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 male veteran endurance runners and 20 controls underwent resting, exercise, and ambulatory electrocardiography. Four athletes and three controls satisfied voltage criteria for left ventricular hypertrophy. The PR interval was longer in the athletes and they had longer mean (SD) treadmill exercise times (19 (4) v 16 (2) min) than the controls. Four athletes but no controls had greater than 2 mm downsloping ST segment depression during exercise. During 48 hour ambulatory electrocardiography the athletes had a consistently lower heart rate but maintained a circadian variation. Profound bradycardia (less than 35 beats/min) occurred in eight athletes but only one control. Eight athletes and two controls had asystolic pauses ranging from 1.8 to 15 seconds. Six athletes had first degree heart block, four had Mobitz II second degree block, and three had complete heart block. Most conduction abnormalities occurred at night and resolved during exercise. Ventricular ectopic activity was not significantly different between the groups. Thus heart block patterns and profound bradycardia are more frequent in older athletes than their youthful counterparts.
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PMID:Electrocardiographic findings in male veteran endurance athletes. 292 52

The efficacy of a once daily, sustained release formulation of verapamil (Verapamil SR, 360 mg) was evaluated in 19 patients with chronic angina pectoris using a double-blind placebo-controlled crossover protocol. Evaluation by exercise testing, 24 hour electrocardiographic ambulatory monitoring and blood drug level assays was performed at the end of each 2 week phase, 21 to 23 hours after the last dose. After the crossover protocol, all patients were given sustained release verapamil for 4 weeks and the evaluation was repeated. Exercise time (mean +/- SEM) increased from 7.4 +/- 0.6 minutes with placebo to 9.6 +/- 0.8 minutes with verapamil (p less than 0.001) and to 9.5 +/- 0.7 minutes (p less than 0.001) after 4 weeks of therapy. The mean time to 1 mm ST depression also increased significantly, from 4.5 +/- 0.4 and 4.8 +/- 0.5 minutes in bipolar leads CM5 and CC5, respectively, with placebo, to 5.5 +/- 0.6 (p less than 0.05) and 6.2 +/- 0.5 minutes (p less than 0.01) with verapamil. Maximal ST depression and rest and peak heart rates were not altered significantly. The mean rate-pressure product was 208 +/- 9.9 with placebo and decreased to 189 +/- 7.7 (p less than 0.05) with verapamil but rose to 200.6 +/- 10.4 (p = NS) after 4 weeks of therapy. The mean hourly heart rates were lower with the drug than with placebo throughout the 24 hour period but there was no significant bradycardia, arrhythmia or heart block.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sustained release verapamil, a once daily preparation: objective evaluation using exercise testing, ambulatory monitoring and blood levels in patients with stable angina. 310 85

Encainide is a class IC antiarrhythmic agent that has been under clinical investigation for the last decade. Laboratory and clinical studies have demonstrated it to be a potent suppressor of ventricular extrasystoles. It is effective in approximately one-half of patients with malignant ventricular arrhythmias. The preliminary experience in patients with supraventricular arrhythmias indicates that the drug is particularly effective in arrhythmias associated with an accessory pathway. Side effects most commonly include blurred vision, nausea, heart block, and proarrhythmic effects. The hemodynamic effect of oral encainide are insignificant in patients with well-preserved left ventricular function. Despite minimal myocardial depression in patients with left ventricular dysfunction, there is the potential for worsening of heart failure. Encainide has a short half-life of 3 hours, but has 2 active metabolites with longer half-lives. No clinically significant drug interaction has been demonstrated with encainide therapy.
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PMID:Encainide: its electrophysiologic and antiarrhythmic effects, pharmacokinetics, and safety. 312 82

