischaemic heart disease (IHD). One or several abnormalities including sinus tachycardia, supraventricular or ventricular ectopic beats, S-T segment depression and T-wave flattening appeared during the procedure; these were more commonly found in patients with IHD. Despite the high incidence of recorded ECG abnormalities, these were transient, and no treatment was needed. However, it seems advisable to have resuscitation equipment and emergency drugs available during balloon dilatation for achalasia, particularly when this procedure is performed in patients with IHD.
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PMID:Continuous electrocardiographic monitoring during balloon dilatation in achalasia. 281 33

The study of the tapes of ambulatory patients who died while wearing Holter devices allows us to know the terminal electrical events of death in these cases and which are the electrical triggering mechanisms leading to the terminal event. From the evaluation of seven published series with 10 or more cases, we can see that the most frequent causes of sudden death are ventricular tachyarrhythmias (84% of cases) and bradyarrhythmias (16%). VF was the most frequent ventricular tachyarrhythmia, usually secondary to VT. The rest were due to torsades de pointes in patients often without heart disease but who were taking antiarrhythmic drugs. The VT leading to VF was often preceded by sinus tachycardia or new atrial tachyarrhythmia. Only a small percentage of patients presented ischemic ST changes. In patients who died due to bradyarrhythmias, this was more often due to sinus depression than to atrioventricular block.
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PMID:Ambulatory sudden cardiac death: mechanisms of production of fatal arrhythmia on the basis of data from 157 cases. 291 68


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