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 effects of the calcium entry blocker diltiazem (iv loading dose 0.4 mg/kg, iv maintenance dose 0.4 mg/min) and subsequent isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right ventricular (RV) and left ventricular (LV) performance (ultrasonic dimension technique), on coronary (electromagnetic flow probes) and systemic hemodynamics, and on electrophysiologic parameters (PR, QRS, QTc intervals) were studied in eight open-chest dogs, anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium. Diltiazem at a plasma concentration of 282 +/- 33 ng/ml (mean +/- SE) caused significant (P less than 0.05) increases in coronary blood flows, and decreases in coronary and systemic vascular resistances with only little effect on global and regional RV and LV function. However, the PR interval increased by 40%, and three animals developed II degrees atrioventricular block type I. At stable diltiazem plasma levels, administration of isoflurane caused dose-dependent decreases in myocardial segment shortening and stroke volume with unchanged LV or increased RV preload, and little changed RV or reduced LV afterload indicating myocardial depression. Coronary and systemic vascular resistances remained unaffected. At the higher concentration of isoflurane (mean inspired 1.3 +/- 0.2%), seven animals developed intermittent sinus node arrests with pauses up to 12 s followed by intermittent junctional escape or sinus rhythms. Similar interactions might develop in patients on diltiazem receiving isoflurane.
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PMID:Cardiovascular and electrophysiologic interactions between diltiazem and isoflurane in the dog. 381 73

After suicidal ingestion of 9 g Propafenone, a 31-year-old woman showed unconsciousness, cerebral convulsions, respiratory depression, sinus arrest, ventricular tachycardia and recurrent atrioventricular block. The maximum Propafenone plasma level was 4,702 ng/ml. Only 67.2 mg of Propafenone were eliminated within 4 h of hemoperfusion. Successful therapy could be achieved by symptomatic intensive care treatment. Additionally, 2 X 25 ml of 20%-saline solution were infused. In this case no efficacy of hemoperfusion in the treatment of Propafenone intoxication could be documented.
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PMID:[Therapy of severe propafenone poisoning--an attempt at elimination by hemoperfusion]. 382 27

To determine the frequency and severity of cardiac arrhythmias in intracranial subarachnoid hemorrhage, 120 nonselected patients were prospectively studied by 24-hour Holter monitoring. Arrhythmias were found in 96 of 107 patients (90%) with adequate Holter recording: ventricular premature complexes in 49, nonsustained ventricular tachycardia in 5, supraventricular premature complexes in 29, paroxysmal supraventricular tachycardia or atrial fibrillation in 9, sinoatrial block and arrest in 29, second-degree atrioventricular block in 1, atrioventricular dissociation in 4 and idioventricular rhythm in 2. Life-threatening ventricular arrhythmias (torsades de pointes-type ventricular tachycardia) occurred in 4 patients, degenerating into either ventricular flutter or fibrillation in 2. ST-segment changes suggestive of acute transitory myocardial ischemia were found in 8 patients (1.5 mm or more of ST depression in 7 patients and 1.5 mm or more of ST elevation in 1 patient). The frequency and severity of arrhythmias were significantly higher in patients studied within 48 hours of subarachnoid hemorrhage; serious ventricular arrhythmias were associated with QTc prolongation more than 550 ms and with hypokalemia less than 3.5 mEq/liter. No correlation was found between age, clinical condition, site and extent of subarachnoid hemorrhage and either the occurrence or severity of arrhythmias. The results of our study indicate an extremely high incidence of arrhythmias, sometimes serious, in subarachnoid hemorrhage, especially in the first 48 hours after hemorrhage. Continuous electrocardiographic monitoring is therefore mandatory.
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PMID:Holter detection of cardiac arrhythmias in intracranial subarachnoid hemorrhage. 382

