Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sick sinus syndrome (SSS) is usually a disease of the elderly produced by idiopathic degeneration of the sinoatrial node. Its initial manifestations range from asymptomatic to nonspecific and include palpitations, fatigue, confusion, and even syncope and sudden death. Electrocardiographic evidence of SSS includes inappropriate sinus bradycardia, sinus pause or arrest, or sinus exit block. These bradyarrhythmias may alternate with tachyarrhythmias, especially atrial fibrillation, to create the tachycardia-bradycardia syndrome. The diagnosis of SSS may be established by electrocardiography or ambulatory monitoring in the majority of cases. Medications such as digoxin, beta-blockers, and calcium blockers may initiate or worsen the manifestations of SSS. Permanent pacing is indicated for symptomatic bradyarrhythmias. Progression of SSS is mostly dependent on the presence and severity of associated coronary or hypertensive heart disease.
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PMID:Update on sick sinus syndrome, a cardiac disorder of aging. 240 55

A 30-year-old pregnant woman was admitted to the Cardiology Research Center with syncope, dizziness, and fatigue on exertion. On ECG complete atrioventricular block was diagnosed. Permanent pacemaker implantation was performed with the guidance of ECG and two-dimensional echocardiography and without the use of fluoroscopy.
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PMID:Permanent pacemaker implantation in a pregnant woman with the guidance of ECG and two-dimensional echocardiography. 244 4

In this report we describe fatigue of the His-Purkinje system during retrograde stimulation of the His bundle by ventricular programmed stimulation. The patient underwent electrophysiologic evaluation for syncope. Antegrade conduction and supraventricular studies were normal with the exception of baseline left bundle branch block. During programmed ventricular stimulation, the patient developed intra-Hisian and infra-Hisian block with symptomatic 3:1 atrioventricular heart block requiring insertion of a permanent pacemaker. This case demonstrates the need for careful study of both antegrade and retrograde conduction properties of the His bundle and atrioventricular node when performing standard His bundle studies in evaluation of syncope.
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PMID:Fatigue of the His-Purkinje system during routine electrophysiologic studies. 245 12

Midodrine, a peripheral alpha-adrenergic agonist, finds use in the clinical management of patients with orthostatic hypotension or hypotension secondary to other clinical conditions or drug therapies. Midodrine is almost completely absorbed after oral administration and undergoes enzymatic hydrolysis to form its pharmacologically active metabolite, de-glymidodrine. In patients with refractory orthostatic hypotension oral midodrine increases standing blood pressure and improves symptoms of orthostatism, such as weakness, syncope, blurred vision and fatigue, without any associated cardiac stimulation. Comparative studies have shown midodrine to be clinically at least as effective as other sympathomimetic agents (norfenefrine, etilefrine, dimetofrine and ephedrine) and dihydroergotamine in this regard. Additionally, midodrine appears to cause less frequent and severe adverse effects associated with alpha-receptor agonism such as piloerection and urinary hesitancy. The most commonly experienced adverse effects--piloerector reactions, gastrointestinal disorders, and cardiovascular complaints--are generally mild and can be controlled by reducing the dosage of midodrine. Thus, midodrine is at least as useful as other currently available options in the management of orthostatic or secondary hypotension, and represents a stepping stone towards optimal therapy.
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PMID:Midodrine. A review of its pharmacological properties and therapeutic use in orthostatic hypotension and secondary hypotensive disorders. 248 Aug 81

Pulmonary hypertension occurs frequently in patients with chronic lung disease and contributes to morbidity and mortality. The most common symptoms are dyspnea, fatigue, chest pain, and syncope; sudden death can occur. Signs of pulmonary hypertension include prominent a-waves in the jugular venous pulse, a prominent P2 and murmur of tricuspid regurgitation. Introduced in 1964, cardiac catheterization is still required for the clinical assessment. Many patients reveal a vasoconstrictive component in their lung vessels that is potentially reversible therapeutically. Accurate noninvasive diagnostic methods and an understanding of the mechanisms causing pulmonary hypertension are necessary, as is appropriate therapy based upon the results.
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PMID:[Pulmonary hypertension. Clinical picture and therapy]. 266 41

Urapidil is a postsynaptic alpha 1-adrenoceptor antagonist with a pharmacodynamic profile similar to prazosin. Unlike prazosin, however, urapidil also has some central activity which may explain the apparent improved tolerability of urapidil, including the absence of first-dose syncope. In clinical trials urapidil therapy resulted in significant reductions in blood pressure in patients with mild to severe essential hypertension, with little influence on heart rate. It is an effective antihypertensive when administered as monotherapy or in combination with beta-blockers and thiazide diuretics. In the few patients with cardiac dysfunction who have been studied to date, urapidil has improved myocardial oxygen consumption, systemic vascular resistance, left ventricular function, cardiac output and pulmonary capillary wedge pressure; however, further study is needed to assess the full therapeutic potential of urapidil in these patients. Urapidil has also been used successfully in the treatment of hypertensive emergencies, including eclampsia and pre-eclampsia, hypertensive crisis and hypertension occurring during general and cardiac surgery, rapidly lowering blood pressure without altering heart rate. Urapidil does not affect lipid or glucose metabolism, nor does it impair renal function. In addition, urapidil may be beneficial to patients with pulmonary hypertension, in whom it dilates pulmonary vascular beds to a greater extent than systemic vasculature, although therapeutic trials have not examined this effect. The most common adverse effects associated with urapidil therapy are dizziness, nausea, headache, fatigue and palpitations; however, these tend to be mild and transient and usually do not require discontinuation of treatment. Thus, urapidil offers a useful alternative to currently available drugs for the treatment of mild to severe hypertension, either as monotherapy or in combination with other antihypertensive drugs.
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PMID:Urapidil. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in the treatment of hypertension. 269 46

