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  • 1
    Electronic Resource
    Electronic Resource
    Influence of Smoking Status on Angiotensin-Converting Enzyme Inhibition–Related Improvement in Coronary Endothelial Function (1999)
    Springer
    Cardiovascular drugs and therapy 13 (1999), S. 201-209 
    Details
    ISSN: 1573-7241
    Keywords: acetylcholine ; angiotensin-converting enzyme inhibition ; coronary disease ; endothelium ; smoking ; vasoconstriction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Summary. Our study evaluated the influence of smoking status on coronary endothelial function in normotensive patients with coronary artery disease who received placebo or the angiotensin-converting enzyme inhibitor quinapril in the TREND study (Trial on Reversing Endothelial Dysfunction). In this retrospective analysis of data from the previously published study, patients were classified as either smokers (n = 23) or nonsmokers (n = 82). Patients underwent coronary angiography at baseline and again after 6 months follow-up. The primary response variable was the net change in acetylcholine-induced diameter of the target coronary artery segments (n = 105) between the baseline and 6-month follow-up angiograms. The secondary response variables were based on analysis of all segments (n = 300) and the mean diameter responses of target and all segments at 6 months. At baseline, coronary artery vasomotor responses were similar in smokers and nonsmokers in the placebo and quinapril groups. There was a significant improvement in the primary response variable for both smokers (P = 0.008) and nonsmokers (P = 0.047) randomized to quinapril compared with placebo. At 6 months follow-up, nonsmokers in the placebo group showed no significant change in the mean vasoconstrictor responses (8.3% vs. 8.0% at acetylcholine 10-4 mol/L), whereas nonsmokers in the quinapril-treated group showed significantly less vasoconstriction (2.7% vs. 13.2%; P = 0.003). Among smokers in the placebo group, vasoconstriction increased nonsignificantly (21.7% vs. 17.2% at baseline) but decreased significantly in the quinapril group (0.5% vs. 17.9%; P = 0.002). These results indicate that ACE inhibition improves the coronary vasomotor response in both smokers and nonsmokers, but that smokers apparently derive greater benefit.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007740008155
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Angiotensin II Formation in Human Vasculature after Chronic ACE Inhibition: A Prospective, Randomized, Placebo-Controlled Study (2000)
    Springer
    Cardiovascular drugs and therapy 14 (2000), S. 55-60 
    Details
    ISSN: 1573-7241
    Keywords: angiotensin ; ACE inhibition ; vasculature ; endothelial factors ; renin-angiotensin system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The QUO VADIS (the effects of QUinapril On Vascular Ace and Determinants of ISchemia) study was a randomized, double-blind, placebo-controlled trial designed to evaluate the effects of long-term angiotensin-converting enzyme (ACE) inhibition on angiotensin II formation in human vasculature. Patients (n 〈 187) scheduled for coronary artery bypass surgery used study medication 27 ± 1 days before surgery. Segments of internal mammary arteries were exposed to increasing doses (0.1 nM-1 µM) of angiotensin I and II in organ baths. The rate of local angiotensin II formation is a function of the reciprocal of the difference between the pEC50's of the dose response curves to angiotensin I and II (−log/mol) and of the area between the curves (units). Quinapril (40 mg) and captopril (3×50 mg) similarly and significantly reduced mean blood pressure compared with placebo (p = 0.04). Difference between pEC50's was 0.90 ± 0.08 in quinapril patients compared with 0.60 ± 0.08 for placebo (p 〈5 0.01); the area between curves was 91 ± 8 for quinapril patients compared with 67 ± 8 for placebo (p = 0.03). Angiotensin II formation was decreased to a lesser extent with captopril and was not statistically different from placebo (p = 0.3); the difference between pEC50's was 0.83 ± 0.15; the area between curves was 84 ± 12. This is the first randomized study to demonstrate that long-term oral treatment with an ACE inhibitor reduces vascular angiotensin II formation in humans.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007843205311
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Activity of Procanbid Procainamide Twice-Daily Formulation, to Suppress Ventricular Premature Depolarizations (1997)
    Springer
    Cardiovascular drugs and therapy 11 (1997), S. 169-175 
    Details
    ISSN: 1573-7241
    Keywords: Clinical trials ; ventricular premature depolarizations ; procainamide-twice daily formulation ; antiarrhythmic ; Procanbid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Procainamide is a class IA antiarrhythmic drug indicated for the treatment of life-threatening or symptomatic ventricular arrhythmias. The current sustained-release formulation requires 6-hour dosing (qid). To improve patient compliance, a new sustained-release formulation for twice-daily (bid) administration has been developed (Procanbid, Parke-Davis). This study assesses the pharmacologic equivalence of the bid and qid formulations in the suppression of symptomatic ventricular premature depolarizations (VPDs). Fourteen centers enrolled a total of 99 patients with frequent symptomatic VPDs (average ≥20 VPDs/hr) who previously responded to and tolerated the procainamide qid formulation. During the first week of the double-blind phase, patients were randomized to either placebo or procainamide dosages of 1000, 2000, or 4000 mg/d (bid or qid formulations). In the second week, the patients were crossed over to the alternate formulation. Seventy-seven patients qualified for the primary activity analysis. The bid and qid formulations showed comparable effectiveness in the suppression of mean VPDs with a linear dose-response relationship. The VPD suppression was not attenuated towards the end of the dosing interval for either formulation. Sixty-eight of these patients entered an optional 1-year extension to receive the bid formulation. Thirty-seven (54%) patients had adverse effects. Of those, 15 (22%) had side effects considered treatment related. Most of the adverse events occurred during the first 6 weeks of treatment. Only a few patients (8%) withdrew as a consequence of treatment with the bid formulation. The overall safety profile of the bid formulation was similar to other formulations, and the procainamide bid formulation has a low proarrhythmic rate (`3%). In conclusion, the effectiveness of the twice-daily formulation of procainamide in the suppression of VPDs is comparable to the currently available qid formulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007736931662
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    Paper (German National Licenses)
    Fulltext
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