Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Paroxysmal supraventricular tachycardia is the most common sustained cardiac arrhythmia in pregnant women. Because nearly 50% of these supraventricular tachyarrhythmias fail to respond to vagal maneuvers, other therapies are used, including electrocardioversion and pharmacologic agents. Propranolol, verapamil, and adenosine have Food and Drug Administration-approved labeling for acute termination of supraventricular tachycardia. Verapamil has been the most commonly used agent in the general population but it has several shortcomings, such as its potential to cause or exacerbate systemic hypotension, congestive heart failure, bradyarrhythmias, and ventricular fibrillation. In addition, verapamil readily crosses the placenta and has been shown to cause fetal bradycardia, heart block, depression of contractility, and hypotension. Adenosine has several advantages over verapamil, including rapid onset, brevity of side effects, theoretical safety, and probable lack of placental transfer. Adenosine ultimately may prove to be the preferred agent for termination of paroxysmal supraventricular tachycardia in the gravid woman.
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PMID:Adenosine in the treatment of maternal paroxysmal supraventricular tachycardia. 149 12

1,1,1-Trichloroethane is a widely used solvent that is annually linked to several cases of sudden death following accidental exposure or abuse. Sudden death is believed to be due to ventricular fibrillation or myocardial depression. The purpose of this study was to investigate the mechanism of myocardial depression by assessing the influence of 1,1,1-trichloroethane on intracellular Ca transients in single neonatal rat ventricular myocytes using spectrofluorometric analysis of fura-2-Ca binding. Cells were exposed to 1,1,1-trichloroethane in Hanks' balanced salt solution aliquoted as a 0.2% DMSO solution by a single pass suffusion in an environmentally controlled chamber. 1,1,1-Trichloroethane (0.25 mM-8 mM) reduced the height of electrically (1 Hz, 60 V, 10 ms) induced Ca transients concentration dependently and reversibly to a maximum of about 50% with no effect on diastolic Ca concentration. Video motion analysis revealed an inhibition of contractility in the same concentration range. 1,1,1-Trichloroethane inhibited cytosolic Ca increase in response to KCl-induced (90 mM) depolarizations and further decreased the limited Ca transients in ryanodine (1 microM) pretreated myocytes. Increased external Ca (5 mM) antagonized the effect of 0.5 mM 1,1,1-trichloroethane on the Ca transients. 1,1,1-Trichloroethane reduced the caffeine (10 mM) releasable Ca pool in myocytes. These results show that 1,1,1-trichloroethane inhibits Ca mobilization during excitation-contraction coupling in ventricular myocytes. An inhibitory action on the influx of extracellular Ca as well as on sarcoplasmic reticulum Ca release and sequestration is likely to be responsible for this action.
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PMID:Calcium transients in isolated cardiac myocytes are altered by 1,1,1-trichloroethane. 151 78

Myocardial ischemia is associated with accumulation of lyso-phospholipids, including lyso-platelet activating factor, the degradation product and precursor of platelet activating factor. These compounds produce cellular and microvascular damage and, in the myocardium, depression of contractility and arrhythmia. The potent platelet activating factor antagonist, WEB 2086, or placebo, was infused (IV) 10 min before constriction of the proximal left anterior descending coronary artery in open-chest dogs. Two protocols were followed: the dose of WEB 2086 was 0.5 mg/kg in those subjected to 20 min ischemia with 10 min reperfusion (n = 40) and 5 mg/kg preceding 60 min ischemia alone (n = 24). There was no significant difference in the number of ventricular premature complexes between WEB 2086 and placebo treated dogs during either period of ischemia. On reperfusion in those surviving 20 min of ischemia, 5 of the 18 WEB 2086 and 9 of the 18 placebo treated dogs developed ventricular fibrillation (NS). After 60 min of myocardial ischemia, there was no statistical difference in histological changes (nuclear swelling, aggregation of chromatin, myofibrillar separation) between groups. Hence, no substantial effect of relatively large doses of WEB 2086 on ischemia-induced histological change or arrhythmia was found in this preparation.
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PMID:The effects of a PAF antagonist on ischemic myocardial damage and arrhythmia in the dog. 151 80

Of 150 consecutive patients with sustained monomorphic ventricular tachycardia (VT) (n = 116) or ventricular fibrillation (VF) (n = 34) late after acute myocardial infarction, 17 had reproduction of their sustained monomorphic VT during exercise testing. Data from these patients (group I) were compared with data from patients without exercise-induced VT (group II). No statistical difference was found between groups I and II with relation to age, sex, number of vessels with greater than 70% stenosis, left ventricular ejection fraction, number of previous myocardial infarctions, inducibility during programmed stimulation and total mortality during follow-up. In group I, only 1 patient (6%) developed ST depression during exercise compared with 47 patients (35%) in group II (p less than 0.01). After a 34-month mean follow-up, 6 patients in group I (35%) and 18 patients in group II (13%) died suddenly (p = 0.02). It is concluded that sustained monomorphic VT is reproduced during exercise in only 11% of patients with spontaneous late sustained monomorphic VT or VF. Electrocardiographic findings do not support ischemia as a triggering mechanism of exercise-induced sustained monomorphic VT. Patients with exercise-induced sustained monomorphic VT have a high incidence of sudden death.
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PMID:Incidence, pathophysiology and prognosis of exercise-induced sustained ventricular tachycardia associated with healed myocardial infarction. 152 40

