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

The effects of propranolol, digoxin and combination therapy (/D) on the resting and exercise ECG were studied in ten normal subjects and 20 patients with coronary artery disease (CAD) given a sequence of oral placebo, propranolol, P/D, digoxin and placebo, for two week periods. Digoxin produced a significant decrease in T-wave amplitude and often resulted in ST segment depression in the resting ECG. Propranolol, digoxin, and P/D tended to decrease the QTc interval and prolong the PR interval. However, CAD patients were more sensitive to PR prolongation than normals while receiving propranolol or digoxin alone. Propranolol therapy did not significantly affect the ST segment of the exercise ECG in the normal subjects or the CAD patients without an ischemic control exercise ECG. By contrast, 50 per cent of the normal subjects developed "false-positive" ischemic ST segment responses to exercise while receiving digoxin of P/D and three of eight CAD patients without ischemic control exercise ST segments had a similar response to digoxin or P/D. In 12 CAD patients with ischemic control exercise ST segments, propranolol did not affect the amount of ST segment depression at the onset of angina or the maximum amount of ST segment depression. Digoxin or P/D both uniformly increased the maximum amount of ST segment depression which was greater with digoxin than P/D. However, the maximum heart rate on P/D was significantly reduced as compared to that on digoxin. It is concluded that (1) CAD patients are more sensitive to propranolol or digoxin-induced AV block than normals, (2) propranolol does not change the magnitude of ischemic exercise ST segment depression, (3) digoxin increases ischemic exercise ST segment depression and results in a high incidence of false-positive exercise tests, and (4) the addition of propranolol to digoxin attenuates the effects of digoxin on the exercise ST segment.
 ...
PMID:The effects of oral propranolol, digoxin and combination therapy on the resting and exercise electrocardiogram. 31 42

A healthy 18-year-old man was admitted to our unit two hours after a suicidal ingestion of 2 gm of verapamil. There was mild hypotension, depression of the sinus node, atrioventricular dissociation, changes of repolarization, and first-degree intranodal atrioventricular block (the His bundle electrogram revealed an atrio-His [A-H] interval of 155 msec). Twenty-four hours after ingestion, the patient was well, and the electrocardiogram was completely normal. This case gave us a good opporturnity to study the electrocardiologic effects of a huge oral dose of verapamil on a healthy young heart.
 ...
PMID:Acute intoxication with verapamil. 42 59

In the case described, necrosis of the atrial musculature led to rupture of the chamber. This was overlooked for 4 days until the patient died of ventricular rupture. This unusual complication of atrial infarction may be amenable to surgical repair if recognised in time. The high gain recording of P waves in the presence of AV block made it possible to evaluate the P wave changes during atrial infarction: (1) changes in the configuration and width of the P wave, probably resulting from intra-atrial conduction defect; (2) depression of the PR segment (0.04 to 0.07 mV); and (3) a previously unrecorded convexity in the first portion of the PR segment, in the leads in which the depression of the PR segment was observed.
 ...
PMID:Atrial infarction leading to rupture. 42 83

The electrocardiographic effects of imipramine hydrochloride at therapeutic plasma concentrations were determined in 44 depressed patients during a 6-week clinical outcome study of depression. During each week of the protocol, i.e., 2 weeks of control and 4 weeks of drug treatment, a standard 12-lead ECG, high-speed, high-fidelity ECG tracings, and a 24-hour continuous ECG recording were obtained. PR, QRS, and QTc intervals, T-wave amplitude, heart rate and frequency of ventricular premature depolarizations (VPDs) were measured. The plasma concentration of imipramine and desmethylimipramine was measured three times a week. Imipramine prolonged the PR (p less than 0.001), QRS (p less than 0.001) and QTc (p less than 0.001) intervals, increased the heart rate (p less than 0.001) and lowered T-wave amplitude (p less than 0.05) during the 4 weeks of treatment. No patient developed high-grade atrioventricular block or severe intraventricular conduction abnormalities. In addition, imipramine had a potent antiarrhythmic action in patients who were recovering from depression. Ten of 11 patients who had more than 10 VPDs/hour had 90% or greater arrhythmia suppression during antidepressant treatment with imipramine at plasma concentrations ranging from 100--302 ng/ml.
 ...
PMID:The electrocardiographic and antiarrhythmic effects of imipramine hydrochloride at therapeutic plasma concentrations. 48 38

