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)

Twenty four hour electrocardiograms in 20 patients with Bartter's syndrome, a disorder associated with chronic potassium deficiency, were analysed for atrial and ventricular extrasystoles, pauses (RR interval greater than 2 s), and heart rate. The 12 lead resting electrocardiogram was also evaluated. There were slight electrocardiographic changes with ST segment depression (greater than or equal to - 0.5 mm) in seven patients, flat or low amplitude T waves in seven, and U waves (greater than or equal to + 1.0 mm) in three patients. The QT interval was prolonged in 18 patients. Nine patients had one or more ventricular extrasystoles in 24 hours. Only two patients had more than 200 ventricular extrasystoles in 24 hours. No patient had ventricular tachycardia. A total of nine patients had one or more atrial extrasystoles in 24 hours, but only one patient had more than 200 in 24 hours. One patient had an attack of non-sustained supraventricular tachycardia. No patient had pauses. Dangerous tachycardia was rare in these patients with chronic potassium deficiency caused by Bartter's syndrome. The general pattern of slight electrocardiographic changes may reflect an adaptation of the myocardium to hypokalaemia. Further studies are, however, needed to determine whether these findings are relevant to long term prognosis.
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PMID:Electrocardiographic findings and frequency of arrhythmias in Bartter's syndrome. 246 81

The clinical features of 10 children, in whom the diagnosis of a cardiac tumor has been made, are reviewed. There were nonspecific systolic murmurs in 9 patients, depression of the S-T segment in the ECG of 7 children, and premature extrasystoles or supraventricular tachycardia in 4 children. X-ray always showed mild to moderate enlargement of the heart, but an abnormal contour could be detected only in 2 of the patients. While findings of cardiac catheterization were unspecific, the diagnosis could be made angiographically in 8 cases. Invasive studies, however, are now only indicated, if a proper diagnosis cannot be made by means of echocardiography. The diagnosis should be suspected in children with a nonspecific murmur, cardiomegaly and ECG-changes. Usually the diagnosis of a cardiac tumor is an indication for operation.
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PMID:[Diagnosis and differential diagnosis of heart tumors in infancy and childhood]. 270 73

The electrophysiologic effects and efficacy of diltiazem were evaluated with programmed electrical stimulation of the heart in 12 patients with supraventricular re-entrant tachycardia (five with atrioventricular nodal tachycardia and seven with circus movement tachycardia the accessory pathway being concealed in 4). Diltiazem was infused over 1 minute at the dose of 0.25 mg/kg and the electrophysiologic parameters were evaluated at 5 and 30 minutes. Diltiazem prolonged the AH interval from 83.5 +/- 58 to 99 +/- 55 msec (P less than 0.05), effective and functional refractory periods of atrioventricular node from 244 +/- 40 to 268 +/- 56 msec (P less than 0.05) and from 432 +/- 124 to 468 +/- 130 msec (P less than 0.005) respectively, lowered the atrial pacing rate inducing second-degree atrioventricular block from 159 +/- 32 to 134 +/- 33 beats/min (P less than 0.005) and decreased systolic and diastolic blood pressure from 143.5 +/- 33 to 132.5 +/- 22 mm Hg (P less than 0.05) and from 90 +/- 15 to 82.5 +/- 9 (P less than 0.05), respectively. Diltiazem prevented the reinduction of the tachycardia in 4 of 5 patients with atrioventricular nodal tachycardia and in 4 of 7 with circus movement tachycardia. The mechanism of action of diltiazem consisted of depression of conduction in atrioventricular node in anterograde fashion while there were no effects on refractoriness of the accessory pathway. The drug was well tolerated with no adverse effects. Diltiazem, therefore, appears an effective and safe drug in the acute treatment of re-entrant supraventricular tachycardia.
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PMID:Intravenous diltiazem in patients with paroxysmal re-entrant supraventricular tachycardia. 272 88

