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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to determine the effect of low-pressure and high-pressure reperfusion, with and without ventricular fibrillation, on the recovery of hypertrophic and normal hearts after hypothermic cardioplegia. Fourteen hearts rendered hypertrophic by valvular aortic stenosis and 18 normal canine hearts were subjected to 1 hour of cardioplegic arrest at 28 degrees C during cardiopulmonary bypass. Each heart was then reperfused at a coronary pressure of either 40 mm Hg (low) or 80 mm Hg (high), initially in the empty beating state and then during ventricular fibrillation. Low-pressure reperfusion produced left ventricular subendocardial ischemia in hypertrophic and in normal hearts, shown by marked depression of subendocardial blood flow, myocardial pH, and myocardial oxygen consumption. In hypertrophic hearts the ischemia was more severe and resulted in a persistent depression of left ventricular function and myocardial oxygen consumption even when coronary pressure was returned to normal levels. High-pressure reperfusion was associated with rapid and complete recovery of myocardial metabolism and function in hypertrophic and in normal hearts. During low-pressure reperfusion, ventricular fibrillation exacerbated ischemia in hypertrophic and in normal hearts. During high-pressure reperfusion, a short period of ventricular fibrillation produced no adverse effects either in hypertrophic or in normal hearts. We conclude that low-pressure reperfusion produces subendocardial ischemia in normal and in hypertrophic hearts even in the empty beating state; in hypertrophic hearts it also impairs recovery of myocardial metabolism and function. The adverse effects of low-pressure reperfusion are exacerbated by ventricular fibrillation.
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PMID:Adverse effects of low-pressure reperfusion after hypothermic cardioplegia in normal and hypertrophic hearts. 183 91

Effects of coenzyme Q9 (25 mg/kg), N6-cyclohexyl adenosine (CHA, 100 micrograms/kg) and their combination were compared in rats with short-term or permanent ligation of the left coronary artery. The following parameters were evaluated in three series of experiments: 1) incidence and duration of ventricular fibrillation and tachycardia during coronary occlusion (10 min) and consecutive reperfusion (5 min); 2) contractility and electrical stability of the heart (ventricular fibrillation threshold) in animals with 2-day myocardial infarction; 3) ischemic myocardial mass after coronary occlusion (5 min) and necrotic tissue mass in 2-day myocardial infarction. The rats were given oral drugs 5 days and 2 hours before the study. All the experiments were performed in open-chest anesthetized (nembutal, 50 mg/kg) rats exposed to ventilation at room air. Both the coenzyme Q9 and CHA significantly reduced the incidence and duration of coronary occlusion and reperfusion arrhythmias, prevented cardiac contractile depression (heart rate.developed pressure) and increased ventricular fibrillation threshold). The effect of coenzyme Q9 was more marked than that of CHA. Coenzyme Q9 substantially reduced necrotic tissue mass while CHA diminished ischemic tissue mass. At the same time the total cardioprotective action of the Q9 + CHA combination was more pronounced than that of them used alone.
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PMID:[Cardioprotective effect of combined use of coenzyme Q9 and cyclohexyladenosine in ischemia, reperfusion and acute myocardial infarction]. 192 Nov 36

Experimental and clinical evidence indicates that high risk for sudden death is significantly correlated with post-myocardial infarction depression in two "markers" of vagal activity, heart rate variability and baroreflex sensitivity. The present experiments were designed to answer some of the questions generated by those findings. In 33 anesthetized cats, the neural activity of single cardiac vagal efferent fibers was recorded in control conditions and after injection of phenylephrine (n = 33), before and during a 1-hour coronary artery occlusion (CAO) (n = 17), and before and after removal of the left stellate ganglion (n = 16). In the first minute after CAO, vagal activity increased by 35% from 1.66 +/- 0.37 to 2.57 +/- 0.62 impulses/sec (p less than 0.01); despite a slight decline, it remained for the entire CAO above the control values, to which it returned after CAO release. Of 17 cats, ventricular fibrillation occurred in nine (susceptible) and eight survived (resistant). Resistant and susceptible cats had different reflex vagal responses to CAO. Whereas the resistant cats had a 48% (p less than 0.01) increase by the second minute of CAO, susceptible cats had no change (-18%, p = NS) in vagal activity. These differences were independent of blood pressure changes. The increase in vagal efferent activity in response to the blood pressure rise induced by phenylephrine (baroreceptive reflex) was more marked in the resistant cats compared with the susceptible cats (+246 +/- 66% versus +80 +/- 14%, p less than 0.025). Just before the injection of phenylephrine, vagal activity was not different between resistant and susceptible cats (1.58 +/- 0.35 versus 1.48 +/- 0.30 impulses/sec, p = NS). In 16 cats, left stellectomy increased cardiac vagal efferent activity by 75% (p less than 0.01), and the reflex vagal activation secondary to phenylephrine was further enhanced (from 2.2 +/- 0.4 to 4.7 +/- 0.7 impulses/sec, p less than 0.001). These data demonstrate that 1) cardiac vagal efferent activity increases in response to acute myocardial ischemia--much more so among the animals destined to survive, 2) before CAO, susceptible and resistant animals can be identified by the vagal response to blood pressure increase (assessed clinically by baroreflex sensitivity) and not by tonic vagal activity (assessed clinically by heart rate variability), and 3) the findings with left stellectomy support the hypothesis that vagal activity decreases after myocardial infarction because of an increase, secondary to abnormal stretch of the cardiac mechanoreceptors, in cardiac sympathetic afferent traffic, which exerts a tonic restraint on vagal outflow.
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PMID:Single cardiac vagal fiber activity, acute myocardial ischemia, and risk for sudden death. 193 62

