Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Models of right ventricular hypertrophy in rats have been created and characterized: Daily injections of triiodothyronine, irradiation of the lung in Brown-Norway rats, chronic myocardial infarction, and pulmonary artery stenosis. A new Millar ultraminature catheter pressure transducer designed for right heart catheterization allowed the measurement of right ventricular function. All models were characterized by an increase in right ventricular systolic pressure, by an elevation in the RNA/DNA ratio in the right ventricle, and by an increase in the right ventricular weight/body weight ratio. Myocytes isolated from the right ventricle 4 weeks after coronary artery ligation had a greater volume and cross sectional area. Similar results were obtained 14 days after pulmonary artery stenosis. In this model, the effect of angiotensin converting enzyme inhibition with ramipril (1 mg/kg, daily) was examined. The increase in right ventricular systolic pressure from 35 +/- 2 mm Hg to 61 +/- 4 mm Hg (without ramipril) was not influenced by ramipril (63 +/- 4 mm Hg), neither was the elevation of right ventricular weight. However, the increase in cell volume and cross-sectional area of myocytes isolated from the right ventricle was less pronounced in the ramipril-treated group (+27% compared to +58% in untreated animals). Thus, angiotensin converting enzyme inhibition with ramipril altered the hypertrophic response at the cellular level.
 ...
PMID:[Right ventricular hypertrophy in rats: effect of ACE inhibitors]. 183 Sep 10

48 patients (aged 50.5 +/- 8.5 years) with proven acute first myocardial infarction underwent coronary angiography 1.6 weeks to 4 years (mean 13.3 weeks) after infarction. No reperfusion interventions were performed, no patient received a longterm therapy with diuretics, glycosides, beta-blockers or ACE-inhibitors. In accordance with the angiographic results, patients were divided into two groups: 25 patients demonstrated a proximal occlusion of one major coronary artery with retrograde contrast filling by non-compromised collaterals; in 23 patients no collateral filling of the distal vessel segment was visible. The contralateral coronary arteries and corresponding LV wall segments were normal. Age, sex distribution, localization of the infarction and infarct related vessel and intraventricular pressures (LVSP = 121.2 +/- 13.5 vs. 122.1 +/- 18.9 mm Hg; LVEDP = 13.1 +/- 5.2 vs. 11.9 +/- 4.1 mm Hg) were not significantly different between both groups. Between both groups patients were compared in whom angiography was performed less than 4, 4-6, and greater than 6 weeks after infarction. In addition, occlusion of the LAD was compared with LCX- and RCA-obstructions both with and without collaterals. Patients with collaterals revealed no significant time dependent changes of the endsystolic (48.1 +/- 11.3; 56.7 +/- 20.5; 43.8 +/- 16.2 ml/m2), enddiastolic (114.9 +/- 30.6; 121.3 +/- 10.8; 99.0 +/- 22.5 ml/m2) volumes and ejection fraction (57.7 +/- 6.5; 53.9 +/- 13.5; 56.4 +/- 9.9%). In contrast in patients without collaterals ESVI increased significantly (44.2 +/- 16.2; 50.8 +/- 17.5; 68.3 +/- 30.9 ml/m2) by an exponential function (y = 28.11 e0.13x; r2 = 0.99; p less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Effect of collateral circulation on the progression of left ventricular dilatation after myocardial infarct]. 183 45

Progressive enlargement following myocardial infarction can be anticipated to adversely effect outcome since prognosis is intimately related to the degree of left ventricular dysfunction and resultant ventricular cavity size. Recent experimental and clinical data have indicated that chronic angiotensin converting enzyme inhibitor therapy can be effective in attenuating the ventricular enlargement which occurs following infarction. These observations have provided a rationale for ongoing large multicenter clinical trials designed to determine whether angiotensin converting enzyme inhibition will be of clinical benefit following infarction. This article reviews the rationale for studies of angiotensin converting enzyme inhibition in post-infarct patients and summarizes the ongoing international research effort to fully define the role of angiotensin converting enzyme inhibition following infarction.
 ...
PMID:Angiotensin converting enzyme inhibition therapy following myocardial infarction. Rationale for clinical trials. 184 Feb 97

The authors investigated the levels of plasma renin activity and aldosterone in patients with a fresh myocardial infarction during the first 24 hours of hospitalization. The values of plasma renin activity and aldosterone were correlated with values of the control group. At the time of admission to the clinic both hormones were significantly elevated, as compared with the control group, in plasma renin activity p less than 0.001 and in aldosterone p less than 0.01. During the subsequent time intervals, i.e. after 3, 6 and 24 hours, the values of plasma renin activity did not change substantially, while the aldosterone values declined during the 6th and 24th hour (significance p less than 0.05). No significant relationship was found between plasma renin activity an aldosterone. With regard to persisting elevated values of plasma renin activity the authors discuss the possible use of blockers of the angiotensin converting enzyme in order to inhibit in the initial stage of a new infarction the formation of endogenous pressor substances.
 ...
PMID:[Renin and aldosterone in the first 24 hours after acute myocardial infarct]. 189 42

Cardiac failure is the principal medium-term complication of myocardial infarction. Changes in left ventricular geometry are observed after infarction, called ventricular remodeling, which, though compensatory initially, cause ventricular failure in the long-term. Experimental and clinical studies suggest that early treatment by coronary recanalisation, trinitrin and angiotensin converting enzyme inhibitors may prevent or limit the expansion and left ventricular dilatation after infarction, so improving ventricular function, and, at least in the animal, reduce mortality. Large scale trials with converting enzyme inhibitors are currently under way to determine the effects of this new therapeutic option. It would seem possible at present, independently of any reduction in the size of the infarction, to reduce or delay left ventricular dysfunction by interfering with the natural process of dilatation and ventricular modeling after infarction.
 ...
PMID:[Ventricular "remodeling" after myocardial infarction]. 191 Mar 27

