Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Treatment of chronic heart failure with ACE-inhibitors has greatly improved the prognosis. In addition to ACE-inhibitors, diuretics seem to be necessary to decrease mortality, whereas the importance of cardiac glycosides has not been demonstrated unequivocally. Nevertheless, modern treatment of chronic heart failure in all stages should be a combination of diuretics, digitalis, and ACE-inhibitors rather than a stepwise addition of drugs depending on the severity of the disease. An increased heart rate leads to increased myocardial O2-consumption, decreased O2-supply, ischemia, and reduced contractility. Betablocker-induced reduction of heart rate does, however, not necessarily improve symptoms or hemodynamic conditions. The optimal heart rate in large failing hearts is not known yet. Probably, it is dependent on the type and severity of myocardial disease or impairment. In this respect, the sarcoplasmatic release and uptake of Ca2+ plays the most important role in the disordered force-frequency-relation in chronic heart failure.
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PMID:[Clinical aspects of differential drug therapy of chronic heart failure]. 129 Mar 10

In a longitudinal study comprising a total of 18 patients, the paradoxical time course of hANP plasma levels, i.e. the reproducibility of the low levels previously reported in cases of extreme cardiac insufficiency after administration of amiodarone, was investigated over a period of 9 months. At the same time, the effect of the degree of cardiac insufficiency and arrhythmia on the secretion of hANP was observed. The patients had been admitted to hospital because of the diagnoses "cardiac insufficiency secondary to cardiomyopathy" or "Grade IVb arrhythmia according to Lown's classification". During in-patient treatment, antiarrhythmic therapy was commenced in all patients. Clinical examinations and determinations of humoral parameters during therapy showed a substantial number of patients, who exhibited no increase in hANP levels despite massive cardiac decompensation. As far as drug therapy of patients with severe arrhythmias secondary to congestive (dilated) cardiomyopathy is concerned, amiodarone has proved to be the drug of choice in combination with digitalis, ACE inhibitors and diuretics. There is a close correlation between the degree of cardiac insufficiency and plasma hANP levels.
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PMID:[Effects of treatment of arrhythmias requiring therapy in dilated cardiomyopathy with amiodarone on alpha human atrial natriuretic peptide]. 141 68

The clinical features of congestive heart failure in the elderly were investigated in 104 patients (57 males, 47 females, mean age of 79.2). Patients were divided into two subgroups, the readmission group, 33 patients who were readmitted within 6 months after discharge, and the non-readmission group. Chief complaints were dyspnea, edema, chest pain, loss of appetite, chest compression, and palpitation. Heart failure was caused by infection, myocardial ischemia, arrhythmia, inappropriate drug usage including poor drug compliance, the use of beta-blockers, excessive intake of sodium, and anemia. Careful use of drug was essential especially in the readmission group. Major underlying heart disease were ischemic heart disease (39.4%), valvular disease (26.9%), hypertensive heart disease (9.6%), with cardiomyopathy, congenital heart disease seen in the minority. There was no statistically significant difference in underlying heart diseases between the two groups. Supraventricular arrhythmias such as atrial fibrillations, paroxysmal atrial fibrillations, paroxysmal supraventricular tachycardias, and premature atrial contractions were noted in 85.3% of the cases. Drugs for treatment were diuretics, digitalis, isosorbide dinitrate, calcium antagonists. ACE inhibitors and alpha-blockers were also used, showing that vasodilators were more extensively used than before. The major complications were hypertension (39.4%), renal dysfunction (27.9%), cerebrovascular disease (26.9%), diabetes mellitus (16.5%), arteriosclerosis obliterans (7.7%). Renal dysfunction, arteriosclerosis obliterans was seen significantly more frequently in the readmission group. The prognosis at one year after admission was significantly worse in the readmission group. In summary, the major underlying diseases were ischemic heart disease, valvular disease, and hypertensive heart disease. Ischemic heart disease was seen more frequently than in previous investigations at our hospital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Congestive heart failure in elderly readmitted patients]. 152 7

The atrial natriuretic factor (ANF) is secreted by the atria in mild and moderate cardiac failure but, during the evolution of the cardiac failure, the ventricles are also recruited and secrete ANF. In order to investigate the relation between plasma ANF and Doppler echocardiographic parameters of severe cardiac failure, the concentrations were measured simultaneously in 20 patients with NYHA Class III and IV cardiac failure (10 due to ischaemic and 10 due to primary dilated cardiomyopathy) despite optimal medical treatment including an angiotensin converting enzyme inhibitor. Overall, there was a weak negative correlation between the plasma ANF concentrations and the decrease in right ventricular surface area (r = -0.58, p less than 0.005, n = 20 patients). This relation was highly significant in ischaemic cardiomyopathy (r = -0.81, p less than 0.002, n = 10 patients) and not significant in primary dilated cardiomyopathy (r = -0.29, NS, n = 10 patients). No relationship was observed between plasma ANF and other echocardiographic parameters (atrial surface area, right and left ventricular dimensions, left ventricular ejection fraction and mass) or with Doppler aortic indices (acceleration, maximum and mean velocities, aortic velocity-time integrals). However, plasma ANF was related to the velocity of mitral regurgitant jets (r = -0.70, p less than 0.01) which is dependent on left ventricular pump function. These results show that plasma ANF concentrations are only related to right ventricular systolic function and the velocity of mitral regurgitation in patients with severe cardiac failure.
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PMID:[Correlations between plasma concentrations of atrial natriuretic factor and right ventricular function in patients with severe cardiac failure]. 153 2

