Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 4676 patients and 1759 patients were treated with lisinopril and nifedipine respectively in a post-marketing surveillance study conducted in general practice in the UK. Patients were followed up for 12 months. Most of the lisinopril patients had hypertension, but a small number (180) had heart failure. Most of the nifedipine patients had uncomplicated hypertension, but some (22.57%) had other cardiovascular disease with or without hypertension. Lisinopril and nifedipine were equally effective in reducing blood pressure. During the study, 1.5% of hypertensive patients assigned to lisinopril died compared with 1.8% of patients assigned to nifedipine, and 15.1% of lisinopril patients compared with 19.7% of patients in the nifedipine group withdrew because of adverse events. Cough, malaise and fatigue, nausea and vomiting were more frequent causes of withdrawal from lisinopril than nifedipine. Conversely, headaches, pallor and flushing, oedema and palpitations caused more frequent withdrawals from nifedipine. Anaemia was more often encountered on nifedipine treatment than on lisinopril. In hypertensive patients, the frequency of first-dose hypotension was similar on both treatments. Serious events occurred in 0.8% and 0.5% of patients given lisinopril and nifedipine respectively. Lisinopril was well tolerated by heart failure patients: 16 patients (8.88%) died and an incidence of 4.44% of serious adverse events was reported, a pattern to be anticipated in such patients; dizziness, giddiness, dyspnoea, cough, nausea and vomiting were the most frequent causes of withdrawal; the incidence of first-dose hypotension was low (2.22%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-marketing surveillance of lisinopril in general practice in the UK. 811 50

We conducted a prospective, double-blind, placebo-controlled multicenter trial in order to evaluate the long-term effects of captopril (50 mg/day), digoxin (0.25 mg/day) and placebo on quality of life, cardiovascular events, clinical symptoms and exercise tolerance in patients with documented myocardial infarction, resulting in regional wall motion abnormalities, and with mild heart failure (NYHA class II to III without treatment) and exercise not limited by angina. 222 patients were studied, 63 were randomized to captopril, 66 to digoxin, 67 to placebo. Follow-up was conducted for two years. Base line characteristics in the three treatment groups were similar. After one year of therapy, digoxin had significantly improved general well-being (p < 0.01 vs captopril), symptom score (p < 0.05 vs captopril and placebo), and vitality (p < 0.05 vs captopril). Digoxin improved NYHA class in 45% as compared to placebo (28%, p < 0.05). Worsening of angina was more frequent with captopril as compared to digoxin (p < 0.05). However, cardiovascular events during follow-up were lower in the captopril group as compared to placebo and digoxin (p < 0.01 captopril vs placebo). No differences between groups were observed in baseline and follow-up exercise tolerance between the three groups. Dizziness during upright tilt and cough were more frequent with captopril as compared to digoxin or placebo. After two years of follow-up (captopril n = 32, digoxin n = 29, placebo n = 27) general well-being was improved with both digoxin and captopril (p < 0.004 and p < 0.03 vs placebo).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril versus digoxin in patients with coronary artery disease and mild heart failure. A prospective, double-blind, placebo-controlled multicenter study. The CADS Study Group. 812 24

We report on eight cases of amiodarone pulmonary toxicity. Main clinical symptoms are acute/subacute dyspnea or progression in some cases. Amiodarone responsibility is difficult to ascertain. Several arguments can be presented: clinical symptoms with dyspnea and/or fever and/or cough, interstitial or in diffusing capacity for carbon monoxide, abnormal broncho-alveolar lavage cytopreparation smear with increased percentage of lymphocytes and polymorphonuclear leucocytes in typical cases; trans-bronchoscopic lung biopsy failed to provided information on amiodarone toxicity in the two patients where biopsy were performed. Differential diagnosis is an essential step to eliminate other possible causes ie pulmonary micro-organism infections, cancer or pulmonary oedema secondary to heart failure. In one case acute pulmonary toxicity occurred early, after introduction of amiodarone, with a proposed immuno-allergic mechanism. In other cases, chronic amiodarone deposition in the lungs can explain clinico-radiologic features. In six cases improvement was observed after discontinuation of therapy within a 6-months period.
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PMID:[Pneumopathy caused by amiodarone in internal medicine: 8 cases]. 819 Oct 72

A 41-year-old patient with chronic myelogenous leukemia in the accelerated phase was treated with mitoxantrone. She developed pyrexia 7 days after receiving the third administration of mitoxantrone. After 3 more days, she experienced dry cough and dyspnea. Bilateral fine crackles were audible, but no signs of heart failure were found. A chest X-ray film revealed diffuse reticulogranular infiltrates bilaterally. An increase in the prednisolone dosage led to an improvement. Specimens of the bronchoalveolar lavage revealed an increase in CD4-/CD8- lymphocytes. The peripheral lymphocytes also expressed neither CD4 nor CD8. Specimens of a transbronchial lung biopsy disclosed thickening of the alveolar wall with infiltration of lymphoid cells.
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PMID:Interstitial pneumonitis possibly due to mitoxantrone. 829 77

