Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Left ventricular systolic dysfunction is associated with neurohormonal activation which contributes to progressive ventricular remodeling and worsening clinical heart failure. Renin-angiotensin-aldosterone and sympathetic nervous systems are activated, not only in patients with clinically overt heart failure, but also in patients with asymptomatic or minimally symptomatic left ventricular systolic dysfunction. Activation of the angiotensin and adrenergic systems produces deleterious effects on systemic and coronary hemodynamics, promotes myocyte hypertrophy and fibroblast growth, and myocyte necrosis and apoptosis. Thus, therapy of heart failure should consist of pharmacologic agents not only to relieve symptoms but also to prevent and attenuate ventricular remodeling and progressive heart failure, thereby improving prognosis. In patients who are symptomatic, ACE inhibitors along with digitalis and diuretics as initial therapy (triple therapy) have the greater potential to improve exercise tolerance and decrease the incidence of treatment failure compared with diuretics alone or a combination of diuretics and digitalis. Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase. ACE inhibitors decrease mortality in patients with heart failure resulting from left ventricular systolic dysfunction. The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated. Long-term adrenergic inhibition with the use of ss-adrenoceptor antagonists added to ACE inhibitors is associated with attenuation of ventricular remodeling, improvement in ventricular function and clinical class and survival of patients with symptomatic systolic left ventricular failure. Thus, initial pharmacotherapy for systolic heart failure should consist of: maximal tolerated dosages of ACE inhibitors;ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema;adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; relatively low dosages of digoxin (serum concentrations of < or = 1.0 ng/dl) if not contraindicated; and diuretics to relieve congestive symptoms. Addition of spironolactone to ACE inhibitors can result in a significant reduction in the risk of sudden death in patients with symptomatic severe heart failure. Myocardial infarction resulting from ischemic heart disease is the most common cause of systolic left ventricular failure and the therapeutic modalities with potential to reduce the risks of myocardial infraction, such as risk factor modification, adequate control of diabetes and hypertension, antiplatelet agents and lipid-lowering agents, should also be included in the initial therapy.
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PMID:Congestive heart failure: what should be the initial therapy and why? 1472 93

Erdheim-Chester disease (ECD) is a non-Langerhans cell histiocytosis usually affecting bone, that may progress to multi-organ involvement, with pulmonary involvement as an indicator of poor prognosis. Herein, we present a 48-year-old man with a 2-year history of progressive exertional dyspnoea, dry cough, malaise and exophthalmos. High-resolution computed tomography showed peripheral interstitial thickening with a lymphangitic distribution throughout both lungs, suspected of representing lymphangitic spread of neoplasia. Transbronchial biopsy specimen and bronchoalveolar lavage were non-diagnostic; thus, a surgical lung biopsy was performed which showed features diagnostic of ECD. Subsequent systematic investigations showed widespread bone involvement, cardiac involvement manifested as left heart failure and renal/perirenal disease. Treatment with pulsed corticosteroids and cyclophosphamide elicited neither clinical nor functional response, with death at 6 months. This case highlights the aggressive nature of ECD when there is pulmonary involvement, as well as problems in diagnosis when there is pulmonary presentation and when systemic disease is asymptomatic.
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PMID:Erdheim-Chester disease: pulmonary presentation in a case with advanced systemic involvement. 1846 Aug 66

We report a familial form of ventricular non compaction in a mother and two of her sons. It was a young man of 25 years who presented with NYHA stage III dyspnea and a cough with bloody sputum. The clinical examination found left ventricular failure. The echocardiogram done showed left ventricular dilatation with large trabeculae separated by deep intertrabecular recesses in both ventricles suggestive of a non-biventricular compaction. It was possible to note from the family screening by echocardiography of the mother and half-brother a left ventricular non compaction while they were asymptomatic. Thus we concluded a familial form of ventricular non-compaction. This is the first familial case described in Senegal.
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PMID:[A familial form of ventricular non compaction in a mother and two of his sons in St. Louis, Senegal]. 2222 66


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