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)

Cardiovascular disease is a leading cause of death in diabetic patients. It has been reported to count for almost 80% of all deaths. About three-fourths of these deaths result from coronary artery disease. Studies have shown that diabetic patients who have had an acute myocardial infarction (AMI) have a mortality of about twice that of nondiabetic patients. Various medications have been shown to improve the prognosis among diabetic patients suffering from ischemic heart disease. They include beta-blockers, thrombolytic agents, aspirin, ACE inhibitors, and lipid-lowering drugs. Experiences indicate that treatment with beta-blockers, thrombolytic agents, and ACE inhibitors is particularly advantageous in diabetic patients who have suffered AMI. Metabolic control also may be of major importance during the acute cardiac event because it is assumed that fatty acid metabolism is increased with a compromised glycolysis not only in ischemic but also in the nonischemic areas. One way to suppress free fatty acid oxidation is by the infusion of insulin-glucose. In the Swedish Diabetes Mellitus and Insulin Glucose Infusion in Acute Myocardial Infarction (DIGAMI) Study, patients with diabetes and AMI were randomized to receive insulin-glucose infusion followed by intensive subcutaneous insulin treatment or to be control subjects. The 1-year mortality was reduced 30% by insulin treatment. Diabetic patients who suffer from coronary artery disease have a particularly adverse prognosis. Previous experiences indicate that treatment with beta-blockers, thrombolytic agents, and ACE inhibitors is particularly advantageous in diabetic patients who have suffered AMI. Aspirin and lipid-lowering drugs should be offered to these patients on traditional indications as well. Metabolic control seems to be of major importance for the outcome.
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PMID:How to improve the cardiac prognosis for diabetes. 1009 7

We studied neuronal pathways for spinal reflexes activated by group-I and group-II muscle afferents in the spinal segments innervating the tail in unanesthetized and spinalized (L1) cats. Experiments were performed on 25 adult cats of both sexes. The effects of stimulating nerves innervating six tail muscles on both sides were recorded from tail motoneurons in the first coccygeal spinal segment (Co1) using glass microelectrodes. Stable recordings were obtained from 150 tail motoneurons. Stimulation of group-1 muscle afferents (stimulus intensity <1.8 T) often produced EPSPs (82/150) after stimulating nerves innervating neighboring tail muscles. Motoneurons innervating the long-tendoned muscles, M. extensor caudae lateralis and M. flexor caudae longus (ECL and FCL), received heteronymous monosynaptic connections from group-I muscle afferents innervating the ipsilateral tail muscles. The motoneurons innervating segmental muscles, M. extensor caudae medialis and M. flexor caudae brevis (ECM and FCB), received heteronymous monosynaptic connections from group-I muscle afferents innervating tail muscles on both sides. The motoneurons innervating tail muscles originated from the Ossa coxae, M. abductor caudae externus and M. abductor caudae internus (ACE and ACI), received monosynaptic connection from group-I muscle afferents innervating most of the tail muscles on both sides. Crossed disynaptic inhibitory pathways activated by primary muscle afferent inputs were observed in ECM, ACE, FCL, and FCB motoneurons. The effects of group-II afferent inputs were not dependent on the kind of motoneuron, and alternative excitatory and inhibitory pathways were not clearly observed in the tail motoneuron pool. It is suggested that variability of the neuronal pathways from group-I and -II muscle afferents to tail motoneurons corresponds to functional relationships among tail muscles, depending on the tail movements.
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PMID:Neuronal pathways for spinal reflexes activated by group I and group II muscle afferents in the spinal segment (Co1) innervating the tail in the low spinalized cat. 1020 66

