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)

A 48-year-old man with severe pectus excavatum presented with incapacitating supraventricular tachycardia, paroxysmal in nature and invariably provoked by exercise. During mild supine leg exercise on a bicycle ergometer an abnormal increase in right heart pressures, particularly in the right atrium, was observed, followed immediately by supraventricular tachycardia. The latter was also shown during upright exercise on a treadmill. Operative correction of the deformity led to complete relief from the dysrhythmia and a normal haemodynamic response on exercise. The pre- and post-operative studies lend support to the conclusion that the sternal depression was the most likely cause of the cardiac abnormality.
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PMID:Pectus excavatum and cardiac dysfunction: a case report with pre- and post-operative haemodynamic studies. 44 3

Changes in electrocardiograms, blood pressure, pH, and partial pressure of gases (Po2 and Pco2) in arterial blood were studied in goats poisoned by urea or ammonium compounds under spontaneous and artificial respiration and in nonconvulsive state. Abnormal electrocardiogram patterns, such as ventricular flutter, ventricular premature beat, atrioventricular dissociation, depression of ST-segment and sinus tachycardia, were all observed after the occurrence of tetanic convulsion. The electrocardiogram pattern seen at the respiratory arrest showed sinus or supraventricular tachycardia; respiratory arrest preceded cardiac arrest in all the goats, but one. Blood pressure was markedly elevated, accompanied with tetanic convulsion. Po2 decreased gradually and the level was below 30 mm Hg (37.0 degrees C) at respiratory arrest and the final opisthotonus. Artificial respiration starting at the final opisthotonus could delay the cardiac arrest. Under nonconvulsive urea-poisoning with gallamine triethiodide and with artificial respiration of air or a mixture of air and oxygen to elevate the Po2 level, changes of electrocardiogram, blood pressure, and Po2 were similar to those seen under convulsive urea-poisoning. The main cause of death was discussed and presumed to be respiratory and cardiovascular failure.
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PMID:Electrocardiographic observation on goats with urea-ammonia poisoning and a consideration on the main cause of death. 60 86

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

Determining safe and effective antiarrhythmic therapy in paediatric patients requires definition of the mechanism of the arrhythmia, determination of associated risk factors for treatment (such as the presence of congenital cardiac defects, myocarditis or cardiomyopathy), and monitoring for potential drug side effects related to the treatment. A number of modalities for non-invasive evaluation of arrhythmias is available, including ECG, 24-hour ambulatory Holter monitoring, and transtelephonic ECG transmission. Arrhythmias requiring medical treatment in children with normal cardiac anatomy and function include supraventricular tachycardia (SVT), ventricular tachycardia (VT) and primary atrial tachycardias. SVT is treated acutely with vagal manoeuvres or drugs which slow AV conduction [adenosine (adenine riboside), edrophonium, phenylephrine or verapamil]. When medical conversion is not achieved, transoesophageal overdrive pacing or direct current (DC) cardioversion may be required. Long term drug therapy for SVT includes first-line treatment with digoxin, verapamil or propranolol. Ventricular tachycardia is managed acutely with DC cardioversion and intravenous lidocaine (lignocaine). Chronic drug regimens include mexiletine, propranolol or amiodarone. In children with structural congenital heart disease or myocardial dysfunction, hazards of drug therapy for arrhythmias include depression of cardiac function, proarrhythmia (drug-induced worsening of arrhythmias), and conduction abnormalities. Care must be taken to choose medication regimens which are likely to be effective with minimum risk of potentiating abnormal haemodynamics or conduction.
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PMID:Cardiac arrhythmias in childhood. Diagnostic considerations and treatment. 172 43

Electrocardiographic (ECG) changes were studied in 120 consecutive subjects during and after upper GI endoscopy done in ambient hypoxia (PO2-120 mmHg) at Shimla (2200 m). No premedication was given to any of the subjects. There were 75 men and 44 women. Fifty three subjects were aged 40 years or below (Group I) and 67 subjects were above 40 (Group II). There were 29 subjects with and 91 subjects without cardiac diseases. Increase in heart rate was seen in 96.6% of subjects. Maximum rise in heart rate was found in cardiac patients. ST depression was seen in 14.2%, T wave inversion in 13.3%, supraventricular tachycardia in 5.8% and ventricular ectopics in 1.6%. ST depression was more frequent in cardiac than in non cardiac patients (P less than 0.001) and T wave inversion was more frequent in women than in men (P less than 0.001). All the changes reverted to normal within 10 minutes. ECG changes notwithstanding, upper GI endoscopy without premedication in the presence of ambient hypoxia is a safe procedure.
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PMID:Electrocardiographic changes during upper gastrointestinal endoscopy in ambient hypoxia. 172 99

