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)

Hypertensive patients undergoing hemodialysis (HPH) have a marked impairment of their large artery distensibility and an increased cardiovascular morbidity. We investigated twelve HPH (8 males, 4 females, 53 +/- 12 years of age, +/- SD) following a single dose of an ACE inhibitor (quinapril 20 mg) comparatively to a placebo in a randomised cross over study over a week (H0 to H172). We measured repeatedly blood pressure and aortic distensibility (carotid-femoral pulse wave velocity, PWV). Statistical analysis was made through repeated measure ANOVA and repeated measure analysis of covariance because of the tight link between pressure and arterial function. Blood pressure decreased (SAP: p < 0.01, DAP: p < 0.001), and PWV was significantly improved independently of the pressure decrease. ACE inhibitor reduces blood pressure in these patients and improves large arterial function independently of the blood pressure changes.
Arch Mal Coeur Vaiss 1994 Aug
PMID:[Pressure-independent improvement of aortic distensibility in hypertensive hemodialysed patients]. 775 59

The authors reports an unrecognised secondary effect, but perhaps not as rare as has been thought, of enalapril: the acute abdomen. Three similar cases have previously been reported. The underlying mechanism is probably the inhibition of degradation of tissue kinins to inactive peptides as in subcutaneous and/or submucous angioneurotic oedema. Todate, this secondary effect has not been reported with other angiotensin converting enzyme inhibitors. The relationship between the acute abdomen and angioneurotic oedema with primary hyperaldosteronism is discussed.
Arch Mal Coeur Vaiss 1994 Oct
PMID:[A rare clinical form of angioneurotic edema caused by enalapril: acute abdomen]. 777 84

Myocardial hypertrophy is an established risk factor for cardiovascular morbidity and mortality. Beyond quantitative and mechanical aspects hypertrophy is associated with alterations in cardiac gene expression, resulting in a more fetal-like myocyte phenotype with a fragile Ca++ homeostasis. Depressed expression of sarcoplasmatic reticulum ATPase is the hallmark of this overload phenotype. Conversely, the gene expression and the activity of sodium calcium exchanger is up-regulated in endstage heart failure. Both alterations contribute to prolonged cytosolic Ca++ transients, disturbed relaxation and, probably, to electrophysiologic instability. Angiotensin II is a growth promoting agent and several lines of circumferential evidence suggest that the local formation of angiotensin II might contribute to the trophic response and phenotype shift in cardiac overload. The cardiac gene expression of angiotensin converting enzyme and angiotensinogen is increased early after cardiac overload and in patients with severe heart failure. Chronic ACE inhibition suppresses plasma and tissue ACE activity, reduces LV hypertrophy and improves long-term survival. The hallmark of the peripheral adaptation in chronic heart failure is systemic vasoconstriction, associated with neurohumoral activation. Several mechanisms are involved in the impaired peripheral perfusion, including increased sympathetic tone and increased vascular stiffness. Recently, data suggest an important role of the endothelium for perfusion of skeletal muscle in heart failure. Endothelium-dependent dilation of resistance vessels is blunted in patients with severe chronic heart failure. Conceivably, this abnormality may be involved in the impaired reactive hyperemia in patients with chronic heart failure. Moreover, alterations of skeletal muscle emerge in chronic heart failure contributing to reduced exercise performance.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1994 Jun
PMID:Heart failure: an update on pathophysiology. 786 17

The objective of classical treatments of cardiac failure (diuretics, digitalis) was to relieve patients' symptoms. Vasodilators and ACE inhibitors also improve morbidity and mortality. The introduction of the latter class of drugs for cardiac failure will, however, lead to a significant increase in the cost of medication at national level. These costs may increase even further in theory due to a predictable increase in the number of patients with cardiac failure (ageing of the general population, improved survival of cardiac patients) and due to the extension of prescription of these drugs to populations of subjects with cardiac failure hitherto relatively undertreated. On the other hand, economies may be realised in the management of cardiac failure related to fewer and shorter hospital admissions and reduced indirect costs or to the suppression of previous, less useful drugs (calcium antagonists, digitalis). Cost-effective analyses with ACE inhibitors carried out in different countries (Canada, netherlands) tend to show that the costs induced by prescription of these drugs are more than compensated by the economies realised by the reduction in hospital admissions. This is even more marked in the treatment of patients with severe cardiac failure. In subjects at low risk, the prescription of ACE inhibitors would not seem to be justified from both the clinical and economic points of view. It is up to each physician to decide the threshold of basic risk below which this treatment becomes "economically" acceptable.
Arch Mal Coeur Vaiss 1994 Jun
PMID:[Economic evaluation of treatments of cardiac insufficiency]. 786 21