Inhibitors of angiotensin converting enzyme (ACE inhibitors) have been introduced more than fifteen years ago into the treatment of hypertension, congestive heart failure, myocardial infarction and diabetic nephropathy. The therapeutic success is related to their action in reduction of plasma and tissue angiotensin II concentrations and potentiation of endogenous kinins. They are able to improve myocardium metabolic status, prevent cardiac hypertrophy, limit myocardial infarct size, and thus prevent heart failure. Since 1987 ACE inhibitors are introduced in the clinical practice in our clinic. We introduced the therapy with lisinopril (Lopril), in 70% of patients among 2855 patients that were admitted in Coronary Care Unit in 1997 and 1998. Lisinopril was introduced as soon as the patient was admitted, together with fibrinolitic, Heparin and Aspirin therapy. Since that time we noticed decrease in postinfarction heart failure in comparison to previous years. We recommend permanent therapy with a small doses of ACE inhibitors in patients with heart infarction.
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PMID:[Converting enzyme inhibitors in acute myocardial infarct and heart failure]. 1035 28

The ability of angiotensin converting enzyme (ACE) inhibitors to lower blood pressure may in part be due to the formation of vasodilatory prostaglandins. Inhibition of prostaglandin synthesis with aspirin may therefore theoretically attenuate the antihypertensive effect of ACE inhibitors. This trial studied the interaction between aspirin (ASA) and enalapril, an ACE inhibitor, and ASA and losartan, an angiotensin subtype 1 receptor antagonist. Seventeen essential hypertensive patients were studied, maintained on a stable dose of either enalapril (n = 7) or losartan (n = 10) monotherapy for > or =12 weeks before and throughout the study. Each patient received a 2-week course of placebo, 81 mg/day ASA, and 325 mg/day ASA, each treatment separated by a 2-week washout period. Blood pressure (BP) and serum thromboxane B2 (TXB2) samples were obtained at the end of each treatment period. Placebo was compared with each dose of ASA for each group. In both the enalapril and losartan groups, mean, systolic, and diastolic BP were unchanged with the addition of ASA. Concentrations of TXB2 were suppressed to <10% in both groups with ASA. This study demonstrates that 81 to 325 mg/day ASA exerts no significant effect on BP in essential hypertensives taking enalapril or losartan.
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PMID:Effect of aspirin on blood pressure in hypertensive patients taking enalapril or losartan. 1048 Apr 71

Risk factor control has been shown to reduce the incidence of coronary events in patients with or without preceding infarction. Secondary prevention should therefore be borne in mind by every cardiologist. In order to test this concept and/or to promote secondary prevention in our country, the following survey was conducted by our working group for epidemiology and prevention. All interventional centres of the country (7 million inhabitants) were asked to report relevant data of 50 consecutive patients with PTCA in a structured questionnaire. Thirteen centres responded and we report the data of 650 patients. The mean proportion of women was 28%, the mean age 61.1 years and the mean stent rate 49.8%. The indications for PTCA varied widely: stable angina 10-74%, unstable angina 10-86%, primary PTCA 0-22%. The risk factor history was distributed as follows: diabetes 12-46% (mean 22.3%), hypertension 32-68% (mean 54.2%), current smoking 6-56% (mean 21.9%), and total cholesterol (TChol) > 200 mg/dl: 30-78% (mean 60.3%). Current lipid values were available for T chol. in 44-100% (mean 84.5%) and for LDL in 4-100% (mean 67.1%). Dietary counselling by a dietician was done in 4-100% of patients (mean 35.6%) Information concerning the hazards of smoking was given to 25-100% (mean 83.6%) of current smokers. Drug treatment at hospital discharge was as follows: 84-100% (mean 93.1%) received ASA, 24-74% (mean 49.8%) ticlopidine, 6-84% (mean 53.3%) nitrates, 34-82% (mean 60.2%) beta blockers, 10-70% (mean 39.5%) ACE inhibitors, 4-74% (mean 4 7.2%) lipid lowering drugs, 7-48% (mean 17.8%) calcium antagonists, 0-12% (mean 6.1%) digitalis and 0-28% (mean 13.6%) diuretics. Follow-up data were collected in 4 centres at 6 months post discharge and were available for 174 patients. Here we found an increase in the prescription of calcium antagonists, digitalis and statins. The following conclusions were drawn at a conference in which all centres participated: lipid values should be available for each patient at PTCA, dietary counselling should be initiated for every patient during hospitalisation (and continued by the family physician) and the national cardiac society should promote guidelines for the use of drugs in which the variation in use is too wide at present. It should be ensured that these guidelines are implemented not only in patients after AMI but also in those after PTCA.
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PMID:[Secondary prevention following coronary intervention. Survey of 13 intervention centers in Austria]. 1051 Aug 42