During paroxysmal supraventricular tachycardia, patients frequently experience chest pain and marked ST segment depression suggesting acute myocardial ischemia. The purpose of this study was to assess whether ST depression during supraventricular tachycardia is caused by myocardial ischemia as reflected by net myocardial lactate production. Twenty-five patients (14 men, 11 women) who had a history of paroxysmal supraventricular tachycardia and a mean age (+/- SD) of 38 +/- 14 years underwent electrophysiologic testing. Twenty-four of these patients had no evidence of coronary disease, whereas one patient had undergone previous coronary bypass surgery. Nineteen patients had orthodromic and six patients had atrioventricular node reentrant tachycardias. A 12 lead electrocardiogram and simultaneous femoral artery and coronary sinus blood samples for lactate determinations were obtained at baseline and at 5 and 10 min of supraventricular tachycardia. Mean baseline heart rate of 83 +/- 12 beats/min increased to 180 +/- 25 beats/min during supraventricular tachycardia. All patients had 1 to 8 mm of ST segment depression in 1 to 9 of the 12 leads. Chest pain occurred in 64% of patients during supraventricular tachycardia. Baseline myocardial lactate extraction was 28 +/- 13% with no significant change at 5 or 10 min of tachycardia. In contrast, in a comparison group of seven patients with known coronary artery disease, atrial pacing at 168 +/- 26 beats/min in five patients resulted in greater than or equal to 1 mm ST depression in 2 to 7 of the 12 leads and a change in lactate extraction from a baseline of 29 +/- 13% to -27 +/- 20% (p less than 0.05) indicating net myocardial lactate production.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of ST segment depression during paroxysmal supraventricular tachycardia. 339 31

During systemic hyperthermia (42 degrees C), depression of ST segments or T wave changes in the left precordial leads were noticed in 56% of patients, and 29% of cases showed right bundle branch block. Supraventricular tachycardia was found in 26% and temporary deviation of mean frontal vector to the left axis was observed in 15%. These changes disappeared following recovery to normal temperature. The ECG findings for any particular patient were similar even during a second period of hyperthermia. Pulse rate became elevated by 1.7 times, and cardiac output became up to 2.4 times higher at 42 degrees C.
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PMID:[Electrocardiographic and hemodynamic changes during systemic hyperthermia (42 degrees C)]. 372 56

The electrophysiologic effects of intravenous diltiazem were evaluated in 10 patients with recurrent supraventricular tachycardias. The tachycardia incorporated an accessory pathway in 7 patients and was due to AV nodal reentry in 3 patients. Diltiazem 0.25 mg/kg was administered intravenously over 5 minutes during sustained supraventricular tachycardia. Programmed electrical stimulation was used to restore sinus rhythm if diltiazem failed to terminate the arrhythmia within 10 minutes. Conduction intervals, refractory periods and tachycardia characteristics were evaluated before and immediately after drug administration. Diltiazem did not significantly modify sinus cycle length, AH and HV intervals. Atrial and ventricular effective refractory periods were similar before and after diltiazem. The effective refractory period of the AV node was prolonged by 42 msec after diltiazem (p less than 0.05). Diltiazem increased the tachycardia cycle length from 320 +/- 41 to 353 +/- 36 msec (p less than 0.01) but terminated the arrhythmia in only 2 patients. After diltiazem, supraventricular tachycardia could not be reinitiated in only 2 patients and the tachycardia initiating window was not significantly reduced (56 +/- 26 to 41 +/- 33 msec). The infusion of diltiazem was accomplished without side effects. Thus, 0.25 mg/kg of intravenous diltiazem produces a modest depression of AV nodal function and is not very effective in terminating supraventricular tachycardia or preventing its initiation in this study population. Further studies using higher doses of intravenous diltiazem would be useful to determine its maximal therapeutic benefit in patients with recurrent supraventricular tachycardias.
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PMID:Electrophysiologic effects of intravenous diltiazem in patients with recurrent supraventricular tachycardias. 384 93

Low-dose (7 mg/kg per day) disopyramide administration to arrhythmic chagasic patients decreased the frequency of ventricular extrasystoles in 4 of 17 patients (24%) and suppressed most complex ventricular arrhythmias in 12 of 15 patients (80%). This assessment was made from 72-h continuous Holter monitoring recorded during the course of this double blind, placebo-controlled randomized crossover study. Seven patients (41%) complained of anticholinergic side effects, but no contractile or conduction system depression was seen. Amiodarone (200 mg) given on a single blind, placebo-controlled basis to 9 of these patients reduced the frequency of ventricular extrasystoles in 6 of 9 patients (67%) and suppressed complex ventricular ectopy in 6 of 7 patients (85%). One patient was unable to tolerate this drug (11%). Both drugs seemed less effective in controlling supraventricular arrhythmias, although disopyramide eliminated paroxysms of supraventricular tachycardia in 9 of 13 (69%) and amiodarone in all 6 patients with this arrhythmia. Amiodarone appears to be a better antiarrhythmic drug for chagasic patients, due to its greater effectiveness and lower incidence of side effects.
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PMID:Effect of low oral doses of disopyramide and amiodarone on ventricular and atrial arrhythmias of chagasic patients with advanced myocardial damage. 390 29

