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)

Quinidine, procainamide and disopyramide are antiarrhythmic drugs in the class 1A category. These drugs have a low toxic to therapeutic ratio, and their use is associated with a number of serious adverse effects during long term therapy and life-threatening sequelae following acute overdose. Class 1A agents inhibit the fast inward sodium current and decrease the maximum rate of rise and amplitude of the cardiac action potential. Prolonged Q-T interval and, to a lesser extent, QRS duration may be observed at therapeutic concentrations of quinidine. With increasing plasma concentrations, progressive depression of automaticity and conduction velocity occur. 'Quinidine syncope' (a transient loss of consciousness due to paroxysmal ventricular tachycardia, frequently of the torsade de pointes type) occurs with therapeutic dosing, often in the first few days of therapy. Extracardiac adverse effects of quinidine include potentially intolerable gastrointestinal effects and hypersensitivity reactions such as fever, rash, blood dyscrasias and hepatitis. Procainamide produces electrophysiological changes that are similar to those of quinidine, although Q-T interval prolongation with the former is less pronounced at therapeutic concentrations. Hypersensitivity reactions including fever, rash and (more seriously) agranulocytosis are associated with procainamide, and a frequent adverse effect requiring cessation of therapy is the development of systemic lupus erythematosus. Of the 3 drugs, disopyramide has the most pronounced negative inotropic effects, which are especially significant in patients with pre-existing left ventricular dysfunction. As with quinidine, unexpected 'disopyramide syncope' at therapeutic concentrations has been described. Anticholinergic side effects are common with this drug and may require cessation of therapy. Disopyramide therapy may unpredictably induce severe hypoglycaemia. Severe intoxication with the class 1A agents may result from acute accidental or intentional overdose, or from accumulation of the drugs during long term therapy. Acute overdose can result in severe disturbances of cardiac conduction and hypotension, frequently accompanied by central nervous system toxicity. Decreased renal function can cause significant accumulation of procainamide and its active metabolite acecainide (N-acetyl-procainamide), resulting in severe intoxication. Mild to moderate renal dysfunction is less likely to lead to quinidine or disopyramide intoxication, unless renal failure is severe or concurrent hepatic dysfunction is present. Management of acute intoxication with class 1A drugs includes gut decontamination with provision of respiratory support and treatment of seizures as needed. Hypertonic sodium bicarbonate, by antagonising the inhibitory effect of quinidine on sodium conductance, may reverse many or all manifestations of cardiovascular toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Poisoning due to class IA antiarrhythmic drugs. Quinidine, procainamide and disopyramide. 228 95

A 64-year-old woman with a history of hypertension for ten years and of syncope 18 month previously visited our Division of Cardiology on 12 June, 1989. The S4 and mitral regurgitation were audible at the apex, and her electrocardiogram showed ST-depression in leads II, aVF, V5-6 and prominent U-wave (PU) in V1-3 when first seen. Then, she was thought to have a posterior myocardial ischemia. PU in V1-3 diminished whereas T-wave increased after nitrate and Ca++ blocker. Ergometer exercise ECG showed ST-depression in II, III, aVF, V4-6 and PU with decreased T-wave in V2-3 with no apparent symptoms. Simultaneously, Tl-201 myocardial imaging demonstrated a transient posterior defect. A silent posterior myocardial ischemia was, therefore, confirmed. Coronary arteriograms demonstrated subtotal obstruction of the proximal left circumflex artery, and the peripheral site was filled by collaterals from the right coronary artery. Angina-induced PU in the right precordial leads proved to be useful in detection of posterior myocardial ischemia, and this marker may also improve the possibility of detection of silent posterior ischemia.
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PMID:[A case of silent posterior myocardial ischemia/left circumflex artery obstruction detected by prominent U-wave in right precordial leads]. 228 23

