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 influence of the new antiarrhythmic agent Propafenon on cardiac conduction and sinus node function was studied by using His-bundle recordings and atrial stimulation in 14 patients with normal and diseases conduction system. Intravenous administration of Propafenon in therapeutic dose (1-2 mg/kg) produced a significant prolongation of the atrioventricular conduction time. Increase of the A-H interval was observed in 13 of 14 subjects during sinus rhythm. Second degree A-V block (Wenckebach form) during atrial stimulation occurred at lower frequencies after administration of the drug. The impulse propagagion within the His-Purkinje system was depressed significantly (H-V interval in 8, H-S interval in 10 of 14 subjects). Propafenon did not cause any alteration in intraatrial conduction, but depression of the sinus node automaticity was noted. Total reversal of the drug induced prolonged atrioventricular conduction and a decrease of the sinus rate was seen after administration of orciprenaline. Beta-adrenergic receptor blocking and local anaesthetic direct membrane actions are discussed as possible cause of the prolongation of atrioventricular and intraventricular conduction.
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PMID:[Effect of the antiarrhythmic agent propaphenone on cardiac conduction. clinical studies using bundle of his electrography]. 23 45

We used intracellular microelectrodes to study the electrophysiological effects of combinations of components of ischemia and their relation to the occurrence of ventricular arrhythmias in the specialized conducting system of isolated canine right ventricles. The middle area of the free wall was exposed to various test solutions in the center compartment of a three-chambered bath; the base and apex of the preparation were superfused with normal Tyrode's solution in the outer control compartments. Hypoxia (Po2 40 mm Hg), lactic acidosis (pH 6.5), and orciprenaline (10(-6) M), either alone or combined, failed to affect the action potential amplitude or the conduction velocity of the subendocardial fibers, and no arrhythmias occurred. The action potential duration and the effective refractory period were markedly prolonged by lactic acidosis. Exposure of the test regions to 15 mM K+ plus orciprenaline resulted in marked decreases in action potential amplitude and conduction velocity. Abnormalities of impulse transmission through the depressed area included high degrees of rate-dependent block, one-way block, warming-up phenomenon, and the Wenckebach phenomenon. Such conditions regularly provoked the appearance of single, sustained, or concealed reentrant depolarizations. The combined effects of hypoxia, 15 mM K+, and orciprenaline resulted in further depression of the already depressed action potential in the depolarized fibers. Our results indicate that regional increases of extracellular K+ may be the predominant factor of the components of ischemia we studied which facilitates the initiation of reentrant arrhythmias.
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PMID:Effects of some components of ischemia on electrical activity and reentry in the canine ventricular conducting system. 42 79

A patient is presented who had two paroxysmal supraventricular tachycardias, one slow and incessant and the other fast. Both paroxysmal tachycardias appeared to be atrioventricular (A-V) reentrant, with anterograde conduction by way of a normal A-V pathway. Two pathways conducting in retrograde manner were demonstrated, characterized by different conduction times (fast and slow), identical abnormal atrial activation sequence and A-V nodal-like properties (retrograde Wenckebach periodicity with rapid ventricular pacing, and depression with ouabain and propranolol). Thus, there appeared to be two anomalous A-V bundles with nodal-like properties conducting in retrograde fashion. Whether the paroxysmal tachycardia was fast or slow depended on which of these pathways was utilized. Spontaneous cure of incessant paroxysmal tachycardia was observed and coincided with unexplained total loss of ability for ventriculoatrial conduction.
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PMID:Multiple reentrant tachycardias due to retrograde conduction of dual atrioventricular bundles with atrioventricular nodal-like properties. 45 41

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.
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PMID:Sinus node recovery time in the elderly. 112 18