Pentoxifylline, a methylxanthine, is an effective modulator of alkylating agents in tissue culture and in human tumor explants in mice. In this Phase I trial, escalating dose controlled release pentoxifylline was administered p.o. 3 times daily for 5 days (15 doses) with a constant dose of thiotepa, 40 mg/m2 i.v. on day 2. Forty-four courses of escalating doses of pentoxifylline varying from 400 to 2400 mg were administered to 22 patients with refractory malignancies. Gastrointestinal toxicity, consisting mainly of nausea and vomiting, was dose limiting at 2400 mg pentoxifylline and subsided completely within 24 h of cessation of the drug. Nongastrointestinal toxicity of this thiotepa/pentoxifylline combination was infrequent and included bone marrow depression and supraventricular tachycardia. Increasing the dose of pentoxifylline did not increase the frequency of these rare toxic effects. Plasma concentrations of pentoxifylline and its major metabolites were determined by gas chromatography. Drug accumulation was noted within a cycle (i.e., by day 5) in only two patients and between cycles in no patient. The recommended Phase II dose of p.o. pentoxifylline is 1600 mg (four 400-mg tablets) when given 3 times daily for 5 days (15 doses) with 40 mg/m2 i.v. thiotepa. Based on an interspecies comparison, this dose exceeds that predicted from mouse models to enhance chemotherapy. This regimen can be safely administered on an outpatient basis, with adequate control of gastrointestinal symptoms achieved by standard antiemetics and intermittent dosing with meals. Phase II trials are required to determine the activity of alkylator/modulator combinations.
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PMID:Phase I trial of escalating pentoxifylline dose with constant dose thiotepa. 211 82

These findings permit the following conclusions on cardiac changes induced by high-performance sports and high levels of training. Sinus bradycardia and AV block can frequently be observed in athletes, but they do not require attention as long as they are asymptomatic or do not produce pauses exceeding 4 seconds. Persistent rather than transient second-degree AV block or Mobitz second- or third-degree AV block is an extremely unusual finding even in athletes and should be considered a sign of organic lesions until proved otherwise. Supraventricular and AV node ectopic beats are not more frequent in athletes than in the general population except for atrial fibrillation. WPW syndrome is of particular importance, since rapid conduction to the ventricle via the accessory AV pathway is possible, especially if there is a tendency toward atrial fibrillation. Likewise caution is required in athletes with hypertrophic cardiomyopathy. Here hemodynamic deterioration must be anticipated with the occurrence of supraventricular tachycardia. Simple ventricular arrhythmias occur among athletes with the same frequency as in the general population, but they usually disappear with exercise. The occurrence of complex ventricular forms of arrhythmia should always prompt cardiologic examination in search of underlying cardiac disease, particularly hypertrophic or dilated cardiomyopathy. The presence of ventricular arrhythmias without evidence of underlying heart disease does not indicate a special or increased risk of sudden cardiac death. A higher incidence of right and/or left ventricular hypertrophy, exercise-reversible ST elevation, and exercise-reversible changes in T waves (T negativity, sharp and/or excessive T waves) can be considered physiologic changes in the ECGs of athletes. These changes correlate closely with the type of sports activity and degree of training and are reversible when the activity is stopped. Horizontal ST segment depression are by contrast very rare in athletes and should always be clarified by cardiologic examination. Exercise-induced sudden cardiac death in athletes is unusual without preexisting heart disease. The cause of sudden cardiac death among athletes less than 40 years of age can be predominantely ascribed to congenital heart diseases (such as hypertrophic cardiomyopathy or coronary anomalies). In athletes more than 40 years of age and with increasing age, coronary heart disease is the most frequent autopsy finding. A corresponding risk stratification should take these partial dangers into account.
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PMID:ECG variants and cardiac arrhythmias in athletes: clinical relevance and prognostic importance. 219 78

