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 amelioration of symptoms and the improvement of long-term prognosis are the main objectives of drug treatment in congestive heart failure [CHF]. Digitalis, glycosides and diuretics can reduce dyspnea and increase exercise tolerance, while their influence on the course of the cardiac failure remains uncertain. Vasodilators, ACE inhibitors in particular, have in contrast not only the desirable symptomatic and hemodynamic effects, but they also delay the deterioration of LV dysfunction and reduce cardiac mortality. Vasodilators, therefore, became first-line drugs in all stages of CHF. In patients with moderate to severe heart failure the addition of diuretics and also of digoxin is usually required. Pharmacological effects, dosage, side effects and specific indications of the various drug groups in CHF are discussed.
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PMID:[Drug therapy of heart failure]. 835 74

Angio-oedema is a recognised complication of angiotensin converting enzyme (ACE) inhibitor therapy, occurring in 0.1% to 0.5% of patients taking captopril, enalapril, or lisinopril. This is the first report of severe angio-oedema complicating therapy with quinapril, a new, long-acting drug. CASE REPORT. A 74-year-old female had been taking quinapril (10 mg/day) and diuretics (fixed combination of triamterene and hydrochlorothiazide) for arterial hypertension for 18 months without any complication. After a fracture of the ankle, the patient received spinal anaesthesia uneventfully for an osteosynthesis. Ten days postoperatively, she noted swelling of the lips and the left half of the tongue. Following intravenous injection of antihistamines and prednisolone, these symptoms regressed. However, a relapse occurred on the 16th postoperative day with rapidly increasing oedema of the lips, face, ventral collar area, and entire tongue. Despite high-dose steroids, dyspnoea developed within 2 h. Direct laryngoscopy was impossible, and a flexible bronchoscope was used for nasotracheal intubation. At this point, the diagnosis of ACE inhibitor-induced angio-oedema was made and quinapril was withdrawn. The patient recovered, tracheal extubation was performed after 48 h, and the later course was uneventful. DISCUSSION. This is the second report of angio-oedema as a postoperative complication in a patient on long-term and previously unremarkable ACE inhibitor therapy. The first reported case occurred immediately after oral intubation and was perhaps precipitated by mechanical irritation. In this case, it is likely that postoperative deterioration of renal function due to dehydration and diuretic therapy was the precipitant, as has been reported in patients on lisinopril without surgery. Despite a significant increase in angio-oedema associated with the use of long-acting ACE-inhibitors, there appears to be a lack of familiarity among anaesthesiologist and other emergency physicians concerning this adverse effect. Withdrawal of the drug is the only effective treatment. High-dose steroids may be helpful, but if there is beginning dyspnoea or stridor, early endoscopically controlled intubation or emergency tracheostomy is essential to avoid hypoxaemia and death, as has occurred in the past.
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PMID:[Life-threatening postoperative angioedema following treatment with an angiotensin converting enzyme inhibitor]. 906 60

Overt congestive heart failure (CHF) has a prevalence of 1% of the population. The predominant symptoms of patients with CHF are fatigue and dyspnoea. Fatigue is thought to result from changes in peripheral muscle metabolism secondary to decrease vasodilative capacity and physical inactivity. An increase of peripheral perfusion by vasodilator therapy and physical activity are therefore recommended. Beside overt decompensation, where dyspnoea results from acute pulmonary congestion due to backward failure, increased physiological dead space ventilation caused by pulmonary ventilation/perfusion mismatch accounts, to a large degree, for dyspnoea, and can be improved by vasodilator therapy. According to the pathophysiology of CHF, normalisation of loading conditions and myocardial inotropy are the parameters addressed by various pharmacological agents in order to alleviate symptoms and slow progression of the disease. Diuretics are rapidly acting and effective agents to improve congestion and decrease filling pressures. Digitalis improves haemodynamics and symptomatology by increasing inotropy and slowing resting heart rate in atrial fibrillation; however, prognostic effects have yet to be proved. The introduction of vasodilators has significantly improved the prognosis of the disease, and the administration of ACE inhibitors in particular has been shown to slow progression of CHF. This results in a substantial decrease in morbidity and mortality. The present article appraises the role of the currently used drugs in the treatment of CHF, considering effects on pathophysiology and clinical outcome and provides an approach to a differential drug regimen.
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PMID:Current guidelines for the treatment of congestive heart failure. 874 Dec 34