Adjunctive therapy is critical in treating acute coronary syndromes. Aspirin, nitrates, beta-blockers, ACE inhibitors, HMG-CoA reductase inhibitors (statins), and intra-aortic balloon pumps all have important roles and should be considered on a case-by-case basis.
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PMID:Adjunctive medical therapy for acute coronary syndromes. 1074 8

The state of pharmacotherapy in the Czech Republic in 1998 was analysed in a group of 548 patients with coronary heart disease and diabetes mellitus. 83.0% of the group were treated by antiplatelet drugs, mostly ASA (with the most frequent dose being 100 mg). 7.3% of the patients were treated by anticoagulation treatment. Beta-blocking agents were used in 56.9% of the group (most frequently metoprolol and atenolol). The optimal dose of metoprolol, 100 mg b.i.d., was used in only 12.4% of the patients treated by metoprolol. Older patients and patients with left ventricular systolic dysfunction were treated significantly less frequently than younger patients or patients without left ventricular systolic dysfunction. ACE inhibitors were used in 52.2% of the patients. The optimal daily target dosages of captopril 100-150 mg were used in only 6% of patients treated by captopril. The optimal target daily dosages of enalapril were used in only 35.1% of patients treated by enalapril. 65% of patients with left ventricular systolic dysfunction were treated by ACE inhibitors. Calcium-channel blockers were used in 24.6% of the patients. However, in 20.1% of patients treated by calcium-channel blockers, shortacting or inadequately retarded nifedipine was used. 69.8% of the patients had total cholesterol values higher than 5.2 mmol/l, 18.1% higher than 6.2 mmol/l and 13.5% of patients had total cholesterol values higher than 7.0 mmol/l. 34.3% of the group were treated by hypolipidemic drugs (most frequently fenofibrate). Statins were used by 45.5% of patients treated by hypolipidemic drugs. When compared to our analysis of pharmacologic treatment in patients after myocardial infarction, performed in 1995, ACE inhibitors and hypolipidemic treatment are used more frequently. However, in spite of this improvement, only about 15% of patients with CHD are treated by statins. Furthermore, 35% of patients with left ventricular systolic dysfunction due to CHD are not treated by ACE inhibitors. Elderly patients with CHD and diabetes mellitus or patients with left ventricular systolic dysfunction due to CHD are less frequently treated than younger patients or those with normal left ventricular systolic function despite the fact that patients at highest risk benefit most from treatment with beta-blocking agents. Also unsatisfactory is the use of not retarded or inadequately retarded nifedipine although data show its use may increase total mortality in CHD patients. By contrast, use of antiplatelet therapy is satisfactory.
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PMID:[Pharmacotherapy in patients with ischemic heart disease and diabetes mellitus in 1998 in the Czech Republic]. 1095 43

