Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Key safety parameters of sotalol were examined in 1,288 patients entered into recent controlled trials of ventricular (85% of patients) or supraventricular arrhythmias (15%). Most patients were middle-aged male Caucasians with significant heart disease. The most serious adverse event was proarrhythmia, occurring in 56 patients (4.3%). Of these, 27 had hemodynamic compromise due to malignant ventricular arrhythmias. Most had a history of sustained ventricular tachycardia, myocardial infarction, congestive heart failure (CHF) or cardiomyopathy, or a combination of these. The other 29 had nonsevere events; 38% continued taking sotalol. Proarrhythmia was manifested by torsades de pointes in 24 of the 56 patients. No universal causal relation was found with commonly associated factors such as bradycardia, hypokalemia and long QT interval. The mean QT and QTc at baseline within 1 week of a severe proarrhythmic event were greater than those of patients not having proarrhythmia. Nineteen patients (1%) discontinued therapy with sotalol because of drug-related CHF. Predisposing conditions included low initial baseline ejection fraction, history of CHF, cardiomyopathy or cardiomegaly, or both, male gender and age greater than 65 years. Heart failure usually occurred within 7 to 30 days of initiating therapy. The most common reason for premature discontinuation of the drug in patients treated for sustained ventricular tachycardia was ineffectiveness (39%), whereas adverse effects were the most common reasons among patients treated for complex ventricular ectopy (21%). Dyspnea and bradycardia were the most common cardiovascular effects, and fatigue, dizziness and asthenia the most common noncardiac, adverse effects. Although frequently reported, these adverse effects resulted in discontinuation of only 1 to 4% of the patients at risk.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical safety profile of sotalol in patients with arrhythmias. 240 37

A series of 5 males and 2 females aged 23-73 yr with carcinoid cardiopathy is presented, all of them with clinical and instrumental signs of liver metastasis. The main clinical signs were dyspnoea and asthenia rendered ingravescent by effort, and, in the later stage, a frank picture of congestive cardiac decompensation. All subjected presented stethoscopic evidence of tricuspid valvulopathy, combined with pulmonary stenosis in 2 cases. The ECG picture displayed a constant reduction in cardiac potentials, together with right branch bundle block in 3 cases. In cases where an echocardiogram was taken, this confirmed tricuspid involvement. The disease progressed in all cases, and four patients died as a result of terminal liver failure.
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PMID:[Carcinoid cardiopathy]. 621 32

In 17 patients (aged 78 +/- 9 years) with symptomatic atrial fibrillation and a slow ventricular response not related to drugs, a resting electrocardiogram and 24-hour Holter recording were obtained before and 5 to 6 days after administration of slow-release theophylline (700 mg/day), and successively every 3 months during the long-term phase. Fourteen patients had organic heart disease, and 13 complained of syncope or presyncope, and 4 of asthenia and easy fatigability. At the steady-state evaluation, theophylline significantly increased resting heart rate (HR) by 42%, mean 24-hour HR by 31% and minimal 24-hour HR by 34%. Cardiac pauses > 2,500 ms disappeared or markedly decreased. The daily number of wide QRS complexes increased. Serum theophylline level was 13 +/- 5 ng/ml. During the follow-up period (20 +/- 18 months), the mean daily theophylline dosage was 450 mg and the mean serum theophylline level 9 ng/ml. Seven patients died: 1 because of heart failure, and 6 because of noncardiac death. One patient complained of a syncopal episode during 1 visit. The drug markedly reduced asthenia and easy fatigability. During the long-term phase, HR increased spontaneously in 3 patients, and the treatment was interrupted. In 2 patients, theophylline had to be discontinued because of gastric intolerance. During long-term therapy, HR was similar to that observed at the steady-state evaluation, despite the reduction in daily dosage. The data suggest that theophylline is an effective therapy in most patients with symptomatic atrial fibrillation and a slow ventricular response.
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PMID:Long-term effects of theophylline in atrial fibrillation with a slow ventricular response. 823 3

