Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various drugs are associated with adverse respiratory disorders (ARDs) ranging in severity from mild, moderate to severe and even fatal. Cardioselective and nonselective beta-blockers, calcium antagonists and dipyridamole can induce asthma. ACE inhibitors are mainly associated with cough. Amiodarone is related to a form of interstitial pneumonitis (IP) which can be fatal, tocainidine and flecainidine to a form of IP, and hydrochlorothiazide to a form of IP and pulmonary oedema. Antiasthmatic drugs can be associated with a paradoxical bronchospasm, while leukotriene antagonists are linked to the development of Churg-Strauss syndrome. Nonsteroidal anti-inflammatory drugs including aspirin (acetylsalicylic acid) may induce asthma. Gold is mainly related to IP, penicillamine to IP, systemic lupus erythematosus, bronchiolitis obliterans, and Goodpasture's syndrome. Acute respiratory reactions to nitrofurantoin include dyspnoea, cough, IP, and pleural effusion while IP and fibrosis are common in chronic reactions. Other antibacterials mainly evoke pneumonitis, pulmonary infiltrates and eosinophilia, and bronchiolitis obliterans. ARDs are similar for most categories of cytotoxic agents, with chronic pneumonitis and fibrosis being the most common. Noncardiogenic pulmonary oedema occurs as the most common respiratory complication in opioid agonist addiction. Psychotropic drugs such as phenothiazides, butyrophenones and tricyclic antidepressants can also induce pulmonary oedema. Oral contraceptives may produce asthma exacerbation, while long term use and/or high doses of postmenopausal hormone replacement therapy increase the risk of asthma. Bromocriptine is mainly associated with pleural effusion, while methysergide is usually associated with pleural effusion and fibrosis. Some anorectic agents have been linked to the development of primary pulmonary hypertension. The possibility of the occurrence of ARDs should be taken into account in each individual patient. Although in most cases the adverse effects are unpredictable, they can be reduced to a minimum or prevented if some drugs are avoided or stopped in time.
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PMID:Drug-induced respiratory disorders: incidence, prevention and management. 1094 76

In non-smokers the underlying causes for chronic persistent cough (CPC) e.g. chronic cough without diagnostic chest X-ray or pulmonary function test--are usually as follows: several common upper airways diseases, bronchial (cough type) asthma, gastrooesophageal reflux or treatment with an ACE (angiotensin converting enzyme)--inhibitor. In 10% of CPC however the cause remains uncertain. We report a 30 year old non-smoker with severe coughing and repeated vomiting for two months. No laboratory or technical data could be collected suggestive of a common cause of CPC: Upper airways disease, bronchial flow limitation or hyperresponsiveness, ACE inhibitor medication, B. pertussis infection, gastrooesophageal reflux disease (by 24 hours pH-probe) were ruled out. Fiberbronchoscopic findings remained unremarkable, except for the bronchial biopsy specimen, which showed moderate eosinophilic inflammation of the mucosa and marked thickening of the subepithelial layer. Since the cough was non-productive, sputum induction with 3 ml nebulised 3% NaCl solution was performed. 28% of the granulocytes were eosinophil stained. A low quality morning sputum (< 1 ml) showed 21% eosinophilia. Thus, the diagnosis of eosinophilic bronchitis was established. 400 micrograms budesonide dry powder inhalations b.i.d. for one week resolved the cough, treatment was stopped after three weeks. No recurrence was seen two months later. Both the cough type asthma and the eosinophilic bronchitis could represent a form fruste of classical bronchial asthma beyond wheezing or dyspnoea, but with the common main symptom: cough. Since hyperresponsiveness and cough are phenotypic hallmarks of cough variant asthma, in eosinophilic bronchitis--beside cough--another two features of asthma are present: eosinophilic inflammation of the mucosa along with sputum eosinophilia and subepithelial layer thickening. Not surprisingly, eosinophilic bronchial inflammation could be shown in patients with cough variant asthma as well, who--up to 56% during a four year-period--develop classic asthma. The long-term outcome of eosinophilic bronchitis is not known, however. Thus, asthma, cough variant asthma and cough due to eosinophilic bronchitis can mirror different phenotypes or phases of the same entity. CPC due to either the cough type asthma or the eosinophilic bronchitis is like asthma fast responding to inhalative steroids. (Induced) sputum staining should be added to the diagnostic armamentarium of CPC.
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PMID:[Eosinophilic bronchitis without asthma--an additional rare cause for chronic persistent cough (CPC)? A 30-year old patient with severe CPC due to eosinophilic bronchitis without asthma or hyperreactivity]. 1144 11

