Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0231807 (exertional dyspnea)
 3,402 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amiodarone, a benzofuran derivative, has proven useful in the control of serious cardiac arrhythmias. We reviewed the English language medical literature to characterize clinical, radiographic, scintigraphic, pathologic, diagnostic, and prognostic data concerning amiodarone pulmonary toxicity. Our review showed that features consistent with amiodarone pulmonary toxicity include exertional dyspnea, fever, and high sedimentation rates, usually in patients taking larger maintenance doses. Positive findings on gallium scan, foamy alveolar macrophages on lung biopsy or bronchoalveolar lavage, and resolution of abnormal chest roentgenogram upon withdrawal of amiodarone and/or institution of corticosteroid therapy support a diagnosis of amiodarone pulmonary toxicity. Conversely, maintenance doses of 400 mg or less daily, normal lung diffusing capacity and bronchoalveolar lavage or lung biopsy specimens without foamy alveolar macrophages are features that make amiodarone pulmonary toxicity unlikely. Amiodarone pulmonary toxicity should be considered in any patient who has new or clinical worsening of respiratory symptoms and/or abnormalities on chest roentgenogram. Congestive heart failure is often present in these patients and must be excluded before a diagnosis of amiodarone pulmonary toxicity can be considered. Amiodarone pulmonary toxicity also needs to be distinguished from pulmonary infection. Therefore, amiodarone pulmonary toxicity remains a clinical diagnosis relying upon a composite of clinical, radiographic, and histopathologic findings.
 ...
PMID:Amiodarone pulmonary toxicity: a multidisciplinary review of current status. 842 20

We previously reported that dyspnea on exertion in patients with congestive heart failure was not associated with pulmonary function ar rest, but was associated with the appearance of the anaerobic threshold and with the respiratory compensation point during exercise. Here we described a study of the influence of aging on the onset of dyspnea on exertion in elderly and in young patients with congestive heart failure. A total of 53 patients were studied: 35 were less than 65-year-old (average age, 47-year-old; 19 men and 16 women) and 18 were more than 65-year-old (average age, 70-year-old; 13 men and 5 women). All patients underwent maximal graded exercise testing on a bicycle ergometer. The workload increased according to a ramp protocol, and perceived exertion was evaluated with the Borg scale. The anaerobic threshold, the respiratory compensation point, and the peak VO2 were recorded. Values of 13 (somewhat hard) and 17 (very hard) on the Borg scale were considered to mark the start of dyspnea on exertion and an increase in dyspnea on exertion respectively. In the young patients, dyspnea on exertion began at about the time that the anaerobic threshold was reached, and it increased at about the time that the respiratory compensation point was reached. In contrast, elderly patients dyspnea on exertion began 70 seconds after the anaerobic threshold was reached, and it increased 30 seconds after the respiratory compensation point was reached. The VO2 at the start of dyspnea on exertion and the VO2 at the anaerobic threshold correlated more closely in the young patients than in the old patients. The same was true of the VO2 at the time that dyspnea on exertion increased and the VO2 at the respiratory compensation point. These findings suggest that elderly patients with congestive heart failure are less sensitive to the stimuli that cause dyspnea than are young patients.
 ...
PMID:[Onset of dyspnea on exertion in elderly and young patients with congestive heart failure]. 874 66

Constrictive pericarditis can be associated with ICD patch electrodes. During a mean follow-up of 24 months, in a population of 35 patients who received ICDs with a patch electrodes configuration, we identified three patients with clinical and hemodynamic signs compatible with this event. Patient 1, a 35-year-old male, underwent implantation of an ICD because of a primary electrical disease complicated by cardiac arrest. Fourteen months later he complained of exertional dyspnea without any signs of heart failure. Right heart catheterization showed high filling pressures and diastolic dip and plateau in pressure curves. Thoracotomy and pericardial exploration were performed. Three months after removal of the patches and insertion of an endocardial lead system, the patient had normal respiration. Patients 2 and 3, who suffered from coronary heart disease without heart failure, exhibited a hemodynamic profile suggestive of constrictive pericarditis: in one patient, 10 months after ICD implantation, associated with right heart failure; and in the other, 18 months after ICD implantation with left heart failure. Patch electrodes were removed in these two patients and replaced by endocardial lead electrodes with subsequent clinical improvement. It is concluded that constrictive pericarditis related to epicardial patch is not an uncommon occurrence during ICD therapy and should be considered in patients who show clinical signs of cardiac decompensation.
 ...
PMID:Symptomatic pericardial disease associated with patch electrodes of the automatic implantable cardioverter defibrillator: an underestimated complication? 899 57