In a group of 37 patients (30 men and 7 women aged from 36 to 67 years, men age 50.3) after a first acute myocardial infarction the frequency was analysed of the episodes of silent myocardial ischaemia with ST depression, and its correlation with arrhythmia was studied during outpatient ECG monitoring and exercise test on cycle ergometer. Outpatient ECG monitoring during 24 hours was done with a recorder Oxford Medilog MR-14 AM System 8-12 weeks after the onset of infarction. In the same patients the exercise test on cycle ergometer (KF-12 Medicor) was done by graded exercise method with workload increasing by 25 Watt every 3 minutes. The test was terminated after achieving 85% maximal heart rate or appearance of limiting signs. Each episode of ST depression by 1.0 mm or more lasting over 1 minute with horizontal or sloping ST depression 80 msec from point J was regarded in both cases as ischaemic. During outpatient ECG monitoring it was observed that 30 out of 37 (81.1%) had 138 episodes of ST depression, including 45 (32.6%) associated with pain and 93 (67.9%) painless (p less than 0.02). The mean maximal ST depression during painful and painless episodes was respectively 3.4 +/- 1.3 mm and 2.9 +/- 1.1 mm (p less than 0.03). Out of 30 patients 7 (23.3%) had 54 episodes of various arrhythmias, with bursts of ventricular ectopic beats, in one patient supraventricular tachycardia and in another one grade II atrioventricular block developed. These patients had also isolated ventricular ectopic beats. In 6 patients (20.0%) arrhythmia was temporarily associated with signs of ischaemia with ST depression.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Arrhythmia and silent myocardial ischemia in patients after myocardial infarction]. 225 Dec 10

Sixteen patients who had manifested ST segment depression during episodes of paroxysmal supraventricular tachycardia (PSVT) were studied with exercise testing in order to detect coronary artery disease and myocardial ischaemia. No ST segment depression was observed during exercise testing in 15 out of the 16 patients tested. Paroxysms of supraventricular tachycardia associated with ST segment depression occurred during exercise testing in three cases. The ST segment depression was immediately apparent, remained constant throughout the supraventricular tachycardia and was almost instantly abolished following conversion to sinus rhythm. Patients with heart rates greater than 250 beats min-1 during PSVT had marked ST segment depression associated with the tachycardia. These results suggest that coronary artery disease and myocardial ischaemia are not involved in the genesis of ST segment depression during PSVT. Tachycardia per se may be the cause of ST segment depression by altering the slope of phase 2 of the ventricular action potential. Retrograde atrial activation may also induce ST segment shifts in some of the cases.
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PMID:Exercise testing for assessment of the significance of ST segment depression observed during episodes of paroxysmal supraventricular tachycardia. 228 27

The purpose of this study was to determine if the known frequency-dependent effects of diltiazem on inward calcium current result in selective actions during supraventricular tachycardia. These effects were evaluated by use of an experimental model of orthodromic atrioventricular reentrant tachycardia (AVRT). AVRT was induced in 15 dogs over a wide range of retrograde conduction times before and after two doses of diltiazem. Diltiazem produced a tachycardia-related suppression of atrioventricular nodal conduction resulting in greater efficacy for faster than for slower AVRTs. The degree of slowing for tachycardias that remained inducible after diltiazem administration was greater for AVRTs with a rapid initial rate (dose 1, 29%; dose 2, 40%) than for slower AVRTs (dose 1, 11%, p less than 0.01; dose 2, 18%, p less than 0.001). Rate-dependent AVRT slowing occurred because of a time-dependent phase of AH interval prolongation after the onset of tachycardia, which was observed only after diltiazem administration. to further clarify the mechanism of diltiazem's selective actions against faster tachycardias, its effects on the minimum pathway for reentry, or wavelength, were examined in four dogs. The ratio of refractory period to revolution time (RP/RT), an index of wavelength, was measured for each AVRT before and after diltiazem administration. Diltiazem increased the positive slope of the relation between RP/RT and the AVRT rate threefold compared with control (p less than 0.05). This rate-dependent effect prevented AVRT when RP/RT became greater than unity. In conclusion, rate-dependent atrioventricular node depression by diltiazem results in greater tachycardia slowing and higher rates of termination during atrioventricular reentrant tachycardias with faster initial rates and shorter retrograde conduction intervals.
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PMID:Antiarrhythmic actions of diltiazem during experimental atrioventricular reentrant tachycardias. Importance of use-dependent calcium channel-blocking properties. 229 37


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