The effects of slow-release gallopamil (100 mg b.i.d.) were studied on exercise-induced ST-segment depression as well as on spontaneous myocardial ischemia detected by long-term electrocardiography (ECG) monitoring for 48 h in 26 patients with coronary artery disease and angina pectoris. Eight patients had to be excluded (because of paroxysmal atrial fibrillation in four patients, development of unstable angina pectoris in three patients, and frequent ventricular premature beats in one patient). In the remaining 18 patients, gallopamil led to an increase of work load (W x min) evaluated by bicycle ergometry, paralleled by an increase of exercise duration until the occurrence of ST-segment depression of > or = 0.1 mV in the nonblinded part of the trial. The number of spontaneous episodes of myocardial ischemia during long-term ECG recording, ranging from 0 to 14 during control, decreased in patients with two or more episodes during control, paralleled by a decrease in the total duration of ischemic episodes and a decrease in the ischemic score (duration of episodes x maximal ST-segment depression). During long-term ECG monitoring, we observed asymptomatic episodes of spontaneous second degree atrioventricular block of the Wenckebach type in three patients. No other adverse effects of slow-release gallopamil were observed. Therefore, these preliminary results of the non-blinded protocol confirm the anti-ischemic effects of slow-release gallopamil given 100 mg b.i.d.; however, these promising results will have to be confirmed in the consecutive double-blind, placebo-controlled part of the trial.
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PMID:Slow-release gallopamil evaluated by exercise test and long-term electrocardiography. 128 62

Disopyramide is a Vaughan-Williams class Ia antiarrhythmic, which is distinguished by its anticholinergic activity, which is due to its active metabolite: mono-N-alkyl disopyramide. In cells with a rapid response, such as those in the His-Purkinje tissue, it depresses conduction. In slow-responding cells (sinus node and Tawara's node) direct depression of conduction and automatism, and anticholinergic stimulation have opposing effects. In terms of clinical electrophysiology, this is a Touboul class IIa compound: and action mainly on the His-Purkinje system involving extension of the conduction time and of the refractory time. Nodal conduction is improved according to measurement of the alternate Wenckebach; according to studies of the denervated heart in transplanted patients, there is a depressant effect on automatism and conduction at all levels, but the vagolytic effect corrects this activity at Tawara's node. Clinical trials have demonstrated the absence of any deterioration, and in some cases and actual improvement of nodal conduction disorders in response to disopyramide and good safety in the presence of non-major intraventricular conduction problems (such as bundle branch block). In practice, these properties mean that moderate nodal conductive disorders and simple bundle branch block do not constitute an obstacle to the use of disopyramide. In junctional tachycardia, it is particularly indicated for use in tachycardia involving an accessory pathway, but is also effective in intranodal tachycardia due to its twofold action.
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PMID:[Effects of disopyramide on normal and pathological atrioventricular conduction]. 129 85

Age effects on responses to calcium channel blockade with nifedipine were studied in isolated Langendorff-perfused Fischer 344 rat hearts. Responses to 25 min of perfusion with nifedipine concentrations of 0, 25, 50, 75, and 100 ng/ml were studied in hearts from 11 mature (6 months) and 13 senescent (23-27 months) male F344 rats. Nifedipine produced significant increases in the atrial cycle length (p less than 0.001), paced atrioventricular (AV) conduction time (p less than 0.001), AV Wenckebach cycle length (p less than 0.001), left ventricular (LV) diastolic pressure (p less than 0.001), and decreases in LV systolic pressure (p less than 0.001) and peak dP/dt (p less than 0.001) in hearts from both mature and senescent rats. Greater decreases in the atrial rate (p less than 0.05) and depression of peak dP/dt (p less than 0.05) were detected in senescent vs. mature rat hearts. No age difference in responses of AV conduction parameters were detected although increases in the AV Wenckebach cycle length appeared to be greater in senescent hearts at concentrations greater than 75 ng/ml.
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PMID:The effects of aging on the electrophysiologic and hemodynamic responses to nifedipine in isolated perfused hearts. 138 Oct 13

