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)

1. Over the last 40 years a range of therapeutic strategies has been introduced for the long term treatment of hypertension. 2. Although safe effective agents are available a significant number of patients are unable or unwilling to take these drugs as long term treatment. 3. Both insufficient efficacy and adverse effects justify the search for new antihypertensive strategies. 4. Recent developments include orally active angiotensin (AT1) receptor antagonists (ARA) which appear to offer the benefits of prevention of angiotensin II effects without the adverse effects of bradykinin potentiation, such as cough, which limit the usefulness of angiotensin converting enzyme (ACE) inhibitors. 5. Imidazoline receptor agonists offer the potential of centrally active antihypertensives without the adverse effects of sedation and dry mouth. Further clinical experience is necessary to confirm whether the clinical efficacy and good tolerability are confirmed with long term use. 6. Both ARA and imidazoline preferring substances offer the bonus of a desirable haemodynamic profile in patients with heart failure and may open new therapeutic avenues in the management of cardiac failure.
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PMID:New therapeutic agents for hypertension. 880 42

A drug surveillance study was performed to determine the tolerance and safety of quinapril in the treatment of patients with stage 1 or 2 hypertension. The trial was noncomparative, open-label, uncontrolled, and nonrandomized. Patients with secondary hypertension, heart failure, other heart diseases, and other serious conditions were excluded. After a washout period of 2 weeks, 752 patients (316 men and 436 women) with diastolic blood pressure (DBP) between 90 and 115 mm Hg and systolic blood pressure (SBP) between 140 and 200 mm Hg were entered into the treatment phase. The mean age of patients (+/- SD) was 53.1 +/- 11.4 years. Patients initially received 10 mg/d quinapril for 4 weeks. For nonresponders, the dosage was titrated up to a maximum of 40 mg. Active treatment continued for 12 weeks. Initial blood pressures (mean +/- SD) were DBP, 102 +/- 6.1 mm Hg, and SBP, 163 +/- 14.4 mm Hg. Final blood pressures were DBP, 83 +/- 6.5 mm Hg, and SBP, 135 +/- 11.6 mm Hg. The response rate for the therapeutic goal (DBP < 90 mm Hg and SBP < 140 mm Hg, or a reduction in SBP > or = 20 mm Hg) was 67.1%; 41 patients did not complete the study. The most common adverse events were cough, headache, and dizziness; only 10 patients (1.3%) failed to complete the study because of adverse events. Quinapril, as used in current private clinical practice, is well tolerated and effective for the treatment of patients with stage 1 or 2 hypertension.
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PMID:Usefulness of low-dose, once-daily quinapril as monotherapy for patients with hypertension. 893 Apr 30

The ACE inhibitors have been found effective in reducing the morbidity and mortality of both post-infarction patients and those with chronic systolic left ventricular dysfunction. However, their use is limited--particularly in elderly patients because of poor tolerance partly due to bradykinin-induced side-effects such as renal dysfunction, first-dose hypotension, and cough. Thus, the introduction of the angiotensin II type I receptor antagonists--that block the effects of angiotensin II without increasing bradykinin concentration--may be particularly important in the treatment of elderly patients. The role of the angiotensin II type I receptor antagonists in patients with systolic left ventricular dysfunction is currently being explored in direct comparison with and in conjunction with the ACE inhibitors. Furthermore, important questions about the most effective dose of ACE inhibitor and ACE inhibitor use in conjunction with aspirin and the NSAIDs still have to be answered. Thus, although we have learnt much about the role of ACE inhibitors in heart failure treatment, we are still at an early stage in the application of this knowledge, particularly in elderly patients.
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PMID:ACE inhibitor use in elderly patients with systolic left ventricular dysfunction: problems and opportunities. 899 96

A 42-year-old man presented with cough, chest pain and dyspnea. The chest roentgenogram revealed a large mass shadow in the right upper and middle lobes with atelectasis and pleural effusion. Massive polypoid tumor extending into the left atrium was diagnosed by computed tomography and two dimensional echocardiography. In order to prevent sudden death and cardiac failure, surgery was performed. At first, the polypoid tumor in the left atrium was removed with a partial resection of the left atrial wall under cardiac arrest using cardiopulmonary bypass. Then, a right pneumonectomy was performed. Episodes of embolism were not observed during surgery. His postoperative course was almost favorable. The size of the tumor in the right lung was 18 x 15 x 8 cm and the one in the left atrium was 6.5 x 4.5 x 3 cm, respectively. Pathological examination of the resected specimen revealed the evidences of large cell carcinoma extending into the left atrium. Local recurrence with S9 metastasis of the left lung were detected 6 months after surgery, and he died 6 months later. It is emphasized that the extended surgery using cardiopulmonary bypass was useful for both prevention of embolism and improvement of quality of life.
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PMID:[A successful removal of T4 lung cancer with its left atrial extension using cardiopulmonary bypass]. 902 67