Chronic heart failure is a well-recognized syndrome in which left ventricular impairment produces a constellation of secondary changes in other organ symptoms leading to symptoms such as muscular fatigue and dyspnoea and objective limitation to exercise tolerance. With modern drug therapy of diuretics and ACE inhibitors, the majority of patients have minimal if any signs of congestion, and yet severe symptomatic limitation remains. This limitation bears little relationship to conventional measures of either left ventricular function or the haemodynamic profile of the patient. The symptoms limiting exercise are predominantly fatigue or dyspnoea, and yet the classical pathophysiological explanations for their genesis now seem inadequate. Recent investigations, as demonstrated, in part, by the research presented in this symposium, attest to the importance of abnormalities in peripheral blood flow and in skeletal muscle in producing both objective limitation to exercise and in explaining the generation of the exercise-limiting symptoms of the syndrome of stable optimally treated chronic heart failure. In addition it is now evident that these muscle changes may in addition have pathophysiological significance for the maintenance of sympatho-excitation during exercise and potentially therefore in the progression of left ventricular remodelling and in the susceptibility to ventricular arrhythmias. This paper presents some of the background evidence which leads to the hypothesis that a feedback loop links changes in skeletal muscle to abnormal reflex cardiopulmonary control which may both limit exercise and be harmful in the progression of the syndrome.
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PMID:The "muscle hypothesis" of chronic heart failure. 893 79

In symptomatic endstage coronary artery disease after full medical therapy (antianginal drugs, betablockers and ACE-inhibitors) further therapeutical options both for the interventional cardiologist with little hope for improvement by PTCA, stent, rotablation and atherectomy and for the cardiac surgeon with bypass surgery and endarterectomy are not available by definition due to the diffuse arteriosclerotic vessel morphology. In those patients one can therefore consider transmyocardial laser therapy (TMR) as the ultimate treatment option. It then is primarily a palliative measure to reduce the patient's symptoms. Improving perfusion and prognosis remains the most important goals, however. TMR can be utilized as the only revascularizing treatment measure or in combination with CABG or PTCA. According to data from international registries, few controlled and several non controlled studies and our own registry in Marburg with now 101 patients improvement of angina and/or dyspnoea can be expected in more than 60% of patients with end stage coronary artery disease (CAD). The patient cohort comprises symptomatic individuals after CABG or multiple PTCAs or with diffuse CAD in diabetes mellitus or with most severe hypercholesterinemia. We consider these above mentioned criteria as the only validated criteria to enter patients with endstage CAD in our controlled study. Hypothetical options for treatment by TMR such as vasculopathies after heart transplantation, cardiomyopathies under the notion of a possible but not proven microangiopathy are not accepted in our institution at present. Before TMR all patients are assessed for their angina class according to the Canadian Cardiac Society (CCS I-IV)) and their exercise capacity according to the New York Heart Association classification (NYHA I-IV) and reassessed regularly after 3, 6 and 12 months. Thallium/Te MIBI scans at rest- and whenever possible at exercise as well as stress echocardiography are carried in the patients to assess symptomatic improvement, alterations in myocardial perfusion and functional efficacy by TMR. By intermediate analysis the 101 patients of our registry more than 60% of the patients had improved their angina class by at least one classe, some patients have improved perfusion as assessed by scintigraphy, which makes at present a trend but not yet a significant difference, whereas central hemodynamics and ejection fraction remained virtually unchanged in most patients reassessed after TMR. In our analysis mortality of the 101 TMR patients was assessed and plotted on Kaplan Meier survival curves. Mortality at 6 months was 11%. When compared to a historical group of patients with identical CCS and comparable NYHA classes, who were worked up in the manner of a case control study, the TMR mortality was marginally but not yet significantly lower than one would expect from these control patients with terminal CAD treated purely by medication: Their 6 months mortality was 14%. Remarkably but not unexpectedly patients with comparable CCS classes, who could still be treated by PTCA and/or CABG had a significantly lower 6 months mortality than TMR patients or patients on antianginal drugs only. The pathophysiological mechanisms for the symptomatic improvement by laser therapy are not yet fully understood. The 1 mm transmyocardial channels created by the CO2 laser have been postulated to permit perfusion from the ventricular cavity and to seek connection to capillaries and vessels present in the malperfused myocardium thus improving the perfusion by newly created connections and sinusoids from the ventricular cavity. Although there is clear evidence for the presence of open channels acutely and within a few days after TMR therapy little evidence in man is as yet available on the question whether the channels remain open in the long run and, if so, whether they can actually improve perfusion to a substantial degree...
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PMID:[Indications for transmyocardial laser therapy]. 906 76