To investigate the electrophysiological properties of ventricular impulse formation after His-bundle ablation in 11 patients, incremental ventricular overdrive stimulation studies were performed. The studies, which were spread over a follow-up period of up to 601 days, were carried out invasively with temporary leads as well as noninvasively with the implanted pacemakers and chest wall inhibition. The overdrive pacing rate was increased in steps of 10 beats/min, and the pacing duration was 2 minutes at each level. Ten out of 11 patients had a reliable ventricular escape rhythm; in the remaining patient, consistently no subsidiary pacemaker function was observed up to 10 seconds. In 83% of the studies, incremental ventricular overdrive stimulation caused progressive suppression of ventricular impulse formation with exponential increase in ventricular recovery time and progressive postrecovery subsidiary pacemaker depression. In the remaining 17%, ventricular recovery time showed a heterogeneous response to overdrive stimulation--as possible cause alterations in the sympathetic tone and limitations attributable to the method used are discussed. The results of this study demonstrate a rate-dependent overdrive suppression of subsidiary ventricular pacemaker tissue. This can be of clinical importance in patients with complete heart block and rate-adaptive pacemakers because sudden pacemaker failure or temporary pacemaker inhibition at high stimulation rates may cause Stokes-Adams attacks not reproducible at lower pacing rates.
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PMID:Subsidiary pacemaker function in complete heart block after His-bundle ablation. 316 98

The relations between reciprocal ST segment depression in the electrocardiogram and infarct size and 10 year prognosis were studied in 315 patients who survived for at least 28 days after a first anterior or inferior myocardial infarction. ST depression was more common in inferior infarcts (72%) than in anterior (37%) ones. It occurred more frequently in complicated infarcts and in the presence of considerable ST elevation. Patients experiencing second or third degree heart block were significantly more likely to show reciprocal changes. The rise in peak cardiac enzyme concentration was higher in patients showing ST depression. In patients with ST depression, peak creatine kinase concentration was 46% higher, aspartate aminotransferase was 39% higher, and lactate dehydrogenase 29% higher after correction for site and complications. A discriminant function analysis selected infarct site, peak aspartate aminotransferase, and magnitude of ST elevation as predictors of the occurrence of ST depression. Age, severity, and smoking status did not significantly improve discrimination. Despite larger increases in peak enzyme concentrations patients with ST depression had marginally fewer subsequent episodes of unstable angina or fatal or non-fatal infarction and a marginally lower 10 year death rate. Neither difference was statistically significant. ST depression occurring early in the acute phase of myocardial infarction is likely to be a reflection of electrophysiological changes taking place at the site of the infarct that is manifested in the contralateral surface of the heart. Other causes, however, such as transient ischaemia at the site of the reciprocal changes or extension of the infarct to contiguous areas cannot be excluded in all cases.
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PMID:The aetiology and prognostic implications of reciprocal electrocardiographic changes in acute myocardial infarction. 370 82

The response of the atrioventricular (AV) junction to brief intense adrenergic stimulation applied during episodes of second degree heart block achieved by acetylcholinesterase paralysis in the AV junction was examined in six dogs. Despite profound depression of AV conduction due to enhanced cholinergic activity, strong local adrenergic stimulation still readily elicited AV junctional tachycardia. Increase in cholinomimetic influences in the AV junction did not prolong transatrial or His bundle-ventricular conduction times. During AV junctional rhythm and retrograde atrial capture (n = 4), neither the sequence of retrograde atrial activation nor the atrial electrogram configurations were altered. In the two remaining dogs the AV junctional tachycardia was associated with AV dissociation. These findings suggest that the acetylcholine-induced depression of AV conduction is located in the AV node region exclusively. More important, however, is the demonstration that retrograde atrial activation originating from a pacemaker located in the AV node or immediate vicinity could actually precede the inscription of the H spike by a considerable amount of time, further suggesting that anterograde conduction from the pacemaker site to the bundle of His is far more depressed by acetylcholine than is the concomitant retrograde conduction from the pacemaker site to the atrium. Thus, inference of the origin of a subsidiary pacemaker from the P wave configuration or the relation of the A wave to the His bundle electrogram, or both, may lead to erroneous conclusions.
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PMID:Atrioventricular junctional tachycardia during heart block. 374 13

To assess the prognostic significance and the clinical implications of the electrocardiographic findings of the first acute myocardial infarction, the in-hospital mortality and complications and three-year follow-up of 180 patients were analyzed. The patients were divided according to the infarction type (transmural, non-transmural), the site, (anterior, inferior including posterior) and the absence or presence of ST depression in leads facing the site of infarction. The peak enzyme concentrations were significantly higher in those with transmural infarcts than in those with non-transmural infarcts, in anterior infarcts compared to inferior infarcts, and in those sites with ST depression than those without. The early complications of cardiogenic shock, congestive cardiac failure, and complete heart block were significantly higher in transmural infarcts compared to non-transmural, while late complications and mortality were the same in all groups and subgroups. This study demonstrated that ECG changes in the first acute myocardial infarction are of prognostic significance for the early clinical course, but cannot predict the late course or subsequent coronary events.
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PMID:The clinical implications of electrocardiographic changes in first acute myocardial infarction. 406 70

