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)

Relieving the symptoms of angina and improving the quality of life and functional status are important objectives in the management of patients with chronic stable angina. A high heart rate induces or exacerbates myocardial ischemia and angina because it both increases oxygen demand and decreases myocardial perfusion. Beta-Blockers are effective at reducing anginal symptoms largely by decreasing heart rate. Physician use and patient compliance may be limited by the side effects of Beta-blockers which include fatigue, depression and sexual dysfunction. Heart rate reduction can also be obtained by the calcium antagonists verapamil and diltiazem and by the new selective heart-rate-reducing agent ivabradine. Ivabradine (Procoralan) is a selective and specific I(f) inhibitor that acts on one of the most important ionic currents for the regulation of the pacemaker activity of sinoatrial node cells. Ivabradine has demonstrated dosedependent anti-ischemic and antianginal effects in a placebo-controlled study. The INITIATIVE trial is a large multicenter trial in which 939 patients with stable angina were randomized to ivabradine or atenolol. The noninferiority of ivabradine was shown in the INITIATIVE trial at all doses and for all criteria including time to limiting angina. The number of angina attacks per week was decreased by two thirds with both ivabradine and atenolol. In another trial of 1,195 patients, time to 1mm ST segment depression was increased by 45 s with ivabradine 7.5 mg b.i.d. and by 40 s with amlodipine 10 mg daily. Unlike beta-blockers, ivabradine is devoid of intrinsic negative inotropic effects and does not affect coronary vasomotion. A whole range of patients with angina may benefit from exclusive heart rate reduction with ivabradine, including those with contraindications or intolerance to the use of beta-blockers and patients that are insufficiently controlled by beta-blockers or calcium channel blockers.
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PMID:Heart rate slowing versus other pharmacological antianginal strategies. 1693 73

Erectile dysfunction affects more than 30 million men in The United States. Since the FDA approved the use of Sildenafil, prescription of this medication has been raising. Adverse events of Sildenafil includes: fatigue, dyspnea, and hypotension. Reported adverse cardiac events associated with the medication use include myocardial infarction, ventricular tachycardia, angina and death, raising concerns about the safety of this agent in patients with coronary artery disease. Published guidelines regarding the management of cardiac patients with erectile dysfunction suggest that Sildenafil may be hazardous in patients with ischemic heart disease. In patients using Sildenafil, myocardial infarctions have been reported to the Food and Drug Administration. Now, we report a patient with myocardial infarction after taking 100 mg of Sildenafil without sexual activity.
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PMID:[Acute myocardial infarction associated to the Sildenafil consumption. A case report and review of the literature]. 1741 Sep 88

Coronary artery fistula (CAF) is a rare congenital anomaly of the coronary arteries in which abnormal connections are present between the coronary artery branch and the cardiac chambers or a major vessel. The incidence of CAF is estimated at 1 in 50,000 live births, and it is detected in approximately 0.2% of the adult population during coronary angiography. Reports of the coincidence of mitral stenosis and CAF are rare in the literature. We report a case of CAF and mitral valve stenosis in a patient with dyspnea and fatigue before valve replacement and surgical radiofrequency ablation. Coronary angiography showed a connection between the right coronary artery and right atrium. A fistula opening into the right atrium is rare in patients with coronary artery anomalies and mitral valve disease. Coronary angiography of the patient 1 month after surgical repair showed that the coronary anatomy was normal and the fistula was occluded. CAF can be diagnosed more frequently if coronary angiography is performed simultaneously with cardiac catheterization to evaluate valve functions or nonatherosclerotic myocardial ischemia in each valvular heart disease case. Surgical repair of CAF is the first-choice treatment to prevent complications and improve quality of life.
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PMID:Right coronary artery fistula draining into the right atrium and associated with mitral valve stenosis: a case report. 1759 85

A case of colchicine-induced rhabdomyolysis is reported. A 79-year-old man with ischemic heart disease, chronic atrial fibrillation, chronic renal failure, hypothyroidism, and gout arthritis was hospitalized because of fatigue, myalgia, and leg weakness, shortly after starting treatment with colchicine. Investigation confirmed the diagnosis of rhabdomyolysis, and discontinuation of colchicine resulted in resolution of clinical and biochemical features of rhabdomylysis. Colchicine-induced rhabdomyolysis is a rare complication, and the postulated mechanisms and risk factors for this severe complication are discussed.
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PMID:Colchicine-induced rhabdomyolysis. 1761 11

Myocardial ischemia is associated with reduced ATP fluxes and decreased energy supply resulting in disturbances of intracellular ion homeostasis in cardiac myocytes. In the recent years, increased persistent (late) sodium current was suggested to contribute to disturbed ion homeostasis by elevating intracellular sodium concentration with subsequent elevation of intracellular calcium. The new anti-ischemia drug ranolazine, a specific inhibitor of late sodium current, reduces sodium overload and hence ameliorates disturbed ion homeostasis. This is associated with symptomatic improvement of angina in patients. Moreover, ranolazine was shown to exhibit anti-arrhythmic effects. In the present article, we review the relevant pathophysiological concepts for the role of late sodium inhibition and summarize the most recent data from basic as well as clinical studies.
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PMID:Mechanism of action of the new anti-ischemia drug ranolazine. 1804 26