Carvedilol competitively blocks beta 1, beta 2 and alpha 1 receptors. The drug lacks sympathomimetic activity and has vasodilating properties that are exerted primarily through alpha 1-blockade. Animal models indicate that carvedilol confers protection against myocardial necrosis, arrhythmia and cell damage caused by oxidising free radicals, and the drug has no adverse effects on plasma lipid profiles. Recent data have confirmed the antihypertensive efficacy of carvedilol in patients with mild to moderate essential hypertension. Carvedilol has similar efficacy to other beta-blocking agents, calcium antagonists, ACE inhibitors and hydrochlorothiazide. Carvedilol also improves exercise tolerance and ischaemic symptoms in patients with stable angina pectoris. Significant reductions in serious cardiac events after acute myocardial infarction and in frequency and severity of ischaemic events in patients with unstable angina have also been demonstrated. Interest in the use of carvedilol in patients with congestive heart failure (CHF) has culminated in the publication of a cumulative analysis of data from 1094 patients with mild to severe CHF who participated in the US Carvedilol Heart Failure Study Program (4 trials). After a median follow-up of 6.5 months, a significant overall reduction in mortality relative to placebo (3.2 vs 7.8%) was revealed in patients who had received carvedilol 6.25 to 50 mg twice daily (plus diuretics and ACE inhibitors). All-cause mortality, risk of hospitalisation for cardiovascular reasons and hospitalisation costs were also reduced significantly (by 65, 28% and 62%, respectively) in these trials. In addition, the Australia and New Zealand Heart Failure Research Collaborative Group showed a 26% reduction in the combined risk of death or hospitalisation with carvedilol 12.5 to 50 mg/day relative to placebo after a mean 19-month follow-up period in 415 patients with CHF (relative risk 0.74). Adverse events with carvedilol appear to be less frequent than with other beta-blocking agents, are dosage-related and are usually seen early in therapy. Events most commonly reported are related to the vasodilating (postural hypotension, dizziness and headaches) and the beta-blocking (dyspnoea, bronchospasm, bradycardia, malaise and asthenia) properties of the drug. Carvedilol appears to date to have little effect on the incidence of worsening heart failure. Concomitant administration of carvedilol with some medications requires monitoring. Carvedilol is therefore likely to have a beneficial role in the management of controlled CHF, but further clinical studies are required to show the place of beta-adrenoceptor blocking therapy in general in this indication, and the position of carvedilol relative to other similar agents. Carvedilol is also confirmed as effective in the management of mild to moderate hypertension and ischaemic heart disease.
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PMID:Carvedilol. A reappraisal of its pharmacological properties and therapeutic use in cardiovascular disorders. 921 Oct 87

To assess te incidence, clinical characteristics and current strategies in the management of patients with acute heart failure, we conducted a prospective survey of all acute medical admissions with heart failure to a district hospital serving a city centre population of 300,000 people in a multiracial community. Of 7451 such admissions, 348 (4.7%) were diagnosed as having acute heart failure: 265 Caucasian (76.1%), 27 black/Afro Caribbean (7.7%), 56 Indo-Asian (16.1%). Complete clinical data were available from 260 patients. The main presenting symptom was dyspnoea in 233 patients (89.6%) and chest pain in 60 patients (23.1%); 139 patients (53.5%) had a history of ischaemic heart disease, 87 (33.5%) hypertension and 49 (18.8%) had diabetes; 103 patients (39.6%) had a previous history of heart failure; 75 patients (28.8%) were in atrial fibrillation. An echocardiogram was performed in 89 patients (34.2%). On admission, ACE inhibition was prescribed to only 78 patients (30.0). The diagnosis of heart failure was stated on the hospital inpatient data sheet (KMR-1) in only 170 patients (65.4%). Following admission, 50 patients (19.2%) died while in the wards. Heart failure is a common problem among acute medical admissions and has a poor prognosis. The KMR-1 diagnosis may underestimate the prevalence of heart failure.
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PMID:Acute admissions with heart failure to a district general hospital serving a multiracial population. 928 63

