Accupril-Accupro scientific update |
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J Renin Angiotensin Aldosterone Syst. 2007 Mar;8(1):13-22.
Donnelly R, Manning G.
Derby City General Hospital, Derby, DE22 3DT, UK.
Angiotensin-converting enzyme inhibitors and coronary heart disease prevention.
The so-called ACE inhibitor drugs
(quinapril and several others) have
been shown in a number of studies to
be beneficial for patients suffering
from many classes of heart problems.
However there are some differences
between the findings of the
different studies which are still
unexplained. The authors review some
of these unresolved questions. / / / / / A number of large randomised controlled trials have shown that angiotensin-converting enzyme (ACE) inhibitors,
compared with placebo or other blood pressure-lowering drugs, improve coronary heart disease outcomes (fatal and
non-fatal myocardial infarction, and coronary revascularisation) in diverse patient groups, e.g. in primary and
secondary prevention, those with and without left ventricular dysfunction, and among hypertensive and
non-hypertensive subjects. An updated meta-regression analysis which included five major trials in patients with
established coronary artery disease (CAD) (EUROPA, INVEST, ACTION, PEACE and CAMELOT) concluded that ACE inhibitor
(ACE-I) therapy has clear benefits in secondary prevention, but there are important and unexplained differences
between trials in clinical outcome, baseline cardiovascular risk, blood pressure changes and trial design which
deserve further discussion of the underlying mechanisms and clinical interpretation. For example, in
placebo-controlled trials the biggest (2022%) reductions in primary end points (including mortality) have been
observed with perindopril and ramipril, whereas trials using trandolapril and quinapril had no effect on survival
or recurrent CAD events. This review summarises and compares the major findings of these recent trials, and
provides further analysis of the underlying mechanisms and clinical significance of secondary CAD prevention with
ACE-I therapy.
Cardiovasc Drugs Ther. 2007 Apr 3
Egido J, Ruiz-Ortega M.
Vascular and Renal Laboratory Fundacion Jimenez Diaz, Autonoma University Madrid, Avda. Reyes Catolicos 2, Madrid, Spain
Anti-inflammatory Actions of Quinapril.
This study looks at the effects
of Quinapril, one of the class of
ACE-inhibitor drugs, in treating a
number of diseases involving
inflammation. / / / / / OBJECTIVE: The role of angiotensin II (Ang-II) in inflammation and the mechanisms through which it exerts this role
are explored. Signaling through angiotensin stimulation of inflammatory cells often amplifies inflammation.
Formation of Ang-II from tissue angiotensin-converting enzyme (ACE) has been shown to be of greater importance in
the development and progression of inflammatory diseases than plasma ACE. CONCLUSION: Quinapril, which is a potent
and selective inhibitor of both plasma and tissue ACE, has demonstrated anti-inflammatory properties in many
disease states such as atherosclerosis, nephritis, scleroderma, diabetes and arthritis, and, thus, offers new
therapeutic possibilities for disease treatment.
Hum Hypertens. 2007 Apr 26;
Aznaouridis KA, Stamatelopoulos KS, Karatzis EN, Protogerou AD, Papamichael CM, Lekakis JP.
1Vascular Laboratory, Department of Clinical Therapeutics, Athens Medical School, Alexandra Hospital, Athens, Greece.
Acute effects of renin-angiotensin system blockade on arterial function in hypertensive patients.
This paper reports results from
an experimental study on the
short-term effects of quinapril and
two similar drugs on detailed
parameters of blood-flow, in patients
suffering from high blood-pressure.
