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)

Five patients were studied 5-13 months after dynamic cardiomyoplasty for refractory heart failure. In two, muscle flap stimulation caused a pronounced increase in cardiac index (mean 55%) and ejection fraction (mean 75%); no patient showed improvement in cardiac filling pressure. 2 years after surgery, one of the patients with haemodynamic improvement died from ventricular fibrillation, and histochemistry of the stimulated muscle flap revealed predominantly fatigue-resistant type I fibres, without evidence of fibrosis. In selected cases, dynamic cardiomyopathy could be of long-term benefit.
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PMID:Preliminary report: follow-up after dynamic cardiomyoplasty. 197 65

Calcium-entry blockers were administered in an attempt to protect myocardium during cardiac arrest due to ventricular fibrillation in mechanically ventilated dogs. An intravenous injection of verapamil, nifedipine, or lidoflazine was administered prior to successively prolonged episodes of ventricular fibrillation, during which no thoracic compression was performed. It is of interest that ventricular defibrillation was more easily obtained after treatment with the three drugs. As previously observed in this model, nine control dogs developed electromechanical dissociation (EMD) after 120 seconds of ventricular fibrillation. In contrast, six of the 11 dogs treated with 0.3 mg/kg of verapamil recovered mechanical systole after 120 seconds of ventricular fibrillation (p less than 0.05). Nifedipine administration also postponed the onset of EMD in three of four dogs. However, lidoflazine postponed the onset of EMD in only one of the eight dogs. The later onset of EMD after administration of verapamil or nifedipine in this model was attributed to myocardial protection by calcium-entry blockers during ventricular fibrillation. Decreased energy utilization during cardiac arrest was considered to be the principal protective mechanism. These observations indicate calcium-entry blockers, and especially verapamil and nifedipine, can be valuable drugs during cardiac resuscitation for ventricular fibrillation.
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PMID:Electromechanical dissociation after ventricular fibrillation: prevention with calcium-entry blockers. 608 70

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of sotalol hydrochloride are reviewed. The chemical name of sotalol hydrochloride is 4'-[1-hydroxy-2-(isopropylamino)ethyl]methanesulfonanilide monohydrochloride. Sotalol is a class III antiarrhythmic that prolongs the action potential and refractoriness of cardiac tissue and has potent nonselective beta-blocking activity. Sotalol is well absorbed after oral administration. The pharmacokinetics of sotalol can be described by an open, linear, two-compartment model. The drug is eliminated primarily by the kidneys; mean elimination half-life is 12 hours. Sotalol has been found to be effective in controlling life-threatening ventricular arrhythmias, including sustained ventricular tachycardia, ventricular fibrillation, and premature ventricular complexes. Although sotalol has FDA-approved labeling for use in the treatment of ventricular arrhythmias only, it is also effective against a variety of supraventricular arrhythmias. Noncardiac adverse effects include fatigue, impotence, depression, headache, nausea, diarrhea, and increased triglyceride levels. Cardiovascular adverse effects include atrioventricular block, bradycardia, hypotension, exacerbation of heart failure, and polymorphic ventricular tachycardia. Overall, 11-21% of patients experience adverse effects; 6-18% of these patients have reactions serious enough to warrant the discontinuation of sotalol therapy. The initial dosage of oral sotalol hydrochloride in adults is 80 mg twice daily or 160 mg once daily; the dosage can be increased every three to four days in increments of 40-160 mg/day to a maximum of 480 mg/day. Sotalol is useful in the control of intractable, life-threatening ventricular arrhythmias, as well as a variety of supraventricular arrhythmias, in patients who do not respond to or are intolerant of more conventional antiarrhythmics.
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PMID:Sotalol: a new class III antiarrhythmic agent. 813 5