Cardiac autonomic neuropathy associated with diabetes can cause silent myocardial ischemia and may influence the way that patients perceive symptoms of acute coronary syndromes (ACS). The purpose of this study was to examine symptoms of ACS in patients with and without diabetes while controlling for length of time with diabetes. A convenience sample of 256 patients from two large medical centers in the Midwest participated. Patients with diabetes comprised 33.2% of the sample and reported significantly less chest pain and more unusual fatigue. Patients with diabetes of longer duration (10 or more years) reported more difficulty breathing than did patients with diabetes of shorter duration (fewer than 10 years). Older patients with the same diabetes status also reported less chest pain. For older patients and for patients with diabetes, lack of chest pain during ACS could delay treatment and is thus a concern.
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PMID:The association of diabetes and older age with the absence of chest pain during acute coronary syndromes. 1818 62

A hiccup is involuntary, paroxysmal inspiratory movements of the chest wall associated with diaphragm and accessory respiratory muscle contractions, with the synchronized closure of glottis. The mechanism underlying this common primitive reflex plays an important role in protecting airways against esophageal aspiration. The hiccup reflex mechanism is based on the afferent pathway (vagus and phrenic nerve and sympathetic fibers innervating chest organs, the abdomen, the ear, the nose and the throat stimulation, and the stimulation of hiccup center in the central nervous system, mainly reflecting psychogenic or metabolic disorders) and the efferent pathway (phrenic nerves). An incidental hiccup is a common problem, usually resolves spontaneously and does not present a clinical issue. The clinical issue arises in the case of pathologic persistent hiccups or symptomatic secondary hiccups which may lead to significant fatigue, insomnia or depression. Generally, pathologic hiccups are associated with considerable discomfort concerning both the "stigmatized" person and his or her personal surroundings in which it evokes different emotions, from amusement through impatience to uneasiness and the suggestion of a medical visit as an expression of concern for a given person. The most common causes of pathologic symptomatic hiccups are nervous system diseases, either the central nervous system (proliferative, angiogenic, inflammatory disorders), or the peripheral nervous system: the irritation of the phrenic nerve (proliferative disorders, goitre) and the vagus nerve (otolaryngologic diseases, meningitis, esophageal, stomach and duodenal diseases, hepatitis, pancreatitis, enteritis). The vagus nerve irritation with subsequent hiccups may be caused by chest disorders (injury, surgery) and heart diseases (myocardial infarction). In the present paper we describe the case of a 62-year-old male with recurrent hiccups associated with exertion as a secondary symptom of myocardial ischemia.
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PMID:Hiccups as a myocardial ischemia symptom. 1847 62

Despite a growing body of evidence suggesting that prolonged strenuous exercise (PSE) is associated with a transient reduction in right (RV) and left ventricular (LV) performance, the exact mechanism(s) responsible for this phenomenon is not fully understood. As such, the primary objective of this article was to critically review the available literature (both animal and human) to provide insight into the potential mechanism(s) responsible for the development of "exercise-induced cardiac fatigue." We pay particular attention to the major mechanisms that have been linked to transient changes in systolic function after PSE including altered loading conditions, myocardial ischemia/damage, altered beta-receptor responsiveness, and altered cardiac autonomic modulation. We also examine the potential mechanisms that may contribute to transient changes in diastolic function often observed after PSE including changes in LV pressure gradients and alterations in intrinsic myocardial relaxation. Although further mechanistic investigations are clearly warranted, several key mechanisms have received support for at least a partial contribution to the transient changes in myocardial performance often observed after PSE.
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PMID:Mechanisms underpinning exercise-induced changes in left ventricular function. 1861 53

Atrial fibrillation (AF) is prevalent in the elderly (affecting 5% of persons aged >or= 65 years and around 10% of those aged >or= 80 years old) and is associated with stroke, heart failure and poor quality of life. The symptoms of AF are palpitations, fatigue, reduced exercise capacity, dyspnea or dizziness. AF is associated with comorbidity, mainly hypertension in outpatients, and ischaemic heart disease and heart failure in hospitalized patients. Two therapeutic strategies are available to treat arrhythmia: rhythm control or frequency control. In many elderly patients with AF, frequency control is an effective option, particularly when there is heart failure, contraindications to antiarrhythmic agents or when cardioversion is not indicated. Anticoagulation is the main measure to reduce stroke risk. If anticoagulation is not appropriate for a patient, antiaggregants can be used, but the benefit is clearly lower than that provided by anticoagulation.
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PMID:[Atrial fibrillation in the elderly]. 1868 21

Inhibition of the persistent or late Na current (INa) using ranolazine (Ranexa) represents a novel mechanism of action that was approved in the United States in 2006 and only recently in the European Union for use in patients with stable angina pectoris. In general, myocardial ischemia is associated with reduced adenosine triphosphate fluxes and decreased energy supply, resulting in severe disturbances of intracellular ion homeostasis in cardiac myocytes. In the recent years, increased late INa was suggested to contribute to this phenomenon by elevating intracellular Na concentration with subsequent rise in diastolic Ca levels by means of the sarcolemmal Na-Ca exchange system. Ranolazine, a specific inhibitor of late INa, reduces Na influx and hence ameliorates disturbed Na and Ca homeostasis. This is associated with a symptomatic improvement of angina in patients unlike other antianginal drugs without affecting heart rate or systemic blood pressure as shown in placebo-controlled studies. Therefore, ranolazine is a useful new option for patients with chronic stable angina not only as an add-on therapy. New clinical and experimental studies even point to potential antiarrhythmic effects, beneficial effects in diastolic heart failure, and under hyperglycemic conditions. In the present article, the relevant pathophysiological concepts for the role of late INa inhibition are reviewed and the most recent data from basic studies and clinical trials are summarized.
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PMID:A novel mechanism for the treatment of angina, arrhythmias, and diastolic dysfunction: inhibition of late I(Na) using ranolazine. 1933 33


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