Quinapril appeared to be more
effective than the other drugs in its
efects on the measured parameters. / / / / / The acute effects of the renin-angiotensin system (RAS) blockers may be important in some clinical settings. To
assess the acute impact of such drugs on arterial function, we studied the effects of captopril 25 mg, quinapril 20
mg and telmisartan 80 mg on 100 hypertensive patients, according to a randomized, double-blind, placebo-controlled
study. Central (aortic) blood pressure (BP) and augmentation index (AIx, a measure of wave reflections), as well as
flow-mediated dilatation (FMD) of the brachial artery and forearm blood flow (FBF) (measures of conduit and
resistance artery endothelial function, respectively), were evaluated before and 2 h after oral drug
administration. Compared to placebo, captopril and quinapril decreased central systolic (by 7.5 mm Hg, P<0.05 and
by 12.3 mm Hg, P<0.001) and diastolic BP (by 4.9 mm Hg, P<0.01 and by 8.4 mm Hg, P<0.001), whereas telmisartan had
no significant effect (P=NS). Additionally, AIx was reduced after quinapril (absolute decrease of 7.2%, P<0.01) and
marginally after captopril (decrease of 4.7%, P=0.07). Only quinapril led to a beneficial change of FMD (absolute
increase of 2.7%, P<0.001). No treatment was related to significant changes of peak hyperaemic or 3-min hyperaemic
FBF. In adjusted analyses, all the favourable alterations induced by quinapril were independent of potential
confounding haemodynamic factors. Our data show that acute RAS inhibition with quinapril (20 mg) may be more
beneficial in terms of arterial function and central haemodynamics compared to captopril (25 mg) or telmisartan (80
mg). Further studies are needed to investigate whether these acute arterial effects of quinapril are clinically
significant.
J Thromb Haemost. 2006 Aug 14;
Undas A, Brummel-Ziedins KE, Potaczek DP, Stobierska-Dzierzek B, Bryniarski L, Szczeklik A, Mann KG.
Department of Medicine, Institute of Cardiology, Jagellonian University School of Medicine, Krakow, Poland.
Atorvastatin and quinapril inhibit blood coagulation in patients with coronary artery disease following a 28-day therapy.
The authors studied the
anti-coagulation effects of two drugs
(quinapril and atovastatin), alone
and in combination with each other,
in treating patients with coronary
heart-disease. Either drug produced
benefits when used alone. However,
the effect of continued therapy with
a treatment involving both drugs
together depended on which of the two
drugs had been used in the initial
phase of treatment. / / / / / Objectives: We evaluated the antithrombotic effects of statins and angiotensin-converting enzyme inhibitor (ACEI) drugs in patients with coronary artery disease (CAD). Methods and Results: Blood coagulation at the site of microvascular injury was assessed in 26 males with CAD before and after quinapril (10 mg/d; n=13) or atorvastatin (40 mg/d; n=13) for 4 weeks and an additional 4 weeks of combined therapy (quinapril + atovastatin). Rates of prothrombin and factor (FV) activation, fibrinogen cleavage, and FVa inactivation showed that both quinapril and atovastatin decreased rates of formation of: thrombin B-chain (by 30.6%, p=0.007 and 34.3%, p=0.003), thrombin-antithrombin complexes (by 30.4%, p=0.0002 and 40%, p=0.001), FV activation (by 19.1%, p=0.03 and 21.8%, p=0.005) and fibrinogen depletion (by 29.2%, p=0.004 and 32.7%, p=0.001). Atorvastatin alone accelerated FVa inactivation (p=0.005). A further 4 weeks of combined therapy enhanced most anticoagulant effects only when atorvastatin was added to quinapril. Conclusions: In CAD patients, atorvastatin and quinapril slowed blood clotting at the site of microvascular injury after 28 days of therapy. Addition of atorvastatin to quinapril, but not quinapril to the statin, enhanced the anticoagulant effects. Our findings might help explain the reduced risk of myocardial infarction or stroke in patients treated with statins and/or ACEIs and the lack of clinical benefits from ACEI added to prior statin therapy in patients at cardiovascular risk.
Clin Cardiol. 2004 Aug;27(8):480-4.
Sipahi I, Tekin G, Yigit Z, Guzelsoy D, Guven O.
Department of Cardiology, Cardiology Institute, Istanbul University, Istanbul, Turkey.
Effect of quinapril on the attenuated heart rate recovery of type 2 diabetic subjects without known coronary artery disease.