The objective of this study was to determine the pumping capability of dynamic cardiomyoplasty during induced ventricular fibrillation. In this acute study of 6 dogs, the pumping capability of the unconditioned left latissimus dorsi (LD) muscle (141 to 292 gm), wrapped around both ventricles, was investigated during induced ventricular fibrillation. Left-ventricular and femoral artery pressure, the ECG and aortic root flow velocity were monitored. Prior to inducing ventricular fibrillation, the ability of the unconditioned LD muscle to augment stroke volume (SV), was quantified as the area under the aortic flow-velocity record. The ventricles were then fibrillated and, after 10 sec, rhythmic 250 msec trains (1/sec) of stimuli (40/sec) were delivered to the thoracodorsal nerve to contract the LD muscle tetanically. In no case could dynamic cardiomyoplasty produce the same SV as when the ventricles were beating normally. In one animal, the SV attained two percent of the normal SV by 5 contractions; in another, the SV reached one percent by 25 contractions. In the remaining animals, the SV varied around 20% of the prefibrillation SV. By 90 contractions, the stroke volume was 10% of the prefibrillation value. The progressive decrease in SV was likely a consequence of LD muscle ischemia and fatigue, since the latissimus dorsi muscle provided low blood flow during the period of fibrillation.
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PMID:Stroke volume with dynamic cardiomyoplasty during ventricular fibrillation in the acute dog. 820 83

According the literature atrio-ventricular blockade (AVB) is the most frequent and well-known symptom of Lyme carditis. Typical signs of complete AVB include fatigue, lethargy and syncope- Morgagni-Adams-Stokes syndrome (MAS). The authors present their results and experience with 5 patients selected from a long-term study (conducted between 1987 and 1998) comprising 58 patients who developed MAS. The authors tried to evaluate the changes especially in the cardiovascular system. They correlated the clinical state with ECG findings, as well as with the levels of the Borrelia burgdorferi antibodies. The following results were obtained: 1) all patients had typical syncope, 2) the clinical course was not complicated (except one patient who developed ventricular fibrillation), 3) two patients had frequent symptomatic and asymptomatic arrhythmia including chest pain and episodic rest dyspnea, 4) subjective difficulties (usually palpitations) correlated with ECG findings (Lown 3a, 3b). The authors also looked for any relationship between clinical difficulties and levels of antibodies. The results obtained with an early permanent pacemaker were less favourable than those reported in the literature. Despite early treatment 2 patients had repeated palpitations and ECG correlates during the next years.
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PMID:Borrelia burgdorferi as a cause of Morgagni-Adams-Stokes syndrome. Long time follow-up study. 1066 10

Based on the national surveys in Japan, the most common symptoms of dilated cardiomyopathy(DCM) were dyspnea, palpitation, general fatigue and edema. Palpitation, dyspnea, general fatigue and anginal pain were common in hypertrophic obstructive cardiomyopathy(HOCM) and hypertrophic non-obstructive cardiomyopathy (HNOCM). Dyspnea was the most common symptom in constrictive cardiomyopathy (RCM). Electrocardiographic findings in DCM were not specific, and ST-T change, wide QRS complex, left ventricular hypertrophy and abnormal Q wave were frequently observed. In both of HOCM and HNOCM, frequent electrocardiographic abnormalities were ST-T abnormality, left ventricular hypertrophy and wide QRS complex. Moreover, abnormal Q wave was frequently observed in HOCM. Ventricular arrhythmia, including fatal ventricular tachycardia or ventricular fibrillation, was frequently found in patients with any type of cardiomyopathy.
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PMID:[Symptoms and electrocardiographic findings in cardiomyopathies]. 1088 83

A 17-year-old male with AML FAB M4 relapsed 4 months after myeloablative conditioning and peripheral blood stem cell transplantation (PBSCT) from an HLA-identical unrelated donor. A second PBSC harvest was infused 2 days after completion of cytoreductive therapy with mitoxantrone 7 mg/m(2)/day i.v. for 3 days (total dose 21 mg/m(2)), fludarabine 30 mg/m(2)/day i.v. for 6 days (total dose 180 mg/m(2)) and Ara-C 125 mg/m(2)/day i.v. for 5 days (total dose 625 mg/m(2)). Neutrophil recovery occurred on day +10 and was associated with GVHD grade III of the skin which was treated with cyclosporin A (CsA) and prednisone. Because of fever of unknown origin and progressive fatigue combined with hypotension on day +15 after second PBSCT, echocardiography was performed which revealed a dramatic decrease in systolic function compared to the status pre-transplant. On the same day acute heart failure with consecutive ventricular fibrillation occurred. Although resuscitation was performed immediately the patient died. The autopsy revealed massive infiltration by donor CD8-positive lymphocytes with concomitant extensive damage of the heart tissue. Acute myocarditis of viral origin was excluded by in situ hybridization and nested PCR techniques. In this patient, myocardial involvement by acute GVHD seems to have triggered a fatal arrhythmia and heart failure.
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PMID:Acute heart failure after allogeneic blood stem cell transplantation due to massive myocardial infiltration by cytotoxic T cells of donor origin. 1124 47