A 68-year-old man experienced systemic pruritus since he was 63 years old, and systemic sclerosis and skin pigmentation were observed when he was 64. When he developed dyspnea the same year, he was admitted and SSc was diagnosed on the basis of the clinical and skin biopsy findings, lung fibrosis on X-P and TBLB findings. At 65, his dyspnea reappeared along with elevated blood pressure, acute renal failure and lung congestion, and he was diagnosed as having a scleroderma renal crisis (SRC) from the clinical and renal biopsy findings. Hemodialysis was started because he showed mental disturbance, and this and other acute symptoms were subsequently reduced. As he showed no recovery from his renal failure, the patient has been maintained on hemodialysis for over four years now. In the meantime, his sclerosis has improved and antinuclear antibody almost disappeared. Hemodialysis appears to be the most likely reason for his improvement, although spontaneous remission, D-penicillamine and angiotensin converting enzyme (ACE) inhibitor therapy may also have contributed, considering the short period and the small amount of drugs given until improvement.
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PMID:[A patient with systemic scleroderma showing improvement during long-term hemodialysis after renal crisis]. 931 Dec 84

A 79-year-old female was admitted to our hospital because of a malignant pleural effusion following mastectomy 4 years ago. In the patient's history arterial hypertension and previous inferior myocardial infarction have been known. Two doses of 20 mg mitoxantrone were installed intrapleurally at an interval of 4 weeks. Six hours after the second mitoxantrone application and the patient had increasing dyspnea with consecutive left heart failure, pulmonary congestion, and a drop of blood pressure. The white-cell count was 14800/mm3. The levels of creatinine phosphokinase (CPK), lactate dehydrogenase (LDH) and serum aspartate aminotransferase (SGOT) were in the normal range. Transthoracic echocardiography showed concentric left ventricular hypertrophy and a markedly decreased fractional shortening, but no left ventricular dilatation. The electrocardiogram showed newly appeared down-sloping ST-segments and inverted T-waves. Clinical recovery was achieved after 6 days by application of oxygen, dobutamine and furosemide followed by angiotensin converting enzyme inhibition and digitalis. In the echocardiographic control examination 14 days later left ventricular function had normalized. The changes of electrocardiogram normalized 4 weeks later.
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PMID:[Mitoxantrone-induced acute left heart failure after intrapleural administration]. 937 56

A 46-year-old man was admitted to our clinic because of acute heart failure. Six years before admission he was pointed out cardiomegary and hematuria. One year later, he was diagnosed as having jugular foramen syndrome. On admission, he had a fever and dyspnea. Pansystolic blowing murmur was audible at the apex. The chest ratio on his chest X-ray was 52.5%. An electrocardiogram showed left ventricular hypertrophy. An echocardiogram showed marked dilatation and severe dysfunction of left ventricle. Radionuclide scanning with technetium 99 m pyrophosphate identified inflammatory change in the apex. Myocardial biopsy showed fibrotic degeneration and IgG deposits in myocardium. Blood examination showed anemia, lymphopenia. positive anti-nuclear antibody (1000 times, shaggy pattern), positive anti ds-DNA antibody and hypocomplementemia. Furthermore, proteinuria was pointed out. Renal biopsy showed focal segmental glomerulonephritis with active necrotizing lesion (type III nephritis). Lupus myocarditis and nephritis was diagnosed. After prednisolone (80 mg/day) was administered. left ventricular function and hypocomplementemia improved. The ACE inhibitor was also used for proteinuria. In spite of a little amount of blood transfusion, he showed hepatic hemosiderosis. We suspect that the cause of hemosiderosis was related chronic inflammation of active lupus. It was treated with Erythropoietin.
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PMID:[A case of lupus myocarditis and nephritis with transient foramen jugular syndrome]. 939 74


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