The authors observe that
sufferers from diabetes are known
have poorer heart-performance in a
particuar detailed aspect, compared
to healthy persons. They hypothesised
that dosage with quinapril would
improve this heart-parameter; and
their experiments proved that this
was in fact true. However, although
in this respect the diabetic patients
appeared to become "healthier", it
remains unproven as to whether they
will actually gain long-term benefits
in terms of survival. / / / / / BACKGROUND: Heart rate (HR) recovery at 1 min is a measure of the vagal reactivation that occurs after cessation of exercise. Despite ample evidence about the association of attenuated HR recovery with increased mortality, pharmacologic modification of this predictor has not been shown. On the other hand, angiotensin-converting enzyme (ACE) inhibitors are known to have vagomimetic activity. HYPOTHESIS: We hypothesized that ACE inhibition would increase HR recovery in a group of subjects known to have reduced HR recovery, namely diabetics. METHODS: Maximal treadmill exercise stress test was performed in 31 type 2 diabetic and 31 nondiabetic male subjects with similar age, body mass index, and hypertensive status. None of the subjects had known heart disease or evidence of myocardial ischemia during the test. The diabetic subjects, after 2 weeks of treatment with quinapril, underwent a second exercise test. A third test was performed 2 to 3 weeks after cessation of quinapril treatment. RESULTS: At baseline, despite similar exercise capacity, the diabetics had a lower HR recovery at 1 min than nondiabetics (25 +/- 8 vs. 31 +/- 8 beats/min, p < 0.01). Quinapril significantly increased HR recovery at 1 min in diabetics (25 +/- 8 beats/min at baseline vs. 28 +/- 8 beats/min with quinapril vs. 25 +/- 7 beats/min off-therapy, p < 0.01 by analysis of variance). CONCLUSIONS: The attenuated HR recovery of type 2 diabetics can be improved by quinapril. Whether the improvement in HR recovery with ACE inhibition can lead to decreased mortality is currently unknown.
Kidney Blood Press Res. 2005 Mar 1;28(2):111-116.
Uchiyama-Tanaka Y, Mori Y, Kishimoto N, Fukui M, Nose A, Kijima Y, Yamahara H, Hasegawa T, Kosaki A, Matsubara H, Iwasaka T.
Department of Medicine II, Kansai Medical University, Osaka, Japan.
Comparison of the Effects of Quinapril and Losartan on Carotid Artery Intima-Media Thickness in Patients with Mild-to-Moderate Arterial Hypertension.
The authors compared the effects
of long-term (1-year) treatment using
quinapril, and another drug of a
different type, in patients with high
blood pressure. They monitored not
only blood-pressure but also another
artery-parameter which is associated
with atherosclerosis. Both drugs were
equally effective in controlling
blood-pressure, but quinapril was
more potent in modifying the other
parameter. However other
atherosclerotic factors did not
change. / / / / / Background: Ultrasonographic evidence of increased carotid intima-media thickness (IMT) is known to be associated with generalized atherosclerosis. Therapeutic blockade of the renin-angiotensin system (RAS) with angiotensin-converting enzyme (ACE) inhibitors reportedly reduces carotid IMT in humans. However, there has been no head-to-head comparison of the effects of ACE inhibitor and angiotensin receptor blocker (ARB), a newer type of RAS inhibitor, on carotid IMT. Methods: 57 hypertensive patients were randomly assigned to treatment with one of two antihypertensive drugs: ACE inhibitor (quinapril; n = 25, group Q) or ARB (losartan; n = 18, group L). Results: After 1 year of treatment, a similar decrease in mean blood pressure was observed in all groups. Carotid IMT was decreased significantly in group Q (10% decrease, p < 0.05) but did not change in group L. There were no significant changes in other atherosclerotic factors between these two groups. Conclusion: Our findings suggest that the antiatherosclerotic effect of quinapril is more potent than that of losartan in hypertensive patients. This effect appears unrelated to the drug's antihypertensive action or to traditional atherosclerotic factors. Copyright (c) 2005 S. Karger AG, Basel.
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Drug category:Hypotensive agents
Accupril-Accupro scientific update
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