Pulmonary alveolar microlithiasis (PAM) is a rare disease characterized by widespread localization of calcispherites in the alveolar spaces. The patients are symptomless for a long time. Nevertheless, this disease slowly develops into pulmonary fibrosis and cardiac failure. The chest X-rays and high-resolution computed tomography strongly point towards a diagnosis of PAM. As for therapeutic approaches, repeated broncho-alveolar lavages (BAL) have been performed with improvement of symptoms but without recovery, and a new oral drug treatment is still under way. We report 2 familial cases of PAM. Both patients underwent chest X-ray examination showing diffuse bilateral micronodular opacities of calcific density. After 5 years, in May 1993, one of them developed exertional dyspnoea, cyanosis, dry cough and was admitted to our Division. Cardiokinetic and diuretic drugs as well as oxygen were administered with satisfactory results. Then repeated BAL were performed. The chest X-ray after 6 months of sodium etidronate (300 mg t.i.d.) administration was unchanged.
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PMID:Pulmonary microlithiasis. Report of two cases. 909 54

Tropical pulmonary eosinophilia (TPE) is considered to be a variant of human filarial infection. The pulmonary manifestations of TPE have been well described. Extra-pulmonary features of the disease, although not commonly seen, have been reported previously. A 9-year-old Malay girl with a history of recurrent cough and wheezing was admitted because of cardiac failure. Physical examination revealed a very sick girl with tachypnoea, central cyanosis, finger clubbing, elevated jugular venous pulse, generalized crackles and rhonchi in the chest, a loud second heart sound and hepatosplenomegaly. A chest radiograph showed cardiomegaly and right pleural effusion. Laboratory investigations revealed hypochromic, microcytic anaemia with persistent blood eosinophilia (absolute eosinophil counts varied from 1.9 to 5.5 x 10(9)/1). The ELISA test for antifilarial IgG antibodies was strongly positive. She responded promptly to treatment with diethylcarbamazine. In summary, this is a patient with TPE who presented with cor pulmonale, probably due to late-stage interstitial pulmonary fibrosis. In order to prevent the long term morbidity of cardiorespiratory disability, the early signs of TPE should be recognized and the infection treated.
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PMID:Cor pulmonale: an unusual presentation of tropical eosinophilia. 917 82

To identify easily ascertainable sociodemographic and health characteristics that are associated with hypoalbuminemia in community-dwelling older persons, we used data from the first National Health and Nutrition Examination Survey. This population-based stratified probability sample survey included 4728 persons aged 55-74 y. We defined hypoalbuminemia in two ways: < 35 g/L (1.2% of the sample) or < or = 38 g/L (7.9% of the sample) and used multivariate logistic models to identify independent predictors of hypoalbuminemia. Older age; receiving welfare; a condition interfering with eating; vomiting > or = 3 d/mo; previous surgery for gastrointestinal tumor; self-reported heart failure; recurring cough attacks; feeling tired or wornout; edentulous, fair, or poor condition of teeth; little or no exercise; a low-salt diet; trouble chewing meat; self-reported protein albumin, blood, or sugar in urine; and current cigarette smoking were independently associated with albuminemia (< or = 38 g/L) or progressively lower albumin concentrations < 40 g/L. Persons with 3-5 of these factors (51.5% of the sample) had an odds ratio of 2.73 (95% CI: 1.64, 4.54) and those with > or = 6 factors (9.4% of the sample) had an odds ratio of 6.44 (95% CI: 3.49, 11.86) of albuminemia < or = 38 g/L compared with those with 0-2 risk factors (39.1% of the sample). These findings suggest that several easily assessed sociodemographic, lifestyle, and disease-related factors are associated with hypoalbuminemia and might be valuable items to include on general health surveys to identify older persons who have this marker of poor health status.
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PMID:Correlates of hypoalbuminemia in community-dwelling older persons. 920 67

ACE inhibitors have been shown to be effective in reducing the morbidity and mortality of patients with left ventricular systolic dysfunction, but their application to clinical practice in this situation is still limited. In part, the failure to prescribe an ACE inhibitor to a patient with left ventricular systolic dysfunction is due to perceptions regarding their side effects, such as cough and renal dysfunction. Relatively few patients with left ventricular systolic dysfunction and a serum creatinine > or = 2 mg/dl receive an ACE inhibitor in clinical practice. In this situation one should consider an agent such as fosinopril, which is metabolized by the liver as well as secreted by the kidney. In patients with moderate renal dysfunction, fosinopril has been well tolerated without an increase in serum creatinine. In patients who develop cough due to an ACE inhibitor, consideration should be given to an angiotensin II type 1 receptor blocking agent, such as losartan. The relative safety and efficacy of an ACE inhibitor compared with an angiotensin II type 1 receptor blocking agent is being explored in a prospective randomized trial (Evaluation of Losartan In The Elderly [ELITE]), as well as the safety and pharmacological effectiveness of adding an angiotensin II receptor antagonist to an ACE inhibitor (Randomized Angiotensin receptor antagonists-ACE-inhibitor Study [RAAS]). There may also be a role for the combination of an aldosterone receptor antagonists and an ACE inhibitor in patients with left ventricular systolic dysfunction. Once an ACE inhibitor is administered to a patient with left ventricular systolic dysfunction it should be continued indefinitely. ACE inhibitors may be of value not only in preventing the progression of heart failure but also in reversing endothelial dysfunction and preventing the development of atherosclerosis and its consequences, such as myocardial infarction.
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PMID:ACE inhibitors in heart failure: prospects and limitations. 921 Oct 22

