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)

The discordance frequently observed between the hemodynamic effects of treatment and change in functional status may be explained by the fact that symptoms are related more to the circulatory changes caused by the heart failure than the heart failure itself. This is why angiotensin converting enzyme inhibitors and controlled exercise training improve exercise capacity of patients with chronic cardiac failure more than inotropic agents and direct vasodilator therapy, partly because of their marked beneficial effect on regional blood flow.
Arch Mal Coeur Vaiss 1990 Nov
PMID:[Influence of medical treatments on the functional status in patients with chronic cardiac insufficiency]. 212 15

The number cardiac transplantation has been dramatically increasing for the last year and the results are satisfactory regarding survival or functional capacity. The observed increase of cardiac transplantation may tend to vulgarize it. However, this intervention should be only considered in a selected group of patients who have no other option. Many reports concerned various technical approach for a clearcut determination of high and low risk population of patients with congestive heart failure. But, considering individual patients, the value of each prognostic parameter remains unresolved. Nevertheless the more discriminant parameters for the prognosis assessment are: the left ventricular ejection fraction, the NYHA class, right heart catheterization data, the functional capacity, the cardiothoracic ratio on chest X ray, the ischemic etiology of the disease. The role of neuro-hormonal determinant such as norepinephrine circulating concentration or cardiac uptake on MIBG imaging should be further investigated, especially for patients treated by ACE inhibitors or beta blockers. Contraindications for cardiac transplantation are less restrictive, nowadays. Concerning patients selected, and waiting for heart transplantation or patients non primary selected survival can be improved by adjusting medical therapy on objective efficacy criteria.
Arch Mal Coeur Vaiss 1990 Nov
PMID:[Cardiac transplantation. Indications, delays, surveillance]. 212 16

Many practical difficulties are encountered by physicians in the medical treatment of chronic cardiac failure. They are related to the choice of drug guided by therapeutic objectives: vasodilators and angiotensin converting enzyme inhibitors are no longer drugs of secondary intention reserved for chronic cardiac failure, but there is no information as to the place of these drugs in early stages of myocardial dysfunction before the appearance of the clinical signs of cardiac failure. Other difficulties are related to the use of many different drugs, to the many secondary effects, sometimes increased by drug interactions; these difficulties are accentuated by the multiplicity of the etiologies of cardiac failure, by the frequency of associated extracardiac disease and by the risks inherent to abnormal myocardial function. In addition, the prescriber must not forget that the drug is not everything in the treatment of cardiac failure and he must be able to recognise the pathology underlying the cardiac failure which may require specific therapy. Finally, the physician must decide the optimal timing for referring patients with very severe cardiac failure for transplantation.
Arch Mal Coeur Vaiss 1990 Nov
PMID:[Practical difficulties in drug prescription in chronic cardiac insufficiency]. 212 18

Left ventricular dysfunction is asymptomatic or paucisymptomatic for a long time. It would be beneficial if progression to the symptomatic stages could be prevented. This is only possible when the abnormal conditions of cardiac load or perfusion which cause the myocardial disease, can be corrected. The treatment of hypertension or valvular disease is an example of this approach. Another approach is to reduce the perverse effects of the neurohormonal adaptations to cardiac failure. The treatment of chronic myocardial infarction by angiotensin converting enzyme inhibitors is an example of this approach.
Arch Mal Coeur Vaiss 1990 Nov
PMID:[Can ventricular dysfunction be prevented or delayed in course?]. 214 70

The spontaneous evolution of 60 patients suffering from recently diagnosed sarcoidosis was compared with their initial biological profile of "activity". 47% of this unselected group of patients belonged to an inactive group (ACE less than 35 nmol/ml/mn and the percentage of alveolar lymphocytes less than 30%). After a mean period of two years of follow up it turned out that the initial bioprofile of activity had no predicted value, even in the absence of any initial elevation of the markers (3 cases out of 28 grew worse). The repeated controls of criteria of activity did not objectively show any concordant change with the outcome in such cases. It is necessary to point out the unfavourable character of very raised ACE activity greater than 50 nmol/ml/mn (7 deteriorations out of 8 cases). It would appear that a systematic search for these criteria should be deferred principally in type 1 lymph node involvement or pulmonary and mediastinal type IIA, all the more so as in practice they have little influence on therapeutic decisions.
Rev Mal Respir 1990
PMID:[Evaluation of the prognosis in sarcoidosis: remission as an issue of biological criteria and current cellular activities (ACE and alveolar lymphocytosis)]. 215 67

This study was undertaken to verify the activity of plasma kininases in hypertension. Male Wistar rats (WIS) were used and three models of experimental hypertension were studied: spontaneously hypertensive rats (SHR), renal hypertensive rats, made according to the method of Goldblatt, DOCA-salt hypertensive rats. Normal Wistar rats, nephrectomized rats and sodium-loaded rats were used as control groups. Plasma from these animals was used to evaluate the kininase activities: kininase II activity (KII) was measured by the hydrolysis of hippuryl-L-histidyl-L-leucine (HHL); kininase I activity (KI) was measured by the hydrolysis of hippuryl-L-arginine (HLA) (CN1 activity) and of hippuryl-L-lysine (HLL) (CN2 activity). The three enzyme activities were characterized by their kinetic constants and the inhibitory pattern of various inhibitors. In normal WIS rats, hydrolysis of HHL proceeds with a Km of 2.55 +/- 0.22 mM and at a Vmax of 0.357 +/- 0.017 mumol/min/ml; the enzyme is inhibited by EDTA, 0-phenanthroline and captopril. HLA has a Km of 6.93 +/- 0.32 mM and a Vmax of 0.748 +/- 0.019 mumol/min/ml while the Km and Vmax values of HLL are 35.8 +/- 1.52 mM and 13.11 +/- 0.40 mumol/min/ml. The hydrolysis of both substrates is inhibited by EDTA, 0-phenanthroline and MERGETPA. KII activity is decreased in WKY and SHR rats (Vmax = 0.241 +/- 0.014 and 0.262 +/- 0.011 mumol/min/ml, respectively). In renal hypertensive rats and DOCA-salt hypertensive rats, the KII activity remained unchanged. CN1 activity was increased in 1K, 1C hypertensive animals (Vmax = 0.866 +/- 0.221 mumol/min/ml) and in DOCA-salt hypertensive rats (Vmax = 1.119 +/- 0.049 mumol/min/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1990 Jul
PMID:[Activity of plasma kininase I and kininase II in hypertensive rats]. 217 85