To determine the electrophysiologic effects of stellate ganglion (SG) block on the human heart, the two SGs were anesthetized separately, with a 24-hour interval between the two procedures, in 13 patients with episodes of supraventricular tachycardia (six had Kent bundles). Left SG block caused: (1) a lengthening of the AH interval, measured at fixed atrial rates of 10 +/- 12 msec (p less than 0.01); (2) a marked depression of the VA conduction in six of the seven patients with measurable VA interval (in two patients it produced complete VA block); (3) a slowing of 20 to 40 msec of the cycle of an electrically induced reciprocating tachycardia; and (4) failure to modify the QT interval duration. In contrast, right SG block produced asymmetric or opposite changes and prolonged the QT interval (7.6 +/- 8.8 msec, p less than 0.05). Atrial and ventricular refractoriness was not significantly altered by SG block. Retrograde effective refractory period of the Kent bundle changed 20 to 60 msec after unilateral SG blockade. Thus, this study suggests that the human conduction system and the Kent bundles receive an appreciable sympathetic influence from the SG. Like experimental studies, we also found an asymmetric response to unilateral SG block and a dominance, in most of our patients, of the left SG. The influence on myocardial refractoriness was less apparent.
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PMID:Electrophysiologic effects of unilateral right and left stellate ganglion block on the human heart. 396 32

Electrophysiologic studies were performed in 11 patients with atrioventricular (AV) nodal reentrant tachycardia (SVT) before and after intravenous administration of 1.5 to 2 mg/kg ethmozin. Initially, 9 of 11 patients had induction of sustained SVT, and two remaining patients had nonsustained SVT and atrial echoes, respectively. Ethmozin terminated induced SVT in six of nine patients. In six of nine patients ethmozin prevented the development of sustained SVT, indicating that ethmozin depressed retrograde fast pathway AV nodal conduction. In four of these patients atrial echoes were abolished. In the two remaining cases ethmozin prevented the induction of nonsustained SVT. In only three of these nine patients was sustained SVT induced. Anterograde fast and slow pathway properties did not significantly change with ethmozin administration. Effective refractory period (ERP) of the ventriculoatrial (VA) conduction system and ventricular paced cycle length producing VA block was 305 +/- 40 (mean +/- SEM) and 347 +/- 38 msec before and 424 +/- 105 and 475 +/- 71 msec after ethmozin administration, respectively (p less than 0.01, n = 8), suggesting depression of retrograde pathway with ethmozin administration. Ethmozin significantly (p less than 0.05) lengthened PA, AH, HV, and PR intervals (36 +/- 11 to 45 +/- 14 msec, 84 +/- 21 to 93 +/- 17 msec, 42 +/- 8 to 50 +/- 7 msec, and 163 +/- 23 to 190 +/- 31 msec, respectively). No significant change was observed in sinus rate, QRS and QT intervals, or ERP of atrium and ventricle. Thus, a single intravenous dose of ethmozin terminated induced SVT and prevented induction of sustained SVT in most patients, reflecting depression of retrograde fast pathway conduction.
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PMID:Ethmozin. II. Effects of intravenous drug administration on atrioventricular nodal reentrant tachycardia. 638 89

Electrocardiographic abnormalities were found in 53 out of 73 patients (72,6%) affected with progressive systemic sclerosis or scleroderma. Along with some modifications of little value, like heart rate increase or decrease, sporadic premature beats, slight ST depression or T-wave flattening, other more important abnormalities were recorded. One patient had atrial fibrillation and one supraventricular tachycardia. In 21 cases (28.8%) conduction disorders were found, including A-V block, right bundle branch block, left anterior hemiblock and bifascicular block. Low QRS voltages were present in 15 cases (20,6%), confined in all but one to the peripheral leads. In 13 patients (17,8%) Q or QS aspects suggesting myocardial necrosis were observed, but a clinical history or clinical picture of myocardial infarction syndrome was lacking in all cases but one. Electrocardiographic patterns of myocardial necrosis in scleroderma may indicate not only myocardial infarction, which seems to be a rather rare occurrence in such disease, but also intraventricular conduction system defects or progressive replacement of myocardium by fibrous tissue.
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PMID:Electrocardiogram in progressive systemic sclerosis. Analysis of 73 cases. 660 93


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