Because the number of patients who require hospitalization for heart failure is increasing, their treatment is often entrusted to physicians operating in Departments of General Medicine. Published data on the in-hospital treatment of heart failure in Italy have not been available up to now, as they are limited only to patients admitted to Department of Cardiology. This study concerns the patients who were discharged from our Hospital after a diagnosis of heart failure (International Classification of Disease--9th Edition, code 428) from January 1 to February 28, 1998. Information collected from patient hospital records included: age, sex, department to which the patient was referred (General Medicine or Cardiology), cause of heart failure, New York Heart Association (NYHA) functional class, symptoms and signs of heart failure, therapy, length of hospitalization and in-hospital mortality. Of the 178 patients identified (82 males--46.1%, 96 females--53.9%, mean age 78 +/- 11 years) 163 (91.6%) were referred to Departments of General Medicine. The cause of heart failure was coronary artery disease in 88 (49.4%) patients, arterial hypertension in 40 (22.4%), primary cardiomyopathy in 28 (15.7%), valvular heart disease in 22 (12.3%). NYHA functional class was reported or deducible from the severity of dyspnea in 57 (32%) patients. In 8 (4.6%) patients symptoms or signs of heart failure were not reported. Chest X-ray was performed in 77.6% of cases, echocardiography in 41%, ambulatory electrocardiography in 10% and coronary arteriography in 5%. Left ventricular ejection fraction was known in 90 (51.6%) patients, in 44 (48.9%) of these it was > or = 45%. ACE-inhibitors were used in 99 (55.6%) patients, but this percentage rose to 63% when considering only patients with left ventricular ejection fraction < 45%. Eighty-five patients were treated with captopril or enalapril; in 52 patients (61.4%) the daily dose of captopril was < 75 mg and that of enalapril was < 20 mg. Diuretics were utilized in 155 (87%) patients, digoxin in 123 (69%), beta-blocker agents in 5 (2.8%) and other vasodilators in 95 (53%). The mean length of hospitalization was 13 +/- 9 days and the overall in-hospital mortality was 18%. In conclusion, the results of this study demonstrate that the patients who are discharged from our hospital with a diagnosis of heart failure are, on the average, very old. The vast majority of these patients are admitted to the Departments of General Medicine. The advanced age of our patients can explain the limited use of ACE-inhibitors and, especially, of beta-blockers.
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PMID:[Treatment of heart failure at a hospital in the north-east of Italy]. 1168 47

Heart failure during the immediate period of an acute myocardial infarction constitutes a major insult to this pathology; since, once installed, it is associate to ventricular dysfunction and expansion of the left ventricle. It can appear either early or delayed. Subsequent to the acute insult, the myocardium is subjected to diverse changes in its anatomical conformation and to diastolic and systolic alterations, which will affect the hemodynamic constants of the patient. Changes in the parietal ventricular architecture as well as at the neurohumoral level will also occur. The clinical signs of heart failure are: dyspnea, pallor, tachycardia, diaphoresis, cold skin, oliguria, somnolence, and gallop, which can be observed at the very beginning of the coronary occlusion. Its clinical identification, through in-hospital studies supported by adequate hemodynamic monitoring, is of utter relevance since it will lead to appropriate and fast treatment. The groups of patients with acute myocardial infarction with high risk for the development of cardiac failure are: patients with extensive Q wave infarction, diabetic, patients over 65 years of age, and those with a history of previous myocardial infarction(s). The cornerstone of treatment must be focused on reducing the myocardial ischemia, which can be achieved through the use of modern therapeutics and, given the case, pharmacological agents, coronary intervention procedures, or cardiac surgery must be taken into account. At present it is known that angiotensin converting enzyme inhibitors, betablockers, inotropics, are useful to improve ventricular function in patients with acute myocardial infarction.
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PMID:[Heart failure in acute myocardial infarction]. 1200 71

From an association of nearly 50 years, the author had diagnosed biopsy proven 200 cases of sarcoidosis in Eastern India during the past three decades. It appears that most of these cases follow a distinct clinical pattern and presentation. The clinical course and prognosis differ considerably from that seen in Caucasians, Afro-Americans, South-African Bantus and Japanese. Males, above 40 years, coming largely from atopic and wealthier section of society (a particular business community with physicians, nurses with their families and other professionals). Patients present with constitutional symptoms (97%) like slow unrecognized fever with little malaise (fever-malaise dissociation in 70%), arthralgia (61%) or lone-myalgia (13%), appreciable loss of weight (33%), irritability, anorexia, respiratory symptoms (93%) like cough, dyspnea, etc., hepatomegaly (43.5%), splenomegaly (32.5%), lymphadenopathy (22%) with raised ESR (91%), hypergammaglobulinaemia (41.5%), hypercalciuria (40.5%), raised serum angiotensin converting enzyme (SACE) in 70.5% advance disease in chest radiograph (68%), positive 67-gallium scan and clinico-radiological dissociation in 81% (alarming looking chest radiograph with few physical signs). Course and prognosis also differ from the West. A different treatment schedule, avoiding oral prednisolone, has been found quite effective.
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PMID:Sarcoidosis: a journey through 50 years. 1243 38

