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 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

The verapamil analog falipamil is a new compound with specific bradycardic action on the sinus node. It differs from verapamil with respect to its electrophysiological and haemodynamic actions. Falipamil causes a slight prolongation of intraatrial and intraventricular conduction, whereas sinuatrial and AV-node conduction is enhanced. The refractory periods of atrial and ventricular myocardium and ventricular repolarization are significantly prolonged, whereas the refractory period of the AV-node is shortened. Falipamil fails to influence any haemodynamic parameter significantly at rest, if heart rate is kept constant. In exercise-induced myocardial ischaemia, changes in haemodynamics reflect changes in heart rate. Increased sinus rate at rest is significantly reduced by falipamil 15%-25%. Around 150 mg falipamil prove aequieffective to about 40 micrograms pindolol. Atropine-induced and catecholamine-induced sinus tachycardia is also significantly diminished. Increased sinus rate during exercise is lowered by about 10%. Through reduction of heart rate, falipamil proves capable of significantly diminishing or even preventing ischaemic ST-segment depression and ischaemia induced increase in pulmonary capillary pressure. Thus falipamil can be used to normalize sinus rate in patients with sinus tachycardia of various origin, particularly in intensive care, in acute ischaemic heart disease, in anaesthesia and in surgery cases.
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PMID:A summary of the acute effects of falipamil in man. 333 May 25

Therapeutic decisions in patients with angina pectoris are traditionally based on the history reported by the patient, since objective evidence of myocardial ischaemia during daily life is often not available. In this study, ambulatory ST segment monitoring was performed in 60 patients with a history of chronic stable angina pectoris, positive exercise test and/or positive coronary angiography, and a correlation was made between the episodes of chest pain and ST segment change. The patients were grouped according to the results of exercise testing and coronary arteriography, and one group was studied with and without antianginal medication. Overall, 195 episodes of angina were noted, only 94 of which (48%) were accompanied by ST segment depression. Pain and ST segment changes were best correlated in patients with a positive exercise test, positive angiography and who were not receiving antianginal medication. In 101 episodes of chest pain, ST segment change could not be identified; in 18 (18%) there was sinus tachycardia, in 12 (12%) ventricular premature beats, and in 71 (70%) sinus rhythm solely. Thus, anginal pain appears not to be the reliable indicator of transient myocardial ischaemia as was previously thought, a finding which supports the use of objective methods in identifying episodes of transient myocardial ischaemia in daily life.
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PMID:The sensitivity of the symptom angina pectoris as a marker of transient myocardial ischaemia in chronic stable angina pectoris. 342 83

Forty three expired cases due to ruptured cerebral aneurysm were studied in electrocardiographic alterations with special reference to other complications of the autonomic nervous system. The cases with past history of ischemic cardiovascular disease had been excluded. The age of the patients ranged between 23 to 79 years old (average 50.1 years old). The clinical condition of the patients according to Hunt & Kosnik classification I in 1 case, II in 11 cases, III in 14 cases, and IV & V in 17 cases. The duration between the aneurysm rupture and admission was within 24 hours in 16 cases, 2 to 3 days in 13 cases, 4 to 7 days in 9 cases, and 2 to 3 weeks in 5 cases. The site of ruptured aneurysms was anterior communicating artery in 12 cases, internal carotid artery in 24 cases, and others in 7 cases. The direct surgeries to the aneurysms were performed in 22 cases, and not done in 21 cases. The electrocardiographic alterations were found as follows: flat or inverted T in 19 cases, prolonged QTc in 33 cases, manifest U in 14 cases, ST elevation or depression in 10 cases, Ta (atrial T) in 10 cases, left ventricular hypertrophy in 8 cases, sinus tachycardia in 7 cases, sinus bradycardia in 12 cases, and arrhythmias with SVPC or VPC (supraventricular or ventricular premature contraction), or sinus arrhythmia in 12 cases. Prolonged QTc, and flat or inverted T were most often found in the cases with ruptured aneurysm of the anterior communicating artery, and next in those with the internal carotid artery, and least often in those with others.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Electrocardiographic alterations in expired cases due to ruptured cerebral aneurysm: correlation with other complications relating to the autonomic nervous system]. 348 74

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Tricyclic antidepressants are among the commonest causes of both non-fatal and fatal drug poisoning in the world. Their toxicity is due to effects on the brain, the heart, the respiratory system and the parasympathetic nervous system. Symptoms usually appear within 4 hours of an overdose and all but the most seriously poisoned patients recover within 24 hours. The most common clinical features are dry mouth, blurred vision, dilated pupils, sinus tachycardia, pyramidal neurological signs, and drowsiness. In severe poisoning, there may be coma, convulsions, respiratory depression, hypotension and a wide range of electrocardiographic (ECG) abnormalities. The most frequent findings on the ECG are prolongation of the PR and QT intervals; the tracing may resemble bundle branch block or supraventricular or ventricular tachycardias. Treatment of poisoning due to the tricyclic antidepressants is essentially supportive, there being insufficient evidence at present to recommend the use of methods to increase elimination of the drug from the body. Gastric aspiration and lavage should be performed if more than 750 mg of drug have been taken. There must be regular monitoring for hypoxia, acidosis and hypokalaemia and these complications should be corrected enthusiastically. Convulsions should be treated with diazepam or chlormethiazole. Muscular paralysis and artificial ventilation should be employed if anticonvulsants are ineffective. Hypotension should be treated firstly by fluid replacement and then with sympathomimetic agents (dopamine or dobutamine). Antiarrhythmic drugs should only be employed if there is evidence of circulatory failure which fails to respond to correction of hypotension. Sodium bicarbonate infusions should be given to cardiotoxic patients who are acidotic and are worth trying even if the patient is not acidotic. Although physostigmine salicylate will reverse most of the features of tricyclic antidepressant poisoning, its effects are short-lived in serious toxicity and it can produce dangerous side effects; physostigmine should therefore be reserved for those patients who have complications of coma or who have resistant cardiotoxicity or convulsions. Drug screening and quantitative determination of tricyclic antidepressant serum concentrations are useful in a minority of patients who have severe, unusual or prolonged symptoms.
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PMID:Poisoning due to tricyclic antidepressant overdosage. Clinical presentation and treatment. 353 21