Exercise testing is an important noninvasive method for the exposure of arrhythmias. It provides complementary information to that obtained from ambulatory monitoring or electrophysiologic testing. By producing a number of important physiologic changes, especially activation of the sympathetic nervous system and an increase in circulating catecholamines, exercise testing provides a more complete assessment. On continuous monitoring, exercise-induced ventricular premature beats may be found in up to 34% of healthy subjects, in 60 to 70% of those with heart disease and in all patients who have experienced sustained ventricular tachycardia. Couplets or nonsustained ventricular tachycardia can be found during exercise in 0 to 6% of healthy subjects, in 15 to 31% of patients with heart disease and in 75% of those with sustained ventricular tachycardia. Even in patients with heart disease, there is only a small risk of inducing sustained ventricular tachycardia or ventricular fibrillation during exercise. The prognostic relevance of exercise-induced ventricular arrhythmias in patients with coronary artery disease or cardiomyopathy has not been clearly established. There appears to be an increased risk, however, in patients with ventricular premature beats as well as ST-segment depression or in patients with repetitive forms of ventricular arrhythmias during exercise which cannot be medically controlled. In healthy subjects, exercise-induced ventricular premature beats are of no prognostic relevance. In particular, for patients in whom arrhythmias are induced by exercise, exercise testing should be used to assess the effectiveness of antiarrhythmic drug treatment. Importantly, serious cardiac toxicity, often not observed at rest or during routine activities, may become apparent during exercise testing. It should be a standard part of arrhythmia assessment and management.
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PMID:Evaluation of cardiac arrhythmias by exercise testing. 169 Jan 68

Three patients under 40-years old who survived cardiac arrest due to ventricular fibrillation were originally diagnosed as having idiopathic dilated cardiomyopathy. Shortly after cardiac arrest, assessment of myocardial function revealed a globally dilated left ventricle in each patient with an estimated ejection fraction between 20% and 30%. Serial assessment of myocardial function, however, showed either normal or near-normal function by 2 weeks postevent. These findings suggest that myocardial stunning due to hypoperfusion during ventricular fibrillation or the effects of transthoracic shocks may result in profound, reversible myocardial depression in survivors of cardiac arrest. Serial evaluation of left ventricular function may be of value in selected survivors of cardiac arrest in order to evaluate time-dependent resolution of myocardial dysfunction and may prevent misdiagnosis of idiopathic dilated cardiomyopathy.
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PMID:Reversible myocardial depression in survivors of cardiac arrest. 169 63

Patients who have sustained greater than or equal to 1 myocardial infarcts are at high risk for sudden death or reinfarction; the risk is highest for those with lowest ventricular ejection fraction, continuing myocardial ischemia and asymptomatic high-density and complex premature ventricular contractions. At present, beta blockers when given prophylactically are the only agents that reduce the incidence of sudden death and reinfarction in survivors of myocardial infarction (MI) in the first 2 years. The beneficial effect was shown to correlate with a reduction in heart rate, the effect being absent or deleterious with beta blockers with marked sympathomimetic activity. The effects of beta blockers on ventricular fibrillation appeared to be dissociated from those on premature ventricular contractions. Trials with calcium antagonists indicate that these drugs had no effect or increased the mortality rate. The divergent effect of beta blockers and calcium antagonists is unexplained but may be due in part to a lack of bradycardiac effect of calcium antagonists; there were no differences in effect among different calcium antagonists. Data from trials involving class I antiarrhythmic agents indicate that agents acting by depression of cardiac conduction are either devoid of effect or produce a modest increase in mortality. Results of the Cardiac Arrhythmia Suppression Trial, employing the newer class I agents flecainide and encainide, were used to determine whether the suppression of premature ventricular contractions in the survivors of acute MI reduces mortality. Flecainide and encainide suppressed premature ventricular contractions greater than 80%, but resulted in an increased mortality rate undoubtedly due to a marked proarrhythmic effect. Whether these data can be extrapolated to all class I agents is uncertain. Preliminary data with class III antiarrhythmic agents suggest that these agents, especially amiodarone, similarly to beta blockers, have the potential to reduce mortality in survivors of MI. Evolving data suggest that in the secondary prevention of morbid events in the survivors of acute MI, the focus must shift away from antiarrhythmic agents that delay conduction and toward beta blockers and antifibrillatory actions resulting from a prolongation of refractoriness.
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PMID:Advantages of beta blockers versus antiarrhythmic agents and calcium antagonists in secondary prevention after myocardial infarction. 169