The long-term acceptability of perindopril in mild-to-moderate chronic heart failure (CHF) was evaluated in a multicenter open study. A total of 320 patients with a mean age of 62 +/- 1 years and CHF of New York Heart Association (NYHA) class I (2 patients), II (204 patients), or III (114 patients) were included after a 2-week run-in period during which time vasodilators were stopped and diuretic and/or digoxin therapy stabilized. Perindopril treatment was started at 2 mg, increasing to 4 mg once daily after 2 weeks if supine systolic blood pressure remained > 100 mm Hg. After this dose titration period, follow-up visits were scheduled at monthly intervals for the first 3 months, then at 3-month intervals with a maximum period of follow-up being 30 months. At the time of analysis, mean duration of treatment was 276 days and 208 patients were treated > or = 6 months. Of the 320 patients, 10 (3.1%) died, 9 (2.8%) were withdrawn for worsening heart failure, and 38 (11.9%) for nonfatal adverse events, including cough (2.8%), dizziness or orthostatic discomfort (1.9%), angina pectoris (1.6%), and cutaneous signs (1.3%). Exercise test duration increased from 516 +/- 14 to 659 +/- 19 sec after 6 months of treatment (p < 0.01). At 6 months, 55.6% of patients improved by at least 1 NYHA class. Supine systolic blood pressure decreased slightly from 137 +/- 2 to 132 +/- 1 mm Hg (p < 0.01) and plasma creatinine levels remained stable from 100 +/- 2 to 102 +/- 2 mumol/liter after 6 months of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acceptability of perindopril in mild-to-moderate chronic congestive heart failure. Results of a long-term open study in 320 patients. 832 69

The effects of cilazapril on exercise tolerance and neurohumoral factors were investigated in old myocardial infarction (OMI) patients with asymptomatic heart failure and reduced left ventricular ejection fraction. Cilazapril (0.5 mg) was administered once daily to OMI patients (n = 20) [NYHA class I, sinus rhythm, ejection fraction by radionuclide scanning < 50% (36.8 +/- 9.1%, mean +/- SD)]. Two weeks later, five patients were excluded from the study because of cough or hypotension, and 15 patients received 1.0 mg cilazapril once daily for the next 6 weeks. Exercise tolerance, neurohumoral factors and ejection fraction were measured in OMI patients before and after administration of cilazapril. Seven age-matched healthy adults served as the controls. OMI patients had latent heart failure because their exercise tolerance values and aldosterone levels were lower and alpha-atrial natriuretic polypeptide levels were higher than those in healthy subjects. In OMI patients, 8 weeks after cilazapril administration, exercise duration increased from 545 +/- 59 to 590 +/- 74 sec (p < 0.05), anaerobic threshold from 17.5 +/- 3.2 to 20.1 +/- 2.8 ml/min/kg (p < 0.05), peak-VO2 from 23.5 +/- 4.7 to 27.1 +/- 4.4 ml/min/kg (p < 0.05), plasma renin activity from 1.34 +/- 1.13 to 5.82 +/- 5.47 ng/ml/hr (p < 0.01) and alpha-atrial natriuretic polypeptide decreased from 100.7 +/- 44.3 to 80.5 +/- 28.0 pg/ml (p < 0.05). In patients with asymptomatic left ventricular dysfunction after myocardial infarction, 8 week's cilazapril administration improved exercise tolerance and neurohumoral conditions.
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PMID:[Effect of cilazapril on exercise tolerance and neurohumoral factors in patients with asymptomatic chronic heart failure after myocardial infarction]. 852 61

1. Angiotensin converting enzyme (ACE) inhibitors are in common use for the treatment of hypertension and heart failure. Whereas they are, in general, well tolerated, a dry cough can develop which, on occasion, requires termination of therapy. The reported prevalence of cough with ACE inhibitor therapy has varied from 0.2 to 25%, depending upon methods of data collection, analysis and symptom reporting. 2. To evaluate the prevalence of cough in Chinese patients receiving ACE inhibitors, interviews were carried out in 191 patients in Hong Kong who were taking therapy which included captopril or enalapril for hypertension or heart failure, and 382 patients matched for sex and age receiving alternative medications which excluded an ACE inhibitor (controls). Patients and controls were interviewed in a blinded manner by the same interviewer using a common adverse-effect questionnaire. 3. Persistent cough was reported in 44% of patients taking an ACE inhibitor (46% of those receiving captopril and 41.8% of patients taking enalapril), and in 11.1% of the controls (P < 0.001). The prevalence of other adverse reactions was similar, with no significant difference between the two treatment groups. The complication of cough was not related significantly to age, sex, underlying disease, drug dosage or smoking status. 4. This study indicates that cough is a common side effect of treatment with ACE inhibitors in Hong Kong Chinese, although in most patients cessation of therapy is not required. Whether Chinese are particularly susceptible to ACE-inhibitor cough requires a formal prospective study comparing Chinese and non-Chinese patients.
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PMID:High prevalence of persistent cough with angiotensin converting enzyme inhibitors in Chinese. 856 96