The prognosis of coronary artery obstruction was studied in patients with Kawasaki disease. Between May 1973 and December 1987, coronary artery obstruction was diagnosed by coronary angiography in 30 patients (21 males, 9 females), of whom, only 8 (26.7%) had clinical symptoms. One patient died after 9 years of illness. Two complained of frequent chest pain, which disappeared after bypass surgery in one case and spontaneously in the other. Five had symptomatic myocardial infarction. Myocardial ischemia was diagnosed in 31.8% by treadmill stress testing, but was well demonstrated in 85.7% by thallium-201 myocardial tomography. Frequent ventricular premature beats, Wenckebach-type atrioventricular block, and ST-segment depression accompanied by chest pain were recognized by 24-h Holter monitoring. In the past, the methods used to determine the prognosis of Kawasaki disease patients with coronary artery obstruction were not adequate. However, the examinations used in this study revealed an improved ability to determine the prognosis in this disease. Myocardial tomography, in particular, provided a more accurate evaluation of myocardial damage. Ventricular arrhythmias seem to be a serious problem in these patients. Therefore, careful observation using these tests, especially myocardial tomography and Holter monitoring, should be done even if the patients are free of symptoms.
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PMID:Long-term prognosis of Kawasaki disease patients with coronary artery obstruction. 258 78

Clonidine can produce symptomatic sinus bradycardia or atrioventricular (AV) block in some patients. Electrophysiologic studies have been performed after intravenous clonidine in patients showing such side effects; these have demonstrated variable depression of sinus and AV nodal function. We have evaluated the electrophysiologic and hemodynamic effects of chronic oral treatment with either clonidine (0.2 to 0.5 mg every 12 hours; n = 7) or another centrally active alpha 2-agonist, tiamenidine (0.5 to 1.5 mg every 12 hours; n = 7), in otherwise healthy hypertensive human volunteers. At dosages that modestly lowered diastolic blood pressure, both agents significantly slowed sinus rate and increased the atrial pacing rate producing AV nodal Wenckebach. Clonidine also significantly increased corrected sinus node recovery time and lowered cardiac output while similar (but statistically insignificant) trends were seen with tiamenidine. We conclude that chronic oral treatment with these alpha 2-agonists depresses sinus and AV nodal function in virtually all subjects, including those without manifest conduction system disease.
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PMID:Electrophysiologic and hemodynamic effects of chronic oral therapy with the alpha 2-agonists clonidine and tiamenidine in hypertensive volunteers. 289 89

In ischemic heart disease, the left ventricle has been considered the main target of an imbalance between myocardial oxygen supply and demand. Accordingly, the approach to ischemia has been directed at the evaluation of the left ventricle. The aim of this study was to assess the relative involvement of the left and right ventricle in patients with isolated right coronary artery stenosis. We studied 20 patients with a clinical history of effort angina (15 male, 5 female, mean age 54.1 +/- 6.2) using radionuclide angiography and atrial pacing. Findings were compared with those of 6 normal subjects that were paced at the maximal heart rate of 150 beats/min. Atrial pacing was interrupted because of diagnostic ST segment depression in 8 patients, Wenckebach type atrioventricular block in 1, chest pain without electrocardiographic changes in 4 and the achievement of the maximal prefixed heart rate of 150 beats/minute in 7. With respect to control conditions, during atrial pacing right ventricular ejection fraction declined from 46.8 +/- 6.8% to 37.4 +/- 8.1% (p less than 0.001), while no significant change was observed in left ventricular ejection fraction values (55.2 +/- 4.5% and 51.1 +/- 10.2% respectively). During atrial pacing, left ventricular peak filling rate increased from 1.77 +/- 0.53 to 4.71 +/- 1.8 end-diastolic volumes/second (p less than 0.0001). Qualitative analysis of regional wall motion showed a right ventricular dysfunction in 19/20 patients; this was prevalent in 9 and involving also the left ventricle in 10; an isolated impairment of the left ventricle was observed in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Right ventricular dysfunction in demand-induced ischemia in patients with isolated right coronary artery disease: a radioisotope study]. 325 39


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