Wilson's disease is a multisystem disorder. Heart involvement in Wilson's disease, however, has rarely been recognized. A prospective study was undertaken of 53 consecutive patients (28 men and 25 women, mean age of 21.4 years) with Wilson's disease. Electrocardiographic abnormalities occurred in 18 of 53 patients (34 percent), including left ventricular hypertrophy, biventricular hypertrophy, early repolarization, ST depression and T inversion, premature atrial or ventricular contractions, atrial fibrillation, sino-atrial block, Mobitz type 1 atrioventricular block, and tremor artifact. In contrast, 26 medical students and 14 carriers of Wilson's disease as control subjects (mean age of 22.6 years) all showed normal ECG. Eight out of 43 patients (19 percent) demonstrated asymptomatic orthostatic hypotension. An abnormal response to the Valsalva maneuver occurred in six of 18 patients (33 percent). There were two cardiac deaths; one died of repeated ventricular fibrillation (the copper content in the myocardium was 2.28 micrograms/g, and in the bundle of His 1.21 micrograms/g wet weight in the autopsy specimen); and the other, of dilated cardiomyopathy. It is concluded that four modes of cardiac manifestations in Wilson's disease include arrhythmias, cardiomyopathy, cardiac death, and autonomic dysfunction. Such possible cardiac involvement should be added to the clinical picture of Wilson's disease involving the hepatic and central nervous system.
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PMID:Cardiac Wilson's disease. 382 52

Sixteen patients with spontaneous angina were studied to assess the relative efficacy of diltiazem (D) at different doses [240 mg/day (D240) versus 360 mg/day (D360)], nifedipine (N: 120 mg/day), and verapamil (V: 480 mg/day), given according to a latin-square protocol. Of the 16 patients, 6 had ischemic attacks with ST elevation, 6 had ischemic attacks with ST depression, 4 showed ST elevation or ST depression in different ischemic attacks. All the patients underwent 24-hour Holter monitoring: at the beginning of the study; during the third day of treatment with D240, D360, N or V; after the withdrawal of each treatment. An atrioventricular block was observed in 2 patients during treatment with V, and in 1 patient during treatment with D240 and D360. In the remaining cases, D and V significantly (p less than 0,05) prolonged the PR interval (D240: + 18%; D360: + 16%; V: + 20%), and reduced the mean daily heart rate (D240: -9%; D360: -12%; V: -11%). The effects of D and V were statistically not different. All the treatments significantly reduced the frequency of the ischemic attacks (p less than 0,05) (D240: -79%; D360: -93%; N: -90%; V: -90%). In particular, D240 reduced by the same percentage (-79%) the frequency of ischemic attacks with ST elevation and ST depression, while D360 completely abolished ischemic attacks with ST elevation and reduced by 79% those with ST depression. Our results suggest that: diltiazem is highly effective in the treatment of spontaneous angina; the efficacy of 360 mg/day of diltiazem is equivalent to that of 120 mg/day of nifedipine and of 480 mg/day of verapamil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diltiazem in spontaneous angina: comparison with nifedipine and verapamil]. 383 Jul 63

A group of 123 consecutive patients with acute transmural inferior myocardial infarction were compared according to the presence or absence of precordial ST segment depression on admission to hospital. There was a significant increase in mean age, peak creatine kinase levels, and the incidence of left ventricular failure and high grade atrioventricular block in the group with precordial ST segment depression. There was also an increase in in-hospital mortality in this group but this difference was not significant. Despite these differences in in-hospital progress, during a follow-up period of over two years there was no difference in long term mortality, recurrence of angina, or subsequent cardiac-related admissions between the two groups.
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PMID:Long term follow-up of inferior myocardial infarction. Prognostic significance of precordial ST segment depression. 386 34