Electrocardiographic (ECG) monitoring was performed on 291 donors during apheresis. Twenty-one donors (7.2%) had clinical symptoms such as discomfort, nausea, chill, numbness, and paresthesia, and 13 of this group exhibited ECG abnormalities, such as tachycardia, bradycardia, and other abnormal wave patterns. The donors with tachycardia and slight bradycardia had no symptoms. Ten donors had moderate to severe bradycardia with pulse rates less than 50 beats per minute; four of them had severe bradycardia (less than 45 beats per minute), and three of the four exhibited severe hypotension, vomiting, fainting, or convulsion. Other abnormal ECG changes, such as supraventricular and ventricular premature contractions, right bundle branch block, ST segment elevation or ST segment depression, and tall, flattened, or inverted T waves were observed in 29 donors (10%). These changes were not associated with symptoms. Only three of these donors complained of discomfort or chest heaviness. The abnormal waves appeared more often in granulocytapheresis donors than in plateletapheresis donors.
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PMID:Abnormal electrocardiographic findings in apheresis donors. 245 70

Frequent or repetitive exercise-induced ventricular ectopic beats are often considered a marker for serious cardiac disease or sudden death, or both. However, the prognostic value of these arrhythmias in an unreferred asymptomatic community-dwelling population over a broad age range is unknown. Of 1,160 subjects aged 21 to 96 years who underwent maximal exercise treadmill testing an average of 2.4 times, 80 (6.9%) developed frequent (greater than or equal to 10% of beats in any 1 min) or repetitive (greater than or equal to 3 beats in a row) ventricular ectopic beats on at least one test. These 80 individuals were significantly older than the group without such arrhythmia (63.8 +/- 12.5 versus 50.0 +/- 16.1 years, p less than 0.0001). A striking age-related increase in the prevalence of frequent or repetitive exercise-induced ventricular ectopic beats was seen in men (p less than 0.0001) but not in women. The prevalence of electrocardiographic abnormalities at rest, exercise-induced ST segment depression and thallium perfusion defects, duration of treadmill exercise, maximal heart rate, systolic blood pressure and rate-pressure product did not differ between these 80 study subjects with frequent exercise-induced ventricular ectopic beats and a control group matched for age and gender. Furthermore, the incidence of cardiac events (angina pectoris, nonfatal myocardial infarction, cardiac syncope or cardiac death) (10% versus 12.5%) as well as noncardiac mortality (each 7.5%) was found to be similar for the study and control groups, respectively, over a mean follow-up period of 5.6 years. No study subjects required antiarrhythmic drugs over this time interval.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence and long-term significance of exercise-induced frequent or repetitive ventricular ectopic beats in apparently healthy volunteers. 247 67

Programmed ventricular stimulation was performed in a 74-year-old patient who had a history of syncope following chest pain. In the baseline state, ventricular tachycardia was not inducible. Immediately following the study protocol, the patient complained of her usual chest pain and ST elevation was documented in lead II with reciprocal ST depression in leads AVF and V1. Programmed ventricular stimulation was repeated (presumably during the occlusive phase of coronary spasm) and a polymorphic ventricular tachycardia with a cycle length of 200 msec was repeatedly induced. Following intravenous nitroglycerin and resolution of chest pain, ventricular tachycardia was not inducible. Coronary angiography with ergonovine testing confirmed coronary spasm of the right coronary artery. We speculate that syncope was caused by ventricular tachycardia following coronary artery spasm. During a 12-month follow-up with calcium blockers and nitrates, there has been no recurrence of chest pain or syncope.
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PMID:Programmed ventricular stimulation during variant angina: report of a case. 248 Dec 84

Experience at University Hospitals of Cleveland with 71 cases of Gardner and Diamond's syndrome of autoerythrocyte sensitization is reviewed. Gardner and Diamond attributed the pathogenesis of the inflammatory bruises typical of this syndrome to sensitization to the stroma of the patients' own erythrocytes, as demonstrated by reproduction of the lesion on intracutaneous injection of erythrocytic stroma. Nearly all the cases my colleagues and I have seen were in adult women, in whom the onset of inflammatory bruising could often be precisely dated, frequently some weeks after an injury or surgical procedure or, more often, severe emotional stress. Bouts of bruising were often preceded by sensations localized to the affected site. Cutaneous responses to the injection of erythrocytes were erratic. The patients described a wide range of both hemorrhagic and nonhemorrhagic complaints, including, among others, severe headaches, paresthesias, repeated syncope, diplopia (sometimes monocular), and "nervousness." Psychiatric studies indicated that patients had overt depression, sexual problems, feelings of hostility, and obsessive-compulsive behavior. The patients had traits that can be described as typical of a hysterical character disorder. Therapy of autoerythrocyte sensitization--that is, psychogenic purpura--has been difficult; in younger individuals, psychiatric therapy has appeared to be beneficial.
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PMID:Psychogenic purpura (autoerythrocyte sensitization): an unsolved dilemma. 248 28