Two patients, a 5 year old boy with progressive hypertrophic obstructive cardiomyopathy and increasing symptoms despite appropriate pharmacologic therapy and an 11 year old girl with symptoms of tiredness and peak instantaneous LVOT gradient of 80 and 90 mmHg respectively were considered for radiofrequency catheter septal ablation, to relieve the left ventricular outflow tract obstruction. Via a femoral arterial approach, the His bundle was initially plotted and marked using the LocaLisa navigation system. Subsequently, using a cooled tip catheter a series of lesions was placed in the hypertrophied septum, commencing distally in the ventricle and proceeding towards the aortic valve, taking care to stay away from the His bundle. The procedure was deemed to be completed when the entire extent of the hypertrophied septum had been treated. In the boy the procedure was complicated by two episodes of ventricular fibrillation, requiring DC cardioversion, but without any neurologic sequelae. The peak to peak gradient between left ventricle and aorta was 50 mmHg and 60 mmHg respectively pre-ablation, and remained unchanged immediately after. Both patients were discharged from the hospital 48 hours later. Serial measurement of serum Troponin T and CK-MB isoenzyme confirmed significant myocardial necrosis. Follow-up echocardiography at 7 days and at 6 weeks post-ablation respectively confirmed a beneficial hemodynamic result, with reduction of left ventricular outflow obstruction and relief of symptoms. In young children, in whom alcohol induced septal ablation is not an option, radiofrequency catheter ablation offers an alternative to surgery, with the benefits of repeatability and a lower risk of procedure-related permanent AV block.
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PMID:Radiofrequency catheter septal ablation for hypertrophic obstructive cardiomyopathy in childhood. 1620 Apr 87

Levosimendan increases the sensitivity of the cardiac fibrils to calcium, favorably affects hemodynamics in patients with heart failure. It is a positive inotrope and a peripheral vasodilator. The elimination half-life of the compound is about 1 hour. The drug decreases pulmonary capillary wedge pressure, increases cardiac output with the improvement in left ventricular ejection fraction leading to symptomatic improvement which includes decreased dyspnea and fatigue. Levosimendan can be used safely with diuretics, nitrates, beta-blockers, digoxin, and angiotensin-converting enzyme inhibitors. The most common adverse effects of levosimendan are headache and hypotension. Prolongation of the QTc interval does not appear to increase the incidence of arrhythmias, including ventricular tachycardia, ventricular fibrillation, and torsades de pointes. Levosimendan is a novel agent in the treatment of decompensated heart failure, representing a newer class of medications aimed at increasing calcium sensitivity. Its properties holds promise for the treatment of heart failure but further large-scale studies will be needed to determine its precise efficacy, safety, as well as the compound's long-term impact on mortality.
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PMID:Levosimendan and calcium sensitization of the contractile proteins in cardiac muscle: impact on heart failure. 1908 50

Gitelman's syndrome, or congenital hypokalemic hypomagnesemic hypocalciuria with metabolic alkalosis, is widely described as a benign or milder variant of Bartter's syndrome and most commonly presents with transient periods of weakness and fatigue, presyncope, vertigo, ataxia, and blurred vision, though aborted sudden cardiac death has also been rarely reported. Despite this there are limited data in the literature regarding the formal cardiac evaluation of patients with Gitelman's syndrome. We present the case of a gentleman with Gitelman's syndrome who initially presented to his primary physician with symptoms suggestive of an upper respiratory tract infection and subsequently survived a ventricular fibrillation (VF) cardiac arrest in the community. We review the literature regarding possible life-threatening cardiac complications in these patients.
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PMID:An unusual presentation of primary renal hypokalemia-hypomagnesemia (Gitelman's syndrome). 2037 Apr 62


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