An hemodynamic study has been performed in eight patients (age 68 +/- 7) suffering from complete atrioventricular block. They had to undergo the definitive implantation of a cardiac pace maker under general anesthesia. The fixed cardiac frequency may help to understand the effect of the anesthetic agent used on the cardiac muscle function. Ketamine is the only agent used directly at an initial intravenous dose of 3 mg.kg-1 followed by a perfusion in a constant rate of 0.20 mg.kg-1. min-1. Hemodynamic data (arterial pressure, pulmonary pressures, thermodilution cardiac output) are performed before induction, then every 5 minutes after induction for a 20 minute period. The absence of respiratory depression (PaCO2: 38 +/- 3 mm Hg) shows that hemodynamic changes are entirely due to ketamine. The peak of these changes takes place after 5 minutes (significant rise (p < 0.05) in systemic and pulmonary resistances, in systemic arterial pressure and in pulmonary arterial pressure). Stroke index decreases moderately. After 20 minutes all the parameters have returned to control values. Use of ketamine is not desirable for two reasons: 1 degree The rise of the afterload may alter the hemodynamic state which can be previously deteriorated in patients suffering from atrio-ventricular block. 2 degree Post-anesthetic agitation can displace the right ventricular electrode.
 ...
PMID:[Ketamine anesthesia for definitive implantation of a cardiac pace maker (author's transl)]. 55 78

The mechanism by which atrial systeole influences the efficacy of ventricular capture by a failing pacemaker was investigated in 12 dogs with atrioventricular heart block. Atrial systole caused facilitation of ventricular capture in eight dogs, and inhibition of capture in 10 dogs. Interpolating atrial extrasystoles caused an enhancement or depression of the hemodynamic performance of the atrial systole that affected the efficacy of the pacemaker stimulus. These interpolation experiments showed that atrial systole influenced the efficacy of capture by a mechanical mechanism and not by an electrotonic mechanism. Atrial systole probably caused motion of the endocardial pacing catheter and/or ventricular myocardium. This motion increased or decreased the contact between the pacing electrode and the endocardium with subsequent changes in the efficacy of capture. In three dogs with pacing through epicardial electrodes, atrial systole had no effect on the efficacy of capture.
 ...
PMID:The influence of atrial systole on ventricular capture by failing artificial pacemakers. II. Experimental observations. 63 87

Studies were performed to determine the chronotropic effect of acetylstrophanthidin during constant infusion through cannulation of the sinus nodal artery. Ten mongrel dogs weighing 13.5 to 18 kg were studied under sodium thiamylal anesthesia. Epicardial atrial and ventricular electrograms were recorded. The sinus nodal artery was cannulated and infused for 20 minutes at a rate of 2 cc/min with a solution containing acetylstrophanthidin, 0.5 microng/cc. Mean results for the group of 10 animals were determined. There was a gradual acceleration of the atrial rate of 45 beats/min after 6 to 8 minutes of infusion. The peak atrial rate of 175 beats/min was achieved by 10 to 12 minutes. This tachycardia persisted for 2 to 4 minutes without atrioventricular block or premature beats. By 12 to 14 minutes, there was a gradual slowing of atrial rate followed by bradycardia, sinus pauses and atrial arrest. Sinus nodal arterial infusion of acetylstrophanthidin produces an initial positive chronotropic effect and, if maintained, a depression of atrial rate and, terminally, atrial arrest. The gradual time course of development and decline of the tachycardia suggests that the "paroxysmal" atrial tachycardia caused by digitalis excess is the result of enhanced pacemaker automatically rather than reentry, and thus is not truly paroxysmal.
 ...
PMID:Chronotropic effect of acetylstrophanthidin infusion into the canine sinus nodal artery. 85 29