Bisoprolol is a highly selective beta(1)-adrenoceptor antagonist. Administration of bisoprolol to patients with chronic heart failure is associated with increases in left ventricular function and reductions in heart rate; increases in heart rate variability are also seen. Two major randomised, double-blind, placebo-controlled, multicentre trials have examined the clinical efficacy of bisoprolol in combination with ACE inhibitors and diuretics in patients with stable chronic heart failure (New York Heart Association class III or IV): the Cardiac Insufficiency Bisoprolol Study (CIBIS; n = 641) and CIBIS II (n = 2 647). All-cause mortality (primary endpoint) was significantly lower in bisoprolol than in placebo recipients in CIBIS II (11.8 vs 17.3%) and was reduced by bisoprolol regardless of dosage. All-cause mortality was also lower in CIBIS (16.6 vs 20.9%) although the difference did not achieve statistical significance. In a meta-analysis of CIBIS and CIBIS II (n = 3 288), a relative reduction of 29% in the incidence of all-cause mortality was seen in bisoprolol versus placebo recipients; this analysis also demonstrated that bisoprolol reduces mortality in patients with chronic heart failure regardless of aetiology or severity. In CIBIS II, there were significantly fewer cardiovascular deaths, admissions to hospital for any reason, or cardiovascular deaths or cardiovascular hospitalisations (combined endpoint) in bisoprolol, compared with placebo, recipients (secondary endpoints). Compared with standard treatment alone, the addition of bisoprolol was a cost-effective option in chronic heart failure in UK, French, German and Swedish pharmacoeconomic studies. Bisoprolol is generally well tolerated in patients with chronic heart failure. In CIBIS II, adverse events occurring more commonly in bisoprolol than placebo recipients, regardless of causal relationship with the study medication, included dizziness, bradycardia, hypotension and fatigue. Bisoprolol recipients were less likely than placebo recipients to experience worsening of heart failure, dyspnoea or tachycardia. In both CIBIS and CIBIS II there was no significant difference between bisoprolol and placebo recipients in the incidence of permanent treatment withdrawal. In conclusion, adding the highly selective beta(1)-blocker bisoprolol to a treatment regimen comprising an ACE inhibitor and a diuretic significantly improves survival in patients with stable chronic heart failure and reduces the need for hospitalisation. The use of bisoprolol in this disorder is generally well tolerated and is cost effective. Thus, bisoprolol should be considered a standard treatment option when selecting a beta-blocker for use in combination with ACE inhibitors and diuretics in patients with stable, moderate to severe chronic heart failure.
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PMID:Bisoprolol: a review of its use in chronic heart failure. 1246 13

From 1989 to 1999, the incidence of cardiac failure appears stable but its prevalence has increased up to three folds. Obesity increases the risk of development of cardiac failure. In genetics, mutations in some proteins of muscular cells may lead to the occurrence of dilated cardiomyopathy. The interest of Brain Natriuretic Peptid was confirmed in case of acute dyspnea or diastolic dysfunction as well as its prognostic role in the functional capacity and the occurrence of sudden death. In the therapeutic field, a great disappointment came from the results of studies on omapatrilat. Despite its advantageous hemodynamic effects, this drug is not more efficacious than any ACE-inhibitor, but with much more side effects. New drugs (levosimendan, nesiritide) appear interesting in the acute heart failure. The short-term as well as long-term effects of cardiac resynchronization are confirmed. Implantable cardioverting defibrillators decrease the mortality of patients with a past history of myocardial infarction with severe left ventricle dysfunction. The artificial heart Jarvik 2000 appears to be hopeful for patients on waiting lists for heart transplantation.
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PMID:[The best of cardiac failure in 2002]. 1261 58

