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)

In a 63-year-old woman with longstanding type I diabetes mellitus, CAD and chronic heart failure, a subacute myocardial infarction developed, together with decompensation of cardiac function and diabetes and concurrent pneumonia. Acute heart failure with acute renal failure on top of diabetic nephropathy, and interstitial pulmonary edema was initially treated with hemofiltration and catechol amines together with antibiotic and perfusor-regulated insulin therapy, and systemic heparinization. Subsequent chronic treatment with digitalis, acetyl salicylic acid, insulin and a combination of an ACE inhibitor and a loop diuretic resulted in an improvement of heart failure to NYHA functional class II where PTCA of coronary multi-vessel disease could be performed with low risk.
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PMID:[Heart failure after myocardial infarct in decompensated diabetes mellitus. Acute therapy with catecholamines--long-term therapy with ACE inhibitor-loop diuretic combination]. 937 33

Preventing the progression of established heart failure can be difficult, as multiple factors contribute to the continual decline of cardiac function. Blunting the activated neurohormonal response to a decreased systolic function is a proven means of slowing progression of CHF. Preventing further CAD and cardiac ischemia may also prove to be an effective mechanism. Two trials with HMGCoA reductase inhibitors lend support to this hypothesis. Studies using ACE inhibitors may also support this notion. Since a major portion of heart failure in the USA is caused by CAD, preventing CHF progression may be related to the prevention of CAD. Using ACE inhibitors and lipid-lowering agents, in addition to standard measures of CAD risk factor modification, may prove useful in future trials to retard the progression of heart failure. Further research and clinical trials involving this method of CHF prevention are warranted.
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PMID:Role of secondary prevention in congestive heart failure due to coronary artery disease. 989 17

The increased risk of cardiovascular disease in diabetic patients is well documented. A greater appreciation for the importance of this fact and regular use of secondary prevention strategies, including aggressive use of HMG-CoA reductase inhibitors or other lipid-lowering agents to reduce cholesterol levels, are clearly indicated for diabetic patients with CAD. If no contraindications exist, ACE inhibitors, beta blockers, and aspirin also should be considered for these high-risk patients.
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PMID:Coronary artery disease and diabetes. 1002 4

Initial pharmacologic therapy for hypertension is low-dose thiazide diuretics, beta-blockers, and ACE inhibitors. Increasing data have confirmed that ACE inhibitors have specific benefit in patients with diabetes, atherosclerosis, left ventricular dysfunction, and renal insufficiency. CCBs are alternative agents for ISH in the elderly and appear to decrease stroke with perhaps less protection against progression of renal insufficiency and proteinuria, CAD mortality and new onset heart failure versus other initial agents, especially ACE inhibitors. ARBs are well tolerated and effective blood pressure lowering agents but have not been confirmed as effective as ACE inhibitors for reducing renal progression, clinical events, or mortality from heart failure. Effective pharmacologic antihypertensive therapy may avoid disabling and undetected cerebrovascular disease, cognitive dysfunction, and disturbing symptoms of elevated blood pressure. Vasopeptidase inhibitor, such as omapatrilat, and endothelin-1 antagonist, such as bosentan, may become future agents approved for the reduction of morbidity and mortality with hypertension. The ALLHAT trial continues to examine the potential benefits and harms of amlodipine versus chlorthalidone and lisinopril in a diverse high-risk population. Based on ALLHAT data, however, doxazosin is no longer an acceptable initial pharmacological agent. Intensive pharmacologic treatment with blood pressure lowering to less than 130/85 mm Hg is recommended with diabetes, renal insufficiency, and heart failure with additional goal of less than 125/75 mm Hg with renal failure and proteinuria greater than 1 g/24 h, based on multiple outcome studies.
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PMID:Update in pharmacologic treatment of hypertension. 1140 10

Life expectancy is increasing even though life span is fixed. There will be almost 35 million Americans over 65 years of age in the year 2030. CAD will account for almost 80% of the deaths in the population with almost 50% of such deaths classified as sudden. Ventricular arrhythmias increase with age and have been shown to be independent markers for premature cardiac death. Therefore, many trials involving the use of antiarrhythmics have been performed, hoping to show an improvement in overall survival. Unfortunately, some of the classical antiarrhythmic agents despite markedly suppressing the arrhythmias, have been shown to be harmful or of no benefit. The use of b-blockers, amiodarone, aspirin, and ACE inhibitors show some potential for benefit in this high risk patient population. The implantable devices are superior to antiarrhythmics in survivors of cardiac arrest.
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PMID:Antiarrhythmic Drug Therapy of Ventricular Tachycardia in the Elderly: Lessons From Clinical Trials. 1141 81