Treatment with ACE inhibitors has improved the prognosis of cardiac failure (CF). The results of CONSENSUS I, SOLVD and V HEFT II show clinical improvement and longer survival with this therapeutic class of drugs. However, the search for the optimal dosage was not undertaken in these trials (a standard dose was fixed at the onset, average dose of enalapril from 15 to 20 mg/day). In clinical practice, patients are prescribed lower doses of ACE inhibitors (enalapril: 7.5 mg/day) than the averages used in large scale trials. In order to optimise the use of ACE inhibitors, the ATLAS study (Assessment of Treatment with Lisinopril and Survival) was undertaken with the precise objective of comparing two dosages (2.5 to 5 mg/day vs 32.5 to 35 mg/day) of lisinopril on the morbidity and mortality of patients with CF. This international, multicenter, randomised, double-blind parallel group trial aims to include 3,000 patients over 18 years of age with NYHA Classes II, III and IV, and an ejection fraction < or = 30% and to follow them up for 3 to 4.5 years. Nearly 30 French centres will participate in this trial. After an initial, open period of evaluation of tolerance (5 mg to 15 mg/day of lisinopril in France), the patients will be randomised to two groups. After randomisation, all patients will receive 5 mg per day of lisinopril. The "high dose" group will receive 20 mg/day for two weeks, then 30 mg/day in addition to the "open dosage". In cases of intolerance, the dosage may be reduced to 20 mg/day or 10 mg/day, or the drug may be withdrawn.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1994 Jun
PMID:[The ATLAS study (Assessment of Treatment with Lisinopril and Survival); justification and objectives]. 786 22

This study concerns 45 patients group one suffering from broncho-pulmonary cancer, the diagnosis was obtained by bronchial biopsies or by transparietal puncture using a scanner: there were 35 non-small cell bronchial carcinomas (CNPC) and 10 small cell bronchial cancers (CPC). The control patients (99 patients) were divided up as follows: 44 pleuro-pulmonary infections (group two) and 55 with respiratory failure of various causes other than infectious episodes (group three). In group one the level for TPA was positive in 30 cases (the threshold value was 90 units per litre), 9 for CA 19.9, 7 for ACE and 9 for NSE. The overall sensitivity was thus better for TPA. There was no correlation between TPA and type of tumour histology nor between the different markers. Their association did not improve the sensitivity. The NSE however, remained the most sensitive test for the diagnosis of CPC with six positive tests out of ten. In the control population, the specificity of TPA (66%) was less than that of ACE (100%) or of CA 19.9 (94%) and the false positives were significantly more numerous in group two: 21 patients had a positive test compared to only 12 in group three. Finally we noticed an increase in the level of TPA contrary to other markers, as a function of the extent of the disease from the carcinoma (CNPC unique). The TPA is thus the most sensitive and it turns out to be better reflector to the extent of the tumour disease than either ACE, CA 19.9 or NSE but this applies uniquely to non-small cell carcinoma.
Rev Mal Respir 1994
PMID:[Importance of serum TPA determination in bronchopulmonary cancer. A comparative study of CEA, CA 19.9 and NSE]. 797 38

Cough is known to be the major respiratory side effect of treatment with angiotensin converting enzyme inhibitors (ACEI). Recently, ACEI have been implicated in drug-induced lung disease. We report a new case of diffuse pneumonitis which occurred during treatment with ACEI. A 73-year-old man was admitted for cough, dyspnea at rest, fever and weight loss. The patient had been treated with the ACEI pirindopril during 6 months for systemic hypertension. Chest radiographs showed reticular infiltrates in the upper lung fields. A CT scan confirmed the infiltrates and showed pleural thickening and airspace opacities. White blood cell counts showed 15,700/mm3 leucocytes with 940 eosinophils/mm3. Transbronchial biopsy was consistent with infiltration of the lung with eosinophils. There was no evidence for another etiology. Once the drug was withdrawn, clinical and radiological abnormalities improved but steroids were required to control symptoms. This report suggests that pirindopril, as captopril, can induce the picture of drug-induced pulmonary disease.
Rev Mal Respir 1994
PMID:[Pneumopathy induced by pirindopril. A case report]. 804 99