Congestive heart failure (CHF) is a progressive disease with multiple possible causes. Systolic heart failure, defined as contractile failure of the myocardium leading to a reduced ejection fraction, is the most common type. Systolic heart failure may result from coronary artery disease, hypertension, a metabolic disorder, infection, or an infiltrative or other disease, or it may be idiopathic. Recognition of CHF can be difficult, especially in elderly patients with several medical conditions. An early clinical sign may be dyspnea on exertion. The extent of workup needed is often indicated by findings on history taking and physical examination. In all patients suspected of having new-onset CHF, a chest film, an electrocardiogram, and left ventricular ejection fraction should be obtained and a search for complicating and causative factors undertaken. Early treatment may halt the otherwise inevitable decline in cardiac function and improve prognosis.
 ...
PMID:Causes of congestive heart failure. Prompt diagnosis may affect prognosis. 900 88

A 67-year-old man was admitted to hospital for the treatment of exertional dyspnea. He suffered from congestive heart failure due to an old inferior myocardial infarction with type B Wolff-Parkinson-White syndrome. Asynchronous wall motion caused by pre-excitation through a right-side bypass tract caused his cardiac function to deteriorate. Catheter ablation of the bypass tract increased the ejection fraction, and improved his symptoms, prior to surgical revascularization.
 ...
PMID:Improved cardiac function after catheter ablation in a patient with type B Wolff-Parkinson-White syndrome with an old myocardial infarction. 985 5

A 29-year-old female with systemic lupus erythematosus (SLE) was admitted because of exertional dyspnea in January, 1996. The diagnosis of SLE was made on the basis of malar rash, discoid rash, polyarthritis, leukopenia, positive antinuclear antibody and focal glomerulonephritis in 1991. She did not have any cardiac symptoms in 1994, when the electrocardiogram (ECG) abnormalities, such as poor R wave progression and right axis deviation, were present. On admission, she developed congestive heart failure without any signs of active SLE. Laboratory findings were unremarkable. There were new ECG abnormalities, such as left atrial overload and low voltage in limb leads. Chest roentgenogram showed mild pulmonary congestion and marked cardiomegaly. Echocardiography showed enlargement and diffuse hypokinesis of the left ventricle. Cardiac catheterization confirmed that the coronary arteries were normal and that the left ventricular function was poor (ejection fraction, 21%). Myocardial biopsy obtained from left ventricle revealed interstitial fibrosis. After furosemide, digoxin and captril were administered with predonisolone (PSL), her symptoms gradually improved. Since the Holter monitoring showed nonsustained ventricular tachycardia, the doses of PSL and mexiletine were increased up to 20 mg and 300 mg daily, respectively. Unexpectedly, she was found dead in her hospital room in May, 1996. The postmortem findings of the heart revealed mild infiltration of inflammatory cells, predominantly lymphocytes, and plasma cells, and interstitial fibrosis, which were consistent with interstitial myocarditis. In this case ECG abnormalities preceded cardiac symptoms, which may suggest that myocarditis subclinically developed. Serum creatinine kinase levels had not been elevated throughout the entire course. While several cases of acute myocarditis associated with a flare of SLE have been reported, there were few cases regarding interstitial myocarditis that chronically progress and can be fatal. This case is thought to be suggestive of elucidating the pathogenesis of lupus myocarditis.
 ...
PMID:[A case of systemic lupus erythematosus with interstitial myocarditis leading to sudden death]. 1043 53

