Drugs online research references
Cardiovasc J S Afr. 2000 Apr;11(2):89-94.
A South African pharmaco-economic analysis of the Acute lnfarction Ramipril Efficacy (AIRE) Study.
Anderson AN, Moodley I, Kropman K.
Anderson Kropman cc., PO Box 1278, Parklands, Johannesburg, 2121, South Africa.
OBJECTIVES: Heart failure (HF) is a serious, prevalent health condition in industrialised countries where the incidence has been on the increase. The economic repercussions are costly, and therefore cost-effective medication is important in the overall management of the condition. It has been shown that angiotensin-converting enzyme (ACE) inhibitors are clinically effective in the management of HF. Ramipril has been shown to reduce mortality and the probability of hospitalisation in post-myocardial infarction (MI) patients. Internationally, the use of this drug has proved to be cost-effective. The objective of this study was to investigate the economic implications of using ramipril in South Africa for post-MI patients with HF. METHODOLOGY: An incremental cost-effectiveness analysis was performed comparing the use of ramipril and placebo in post-MI patients with HF who were receiving standard therapy. The economic impacts included drug acquisition costs and savings on hospitalisation; these were evaluated based on the clinical benefits of using ramipril in terms of life-years gained (LYG). The cost-utility of the use of ramipril was determined to provide an incremental cost per quality-adjusted life-year (QALY). Sensitivity analyses were performed on the major economic variables; discounting of future costs and savings was performed at rates of 0%, 5 % and 10 %. RESULTS: The use of ramipril results in an incremental cost/LYG of R16 808 and a total incremental cost per patient per month of R107 over 3.8 years. When the quality of life of the patients is taken into account, the cost-utility analysis shows an incremental cost/QALY of R21 382 for those younger than 65 years of age and R18 029 for those older than 65 years. The pharmaco-economic model was robust and consistent when tested at the extremes of the major variables, including costs, savings and discount rates. CONCLUSION: The results indicate that it is cost-effective to administer ramipril in addition to standard therapy for post-MI patients with HF in South Africa.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11447469&dopt=Abstract [PubMed - as supplied by publisher]
medinf.mu-luebeck.de
The potentiation of kinin actions represents a cardioprotective property of ACE inhibitors. Although a clear contribution to this effect is related to the inhibition of bradykinin (BK) breakdown, the high efficacy of potentiation and the ability of ACE inhibitors to provoke a B(2)-receptor-mediated response even after receptor desensitization has also triggered hypotheses concerning additional mechanisms of kinin potentiation. The application of kinin analogues with enhanced metabolic stability for the demonstration of degradation-independent mechanisms of potentiation, however, has yielded inconsistent results. Therefore, the relation between the susceptibility of B(2)-agonists to ACE and the potentiation of their actions by ACE inhibitors was investigated with the use of minimally modified kinin derivatives that varied in their degree of ACE resistance. The B(2)-agonists BK, D-Arg-[Hyp(3)]-BK, [Hyp,(3) Tyr(Me)(8)]-BK, [DeltaPhe(5)]-BK, [D-NMF(7)]-BK, and [Phe(8)psi(CH(2)-NH)Arg(9)]-BK were tested for degradation by purified rabbit ACE and for their potency in contracting the endothelium-denuded rabbit jugular vein in the absence and presence of ramiprilat. Purified ACE degraded D-Arg-[Hyp(3)]-BK and [Hyp,(3) Tyr(Me)(8)]-BK at 81% and 71% of BK degradation activity, respectively, whereas other peptides were highly ([DeltaPhe(5)]-BK) or completely ([D-NMF(7)]-BK, [Phe(8)psi(CH(2)-NH)Arg(9)]-BK) resistant. The EC(50) of BK-induced venoconstriction (1.15+/-0.2 nmol/L) was reduced by a factor of 5.7 in the presence of ramiprilat. Likewise, D-Arg-[Hyp(3)]-BK and [Hyp,(3) Tyr(Me)(8)]-BK were both significantly potentiated by a factor of 4.4, whereas the activities of the other agonists were not affected. Ramiprilat exerted no influence on the maximum contraction induced by any of the agonists. It is concluded that the potentiation of kinin analogues during ACE inhibition correlates quantitatively with the susceptibility of each substance to degradation by ACE. As such, no evidence of degradation-independent potentiating actions of ACE inhibitors could be obtained.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11463775&dopt=Abstract
J Hum Hypertens. 2001 Jul;15(7):463-70.
Right atrial function in hypertensive patients: effects of antihypertensive therapy.
Dernellis J.
Department of Cardiology, Vostanion Hospital, Mytilini, Greece.
OBJECTIVES: The effects (16 weeks) of oral antihypertensive drugs on right atrial (RA) function were evaluated by two-dimensional and Doppler echocardiography in 64 patients with mild-to-moderate essential hypertension. Thirty-two age- and sex-matched normal subjects served as controls. BACKGROUND: Hypertension alters the diastolic properties of the left ventricle and disturbs the left atrial contractile activities. RA performance may also alter in essential hypertension. METHODS: From the tricuspid flow velocity curves the E/A ratio, the velocity-time integrals (Ei and Ai, respectively) as well as the sum, TTi = Ei + Ai, were measured. RA active contribution (RAAC) was expressed as the ratio RAAC = Ai/TTi. RESULTS: RA-A/E ratio, RA-Ai and RAAC were increased while RA-TTi were decreased in hypertensives compared to controls, P < 0.0001 for all comparisions. After therapy TTi increased (from 13.2 +/- 1.6 to 16.2 +/- 2.0 cm with ramipril, and from 12.9 +/- 1.1 to 14.4 +/- 1.2 cm with amlodipine, P < 0.001) and RAAC decreased (from 0.19 +/- 0.01 to 0.13 +/- 0.01, with ramipril and from 0.19 +/- 0.01 to 0.16 +/- 0.00, with amlodipine P < 0.001) while RA dimensions did not change. the decrease in RAAC was significantly greater with ramipril (P < 0.001) and was significantly influenced by the decrease in left ventricular mass (P < 0.001) and right ventricular relaxation (P < 0.001). CONCLUSIONS: RA function is deteriorated in patients with essential hypertension. The fall in the arterial blood pressure produced by antihypertensive treatment was associated with improved RA performance and reduced left ventricular mass without changes in RA dimensions. The left ventricular mass and the right ventricular relaxation influenced the changes in RA performance.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11464255&dopt=Abstract
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