The nature of most syncopal episodes, previously unknown, was recently elucidated by new diagnostic techniques such as the use of the tilt test. The vasovagal syncope can be clinically diagnosed by means of the tilt test. The transitory loss of consciousness during prolonged orthostasis is typically associated with sudden hypotension and bradycardia, which are commonly preceded by relative tachycardia and by premonitory symptoms such as pallor, nausea, asthenia, yawns, hyperventilation, mydriasis, humming, lasting several minutes. The nature of the vasovagal reflex is now better understood: in subjects with vasovagal syncope, during prolonged orthostasis, it was observed a fall in the venous return, inducing an increased sympathetic drive to the heart (with positive inotropic and chronotropic effect) and a lower ventricular filling. The powerful contraction around an almost empty cardiac chamber induces the activation of ventricular mechanoreceptors, and through a reflex mechanism, a sudden increase in the vagal and a sudden reduction in the sympathetic drive. These autonomic changes are responsible for a sudden hypotension and bradycardia. The discussion is still open about the origin of the reduced venous return: it probably originates from a redistribution in the blood volume, due to a venous pooling in the lower limbs or from a reduced muscle tone, because many subjects with vasovagal syncope are slender and with less developed muscle apparatus. Others suggest that a reduction in the sympathetic drive to the vessels, responsible for a progressive hypotension in the minutes preceding syncopal episodes, is the origin of the reduced venous return. In this review a diagnostic pattern for the assessment of the vasovagal syncope is suggested. The medical history, clinical examination, electro- and echocardiogram, chest x-ray identify two main groups of patients (with or without cardiopathy) who will follow different diagnostic protocols. The therapy of vasovagal syncope, which is based on beta-blockers, scopolamine, dysopiramide and plasma expanders, is reviewed.
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PMID:[Vasovagal syncope]. 851 54

A twenty-four-year-old, white, athletic woman, free of heart disease, experienced an episode of fear when she was assaulted in the street without physical injury while under-going twenty-four-hour Holter monitoring. She developed an important sympathetic response in which, besides the symptoms characterized by palpitations, chest pain, dyspnea, asthenia, dizziness, nausea, and profuse cold sweating, she had an episode of paroxysmal atrial tachycardia. The causes and mechanism of this not well-documented event in humans are discussed.
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PMID:Paroxysmal atrial tachycardia recorded by Holter monitoring during an episode of fear. A case report. 868 68

Paroxysmal supraventricular tachycardia (SVT) may have numerous electro-physiologic mechanisms. The most common type of SVT is AV-nodal reentry tachycardia (60%) followed by the bypass tract-mediated SVT (preexcitation. 30%) and a smaller group (10%) comprising paroxysmal atrial flutter or fibrillation and atrial ectopic tachycardia. In persons with otherwise normal hearts symptoms are usually mild and include palpitations or an uneasy feeling in the chest. But some describe precordial pain. Weakness, dizziness, nausea, vomiting, and even syncope. Whenever possible a 12-lead-ECG during an episode of SVT should be obtained. If not possible the use of several Holter-ECG or of an event-recorder may be helpful. Conversion of a SVT can be accomplished by vagal maneuvers or intravenous adenosine (6-18 mg bolus injection). Further diagnostic procedures should prove or rule out a significant structural heart disease. Therapeutic options (expectative, pharmacological prophylaxis, invasive electrophysiologic testing and catheter-mediated modification or ablation) are chosen according to the objective threat (e.g. ventricular fibrillation due to 1:1 conducted atrial fibrillation in a preexcitation syndrome) and the subjective complaints. Definitive healing of the AV-nodal reentry tachycardia and the bypass tract-mediated SVT can be achieved by use of catheter-mediated modification or ablation in 95 to nearly 100%.
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PMID:[Modern therapy of paroxysmal supraventricular tachycardia]. 1009 47

Dyspnea is a frequent and devastating symptom among advanced cancer patients and is often difficult to control. However, there has been considerably less emphasis in the literature on the appropriate characterization and management of this symptom than of other cancer-related symptoms. The purpose of this paper is to review issues relating to the prevalence, causes, prognosis and treatment of dyspnea in patients with advanced cancer. A Medline search of the literature published from 1966 to February 1999 was conducted. Dyspnea occurs in 21-78.6% of advanced cancer patients and is reported to be from moderate to severe in 10-63% of the patients. The frequency and severity of dyspnea increase with the progression of the disease and/ or when death is approaching. Lung cancer patients with dyspnea have shorter survival than patients with other types of cancer. Dyspnea can be a direct effect of the cancer, an effect of therapy or not related to the cancer or therapy. In addition to cancer, patients may suffer from chronic obstructive pulmonary disease, congestive heart failure, nonmalignant pleural effusion, pneumonitis, air flow obstruction, or bronchospasm associated with asthma. In the absence of lung or heart disease, dyspnea may be a clinical expression of the syndrome of overwhelming cachexia and asthenia or of severe asthenia. Many different causes may co-exist in a patient. Whenever possible, an attempt should be made to treat underlying cancer. Radiotherapy and chemotherapy may relieve dyspnea also in patients who fail to achieve a major objective response. Symptomatic measures in addition to specific treatments for the underlying cancer and/or other pulmonary and cardiovascular diseases are indicated. Oxygen therapy has proved effective in hypoxemic and nonhypoxemic patients. The role of transfusion therapy to relieve anemia-related dyspnea in advanced and terminal cancer patients is still controversial. Oral, subcutaneous and intravenous opioids are effective but underused in these patients, whereas currently available evidence does not support the clinical use of nebulized opioids. While benzodiazepines are frequently used in patients with dyspnea, these drugs were ineffective in four out of five randomized controlled trials. Other components of the symptom expression are better managed by supportive counseling, occupational therapy or physiotherapy. While the mechanism of breathing and the consequences of different pathologic conditions for both respiratory function and gas exchange are well known, the genesis and pathophysiology of dyspnea as a symptom are much less well understood. Palliative care assessment should be focused on dyspnea as a symptom rather than on the functional and gas exchange abnormalities. Increased research on the appropriate management of dyspnea is needed.
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PMID:Management of dyspnea in advanced cancer patients. 1042 43