One hundred and sixty four (164) patients were evaluated. Sixty (60) with Sickle cell disease (SSHg.) and ninety seven (97) with Trait (ASHg.); seventeen (17) were normal control group. The study confirmed that the incidence of cardiomyopathy in Trait (ASHg.) is greater than reported by other clinical investigations. Cardiac arrhythmia, atrial fibrillation, premature ventricular contractions, bundle branch blocks, and T and ST modifications with sub epicardial isquemia were most significant electrocardiographics changes. The possibility of myocardial infarction in SS patients with low or normal hemoglobin is significant. M-Mode and 2-D echo, demonstrated similar end diastolic volumes in AS and SS patients in which cardiomyopathy were diagnosticated. Patients with cardiac failure, treated with cardiotonics, diuretics and ACE were compensated most frequently. To prevent hemosiderosis, antioxydant (alfatocoferol and Ubiquinones) were used with satisfactory response.
 ...
PMID:[Echocardiographic assessment of patients with sickle cell anemia]. 192 6

Angiotensin converting enzyme inhibitor therapy decreases the production of the vasoconstrictive angiotensin II and reduces the degradation of certain kinines of vasodilatator action. Of captopril, enalapril, and lysinopril marketed abroad, only captopril of shorter action is available in Hungary. Angiotensin converting enzyme inhibitors are new means for the therapy of hypertension and congestive heart failure. Captopril seems to be effective at an early stage of heart failure. It slows down or even inhibits the progression of heart failure. New aspects of therapy have been revealed. It may be successfully used in angina pectoris, for the prevention of reperfusion arrhythmias accompanying myocardial infarction, for the treatment of renoparenchimal renal diseases, diabetic nephropathy. The side-effects, interactions, and dosage of angiotensin converting enzyme inhibitors have also been discussed.
 ...
PMID:Angiotensin converting enzyme inhibitor therapy. 194 79

Treatment of hypertension in patients with NIDDM should be administered with special attention not to increase insulin resistance nor to impair insulin secretion capacity. The coexisting risk for coronary artery disease and myocardial infarction should not be increased by undesired drug effects on the plasma lipoprotein profile. Late lesions of diabetes mellitus (nephropathy, neuropathy) have also to be taken into account. Consequently angiotensin converting enzyme inhibitors, if necessary combined with calcium channel blockers, should be administered first. If blood pressure is thus not sufficiently controlled, alpha-adrenergic blockers, vasodilating agents or sympatholytics may be added. Once insulin treatment is installed, or if required for other reasons (nephropathy, congestive heart failure, cardiac arrhythmia), also diuretics and beta-adrenergic blockers are indicated in antihypertensive treatment of diabetic patients.
 ...
PMID:[Hypertension in type II diabetes mellitus]. 195 Mar 78

ACE inhibition may be useful in several manifestations of ischaemic heart disease, such as heart failure due to ischaemic cardiomyopathy. Recent evidence suggests that these effects may also be present in normotensive patients with ischaemic heart disease without heart failure. Theoretically, converting-enzyme inhibition, through coronary and systemic vasodilating effects and negative inotropic properties, should have a favourable effect on the myocardial oxygen supply/demand ratio and, hence, affect the incidence and severity of myocardial ischaemia. It is doubtful, however, whether these cardiac and extracardiac properties of ACE inhibitors really underlie its potential antiischaemic effects, at least in the average patient with ischaemic heart disease without concomitant heart failure and hypertension. Recent animal and human studies indicate that converting-enzyme inhibitors may modulate myocardial ischaemia by reducing ischaemia-induced circulating neurohumoral activation. It has been shown that, depending on the severity of ischaemia, the circulating renin-angiotensin system may become activated together with an increase in circulating catecholamine levels. ACE inhibition suppresses this neuroendocrine stimulation during ischaemia and modulates subsequent systemic and, presumably, also coronary vasoconstriction. In addition to these effects on circulating neurohormones, ACE inhibition could affect myocardial ischaemia through a number of local actions, e.g. modulation of tissue (cardiac) angiotensin II formation and bradykinin breakdown, stimulation of prostaglandin synthesis and, in the use of sulphydryl compounds, by affecting EDRF formation. Whether ACE inhibitors have clear antiischaemic effects in all clinical conditions is uncertain. Their efficacy to limit exercise-induced ischaemia has been questioned. In contrast, pacing-induced ischaemia in patients at rest is clearly prevented by ACE inhibition. This differential effect may be related to a more pronounced difference in circulating neurohormones during exercise per se. It also suggests that ACE inhibitors may be particularly useful as (additional) antiischaemic therapy in patients with angina at rest, e.g. unstable angina and the acute phase of myocardial infarction.
 ...
PMID:Neurohumoral activation during acute myocardial ischaemia. Effects of ACE inhibition. 197 98

The authors deplore a recent incident that highlights the impact of the media and the pharmaceutical industry on the practice of medicine. The publication of a study comparing the changes in cholesterol levels and glucose metabolism of hypertensive patients treated with a diuretic and with an angiotensin converting enzyme inhibitor (captopril) was publicized by the pharmaceutical company that manufactures the latter drug. Alarmed by popular media reports that diuretics could raise heart attack risks, thousands of hypertensive patients being treated with diuretics contacted their physicians. A decrease in the number of new prescriptions for oral diuretics occurred in the months after the study's release. Citing data to show that diuretic therapy is still safe, effective, and relatively inexpensive in the management of hypertension, the authors call for physicians to take a stand against prescribing pressures generated by the media and by pharmaceutical industry promotion campaigns.
 ...
PMID:Who really determines your patients' prescriptions? 198 36


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>