Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CLINICAL TRIALS WITH VERAPAMIL AND TRANDOLAPRIL: In the Danish Verapamil Infarction Trial II, verapamil improved survival in patients without heart failure but had no effect in patients with heart failure who were receiving diuretic treatment. In the Acute Infarction Ramipril Efficacy study ramipril improved survival in patients receiving diuretic treatment but had no effect in patients not receiving diuretics. COMBINATION WITH THERAPY WITH VERAPAMIL AND TRANDOLAPRIL: By combining verapamil with trandolapril we hypothesized that we could obtain an improvement in left ventricular function and prevent cardiac events. In an open study of 14 patients with angina pectoris and left ventricular ejection fraction below 40%, treatment with trandolapril-verapamil significantly improved left ventricular function. In a double-blind randomized study of 100 postinfarct patients with congestive heart failure the cardiac event rate was significantly lower in verapamil-trandolapril-treated than in the trandolapril-treated patients. These results indicate that the combined treatment with verapamil and trandolapril might be beneficial in patients with ischaemic heart disease and congestive heart failure.
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PMID:Congestive heart failure and ischaemic heart disease treated with trandolapril and verapamil. DAVIT Study Group. Danish Verapamil Infarction Trial. 953 1

Costs of providing a particular medical service can be measured, but it is more difficult to assess whether the service provides good value for the money spent. Rigorous trials have demonstrated the health benefits connected with interventions for treatment and prevention of cardiovascular disease (CVD), and in-depth analyses of the costs associated with many of those interventions have been performed. Careful use of terminology clearly differentiating among cost-minimization (relative costs of proved equivalent therapeutics), cost-effectiveness (lives saved or years of life added), and cost-benefit (total net effect in monetary terms) analyses is warranted. Although trials commonly assess clinical effectiveness as reductions in mortality or CVD-specific outcomes, improvement in quality of life may be equally important and is expressed in quality-adjusted life-years. Comparisons between therapies can be assessed as a cost-effectiveness ratio. Extensive cost-effectiveness studies have been conducted on many important cardiovascular therapies: (1) beta-blockers and diuretics for multiple CVD outcomes, mortality, and prevention of recurrent myocardial infarction (MI); (2) statins for both primary and secondary prevention of CVD; (3) enalapril for prevention and treatment of congestive heart failure; (4) tissue plasminogen activator treatment of acute MI; (5) coronary artery bypass graft for left main, single-, and 2-vessel coronary artery disease, or severe angina; (6) physician counseling for smoking; and (7) radiofrequency ablation therapy for Wolff-Parkinson-White syndrome. Therapies considered economically attractive include (1) secondary prevention with statins in hyperlipidemia, (2) smoking cessation programs, (3) primary prevention in treatment of high blood pressure with diuretics and beta-blockers, (4) primary prevention with regular exercise programs, (5) secondary prevention with cardiac rehabilitation, and (6) postinfarction treatment with beta-blockers and angiotensin-converting enzyme (ACE) inhibitors. A recent cost-minimization analysis has been performed showing aspirin to be a "best buy" therapy for secondary prevention of CVD. The Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) and Telmisartan Randomized Assessment Study in ACE-I Intolerant Patients with Cardiovascular Disease (TRANSCEND) program provide potential opportunities for both cost-minimization and cost-effectiveness analyses.
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PMID:How cost-effective are new preventive strategies for cardiovascular disease? 1278 5

Angiotensin (Ang) II is now recognized to be a mediator of a wide variety of inflammatory processes. This study investigated renin-angiotensin system (RAS) components and a number of inflammatory mediators in left ventricular biopsies from 2-vessel disease unstable angina (UA) (n=43) and stable angina (SA) (n=15) patients undergoing coronary bypass surgery. Biopsy samples from 6 patients undergoing valve replacement for mitral stenosis served as controls. UA patients were randomly assigned to angiotensin-converting enzyme (ACE)-inhibitor (ramipril), AT1 antagonist (valsartan), or placebo and treated during the 5 days preceding coronary bypass surgery, performed from 6 to 9 days after coronary angiography. During coronary angiography coronary blood flow was measured and samples were obtained from aorta and coronary sinus for determination of Ang I and Ang II gradients. The hearts of UA patients produced Ang II in a greater amount than in SA patients (P<0.01). UA biopsy samples showed numerous DR+ cells, identified as lymphocytes, macrophages, and endothelial cells. Reverse-transcriptase polymerase chain reaction showed overexpression of AGTN, ACE, and AT1-R genes, as well as upregulation of TNF-alpha, IL-6, IFN-gamma, and iNOS genes (P<0.01), with no differences between nonischemic and potentially ischemic areas. AGTN, ACE, and cytokine genes were mainly localized on endothelial cells. Ramipril and valsartan markedly decreased the expression levels of TNF-alpha, IL-6, and iNOS, and, to a lesser extent, of IFN-gamma genes, but did not affect the number of DR+ cells, with no significant difference between the 2 treatments. These results show that locally generated Ang II amplifies the immunomediated inflammatory process of coronary microvessels occurring in unstable angina.
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PMID:Cardiac angiotensin II participates in coronary microvessel inflammation of unstable angina and strengthens the immunomediated component. 1521 17

Acute coronary syndrome (ACS) is a clinical syndrome caused by acute myocardial ischemia and a severe stage of coronary atherosclerosis heart disease. The aim of this study was to clarify whether ramipril was a therapeutic agent against monocyte chemoattractant protein 1 (MCP-1), interleukin 18 (IL-18), and interleukin 10 (IL-10) in elderly patients with ACS. A total of 190 subjects including 72 elderly patients with ACS (78.1% male, mean age 67.12 +/- 5.06 years), 60 elderly patients with stable angina pectoris (76.9% male, mean age 68.00 +/- 4.52 years), and 58 healthy volunteers (77.8% male, mean age 65.96 +/- 4.18 years) were recruited into the study. Serum MCP-1, IL-10, and IL-18 were determined in 132 elderly patients by enzyme-linked immunosorbent assay (ELISA) before and after treatment with low doses of ramipril (2.5-5 mg/day), and were determined in 58 healthy volunteers. The levels of serum MCP-1 and IL-18 were much higher in elderly patients with ACS than those in elderly patients with SAP and healthy volunteers. After treating with ramipril, the levels of MCP-1 and IL-18 were decreased in elderly patients with ACS. Moreover, ramipril significantly increased serum IL-10 in elderly patients with ACS. Ramipril plays an important role in elderly patients with ACS. With decreasing MCP-1 and IL-18, it can ameliorate cytokine-associated cardiac damage. This study may provide a new recognition of angiotensin-converting enzyme inhibitor for the treatment of ACS.
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PMID:Effects of ramipril on serum monocyte chemoattractant protein 1, interleukin-18, and interleukin-10 in elderly patients with acute coronary syndrome. 2033 66