At present only two drugs are approved for long-term treatment of obesity. Sibutramine inhibits the reuptake of serotonin and norepinephrine. In clinical trials it produces a dose-dependent 5-10% decrease in body weight. Its side effects include dry mouth, insomnia, asthenia, and constipation. In addition, sibutramine produces a small increase in blood pressure and pulse that is a contraindication to the use of this drug in some individuals with heart disease. Xenical is the other drug approved for long-term use in the treatment of obesity. It works by blocking lipase and thus increasing the fecal loss of triglyceride. One valuable consequence of this mechanism of action is the reduction of serum cholesterol that averages about 5% more than can be accounted for by weight loss alone. In clinical trials it produces a 5-10% loss of weight. Its side effects are entirely due to undigested fat in the intestine that can lead to increased frequency and change in the character of stools. It can also lower fat-soluble vitamins. The ingestion of a vitamin supplement before bedtime is a reasonable treatment strategy. The effect on weight loss during long-term trials with these two drugs is shown in Figs 7 and 8 above. Also in this figure is data on phentermine used in trials of six months or more. Although there were differences in mean weight losses with these drugs, when the placebo effect was taken into account they all had a surprisingly similar magnitude of weight loss.
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PMID:Drug treatment of obesity. 1172 27

The scimitar syndrome or pulmonary venolobar syndrome is a rare, complex and variable malformation of the right lung characterized by an abnormal right sided pulmonary venous drainage in the inferior vena cava, malformation of the right lung, abnormal arterial supply and sometimes cardiac malformations. We present a case in which this diagnosis was suspected on an abnormal routine chest radiograph in a 38-year-old asymptomatic woman. Most patients are asymptomatic; symptomatic patients have a marked left-to-right shunt or a severe congenital heart disease. They usually suffer from shortness of breath, asthenia or repeated chest infections. Usually, the posteroanterior chest radiograph can confirm the diagnostic. It shows the abnormal vein draining into the inferior vena cava as a curved vascular shadow with a scimitar like appearance. However, in some cases, when the scimitar vein is masked by the overlying cardiac shadow, computed tomography, angiography and magnetic resonance imaging can be helpful by showing the abnormal vein and its insertion into the inferior vena cava. Scimitar syndrome seldom necessitates surgical intervention. However, repeated lung infections can sometimes require lobectomy or pneumonectomy, left-to-right shunt vascular surgery to redirect the scimitar vein into the left atrium.
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PMID:[An unusual opacity of the right base]. 1463 83

To determine which of the many clinical parameters routinely collected influence mortality in patients with low left ventricular ejection fraction (LVEF) (< 45% at radionuclide ventriculography), 128 elderly patients (mean age 79 +/- 3 years) with various heart diseases were prospectively followed for 3 years. Twenty-eight-percent had coronary heart disease, 16% hypertensive heart disease, 7% valvular heart disease. The remaining 62 patients (48%) made up a group comprising patients with primitive cardiomyopathy, cor pulmonary with no evidence of coronary heart disease, valvular disease or hypertensive heart disease. Thirty-four-percent of all patients were classified as having congestive heart failure (CHF). Age, sex and 37 clinical variables were analyzed using a Cox proportional model. Forty-four patients died, 36 (82%) of sudden cardiac death. Ten characteristics at study entry predicted an increased mortality risk: S3 gallop, number of clinical signs >or= 3, LVEF <or= 25%, New York Heart Association (NYHA) class >or= III, dyspnea, digoxin treatment, rales, number of symptoms >or= 4, asthenia, associated pulmonary disease. Long-term survival of very elderly patients with low ejection fraction is related to the functional capacity, the severity of symptoms and the number of clinical signs. Moreover a LVEF <or= 25% selects a subgroup of patients at higher risk. Our results suggest that these variables may influence the long-term survival of elderly patients with heart disease. Further studies with a greater number of patients are necessary to better delineate the prognostic value of the clinical and instrumental variables routinely collected in these patients.
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PMID:Clinical determinants of long-term mortality in elderly patients with heart disease. 1537 99


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