In a double-blind study, 49 elderly patients with primary major depression, with or without cardiovascular disease, were treated with maprotiline or doxepin. Holter monitors, 12-lead ECGs, and orthostatic blood pressure measurements were used. Maprotiline was associated with decreased PVCs in patients with a "high" baseline rate, while doxepin was associated with increased PVCs in this group. There were no significant differences in orthostatic blood pressure changes between treatment and nontreatment phases or between the two drugs. Small but significant increases in heart rate and prolonged PR interval were noted with both drugs. QRS interval was prolonged by maprotiline but decreased by doxepin. Neither drug produced untoward effects in patients with stable angina or an old myocardial infarction. Maprotiline may have an antiarrhythmic effect which could be beneficial in the treatment of depression with concomitant PVCs. Conversely, doxepin may be more appropriate for depressed patients with heart block or intracardiac conduction delays. Further research is necessary to confirm these suggestions.
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PMID:Comparative cardiac effects of maprotiline and doxepin in elderly depressed patients. 620 85

Since verapamil and contrast media both cause depression in the electrophysiologic function of the heart and both may exert these effects by actions on ionic calcium, the possible interaction of verapamil and intracoronary contrast media on atrioventricular conduction was studied in six dogs using surface electrocardiography and HIS bundle electrogram. The effects of intracoronary injection of standard ionic media (Renografin 76) and low osmolal contrast media (Hexabrix and Hexabrix with calcium [8 mEq/L]) were compared. Each contrast media was assessed in the normal state and at four increasing doses of verapamil (0.125, 0.25, 0.5, and 1.0 mg/kg). The PR and AH intervals were substantially prolonged by intracoronary injection of Renografin 76 in the presence of a 1.0 mg/kg dose of verapamil (172 +/- 41 msec to 724 +/- 48 msec, P less than 0.05 for PR interval, and 182 +/- 41 msec to 734 +/- 51 msec, P less than 0.05 for AH interval), with most animals developing second degree heart block (Mobitz, type I). There was no change in the HV interval. Hexabrix and Hexabrix with calcium did not cause significant changes in PR or AH intervals at similar doses of verapamil. Thus, standard ionic contrast causes severe inhibition of atrioventricular conduction in the presence of verapamil, whereas low osmolal contrast media cause no significant negative dromotropic effects either in the presence or absence of verapamil. The osmolality of contrast media is an important mechanism responsible for the depression in atrioventricular conduction attending intracoronary contrast media in the presence of verapamil.
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PMID:Combined actions of verapamil and contrast media on atrioventricular conduction. Influence of osmolality of the media. 646 25

This study was designed to compare the direct actions of bupivacaine and lidocaine on the isolated perfused guinea pig Langendorff heart preparation. Sixty min after mounting, either bupivacaine HCl (0.3 or 3 micrograms/ml) or lidocaine HCl (10 or 30 micrograms/ml) was added to the perfusate, and the effect (if any) was compared to untreated control values 30, 60, and 90 min later. Although the highest concentrations of both drugs invariably produced statistically significant reductions in heart rate, df/dt, coronary blood flow, and myocardial oxygen consumption (MVO2), these reductions were consistently greater after bupivacaine. Moreover, arrhythmias occurred in 6 of 12 preparations in those hearts exposed to 3 micrograms/ml of bupivacaine. Most often these arrhythmias consisted of heart block and bi- or trigeminy. Additional studies indicated that the reduction in coronary blood flow and MVO2 produced by 3 micrograms/ml of bupivacaine was a consequence of its direct negative inotropic and chronotropic action. Although the myocardial depression produced by bupivacaine and lidocaine could be reversed readily by substituting fresh perfusate, increasing the extracellular calcium concentration in stepwise increments did not augment the negative inotropic or chronotropic effect produced by 3 micrograms/ml of bupivacaine or 10 micrograms/ml of lidocaine. We conclude that 3 micrograms/ml of unbound bupivacaine is more cardiotoxic than 30 micrograms/ml of unbound lidocaine in this model.
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PMID:Comparative cardiotoxicity of bupivacaine and lidocaine in the isolated perfused mammalian heart. 673 75


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