Arrhythmias are frequent and associated with a poor prognosis, especially when they arise from the ventricle. Although the correction of predisposing factors and improvement of hemodynamic conditions are essential, the use of antiarrhythmic drugs in this context poses problems. The treatment of even complex ventricular extrasystoles has not been shown to effectively prevent the serious arrhythmias responsible for sudden death. Depression of left ventricular function and: Or proarrhythmic effects of antiarrhythmic therapy in some patients, probably offset the benefits observed in others. The treatment of atrial arrhythmias remains traditional: reduction by drugs or electrotherapy and prevention of recurrences, or simply slowing the ventricular response. Sustained ventricular tachycardia and resuscitated ventricular fibrillation should be managed more aggressively, not by empirical antiarrhythmic treatment but by medical therapy guided by the results of electrophysiological studies, and, when this fails, by non-medical treatment: fulguration, implantable defibrillator, antiarrhythmic surgery, or even cardiac transplantation.
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PMID:[Treatment of arrhythmias in chronic cardiac insufficiency]. 198 Jan 88

In Denmark, 6,000-10,000 persons die annually from sudden cardiac death. The majority of these die on account of ventricular fibrillation. A patient is presented here who suffered from recurrent lipothymic seizures which were primarily diagnosed as epilepsy. On account of absence of paraclinical documentation and because of suspected depression, treatment with a cyclic antidepressive agent was commenced, which further increases the tendency to sudden cardiac death. The patient was then brought to hospital with Lidocaine-resistant ventricular fibrillation which responded partly to Ajmalin and partly to Disopyramide. The lipothymic seizures were then interpreted as being precipitated by intermittent malignant episodes of cardiac arrhythmia. During the subsequent six months, the patient has felt well and has been free from lipothymic seizures while receiving 200 mg Mexiletin thrice daily. Attention is drawn to the value of Holter monitoring in the investigation of lipothymic seizures. Lidocaine (despite the existence of resistant cases) must still be considered to be the preparation of first choice on account of extensive knowledge about and confidence in the preparation.
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PMID:[Recurrent ventricular tachyarrhythmias primarily diagnosed as epilepsy]. 202 54

By means of Langendorff method the isolated rat heart was perfused with Krebs Henseleit solution. Following ligation of the left descending coronary artery for 10 min the heart was reperfused for 3 min. The incidence of ventricular fibrillation in the reperfusion period was 100%, and the normal sinus rhythm time was shortened to 29 s within 3 min of reperfusion. Administration of lipoic acid (6.8 X 10(-6)-1.7 X 10(-4) mol/L) to the perfusate significantly reduced the incidence of ventricular fibrillation to 33-50% and prolonged the normal sinus rhythm time to 97-107 s. APA, RP, and Vmax recorded from the guinea pig papillary muscle were depressed due to the deleterious effect of xanthine oxidase and hypoxanthine free radical generating system. Under the treatment of lipoic acid (3.5 X 10(-5) mol/L), the depression of APA, RP, and Vmax were significantly relieved. This confirms that lipoic acid treatment, owing to its free radical scavenger effect, is able to protect myocardium from free radical induced electrophysiological abnormalities, and consequently decrease the incidence of malignant arrhythmias.
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PMID:[Effects of lipoic acid on reperfusion induced arrhythmias and myocardiac action potential alterations induced by free radical generating system]. 206 84

In order to evaluate perioperative electrical cardiac disturbances and ST segment changes, 42 patients (38 M, 4 F, aged 57 +/- 6 ys) were studied using 24-hour Holter monitoring before, during and after coronary bypass surgery. In the 4-6 hours before cardioplegic arrest, 38% of patients had ST segment changes. No patient and malignant arrhythmias. The injection of cold cardioplegic solution was followed by bradycardia, ventricular tachycardia, ventricular fibrillation and isoelectric line within 2-4 minutes. After aortic declamping, 30 patients were defibrillated. Impulse formation and conduction disturbances, found in 55% of patients, solved themselves in 1 to 60 minutes. Bundle branch block continued in just 4 cases. A total of 59% of patients had ST segment elevation for 14 +/- 14 minutes and 19% had ST segment depression for 19 +/- 20 minutes. Successive transient ST segment changes were detected in 38% of patients. Sustained ventricular tachycardia occurred during 2 ischemic episodes. Impulse formation and conduction disturbances were not related to the duration of cardiac arrest or ventricular fibrillation, but were more frequent and lasted longer in patients with incomplete revascularization. Transient ST segment depression far from aortic declamping correlated with preclamping ischemia. Transient ST segment elevation correlated with incomplete revascularization. We concluded that ECG signs of intraoperative damage were reversible. Moreover, perioperative transitory ischemia was frequent but could be prevented by coronary active drug administration. On the other hand incomplete revascularization was associated with electrical disturbances and ischemia.
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PMID:[Intra- and perioperative arrhythmia and ischemic signals in myocardial revascularization patients]. 209 May 45