Determination of defibrillation thresholds (DFTs) and implantable cardioverter defibrillator (ICD) testing requires repeated inductions of ventricular fibrillation (VF) and defibrillation attempts using known energy outputs. Little is known about the individual and cumulative effects of repetitive brief episodes of VF and hypoperfusion on cerebral function. The potential clinical utility of quantitative electroencephalographic (QEEG) monitoring during intraoperative ICD testing, by using processed 19-channel EEG (0.5-35 Hz bandwidth), was examined in ten anesthetized patients, five males and five females (mean age 62 +/- 10 years), who underwent ICD implantation and testing. Ischemic QEEG patterns were defined as those with a 3 standard deviation increase (P less than 0.01) in absolute delta (1.5-3.5 Hz) power persisting for greater than or equal to 2.5 minutes. The majority (80%) of the VF episodes (70) were accompanied by QEEG "slowing" (doubling of the pre-VF low frequency delta waves amplitude). All the patients (5/5) experiencing greater than 6 VF episodes showed a statistically significant increase in the low frequency amplitude. In contrast, this EEG abnormality was apparent in only one of five patients experiencing less than 6 VF episodes. These results suggest a cumulative QEEG depression associated with ICD testing. QEEG may provide an objective means for establishing an individualized upper safe limit of DFT testing and the total number of induced VF episodes.
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PMID:Is defibrillation testing safe? 172 Nov 96

Intracoronary injection of papaverine is used to determine coronary flow reserve in patients. The present study was to investigate the effect of papaverine on the performance of myocardium with reduced flow reserve. In nine anaesthetized open-chest dogs a bypass from the aorta to the left circumflex coronary artery (LCX) was established. Left ventricular end-diastolic and aortic pressure, dP/dt, stroke volume, LCX blood flow, and ECG were monitored. The performance of a segment of subendocardial wall supplied by the LCX was assessed by sonomicrometry. Peak reactive hyperaemia after 15s bypass occlusion was 1.44 +/- 0.09 times the baseline flow (41 ml/min), indicating reduced coronary flow reserve. Papaverine was injected into the bypass (0.3, 0.6, 1.2, 2.5, 5.0 mg/ml, 1 ml in 15s). The maximum LCX flow following PAPA 0.3 mg was comparable to peak reactive hyperaemia, but 10-15% higher after injection of 0.6-5.0 mg papaverine. Systolic shortening of the myocardium (control: 17.5% of end-diastolic length) became reduced in a dose-dependent fashion (5-25%) for about 1 min following papaverine injection. Stroke volume (control: 0.94 +/- 0.12 ml/kg) was reduced by about 8%, left ventricular end-diastolic pressure (control: 6.2 +/- 0.8 mmHg) increased by 15%, and dP/dtmin (control: 1850 +/- 150 mmHg/s) was curtailed by 15-25%. The ECG showed a transient T inversion and S-T depression following papaverine administration and in one experiment ventricular fibrillation occurred after the injection of 2.5 mg papaverine. The observed effects of intracoronary papaverine are consistent with the theory of transient subendocardial ischaemia arising from a redistribution of blood flow from the subendocardial to the subepicardial layers, because of greater vasodilatory capacity in the latter than in the former.
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PMID:Global and regional ventricular function following intracoronary application of papaverine. 177 71

In order to minimize heat loss cold stress induces peripheral vasoconstriction via the sympathetic nervous system. This effect is most pronounced in the extremities. Vasoconstriction does not appear in the head-neck region--a fact of great importance in emergency situations. In order to compensate for heat loss shivering is an early event, where involuntary muscle contractions increase metabolic rate 2-6 fold. Early tachycardia and elevated blood-pressure, followed by progressive bradycardia and lowered pressure are common cardiovascular effects of hypothermia. Death due to ventricular fibrillation or asystole occurs between 28 degrees-25 degrees C. Cold stress causes an osmolal diuresis with sodium and chloride as the main constituents. The natriuresis is of tubular origin and could be due to impaired autoregulation in the kidney and/or depend on the natriuretic polypeptide. The augmented urine flow decreases blood volume, lowers physical working capacity and increases blood viscosity--all negative events in a hazardous situation. Sudden immersion initiates hyperventilation for 1-2 minutes with an increasing risk of drowning. Thereafter ventilation decreases to rates consistent with metabolic requirements. In severe hypothermia carbon dioxide retention causes respiratory and metabolic acidosis. Hypothermia induces progressive depression of mental functions starting with apathy and bizarre behaviour and ending in lethargy and coma often between 30 degrees-28 degrees C. The paradoxal feeling of heat with undressing in agony could depend on cerebral receptor disturbances.
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PMID:Human physiology under cold exposure. 181 74


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