Arterial hypertension is a major risk factor for the clinical syndrome of angina pectoris, in which the ECG is abnormal but the coronary arteries are normal. Structural and functional abnormalities in coronary circulation as well as extravascular factors (eg, left-ventricular hypertrophy, fibrosis with diastolic dysfunction) compromise the adequate ratio of coronary blood flow to oxygen demand causing angina, dyspnea, and major cardiac events. Recent studies stress the importance to functional disturbances of coronary microvasculature leading to profound morphologic changes associated with impaired coronary conductance. In patients without epicardial coronary stenosis hypertensive microvascular disease can be qualitatively assessed by noninvasive diagnostic approaches based on new Doppler echocardiography techniques and may also be monitored by widely available stress tests. For ultimate quantitative assessment, invasive procedures are still required. Beyond guidelines to control blood pressure in hypertensive individuals, restoration of functional and structural integrity of the coronary microvasculature represents the ultimate therapeutic goal in hypertensive patients with coronary insufficiency and without angiographic evidence of atherosclerosis. Concomitant factors reducing coronary conductance such as left-ventricular hypertrophy and diastolic dysfunction should be reversed in parallel. Currently, therapeutic intervention in the renin-aldosterone-angiotensin-II-system using ACE inhibitors, angiotensin receptor blockers, and low doses of aldosterone antagonists represent the most promising strategy to achieve these goals. Using the knowledge of these recent results we should refine the overall management of our hypertensive patients with coronary insufficiency but without atherosclerosis.
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PMID:Management of the hypertensive patient with coronary insufficiency but without atherosclerosis. 1285 22

Elevated blood pressure is a risk factor for a variety of cardiovascular disorders, including coronary heart disease, peripheral vascular disease, cardiac failure and cerebrovascular disease. The prevailing view is that an elevated systolic rather than diastolic blood pressure is the major contributor in mortality and morbidity attributed to cardiovascular disorders. Isolated high systolic blood pressure, especially in the elderly, is a major risk factor and should undoubtedly be a target for drug treatment. In the general population, systolic and diastolic blood pressure are highly correlated, and thus it is difficult to dissociate the effects of these two components of the blood pressure and specifically ascribe cardiovascular risk factors to just elevated systolic blood pressure. Therefore, the goal in therapy of an individual with hypertension must be to reduce elevated systolic and diastolic blood pressure in order to reduce mortality and morbidity. ACE and neutral peptidase inhibitors are a new class of drugs that may be beneficial in the treatment of patients with hypertension and heart failure. They may also be useful in the treatment of diabetic patients with hypertension and/or heart failure. Drugs of this class are dual inhibitors of ACE and neutral endopeptidase, and are capable of affecting vascular tone and fluid balance. They are capable of producing vasodilatation by virtue of inhibiting the production of angiotensin II, degradation of natriuretic peptides and bradykinin. They also appear to promote natriuresis and diuresis by amplifying the actions of natriuretic peptidase and reducing aldosterone effects. In addition, they should also attenuate trophogenic actions of the renin angiotensin system and the sympathetic nervous system. Omapatrilat is one drug that appears to be at the advanced stages of clinical development. This drug has been shown to be quite effective in the treatment of hypertension. Evidence also seems to indicate that treatment with omapatrilat results in a higher tendency towards preventing death and worsening heart failure when compared with treatment with a pure ACE inhibitor in patients with advanced heart failure. Overall safety with omapatrilat appears to be good, but like other ACE inhibitors the incidence of cough is higher when compared with placebo. Other common adverse effects noted are headaches, facial flushing/warm sensation, dizziness, nausea and dyspnoea. Of greater concern is the occurrence of angio-oedema, the true incidence of which remains to be fully established as part of the published medical literature.
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PMID:Dual ACE and neutral endopeptidase inhibitors: novel therapy for patients with cardiovascular disorders. 1501 94

This article contains a series of reports on recent research developments in the field of heart failure. Reports of key presentations made at the European Society of Cardiology meeting, held in Vienna, Austria, between 30 August and 3 September 2003 are reported. In the CHARM study, candesartan reduced cardiovascular deaths and hospital admissions for heart failure, both in patients who were already taking an ACE-inhibitor and in those who were ACE intolerant. However, results in patients with preserved left ventricular function were less conclusive. The BASEL study supports the use of B-type natriuretic peptide testing to confirm the diagnosis of heart failure in patients presenting with acute dyspnoea. In EUROPA, the largest ever study of secondary prevention of coronary artery disease, long-term treatment with perindopril reduced the incidence of cardiovascular death, myocardial infarction (MI) and cardiac arrest. The ESTEEM study showed that the oral thrombin inhibitor ximelagatran plus aspirin was more effective than aspirin alone in the prophylaxis of major cardiovascular events following MI.
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PMID:Clinical trials update from the European Society of Cardiology: CHARM, BASEL, EUROPA and ESTEEM. 1460 10


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