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)

Survivors of out-of-hospital ventricular fibrillation (VF) are at high risk for recurrent VF, probably reflecting continued myocardial electrical instability. In this study 12-lead ECGs of 125 VF survivors with coronary heart disease were examined and compared to those of 98 ambulatory post-MI patients. The study was part of an effort to define clinical identifiers of patients likely to develop sudden cardiac death. Ventricular fibrillation survivors were commonly had premature ventricular complexes (PVCs):30% versus 13% (P less than 0.01). In addition, ECGs of VF survivors showed a significantly greater prevalence of ST-segment depression (46% versus 10%), T wave flattening (52% versus 26%), and QTc prolongation (35% versus 18%). It is proposed that these repolarization abnormalities represent asynchronous repolarization, which together with frequent PVCs, may set the stage for re-entrant ventricular dysrhythmias and ultimately VF. It is also possible that repolarization abnormalities together with premature ventricular contractions might serve as markers of patients with coronary heart disease who are at increased risk for sudden cardiac death.
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PMID:Repolarization abnormalities in survivors of out-of-hospital ventricular fibrillation. 7 73

The antiarrhythmic activity of flecainide acetate (R-818), 2 mg/kg, was investigated in anesthetized, open-chest pigs. Ventricular arrhythmias were provoked by reducing the flow in the left anterior descending coronary artery (LAD) to 25% of control during 30 min. During this period ventricular fibrillation occurred in 33% (11 out of 33) of control animals against 12.5% (1 out of 8) of animals treated with flecainide. Ventricular tachycardias were seen in 42% (14 out of 33) of the untreated animals as compared to none of the animals previously treated with flecainide. Total number of ventricular arrhythmias was significantly lower in the treated than in the untreated animals (p less than 0.05). However, when the LAD was occluded completely at its distal part, ventricular fibrillation occurred in all animals (5 untreated and 6 pretreated with flecainide). Time to onset of ventricular fibrillation was the same for both groups of animals, despite a lower incidence of preceding ventricular arrhythmias in the pretreated group. Flecainide depressed myocardial contractility (LVdP/dt max), caused hypotension, and increased QRS width. Both myocardial depression and widening of QRS are related to arterial plasma levels of flecainide. Therefore, a slower infusion rate than the 1 mg/kg per minute used in this study is advisable when myocardial function is impaired.
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PMID:Antiarrhythmic and hemodynamic actions of flecainide acetate (R-818) in the ischemic porcine heart. 9 25

A technique for measuring the maximum contractile element velocity (Vpm) of the myocardium was developed, verified, and employed in patients to allow accurate intraoperative assessment of the adequacy of myocardial protection. Four groups of patients were studied. Ten patients had coronary artery bypass grafts (CABG) with cardioplegia; 13 had CABG with coronary perfusion, ventricular fibrillation at 28 degrees C, and aortic clamping for distal anastamoses; 6 had aortic valve replacement (AVR) with cardioplegia; and 7 had AVR with coronary perfusion to the beating heart. For cardioplegia, a solution of 5% dextrose in 0.2% saline at 4 degrees C with 25 mEq of potassium chloride and 12.5 gm of mannitol was infused initially, followed by 500 ml every 30 minutes. Clinically all patients did well, and there were no deaths. Patients having CABG with intermittent coronary perfusion during ventricular fibrillation had significant (p less than 0.01) depression of Vpm from 38.3 to 30.8 sec-1 while Vpm in patients having CABG with cardioplegia was unchanged. Patients having AVR with continuous coronary perfusion or with cardioplegia (average anoxia time, 70.4 minutes) had no significant change in Vpm. We conclude that this cardioplegic solution provided adequate protection of myocardial function for up to 105 minutes of continuous aortic clamping in humans. The depression in Vpm observed following CABG with intermittent coronary perfusion is consistent with previous suggestions that this combination is detrimental because of maldistribution of coronary blood flow during ventricular fibrillation.
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PMID:Effects of cardioplegic solution on human contractile element velocity. 31 64

Trichloroethylene (TCE) has been an industrial chemical of some importance for the past 50 years. First synthesized by Fischer in 1864, TCE has enjoyed considerable industrial usage as a degreaser and limited medical use as an inhalation anesthetic and analgesic. This TCE overview provides a narrative survey of the reference literature. Highlights include history, nomenclature, physical and chemical properties, manufacture, analysis, uses, metabolism, toxicology, carcinogenic potential, exposure routes, recommended standards, and conclusions. Chemically, TCE is a colorless, highly volatile liquid of molecular formula C2HCl3. Autoxidation of the unstable compound yields acidic products. Stabilizers are added to retard decomposition. TCE's multitude of industrial uses center around its highly effective fat-solvent properties. Metabolically, TCE is transformed in the liver to trichloroacetic acid, trichloroethanol, and trichloroethanol glucuronide; these breakdown products are excreted through the kidneys. Most toxic responses occur as a result of industrial exposures. TCE affects principally the central nervous system (CNS). Short exposures result in subjective symptoms such as headache, nausea, and incoordination. Longer exposures may result in CNS depression, hepatorenal failure, and increased cardiac output. Cases of sudden death following TCE exposure are generally attributed to ventricular fibrillation. Current interest in TCE has focused on recent experimental data that implicate TCE as a cause of hepatocellular carcinoma in mice. No epidemiological data are available that demonstrate a similar action in humans. The overall population may be exposed to TCE through household cleaning fluids, decaffeinated coffee, and some spice extracts. The NIOSH recommended standard for TCE is 100 ppm as a time-weighted average for an 8-hr day, with a maximum allowable peak concentration of 150 ppm for 10 min.
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PMID:Trichloroethylene. I. An overview. 40 97