Experiments were performed on the isolated rabbit hearts and also on the hearts with complete atrioventricular block; a study was made of the effect of an excess or deficiency of the sulfhydryl groups on the automatism of the cardiac pace makers. Unithiol and cysteine in concentrations of 1-10(-6)-1-10(-4) g/ml were used as donors of sulfhydryl groups; deficiency of these groups was induced by the alloxan administration in concentrations of 1-10(-5)-5-10(-5) g/ml. Changes in the sulfhydryl group content produced no marked effect on the automatism of the synoatrial node. An excess of sulfhydryl groups promoted poststimulation depression of the automatism of the potential pace makers of the cardiac ventricles and could lead to the origination of Luciani's periods. On the contrary, in case of a deficiency of the sulfhydryl groups there was a sharp elevation of the automatism of the ventricular pace makers, the atrioventricular conduction became disturbed, and the poststimulation depression of the automatism became considerably diminished. Disturbances of the cardiac activity caused by the sulfhydryl group deficiency were completely eliminated by unithiol or cysteine.
 ...
PMID:[Effect of sulfhydryl compounds on the automatism of the pacemakers]. 102 91

Measurement of the sinus node recovery time has been proposed as a diagnostic tool for recognition of the sick sinus syndrome. The latter is most frequently encountered in elderly patients with hypertension, coronary heart disease, and atherosclerosis. In order to provide normal values for the sinus node recovery time in this particular population group, atrial pacing studies were carried out in 30 subjects over 50 years of age, all with peripheral vascular disease and some with angina pectoris (10), residua of infarction (6), or hypertension (7). On stimulation, 7 patients maintained a I:I atrioventricular conduction up to the rate of 180/min. Second degree atrioventricular block developed in all other cases. On six occasions, Wenckebach's periods appeared at the relatively slow pacing rate of 120/min. The maximum postoverdrive pause ranged from 680 to 1600 ms with an average of 1100 ms plus or minus 190 (10). For each pacing speed, a correlation was found between the duration of the pause and the control intrinsic cardiac rate, longer pauses being associated with longer resting PP intervals. Beyond 120/min, the duration of the pause was seen to shorten progressively as the driving rate was increased. Finally, the behavior of the sinus node pacemaker following interruption of pacing showed individual variations. After pacing at relatively slow rates, a prompt return to near control values was consistently observed, whereas, after fast rates of driving, a phase of secondary depression developed in about one-half of the studied cases.
 ...
PMID:Sinus node recovery time in the elderly. 112 18

Intravenous injection of the thermostable direct hemolysin (lethal toxin) produced by Vibrio parahaemolyticus caused rapid death of rats. Studies by electroencephalography and electrocardiography showed that after intravenous injection of the toxin the electroencephalogram remained normal for quite a long time after the heart of the animals had stopped beating. Depression of intraatrial and intraventricular conduction of electrical activation, including atrioventricular block, was observed in electrocardiograms of animals injected with the toxin. The toxin was also found to be toxic to cultured mouse heart cells. When it was added to the medium, the beating rhythm of the cultured heart cells increased temporarily and then soon stopped abruptly. The effect of the toxin on cultured mouse heart cells was blocked by preincubation of the toxin with a ganglioside mixture. From these results it is concluded that the thermostable direct hemolysin (lethal toxin) had cardiotoxic activity, and thus administration of the toxin causes rapid death of animals.
 ...
PMID:Demonstration of the cardiotoxicity of the thermostable direct hemolysin (lethal toxin) produced by Vibrio parahaemolyticus. 124 68


1 2 3 4 5 6 7 8 9 10 Next >>