Based on analysis of 399 symptomatic patients with mitral valve prolapse (MVP) and the reported experience of others, we developed a clinical classification in order to improve nosology, provide better identification and promote insight into the mechanism of symptoms in patients with MVP. The heading of anatomic MVP designates those in whom symptoms or complications were primarily or directly related to valvular dysfunction and the heading of MVP syndrome designates those patients in whom symptoms cannot be explained on the basis of valvular dysfunction alone. Patients with MVP syndrome present with a symptom complex which results from various forms of neuroendocrine or autonomic dysfunction; the most common symptoms include chest pain, palpitations, cardiac arrhythmias, orthostatic phenomena, syncope, presyncope, fatigue, exercise intolerance, dyspnea and neuropsychiatric symptoms (Table 1). Mechanisms underlying the condition have been shown to include increased adrenergic activity, disturbances of catecholamine regulation, hyperresponsiveness to adrenergic stimulation, anomalous beta-adrenergic receptors, dysfunction of the parasympathetic portion of the autonomic nervous system, disturbances in renin-aldosterone regulation, decreased intravascular volume, diminished left ventricular diastolic volume in the upright position as well as abnormal secretion of atrial natriuretic factor (Table 2). In MVP syndrome, alterations of the heart, kidney, the adrenals and the autonomic nervous system coexist and interact, creating a complex "neuro-endocrine cardiovascular process" which may account for many of the symptoms otherwise unexplained on the basis of the valvular abnormality alone.
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PMID:Mitral valve prolapse syndrome: neuro-endocrinological aspects. 284 39

The overall effect of zotepine was a "slightly improved" or better response in 20 patients (64.5%), "unchanged" in 10 (32.3%) and "worsened" in 1 (3.2%). Zotepine exhibited some degree of improvement in 54.5% of patients unresponsive to prior drugs. The onset of effect of zotepine was within one month in 19 patients. The improvement rate in the hebephrenic type (66.7%) was almost the same as in the paranoid type. The improvement rate classified by psychopathology was highest for hypobulia, followed by restlessness-excitement and hallucination, depressive mood, hypochondria and delusion. The side-effects were subjective complaints, such as general fatigue, dryness of mouth, sleepiness or fainting in a small number of cases. There was a slight increase in S-GPT in one patient and a slightly increased blood platelet count, also in one patient. Serial EEG changes associated with zotepine studied in another 17 chronic schizophrenics could be classified into three groups: those with increased slow waves, those with enhanced alpha waves and those with unchanged EEGs. There was a positive correlation between the incidence of slow waves and higher plasma levels of zotepine.
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PMID:Clinical and EEG studies of zotepine, a thiepine neuroleptic, on schizophrenic patients. 288 87

An intense vaso-vagal reaction characterizes all the reflex induced cardiovascular syncopes. In these syndromes the vagal cardio-inhibitor effect on heart rate is more evident than the vasodilatation and fall in blood pressure. The vasodepressor mechanism is uncommon even in carotid sinus syndrome. We have studied 6 male patients, age range 56-73 years (mean age: 64) with recurrent vasodepressor syncopes. The following were always present during such episodes: generalized malaise, profound fatigue, pallor, cyanosis, copious sweating, lack of peripheral pulses, severe fall in blood pressure (BP) (systolic BP less than or equal to 50-60 mmHg or unrecordable), mental disorientation and/or syncope. The first diagnosis in our patients was carotid sinus syndrome, but, the clinical picture was quite different from classic carotid sinus syndrome: triggering factors were not present, the vasovagal episodes were longer, the syncopes more frequent and severe, and the VVI pacing uneffective. Further investigations, including computerized axial tomography, showed--in all these patients--a malignant tumour originally localized in or near the parapharyngeal space. We think that the symptoms of our patients can be attributed to parapharyngeal tumour and that the parapharyngeal space lesions are able to cause severe vasovagal attacks and syncope. The pathogenetic mechanism in this syndrome, due to neural irritation of the glossopharyngeal afferent fibres, is similar to the glossopharyngeal neuralgia-asystole syndrome, but it obviously doesn't involve pain-pathways since none of our patients had pain. Therefore, this syndrome differs from glossopharyngeal neuralgia- asystole syndrome in the presence of tumours and in the absence of neuralgia and initiating factors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A new reflex cardiovascular syndrome: recurrent vasodepressive syncope caused by lesions or tumors of the parapharyngeal space. Etiopathogenesis, clinical picture, differential diagnosis with carotid sinus syndrome and glossopharyngeal neuralgia-asystole syndrome. Therapy by intracranial resection of the 9th cranial nerve]. 319 43

Elevation of pulmonary arterial pressure may be secondary to many diseases of the lungs, chest wall, and heart. From a pathophysiologic viewpoint, pulmonary hypertension is secondary to vascular obstruction, vasoactivity, increased circulation, and passive forces. Clinically, the entities that result in secondary pulmonary hypertension present with a picture that identifies the primary disease. Patients with primary pulmonary hypertension may be difficult to identify. Pulmonary hypertension may present early with dyspnea and fatigue, while syncope and hemoptysis are late symptoms. In many instances, pulmonary hypertension can be diagnosed utilizing physical examination and noninvasive tests. Eventually, right heart catheterization is necessary to confirm the diagnosis and to monitor trials of therapy with vasodilators. Treatment may be specific (closure of a septal defect, thromboendarterectomy) or generic (vasodilators). These have been used recently for both secondary and primary pulmonary hypertension in an effort to reduce pulmonary vascular resistance, thereby decreasing right ventricular afterload and improving cardiac output and oxygen delivery. The success of these treatments has not been demonstrated.
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PMID:Pulmonary hypertension: etiology and clinical evaluation. 333 61


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