Diabetes mellitus is a risk factor for coronarosclerosis and for high mortality after myocardial infarction (MI). The causes of this high mortality are: more extensive and premature coronarosclerosis, more frequent left ventricular dysfunction, worse glycemic control with increased myocardial oxygen consumption, sulfanylurea drugs before and during MI. The results of a multicenter study (DIGAMI) and other studies suggest that a better control of diabetes using intravenous infusion of insulin and glucose, followed by long-term (3 months) intensive insulin therapy subcutaneously, improves long-term prognosis after MI. The relative reduction of mortality at the end of follow-up (3.4 years) is 28%. Thrombolysis reduces mainly mortality in hospital,s period and does not provoke retinal haemorrhages. Aspirin lowers the relative risk of mortality to 0.72. The beta-blockers are less used in diabetic patients because they probably alter diabetic control, lipid profile and "mask" the hypoglycemic symptoms, but the results of the beta-blocker's effect concerning reduction of mortality are convincing. ACE inhibitors and statins also reduce mortality in diabetics with MI, via beneficial influence of endothelial dysfunction. The ATMA study registers reduction of rhythmogenic mortality by 29% with amiodarone in high risk of arrhythmia after MI. The invasive methods of treatment in diabetes are accompanied by higher risk of reobstruction. The attempt to reduce this tendency is realizable with intracoronary stents, glycoprotein IIb/IIIa inhibitors and aggressive early treatment of all other risk factors.
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PMID:[Diabetes mellitus and myocardial infarct--new answers and questions]. 1098 72

Coronary artery disease is still the no. 1 killer in the developed countries and must thus be detected and treated at an earlier stage. If coronary artery disease is advanced, patients have to be examined regarding the need for revascularization. For secondary prevention, of course, an optimal change of life style and optimal medical treatment of risk factors is mandatory. Independent of the optimal risk factor modification, all of these patients (according to the rules of evidence-based medicine) should take ASA, statins, beta blockers and ACE-inhibitors, if no contraindications or intolerance are present. Therefore, the problem in secondary prevention is not how to identify these patients, but rather how to fulfill their needs. In our own survey in patients with known coronary artery disease referred for PTCA (including patients with post myocardial infarction previous PTCA or bypass surgery), only 89% were on ASA (or clopidogrel), 51% on lipid lowering drugs (46% on statins), 65% on beta blockers, and only 43% had an ACE-inhibitor (MUNICH data in Figures 1 to 4). The analysis of published literature is also depicted in Figures 1 to 4. Until 1996, patients with known coronary artery disease took ASA in only 26% of the cases but later on it was 77 to 100% (Figure 1). Lipid lowering drugs (especially statins) are prescribed in only 13 to 77% (Figure 2), beta blockers in only 30 to 80% (Figure 3) and ACE-inhibitors in only 10 to 72% (Figure 4). In 2 major studies, a decrease in the rate of intake of these drugs during the follow-up years has been documented. The "ideal tablet" for secondary prevention contains ASA (100 mg), a statin (e.g. for most statins 40 to 80 mg), a beta blocker (e.g. metoprolol 100 mg or bisoprolol 10 mg) and an ACE-inhibitor (e.g. ramipril 10 mg). So this ideal "SPM" ("secondary prevention mix") tablet contains 160 to 300 mg of drugs. In conclusion, the analysis of published data for Europe and the USA shows that--in contrast to the statements of politicians and health care insurance companies--we are not overtreating but rather undertreating our patients regarding medications for secondary prevention.
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PMID:[Undertreatment in secondary prevention of patients with coronary heart disease after revascularization]. 1107 20

Myocardial infarction is the leading cause of death among persons with diabetes. Recent advances in the understanding and treatment of cardiovascular disease in diabetes have made it increasingly important to tailor therapy when treating this high-risk population. Because patients with diabetes are at significantly higher risk for complications and death from MI, these patients are most likely to benefit from early and aggressive therapeutic intervention. Strong recommendations can be given for the use of beta-blockers, ACE inhibitors, and thrombolysis when indicated in the management of acute MI in the diabetic patient. Acetylsalicylic acid is also likely to be beneficial with little risk of adverse events in this setting. In the absence of more definitive data, cautious use of mechanical intervention in diabetic patients is recommended. The use of intravenous insulin therapy may benefit diabetic patients during the acute phase of MI, but more definitive studies are required before it can be recommended for broad use.
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PMID:Managing myocardial infarction in the diabetic patient. 1114 65


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