Fosinopril is the prodrug of the active diacid ACE inhibitor fosinoprilat. In patients with heart failure, fosinopril reduces pulmonary capillary wedge pressure, mean arterial blood pressure, mean right atrial pressure and heart rate, and increases stroke volume index and cardiac index. The drug has compensatory dual elimination routes via renal and hepatic systems and accumulates to a lesser extent than enalapril and lisinopril in patients with chronic renal insufficiency with or without heart failure. Comparative studies of 3 or 6 months' duration with fosinopril 10 to 40 mg/day have demonstrated clinical efficacy significantly superior to that of placebo in patients with heart failure [mostly New York Heart Association (NYHA) functional class II or III]. Fosinopril treatment consistently increased exercise duration and improved heart failure symptoms in these patients. Significantly fewer fosinopril than placebo recipients withdrew or were hospitalised because of worsening heart failure. Additionally, significantly more fosinopril than placebo recipients showed improvement, and fewer patients had deteriorated, in terms of NYHA functional class. Fosinopril and enalapril showed similar clinical efficacy over 6 and 12 months' treatment in patients with NYHA functional class II to IV heart failure. As yet, there are no data showing a mortality benefit with fosinopril. Fosinopril was well tolerated in clinical trials in patients with heart failure. Dizziness (11.9 vs 5.4% for placebo), cough (9.7 vs 5.1%) and hypotension (4.4 vs 0.8%) were the most commonly reported adverse events. In 6- or 12-month comparative studies, fosinopril therapy was associated with a lower incidence of dizziness and hypotension, but a higher incidence of vertigo, than enalapril therapy. 0.8% of patients discontinued the drug because of cough, which occurred to a similar extent with fosinopril and enalapril. Thus, based on available clinical evidence, fosinopril is an effective and well tolerated option for the management of patients with heart failure. Although clinical data are limited, fosinopril may be especially useful in patients with renal or hepatic impairment.
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PMID:Fosinopril. A review of its pharmacology and clinical efficacy in the management of heart failure. 921 Oct 84

As a net effect of ACE-inhibitors and AT1-receptor antagonists on the renin-angiotensin system (RAS) cardioprotection due to vasodilative (reduction of blood pressure, afterload reduction), antiproliferative (reduced cell growth, reduction of "vascular" and/or "ventricular remodeling", reduced formation of extracellular matrix), as well as antiadrenergic actions and due to the stimulating effect on natriuresis, reduction of blood pressure, preload reduction can be expected. These aims of therapy have mostly been confirmed for the action of ACE-inhibitors by experimental and clinical studies but except for the treatment of arterial hypertension and few preliminary reports concerning the treatment of cardiac dysfunction, no comparable data are available for AT1-receptor antagonists. To date, an antithrombotic and profibrinolytic action could only be demonstrated for ACE-inhibitors. This effect has been discussed to be responsible for the improvement of long-term prognosis in patients with coronary artery disease. Despite the similar spectrum of action there exist important differences between ACE-inhibitors and AT1-receptor antagonists that might underline the need of an individual use of these drugs: the dual action of ACE-inhibitors on the RAS and the kinin system bears many benefits but has been also shown to be accompanied by side-effects, mainly chronic dry cough, in a relatively high percentage of patients thus leading to discontinuation of therapy in 8-14%. This respective side-effect can be prevented by the use of AT1-receptor antagonists. It has been discussed whether the incomplete action of ACE-inhibitors on AT1-receptor-mediated effects is at least in part responsible for the efficacy of this drug which is relatively high (75-80%) as compared to other substances. Due to their direct action, AT1-receptor-blockers might also be of high effectiveness for the treatment of severe heart failure. A combination of the ACE-inhibitor-mediated activation of the kinin-system with the more specific blockade of AT1-receptors by AT1-receptor antagonists might be of benefit and is currently under investigation. Finally, it has been discussed that the increased AT II concentration in case of AT1-receptor-blockade activates AT2-receptor-mediated mechanisms thus leading to an additive vasoprotective effect.
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PMID:[Pathophysiological mechanisms of the renin-angiotensin system and its pharmacologic modification by ACE inhibitors or angiotensin II (type 1) receptor blockers in cardiovascular diseases]. 923 95


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