Angiotensin-converting enzyme inhibitors (ACE-I) have been proven to be effective in reducing morbidity and mortality in patients with heart failure or post-myocardial infarction left ventricular dysfunction. Despite evidence from several large-scale randomized trials, the use of ACE-I in patients with heart failure remains relatively low. In part, the failure to achieve more widespread use of ACE-I in patients with heart failure may be due to physician's perceptions of the side effects associated with ACE-I, such as angioedema, renal dysfunction, cough, and hypotension. Many of these side effects are thought to be due to ACE-I-induced bradykinin accumulation. It is possible to inhibit the effect of angiotensin II without increasing bradykinin levels using an angiotensin II type I blocking agent such as losartan. How effective losartan is compared with an ACE-I is uncertain, however. Some of the beneficial effects of ACE-I have been attributed to bradykinin accumulation, and therefore ACE-I might have an advantage compared with an angiotensin II type I receptor antagonist such as losartan. On the other hand, angiotensin II may be produced by non-ACE-I-dependent mechanisms, which would suggest that an angiotensin II type I receptor blocking agent would be advantageous. To determine the relative safety and efficacy of an ACE-I, which results in bradykinin accumulation and inhibitors of angiotensin II, versus an angiotensin II type I receptor blocking agent, which does not result in bradykinin accumulation, we have begun the Evaluation of Losartan In The Elderly (ELITE) trial, which will compare the safety and efficacy of captopril and losartan in elderly patients with heart failure.
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PMID:Angiotensin II receptor antagonists in heart failure: rationale and design of the evaluation of losartan in the elderly (ELITE) trial. 857 52

Cough accompanied by an increased sensitivity of the cough reflex is the most common symptom of inflammatory airway disease. This symptom is also frequently reported in patients receiving angiotensin-converting enzyme (ACE) inhibitors as therapy for heart failure or hypertension, although the underlying mechanism is unknown. We have investigated the possibility that the inflammatory peptide bradykinin, normally degraded by ACE, causes sensitization of airway sensory nerves and an enhancement of the cough reflex in conscious guinea pigs. Treatment of guinea pigs for two weeks with captopril led to an increased cough response to inhaled citric acid, which was prevented by concomitant treatment with the bradykinin receptor antagonist icatibant. A similar icatibant-sensitive enhancement of citric acid-evoked cough was seen in untreated animals after prior inhalation of bradykinin, although cough evoked by hypertonic saline was unaffected. In electrophysiological studies performed in vitro, responses of single vagal C fibers to capsaicin, applied to receptive fields of single-fiber units in the trachea, were also markedly increased after perfusion with bradykinin, whereas A delta fiber responses to hypertonic saline were unaffected. These results indicate that bradykinin-evoked sensitization of airway sensory nerves may underlie the pathogenesis of ACE-inhibitor cough. Bradykinin receptor antagonists may be of benefit in treating chronic cough seen with this and other inflammatory conditions.
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PMID:Bradykinin-evoked sensitization of airway sensory nerves: a mechanism for ACE-inhibitor cough. 867 30

A 49-year-old woman was admitted to our hospital because of coughing and dyspnea. A chest roentogenogram showed emphysematous changes and a diffuse reticular shadow. A high-resolution CT scan of the chest showed many small cysts throughout the lungs. Lymphangiomyomatosis was diagnosed after examination of a specimen obtained by transbronchial biopsy. Abdominal distention due to chylous ascites developed during the hospital stay despite anti-estrogen therapy. Because the ascites was resistant to conservative therapy, we decided to begin peritoneo-venous shunting with a Denver Shunt system. After the operation, the abdominal distention was controlled for 1 year and 11 months, at which time the patient died of respiratory and heart failure with pneumonia. At autopsy, the shunt was patent and functional although about 900 ml of serous ascites fluid was present. An adenocarcinoma was found in the upper lobe of the right lung, but it may not have been related to the lymphangiomyomatosis. Peritoneovenous shunting with a Denver Shunt can be used to treat chylous ascites due to lymphangiomyomatosis when conservative therapy is insufficient.
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PMID:[Lymphangiomyomatosis with chylous ascites treatment successfully by peritoneo-venous shunting]. 875 14


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