We have previously reported that antioxidant drug intervention protects against magnesium deficiency-induced myocardial lesions. In the present study, Golden Syrian male hamsters were fed either a magnesium-deficient diet or a magnesium-supplemented diet. Animals from each group received sulfhydryl-containing angiotensin converting enzyme inhibitors: captopril, epi-captopril (a stereoisomer of captopril), and zofenopril* (arginine blend of zofenopril containing a free SH group); another group of animals received the non-sulfhydryl-containing angiotensin converting enzyme inhibitor enalaprilat. The animals were killed after 14 days, and their hearts were isolated for morphological and morphometric analyses. Hematoxylin and eosin-stained sections were examined by a computer image analysis system for a morphometric determination of the severity of myocardial injury. Captopril reduced both the density of lesions, from 0.32 to 0.08 lesions/(mm2) (p less than 0.01), and the area fraction of lesions, from 7.42 x 10(-4) to 2.03 x 10(-4) lesion area/(mm2) (p less than 0.01), as well as the degree of inflammatory infiltration around the blood vessels. Epi-captopril and zofenopril* were virtually equipotent to captopril, but enalaprilat afforded only slight (nonsignificant) protection. These results indicate that a significant component of the protective effect of captopril in this model was attributable to its sulfhydryl moiety, rather than solely due to the inhibition of the angiotensin converting enzyme. These data further support our previous findings of possible free radical participation in cardiomyopathy due to magnesium deficiency.
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PMID:Captopril protects against myocardial injury induced by magnesium deficiency. 165 86

Treatment of patients with heart failure due to major ventricular systolic dysfunction should aim not only at symptomatic but also at prognostic improvement. If correction of the underlying problem is not possible, treatment should slow down the progression of cardiac failure and eliminate triggers for sudden cardiac death due to electromechanical dissociation or arrhythmias. In every patient with chronic congestive heart failure screening for myocardial ischemia and complete revascularization is mandatory, if possible. In patients with coronary artery disease and diminished systolic function, beta-blockade may improve prognosis by reducing ischemic events and sudden cardiac death. The incidence of life-threatening arrhythmias in patients with heart failure may be reduced by eliminating facilitating factors like electrolyte disturbances, altered autonomic tone and raised intracardiac pressure rather than by antiarrhythmic medical treatment itself. One of the most important prognostic aspects in treatment is the interference with the development of the cardiomyopathy of overload, uniformly observed in chronic congestive heart failure. Modification of mechanical and neuroendocrine stimuli may postpone myocardial hypertrophy and interstitial hyperplasia as a consequence of altered gene expression. Early treatment with ACE inhibitors and in certain patients with betablockers are the most promising strategies to delay the progression of the disease. In contrast, positive inotropic drugs, including digitalis and phosphodiesterase inhibitors, do not improve prognosis. Calcium antagonists should also be used with restriction, as Verapamil and Diltiazem, but also Nifedipine may adversely affect the outcome in congestive heart failure patients.
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PMID:[Prognostic aspects in the treatment of chronic heart insufficiency]. 173

The primary hereditary cardiomyopathy of the Syrian hamster is a particularly interesting model of experimental cardiomyopathy 1) because of its slow progression to cardiac failure unlike acute experimental volume and pressure overloading; 2) because of the reproducibility and predictable nature of the mechanical, biochemical and electrophysiological abnormalities observed at each stage of the disease; 3) because of involvement of other muscle groups, and particularly, skeletal muscle. The physiopathology is not fully understood but a disturbance of intracellular calcium homeostasis appears to play a major role. From the therapeutic point of view, a number of calcium antagonists have been shown to be effective in restoring myocardial function, but they have no effect on skeletal muscular lesions. Recently, early prophylactic intervention with therapeutic doses of perindopril has been shown to prevent the decrease of certain parameters of myocardial contractility in vitro in the dilated group, before the appearance of any signs of cardiac failure. This study also showed that angiotensin converting enzyme inhibitors had no intrinsic negative inotropic effects.
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PMID:[Cardiomyopathy in the Syrian hamster. Physiological and therapeutic aspects]. 179 30

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.
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PMID:[Echocardiographic assessment of patients with sickle cell anemia]. 192 6

In acute as well as in chronic ischemic heart disease, congestive heart failure indicates a poor prognosis. Treatment after acute myocardial infarction should differentiate between specific subsets. In cardiogenic shock due to extensive ischemic damage, acute revascularization by PTCA or CABG improves the otherwise poor outcome substantially. In congestive heart failure, pre- and afterload reduction by nitrates should be combined with dopamine if systolic blood pressure is below 100 mmHG or dobutamine if an inotropic substance is necessary despite systolic blood pressure greater than 100 mmHg. Amrinone is a potent alternative which combines positive inotropic and vasodilating properties. In chronic ischemic heart disease, congestive heart failure is a clearly defined indication for complete revascularization, if possible. As to drug treatment, progression of the disease characterized by a cardiomyopathy of overload as well as neurohormonal and peripheral maladaptation should be stopped in parallel with symptom relief. Therefore, ACE-Inhibitors are combined very early with diuretic treatment, and digitalis should be added in refractory patients.
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PMID:[The treatment of heart insufficiency in coronary heart disease]. 192 14

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.
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PMID:Neurohumoral activation during acute myocardial ischaemia. Effects of ACE inhibition. 197 98


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