Perindopril has been studied in groups of normal young and elderly subjects, in patients with hepatic cirrhosis and in hypertensive patients. Plasma concentrations of perindoprilat are increased and renal clearance reduced in elderly subjects, resulting in an increase in the acute pharmacodynamic effect of perindopril. Compensated hepatic cirrhosis does not have any independent effect on the pharmacokinetics of perindopril. After intravenous administration, perindoprilat concentrations show multiexponential decay with a terminal half life of over 30 hours associated with sustained inhibition of ACE. During repeated dosing there is little accumulation of drug, and no evidence of increased haemodynamic effect after chronic treatment in hypertensives. The therapeutic consequences of these findings are: binding of perindoprilat to ACE prolongs the haemodynamic effect, giving the option of once daily administration; despite the long terminal elimination half life of the drug, significant accumulation is not a problem during chronic treatment; increased plasma concentrations of active metabolite in the elderly and reduced renal elimination may require reduced doses to be used; further dose adjustment in compensated hepatic cirrhosis is not routinely necessary.
Arch Mal Coeur Vaiss 1989 May
PMID:Pharmacokinetics of perindopril: therapeutic consequences. 250 11

The main vasodepressor hormone systems are the kallikrein-kinin systems and the vascular prostacyclin. Kallikreins release kinins which are the biological active compounds of the kallikrein-kinin systems. Kinins are one of the most potent vasodilators reducing systemic blood pressure by diminution of vascular resistance. The reduction in blood pressure is strongly dose related. Prostacyclin develops similar effects on blood pressure as kinins. There is a close relationship between kinins and prostacyclin since kinins stimulate prostacyclin synthesis very effectively. In arterial hypertension there is a lack in kallikrein-kinin and prostacyclin activity. This could also be shown under experimental conditions in spontaneously hypertensive and in Dahl salt-sensitive rats. In clinical studies these experimental results were confirmed in primary hypertension. The blood pressure response to exogenous vasodepressor hormones is increased in hypertensives suffering from reduced endogenous vasodilator activity. In the knowledge of reduced vasodilator activities in primary hypertension the stimulation of kinins by prostacyclin will be of major interest in the management of primary hypertension. In the last years some drugs have been investigated with regard to their kinin prostacyclin stimulating effect, but only angiotensin converting enzyme inhibitors, linolenic acid and cicletanin seemed to induce therapeutic prostacyclin stimulation. However, it remains unclear whether these drugs develop their blood pressure lowering effect by stimulation of the discussed vasodilators or by some other effect.
Arch Mal Coeur Vaiss 1989 Nov
PMID:Role of kinins and prostacyclin in blood pressure regulation. 251 56

The new orally active angiotensin converting enzyme (ACE) inhibitor perindopril was evaluated in normotensive men. Doses of 2 to 16 mg were given once a day for up to one week. Single oral doses of perindopril were found to blunt the pressor response to exogenous angiotensin I in a dose-dependent manner. The drug-induced ACE inhibition, as estimated by the measurement of plasma ACE activity, was maximal 4 to 8 hours post drug intake. ACE activity was still importantly reduced 24 hours after dosing. Plasma levels of angiotensin II and aldosterone decreased significantly whereas plasma renin activity and blood angiotensin I levels rose during peak ACE inhibition induced by the 4 and 8 mg doses. However, circulating levels of angiotensin II returned to baseline 24 hours after dosing, both on the first day of treatment and after one week of administration. ACE inhibition with perindopril did not affect blood pressure and heart rate in any consistent manner. There was no evidence for drug accumulation during repeated administration. The novel ACE inhibitor was well tolerated and produced no change in routine laboratory tests. The long-acting ACE inhibitor perindopril appears therefore to be effective when given orally in a dose range of 4 to 16 mg.
Arch Mal Coeur Vaiss 1989 May
PMID:Experience with perindopril in normal volunteers. 254 99

In the presence of prevalent bone metastases, the precise histo-pathological diagnosis of the primary tumor is often difficult. The authors study the diagnostic value of systematic serum assay of a series of tumoral tracers (ACE, AFP, PAP and PSA, SCC, CA 19:9, CA 15:3, CA 125) which until now were used in evolutive and therapeutic monitoring. 34 patients were selected for this preliminary retrospective study (including 20 with a demonstrated histopathological diagnosis). 70 p. cent of prevalent bone metastases express a target tracer corresponding to the initial location. In some cases, an elevated tracer, because of its specificity, may bring about a diagnostic or therapeutic decision (always according to the context). No conclusion may currently be drawn in case of discordance between the anatomo-clinical context and the "profile" of the markers (1 case in our series).
Rev Rhum Mal Osteoartic 1989 Jun
PMID:[Systematic study of various tumoral markers in prevalent bone metastasis]. 275 18


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