The syndrome of congestive heart failure occurring secondary to diastolic dysfunction accounts for the major pathophysiologic mechanism in up to one-third of patients who present with dyspnea on exertion and pulmonary congestion. Diastolic dysfunction is characterized by an alteration in the normal diastolic pressure-volume relationship while systolic function may be normal. It is manifested by impairment in the left ventricle's ability to relax and fill completely during diastole at normal low ventricular pressures. This subset of heart failure is most commonly associated with concentric left ventricular hypertrophy and ischemic states. Symptom presentation is similar to that associated with systolic dysfunction as are rates of rehospitalization. Diagnosis is made based on data obtained from invasive and noninvasive procedures. Unlike in the setting of systolic dysfunction, however, there are no large-scale randomized clinical trials evaluating drug efficacy that could be used to guide treatment for the management of diastolic dysfunction. Treatment recommendations, therefore, are empiric. Identifying and aggressively treating potentially reversible causes is a priority. Many of the same drugs used in the management of heart failure associated with systolic dysfunction are also used in the setting of diastolic impairment; however, dosages and rationale for administration may differ. Nursing interventions too are similar. Monitoring response to medications, especially in the acute setting, and comprehensive patient education are paramount. Much is yet to be learned about the management of diastolic dysfunction.
 ...
PMID:Heart failure with preserved LV function: pathophysiology, clinical presentation, treatment, and nursing implications. 1090 2

A 36-year-old Japanese man was hospitalized with coughing and exertional dyspnea (NYHA class I). He was diagnosed as having congestive heart failure, and was treated with diuretics and a beta-adrenergic blocking agent. He responded well to the treatment and his symptoms completely disappeared within a few days. Based on his clinical, laboratory, and molecular genetic findings, he was diagnosed as having X-linked dilated cardiomyopathy (XLDCM). He was found to have a large deletion in the dystrophin gene, involving exons 45-55. This is the first report on a Japanese XLDCM patient with a mutation in the central hot-spot region of this gene.
 ...
PMID:X-linked dilated cardiomyopathy with a large hot-spot deletion in the dystrophin gene. 1181 47

The authors describe the challenging case of a 46-year-old patient who presented with a 2-week history of exertional dyspnea, paroxysmal nocturnal dyspnea, and orthopnea. He was found to have left ventricular failure and atrial fibrillation with a rapid ventricular rate. Initial work-up revealed dilated cardiomyopathy with marked left ventricular dysfunction, without any obvious cause. He received standard medical therapy for left ventricular dysfunction and his symptoms improved. Electrical cardioversion to sinus rhythm and maintenance resulted in complete recovery of left ventricular function within 6 months. (c)2001 CHF, Inc.
 ...
PMID:Difficult cases in heart failure: reversible cardiomyopathy due to atrial fibrillation in a 46-year-old patient. 1182 82

Trastuzumab is a monoclonal antibody used for the treatment of metastatic breast carcinoma in women whose tumors overexpress the HER2 protein. Cardiotoxicity has been reported to occur with trastuzumab when administered alone and in combination with antineoplastic agents, particularly anthracyclines. The risk of cardiotoxicity with trastuzumab has been reported to be 4% with monotherapy and 27% when administered in combination with an anthracycline and cyclophosphamide, but to the author's knowledge severe outcomes, such as death or permanent disability, are uncommon. The majority of reported cardiac effects are mild to moderate, nonspecific, and medically manageable. Signs and symptoms are similar to those observed in patients who develop anthracycline-induced cardiomyopathy and include tachycardia, palpitations, and exertional dyspnea, which may progress to congestive heart failure. The pathogenesis and histologic changes responsible for trastuzumab-associated cardiotoxicity currently are under investigation. Unlike anthracycline-induced toxicity, trastuzumab-associated toxicity usually responds to standard treatment or the discontinuation of trastuzumab, and there is no evidence that the toxicity is dose related. Current methods for the early detection of cardiotoxicity in trastuzumab-treated patients are similar to those used in anthracycline-treated patients. Cardiac function is established at baseline and monitored regularly during treatment by physical examination and measurement of left ventricular ejection fraction. The majority of patients improve with proper treatment, and some are able to continue to receive trastuzumab.
 ...
PMID:Trastuzumab-associated cardiotoxicity. 1223 30


<< Previous 1 2 3 4 5 6 7 8 Next >>