In this investigation associations of gene complexes consisting of seven candidate for coronary atherosclerosis (ACE, AGT, NOS3, APOA1, MTHFR, PLAT, F13) with risk factors for CAD (lipid levels, blood pressure, body mass index (BMI)) were studied in Russian population. 94 male patients with CAD proven by angiography and 131 healthy individuals were involved in the case-control study. We observed a significant contribution of gene combinations ("ensembles"). ACE-MTHFR, ACE-F13, ACE-AGT-MTHFR in the variability of the total cholesterol and LDL-cholesterol levels. The "Ensembles" ACE-AGT-MTHFR were associated with variability of three atherogenic risk factors (LDL, BMI, cholesterol total). Two-locus gametic disequilibrium was analysed between gene polymorphisms. NOS3 and ACE, NOS3 and APOA1 were in gametic disequilibrium in the control group. Polymorphic markers of ACE and F13, NOS3 and F13, ACE and PLAT loci were in gametic disequilibrium in the patients. Both approaches (association analysis and gametic disequilibrium) revealed the same gene combinations contributing to the CAD risk factors. NOS3 and APOA1 markers were in gametic disequilibrium in the patients and both of them were associated with LDL. F13 and AGT were associated with systolic and diastolic blood pressure and two-locus gametic disequilibrium between F13 and AGT polymorphisms observed in the patients.
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PMID:The estimation of gametic disequilibrium between DNA markers in candidate genes for coronary artery disease (CAD) and the associations of gene complexes with risk factors for CAD. 1150 73

Hypertension and hypercholesterolemia, two major risk factors for atherosclerotic disease, frequently coexist in patients with hypertension and CAD. Data from clinical studies suggest the existence of lipoprotein-neurohormonal interactions that may adversely affect vascular structure and reactivity. Data from preclinical studies suggest that RAS may be upregulated by abnormal lipids, most likely via production of ox-LDL. On the other hand, activation of RAS leads to release of ROS and transcriptional upregulation of LDL and ox-LDL uptake in macrophages, smooth muscle cells and endothelial cells. These findings extend our understanding of the interplay among risk factors to synergistically increase cardiovascular risk, and of the anti-atherosclerotic effects of local ACE inhibition to reduce cardiovascular risk. Trials aimed at modifying RAS along with drugs lowering total- and LDL-cholesterol levels and inhibitors of oxidative modification of LDL-cholesterol will address the clinical relevance of this biological interaction.
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PMID:Interactions between the renin-angiotensin system and dyslipidemia: relevance in atherogenesis and therapy of coronary heart disease. 1175 48

In the past era, we held high-grade arterial stenosis responsible for the acute complications of atherosclerosis. These concepts are being reassessed. Qualitative rather than quantitative aspects of plaques (e.g., inflammation rather than plaque size) have been established as decisive determinants of their probabilities to cause acute complications. Numerous beneficial effects of statins have been demonstrated. These include lipid lowering, plaque stability, enhanced endothelial function, and antiplatelet, antiatherothrombotic, and antimacrophage activities. However, the successful medical management of CAD is also multifactorial and in addition to use of statins include beta-blockers, ACE inhibitors, and aspirin, as well as blood pressure control, diet, and exercise (see [figure: see text] Figure). The results have been not only the preventions of acute complications of atherosclerosis, but also the successes in stabilizing acute coronary events and preventing infarctions.
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PMID:Seminal changes in the management of the acute coronary event: current concepts. 1252 41

Women are underrepresented in clinical trials. Lower doses of beta-blockers are required for Southeast Asians. ACE and ARB's are teratogenic in the second trimester. Torsades de Pointes is more common in women related to a longer QT-interval. Lower dose OCPs decrease the risk of MI, stroke and thrombosis. HRTs are not effective for CAD prevention.
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PMID:Gender, ethnicity, and genes in cardiovascular disease. Part 2: implications for pharmacotherapy. 1278 34

The precise molecular mechanism for the development of cardiac allograft vasculopathy (CAV) after heart transplantation is not known. We, thus, hypothesize that increased activity of renin-angiotensin system (RAS) is important for the progression of CAV. There is evidence to support this concept. RAS via its principal effector molecule, angiotensin II exerts multitude of actions on vascular structure and function including regulation of vasomotor tone, cell growth/apoptosis, fibrosis and inflammation, which are particularly relevant to the genesis of atherosclerotic lesions. Risk factors, which increase predisposition to CAD, are known to activate tissue RAS and thus influence its progression. Importantly, CAD risk factors are also associated with accelerated CAV progression after transplantation. Whereas angiotensin converting enzyme (ACE) gene polymorphism increases the predisposition, pharmacological inhibition of RAS seems to reduce the incidence of CAV. These observations may support our hypothesis, provide a plausible explanation for the molecular mechanisms underlying the development of accelerated CAV and has predictions that can be tested.
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PMID:The renin-angiotensin hypothesis for the pathogenesis of cardiac allograft vasculopathy. 1519 9


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