The level of arterial pressure is not the sole determinant of cardiac adaptation to hypertension. In order to identify other factors (such as preload as well as neuro-humoral factors) we categorized by M-mode echocardiography, 192 never treated patients with mild to moderate hypertension of short duration, according to values of end-diastolic relative wall thickness (RWT) and left ventricular mass index (LVMI). Mitral regurgitation was excluded in all patients by Doppler echocardiography. Among hypertensive patients, LVMI and RWT were normal in 43% (group 1), whereas 20% had increase RWT with normal LVMI "concentric remodeling" (group 2), 24% had concentric hypertrophy (increase both LVMI and RWT) (group 3) and 13% had increased LVMI with normal RWT (eccentric hypertrophy) (group 4). Results presented as means +/- SD. [table: see text] In addition the acute response after ACE-inhibition (captopril 50 mg) of mean arterial pressure was significantly attenuated in group 4 when compared with group 1. These results suggest that the effect of arterial pressure on the heart may be modulated by volume overload (low PRA and high CI) in hypertensive patients with eccentric LV hypertrophy with normal LV function.
Arch Mal Coeur Vaiss 1993 Aug
PMID:[Patterns of left ventricular adaptation to arterial hypertension]. 812 6

The effects of de-endothelialization and angiotensin II (A II) on smooth muscle cell (SMC) growth are still controversial. Cell culture experiments suggest an hypertrophic effect of AII, whereas in vivo experiments in de-endothelialized arteries using angiotensin converting enzyme inhibitors suggest a possible role of AII on proliferation and/or migration of SMC. Phenotype of SMC in culture does not necessarily reflect that in the whole organ. Yet, in vivo models are too complex to permit conclusions as to the proper effect of AII or endothelium. Therefore, we examined the effect of de-endothelialization and AII on SMC growth in an organ culture of vessel wall. Rabbit thoracic descending aortas (n = 42) held at their in vivo length, perfused at 40 ml/min and pressurized to 70 mmHg (P70) were maintained in DME medium supplemented with 20% fetal calf serum for periods of time varying between 0 and 15 days. In another group (n = 26), aortas were relaxed and not pressurized (P0). In each group, some arteries were de-endothelialized; 21 arteries were exposed to AII (10(-6) M) and indomethacin (10(-5) M) during the incubation. SMC proliferation was evaluated by 3H-thymidine uptake by the vessel wall. Statistics were performed using covariance analysis. In P0 group, de-endothelialization or AII had no effect on the vessel wall. In P70 group, de-endothelialization or led to a significant increase in media area which was reported to extracellular matrix synthesis and in 3H-thymidine uptake (p < 0.005) which peaked at 3-5 days and returned to basis levels at 6-8 days. All had no effect on 3H-thymidine uptake (p = 0.516) in P70 group. Our results obtained in rabbit aortic organ culture suggest that de-endothelialization induces SMC growth depending on pressure and/or wall stretching. AII, per se, had no additional effect on SMC growth in this model.
Arch Mal Coeur Vaiss 1993 Aug
PMID:[Effects of de-endothelialization and angiotensin II on the vascular remodeling in a model of rabbit aorta organ culture]. 812 27

The present experiment was undertaken to examine the relationship between plasma renin activity and the concentration of angiotensin converting enzyme (ACE) in plasma and renal brush border of Wistar Kyoto rats. Different experimental models known to have opposite effects on plasma renin activity were used: changes in salt intake, the deoxycorticosterone acetate (DOCA) and DOCA-salt models and the two-kidneys one clip (2K1C) model. Two weeks after the start of these experimental series, the rats were killed. At this time, blood pressure did not differ from control group, even in the 2K1C and DOCA-salt groups. As expected, PRAs were highest in the 2K1C and depleted salt groups and lowest in the DOCA, DOCA-salt and high salt groups. No relationship between this wide variation in PRA and change of ACE activity in both plasma and renal brush border could be observed. In the plasma, ACE activity in sodium-depleted rats was slightly decreased whereas no change occurred in the other models. In the kidney, DOCA treatment led to increased ACE activity in the brush border only if the animals were maintained on a high salt intake. DOCA or NaCl alone failed to have this effect. In the 2K1C model, the clipped kidneys exhibited increased brush border ACE activity whereas the unclipped kidneys did not show any significant variation in ACE activity, when compared to sham operated rats. In summary, on one hand these findings show that variations in ACE activity were linked neither to hypertension nor to changes in PRA.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1993 Aug
PMID:[Plasma renin activity and angiotensin converting enzyme of renal brush borders]. 812 36


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