Electrocardiographic (ECG) changes were studied in 82 adult patients with a mean age of 49 years undergoing microlaryngoscopy. The patients were pretreated with practolol 0.15 mg/kg i.v. 5 min before induction of anaesthesia with thiopental. Anaesthesia was maintained with nitrous oxide in oxygen, fentanyl and suxamethonium-infusion. ECG changes occurred in 49% of the patients before anaesthesia and procedure. Pre-existing ECG changes increased or new changes occurred in 39% of the patients during intubation and in 38% during the procedure. The most common preanaesthetic ECG changes were flat or negative T-wave (18%), sinus tachycardia (13%), ischaemic S-T segment depression (8.5%) and intraventricular conduction disturbance (8.5%). ECG changes during intubation were sinus tachycardia (16%), ventricular ectopic beats (12%), supraventricular ectopic beats (10%) and ischaemic S-T segment depression (10%). The most common changes during microlaryngoscopy were supraventricular ectopic beats (16%), T-wave flattening or inversion (15%), ischaemic S-T segment depression (11%) and sinus bradycardia (10%). In all patients ECG changes disappeared without any special treatment. Unlike our earlier identical study without practolol pretreatment, neither sinus tachycardia nor junctional rhythm occurred during microlaryngoscopy in the present study. The results suggest that practolol pretreatment before microlaryngoscopy is especially useful when sinus tachycardia and junctional rhythm should be avoided.
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PMID:Electrocardiographic changes during microlaryngoscopy in practolol-pretreated patients under balanced anaesthesia. 370 99

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 +/- 18 vs 117 +/- 18 beats/min, p less than 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, myocardial ischemia frequently develops during daily life; silent ischemia is an important component of this syndrome; and increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.
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PMID:Transient myocardial ischemia during daily life in patients with syndrome X. 378 14

One hundred twelve patients in preterm labor were followed prospectively, with electrocardiograms taken before ritodrine therapy and at 6 and 24 hours of treatment. Ninety-six percent of patients developed sinus tachycardia. Other changes were seen in 79% of the study group. These changes included ST segment depression in 70%, T wave flattening or inversion in 55%, and prolongation of the QT interval in 35% of our sample. None of the electrocardiograms showed the presence of a significant axis deviation, a change in QRS interval, or arrhythmia. No correlation was seen between symptoms of ischemia and electrocardiographic changes. A drop in potassium concentration was noted initially, but a direct correlation between potassium concentrations and frequency of electrocardiographic changes was not present. We conclude that the electrocardiographic changes that are often observed during myocardial ischemia may be frequent in asymptomatic patients treated with ritodrine and that these changes may be a physiologic expression of ritodrine-induced tachycardia or hypokalemia. The validity of the use of the presence of electrocardiographic changes as the only criterion for discontinuation of ritodrine therapy is questioned.
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PMID:Electrocardiographic changes associated with ritodrine-induced maternal tachycardia and hypokalemia. 396 85

Although overdoses of tricyclic antidepressant are known to produce both sinus tachycardia and ventricular tachyarrhythmias in man, these have been assumed to occur by independent mechanisms. This study was designed to evaluate the relationship of ventricular activation frequency to the cardiotoxic effects of amitriptyline. When amitriptyline was infused into dogs with formalin-induced atrioventricular (AV) block to evaluate a broad range of pacing frequencies, the drug produced dose-related QRS prolongation that was markedly frequency dependent. Similar frequency-dependent depression of the maximum rate of depolarization (Vmax) was noted for canine Purkinje fibers superfused with amitriptyline in vitro. The time constant of recovery from amitriptyline-induced block was dose independent and averaged 228 msec in vivo and 216 msec in vitro. When amitriptyline was infused into dogs with intact AV conduction, sinus tachycardia occurred within 15 min, followed by progressive QRS prolongation and ventricular tachyarrhythmias after an average 29 min. Slowing of sinus rate by vagal stimulation (seven dogs) or intravenous metoprolol (five dogs) reproducibly reversed the QRS prolongation and ventricular tachyarrhythmias caused by amitriptyline. These studies show that amitriptyline produces frequency-related depression of ventricular conduction in vivo, with a time dependence similar to effects on the maximum rate of depolarization in vitro. Interventions that slow heart rate reverse the adverse effects of amitriptyline on ventricular conduction and cardiac rhythm.
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PMID:Frequency-dependent effects of amitriptyline on ventricular conduction and cardiac rhythm in dogs. 402 83


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