Sudden unexpected nocturnal death syndrome (SUNDS) is a distinct clinical entity in previously healthy, young, Southeast Asian males. It is well known in the Philippines and more recently recognized in the U.S. by nonspecific autopsy findings, with no evidence of underlying disease and absence of toxic drug or alcohol levels. In 1973-89, 14 cases of apparent SUNDS came to coroner's autopsy in the Commonwealth of the Northern Marianas (CNMI) and Guam. All 14 cases, with the exception of one Yapese, were previously healthy, male Filipinos, aged 23 to 55, who were either found dead in bed, or described by their colleagues as having nocturnal seizure activity consisting of gurgling, frothing, and tongue biting immediately prior to death. Autopsy findings showed no anatomic findings to account for death. Comprehensive serum and urine drug analyses were negative. All decedents showed absence of significant atherosclerosis or grossly detectable structural cardiac anomaly, while four showed cardiomegaly. Migrants from Southeast Asia carry with them a pre-disposition to this syndrome, which appears to decline with longer residence in the new country. The mechanism of death in SUNDS is believed to be ventricular fibrillation, possibly precipitated by sudden sympathetic discharge. Studies suggest at least some deaths may be associated with an abnormal cardiac conduction system. Acute pancreatitis has been a finding in some series, but not our cases. Why the condition is virtually limited to males and seemingly sleep-triggered, has not been adequately explained. Stress and depression are believed to be predisposing factors.
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PMID:Sudden unexpected nocturnal death syndrome in the Mariana Islands. 188 84

The influence on contractile force (CF) and the propensity for ventricular fibrillation (VF) from infusing the non-ionic contrast medium iohexol during normal (75 cm H2O) and reduced perfusion pressure (35 cm H2O) were investigated in the isolated rabbit heart. Both during normal and reduced perfusion pressure iohexol (150 mg I/ml) with oxygen saturation caused a smaller reduction of CF than iohexol without oxygen. During reduced pressure iohexol with sodium addition (28 mM NaCl) caused less depression of CF than iohexol without sodium. The combination of sodium addition and oxygen saturation had the least influence on CF. Iohexol (350 mg I/ml) without sodium had a similar fibrillatory propensity during both normal and reduced pressure. Enriching iohexol with 28 mM NaCl decreased the risk of VF. The decrease was similar during both normal and reduced pressure. The risk of VF from oxygen saturation of iohexol (350 mg I/ml, without sodium) was similar during both normal and reduced pressure. It is concluded that a small addition of sodium and/or oxygen saturation of a non-ionic monomeric contrast medium have beneficial effects on the heart both during normal perfusion pressure and during ischemia.
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PMID:Sodium addition and/or oxygen saturation of iohexol during normal and reduced perfusion pressure. Effects on contractile force and risk of ventricular fibrillation in the isolated rabbit heart. 226 4

The currently available automatic implantable cardioverter-defibrillator has proven highly successful for termination of ventricular tachycardia and fibrillation. Newer devices, however, permit lower energy shocks to be delivered initially and longer episodes of arrhythmia to occur before shocks are delivered. These changes may result in longer durations of arrhythmia before successful termination. Little is known about the effects of the duration of ventricular fibrillation on the efficacy of defibrillating shocks. In this study, we examined the efficacy of defibrillating shocks in 22 patients undergoing automatic implantable cardioverter-defibrillator implantation or generator change. Defibrillating shocks ranging from 300 to 600 V (5.9-24.2 J) were delivered in matched pairs after 5 and 15 seconds of ventricular fibrillation. For the 300-V shocks (5.9 J), defibrillation was accomplished in 82% of patients when the shocks were given after 5 seconds of ventricular fibrillation and in only 45% of patients when the shocks were delivered after 15 seconds (p less than 0.01). At higher energies, there was no difference in the efficacy of defibrillation shocks delivered after 5 compared with 15 seconds of ventricular fibrillation. The postshock aortic, systolic, and diastolic blood pressures were significantly lower when the shocks were given after 15 seconds of ventricular fibrillation than after only 5 seconds. We conclude that the duration of ventricular fibrillation affects defibrillation efficacy especially at energies that are relatively low compared with maximal device outputs and that longer episodes of ventricular fibrillation cause more postshock hemodynamic depression. These observations have implications for defibrillation threshold testing at the time of device implantation and for the design and programming of future automatic implantable antitachycardia devices.
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PMID:Effect of duration of ventricular fibrillation on defibrillation efficacy in humans. 233 63


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