The results of 1,680 consecutive urine and serum toxicologic screens from 1,120 patients, performed in a children's hospital during a 19-month period were surveyed. Among this sample, 52 (4.6%) patients had specimens that contained cocaine and/or metabolite. Fifteen specimens contained ethanol, a benzodiazepine, or a narcotic in addition to cocaine. Four patients were neonates, whereas three were infants from 1 to 7 months of age. The remaining 45 patients were adolescents with a mean age of 19 years. Among the adolescents, 11 had a significant chronic illness. In 19 patients (37%), cocaine exposure was unsuspected until the results of testing for toxic substances were known. The reasons for hospital evaluation included depression/attempted suicide in 19 patients, seizure in five, chest pain in 5, motor vehicle accident in three, syncope in three, abdominal pain in two, pneumomediastinum in two, accidental self-immolation in one, and apnea in one. Twenty patients required medical hospitalization for a total of 268 patient-days. One patient, a neonate, died. There is a striking prevalence of cocaine exposure in the pediatric age group. Among adolescents, this exposure may occur despite the presence of chronic illness. Although the age distribution appears bimodal, infants and young children may also have unsuspected exposure to this toxin. Greater awareness of cocaine exposure in childhood will be needed by primary and tertiary care pediatricians to identify affected children and provide appropriate intervention.
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PMID:Cocaine exposure among children seen at a pediatric hospital. 278 99

A sixty-six-year-old man with severe aortic stenosis, in whom simultaneous and continuous monitoring of the electrocardiogram and arterial blood pressure was performed immediately before, during, and following recovery from exercise-induced syncope, is reported. During exercise the patient developed anginal pain associated with a gradual fall of arterial blood pressure followed by syncope. At the onset of the syncope, arterial blood pressure was extremely low, and the electrocardiogram showed sinus tachycardia. It was assumed from these findings that profound hypotension, induced by peripheral vasodilatation and ischemic myocardial depression leading to inappropriately low cardiac output, was the underlying factor mainly responsible for the occurrence of exercise-induced syncope in the present case.
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PMID:Simultaneous monitoring of electrocardiogram and arterial blood pressure during exercise-induced syncope in a patient with severe aortic stenosis--a case report. 291 63

Inferolateral ST depression, T wave inversion, and QT prolongation have been frequently described in reports of largely symptomatic mitral valve prolapse (MVP) patients, but not in a recent population-based survey of mainly asymptomatic subjects with MVP. To learn if there is a relationship between these ECG changes and symptoms, physical findings or hemodynamic sequelae, we reviewed ECGs from 119 patients, ages 18 to 60 years who had MVP diagnosed by echocardiography. Seventy-four percent had symptoms characteristic of MVP. ST-T changes were found as frequently in asymptomatic patients (29%) as in those symptomatic (27%), and did not identify those with hemodynamic sequelae of MVP (apical systolic murmurs, Doppler-defined mitral regurgitation, or left atrial enlargement). QT prolongation was found more frequently in the symptomatic group (25% vs 10%) but did not predict syncope. When compared to the expected 0.9% prevalence of ST abnormalities in a normal population, ST-T changes and QT prolongation are indeed frequent in MVP, but are not useful in identifying clinically important subsets.
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PMID:Repolarization abnormalities in mitral valve prolapse. 359 11

The case is described of a 43 year old woman with spasmophilic syndrome. For 12 years she had suffered from fainting fits, marked morning asthenia, anxiety, depression, widespread arthromyalgia, blood pressure fluctuations, precordial pains, paresthesia and painful nocturnal cramp. This clinical picture appeared in a subject with a double left kidney and stones in the supernumerary ureter, enlargement of the pancreatic head and tail revealed by a CAT scan and an earlier cholecystectomy. Given the multiplicity of symptoms diagnosis was necessarily by a process of elimination. The data providing grounds for optimism were a positive Chvostek's sign, stable calcium phosphorus profiles, a reduction in ionised calcium and favourable eletromyographic readings.
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PMID:[A case of spasmophilic syndrome]. 360 Nov 38


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