Toxic cardiomyopathy may result in fatal arrhythmias. To develop a model to study ventricular fibrillation and asystole, we investigated the effect of cantharidin in the production of cardiac arrhythmias and myocardial damage. Conscious albino rabbits, weighing between 1.8 to 2.8 kg received an intravenous bolus injection of cantharidin ranging from 0.6 to 1.9 mg/kg or a control injection of solvent. The electrocardiogram was continuously monitored on tape before and after injection for extended periods of time. Dose-related effects were observed with the following: 1) presence, magnitude and duration of ST depression after injection; 2) occurrence of fatal arrhythmias; 3) survival time (high doses were usually fatal within 3 hr); and 4) electron microscopic evidence of mitochondrial swelling, intramitochondrial granules and myofibrillar degeneration. The most common arrhythmias associated with the high doses of cantharidin were frequent ventricular ectopics, ventricular tachycardia, ventricular fibrillation or asytole. The arrhythmias could not be explained by alterations in blood pressure, electrolytes or blood gases. These findings show the cardiotoxic properties of cantharidin and its ability to produce fatal cardiac arrhythmias. Thus, it may serve as a model to study sudden death and the efficacy of antiarrhythmic drugs.
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PMID:A model of cardiac arrhythmias and sudden death: cantharidin-induced toxic cardiomyopathy. 44 46

The electrophysiologic effects of ethmozin on canine myocardium were studied in anesthetized open-chest animals and in superfused Purkinje fibers. On selective injection into the sinus node artery and the posterior septal artery the drug caused no changes in the sinus node length and atrioventricular conduction, respectively. Intravenous infusion of 4 mg/kg ethmozin led to an increase of right and left ventricular diastolic excitability threshold and refractory period. Intravenous administration of 3--5 mg/kg ethmozin caused marked increase in conduction delay in which the ischemic zone of the left ventricle during acute coronary artery occlusion, which was associated with ventricular fibrillation in 50% of the dogs. In vitro, 1 x 10(-6) g/ml ethmozin shortened the Purkinje fibers' action potential duration whereas a dose of 1 x 10(-5) g/ml reduced the rate of phase 0 rise and slightly reduced the action potential amplitude. Ethmozin in a dose of 1 x 10(-7) g/ml increased transiently the isometric developed tension of false-tendon preparations. Higher concentrations caused marked depression of contractility. These observations suggest depression of the fast current by ethmozin. However, further studies are needed to elucidate its effect on action potential duration and false-tendor contractility.
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PMID:[Electrophysiologic effect of ethmosine on the dog's myocardium]. 45 16

Two patients known to have coronary artery disease died suddenly outdoors while active. Neither had symptoms or signs of acute myocardial infarction. They were being monitored by continuous tape recording of the electrocardiogram at the time of death. In one patient the cause of death was cardiac arrest, preceded by bigeminy and multiform ventricular ectopic beats, in the other ventricular fibrillation preceded by atrial fibrillation, multiform ventricular ectopic beats, and ST depression. These observations are added to the limited reported cases in which the mechanism leading to sudden death outside the hospital is recorded.
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PMID:Two monitored cases of sudden death outside hospital. 65 36

In forty patients with normal coronary arteries, the electrocardiographic changes secondary to Urografin 76 and Hypaque 85 injection into both coronary arteries were monitored. Hypaque caused significantly greater prolongation of the PR interval (p less than 0.001), depression of the ST segment (p less than 0.05) and depth of T wave inversion (p less than 0.05). These effects were more noticeable during right coronary artery injection. Both contrast media slowed the heart rate equally during right and left coronary artery injection. In the absence of coronary arterial disease the ECG changes secondary to contrast media injection probably reflect a direct toxic effect. It is possible that premedication with atropine will reduce these effects. Urografin 76 appears the less toxic of the two media, although one case of ventricular fibrillation occurred with each.
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PMID:Contrast media during coronary arteriography: electrocardiographic changes in the presence of normal coronary arteries. 70 21

Electrographic changes associated with cyclical reduction of blood flow in partially constricted one or two coronary arteries of anesthetized dogs were examined. In the preparations with single vessel constriction, cyclical ST elevation occurred along with cyclical reduction of coronary blood flow below 25% of the control value. The ST elevation was associated with reciprocal ST depression in the contralateral ventricular surface. In the preparations with double vessel constriction, cyclical reduction of flow frequently occurred in both vessels. The reduction of flow in one vessel occurred not synchronously with that in another vessel in the majority of preparations. The reduction of flow in both vessels was associated with ST elevation in the corresponding areas of the left ventricle. Premature ventricular contractions frequently occurred at the beginning of or immediately after disappearance of ST elevation, or when ST elevation persisted for more than 10 min. Ventricular fibrillation frequently occurred in the preparations with double vessel constriction.
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PMID:Electrographic changes associated with cyclical reduction of coronary blood flow. 73 74

A man with known coronary heart disease underwent treadmill exercise testing to determine his functional capacity. The test was negative for ischemia. Ventricular ectopic activity was noted at rest and in the recovery period. On the same day, while viewing a sporting event at home, the patient died suddenly. An ambulatory electrocardiographic recording documented ventricular fibrillations as the terminal mechanism. Ventricular ectopic activity and heart rate increased in the two hours prior to death, and ischemic ST-segment depression was noted at the time of the terminal arrhythmia. It is postulated that myocardial ischemia and catecholamine response lowered the threshold to ventricular fibrillation, thus facilitating the emergence of the fatal arrhythmia.
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PMID:Sudden death during ambulatory monitoring. Clinical and electrocardiographic correlations. Report of a case. 83 Feb 11


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