The effects of three purine derivatives of adenine, adenosine triphosphate (Striadyne), purified adenosine triphosphate and adenosine, on conduction tissue, were studied in closed chest dogs with endocavitary recording catheters. The dogs were anaesthetised with pentobarbital and ventilated, then three bipolar catheters were positioned to allow atrial pacing and recordings of atrial and His bundle potentials. The purines studied were administered by rapid bolus intravenous injection. The dosage was identical based on a predetermined dose-response curve (dose of 2 mg/kg). The study of the effects on atrioventricular conduction was carried out before and after administration of antagonists: atropine, 0.08 mg/kg and aminophylline, 10 mg/kg. Twelve dogs were studied for each purine: 6 with initial premedication with atropine and then aminophylline, and 6 with the inverse sequence. Lengthening of AV conduction was due exclusively to nodal depression. No variation in the HV interval was observed (HV = 35 +/- 4 ms). Lengthening of AH interval was observed very soon after injection of the drugs (5 to 10 seconds) with a peak effect between 20 and 40 seconds. Reversion to the initial value always occurred in under 2 minutes. In the model studied, Striadyne and purified adenosine triphosphate were much more powerful than adenosine, both in intensity and duration; high degree AV block was obtained in 10 out of 12 cases with Striadyne and in 8 out of 12 cases with purified adenosine triphosphate, but in only 2 out of 12 cases with adenosine. The use of specific antagonists demonstrated the different modes of action of the three purines.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mode of action of purinergic derivatives of adenine on auriculo-ventricular conduction. Experimental study in dogs]. 391 75

Associated electrophysiologic abnormalities and site of delay were studied in 20 patients, aged 1.5 to 16.5 years, with congenital heart disease and first-degree atrioventricular (AV) block (PR interval above the 98th percentile for age and heart rate). Eight of the 20 patients with first-degree AV block were studied after 1 or more cardiovascular operations. Refractory periods of the atrium, AV node, His-Purkinje system and ventricle were determined. As a further test for AV nodal integrity, rapid atrial pacing was performed and the cycle at which Wenckebach periodicity occurred was noted. Four groups were identified. Group I included 4 patients (20%) with intraatrial conduction delay (long PA interval). Three patients had depressed sinus nodal function and 1 had depressed AV nodal function. Group II included 7 patients (35%) with AV nodal delay (long AH interval). One patient had sinus nodal depression and 2 had AV nodal depression (prolonged AV nodal refractory period or Wenckebach at a long paced cycle length). Group III included 3 patients (15%) with His-Purkinje delay (long HV interval). Measured functions were normal in all patients. Group IV included 6 patients (30%) with normal or high normal intracardiac intervals with long PR. One patient had sinus nodal dysfunction, 2 patients had long atrial refractory periods, 1 had AV nodal depression; 2 had long refractory period of the His-Purkinje system, and 1 had long ventricular refractory period. Atrial flutter was induced in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Site of conduction delay and electrophysiologic significance of first-degree atrioventricular block in children with heart disease. 399 64

The prognostic value of discharge ECG was studied in 457 patients after their first acute myocardial infarction. Thirteen different ECG variables were studied on the discharge ECG. When cumulative 4-year survival rates were calculated by standard life-table method for each variable individually, the following variables had statistically significant prognostic power: PTF (P terminal force), PTFA (P terminal frontal axis), AF (atrial fibrillation), ST depression, ST elevation, QRS duration, and the combination block (LBBB/RBBB + LAHB/LPHB). The variables with no statistically significant predictive power were: QTc, LBBB or RBBB, LAHB or LPHB, AV block, T wave angle, T negativity, and sigma R. The relative risks for the most important variables in the discrete life-table model were: PTF 3.4, QRS duration 3.3, ST depression 2.6, PTFA 2.5, and ST elevation 2.2. In further analysis a model with only three ECG variables (PTF, ST depression, and ST elevation) was developed which stratified the study population in categories with 1.9% to 75.5% estimated 4-year survival rates.
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PMID:The mortality predictive power of discharge electrocardiogram after first acute myocardial infarction. 400 34

A 61-year-old man presented with symptomatic 2 degree Mobitz II AV block in association with bifascicular block. Ventricular pacing resulted in temporary depression of AV conduction. The extent of pacing-induced AV block varied directly with the duration and rate of ventricular pacing. Intracardiac recordings proved that the site of spontaneous and pacing-induced AV block was distal to the His bundle. Possible mechanisms by which this phenomenon may arise and several implications of practical importance are discussed.
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PMID:Depression of distal AV conduction following ventricular pacing. 617 98


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