c'est ma conviction à la lecture de nombreuses conf ou articles à ma disposition
Voilà en partie la conclusion de l'article paru dans le journal of cardiology 09/09 ,certains vont le découvrir ,d'autres le connaissent déjà
"In patients with osteoarthritis and hypertension, the nondetrimental
impact of naproxcinod on BP is probably due to
its NO-donating properties. As noted previously,1,8 naproxcinod
is rapidly cleaved to naproxen and an NO-donating
moiety. The exogenous release of NO would be expected to
reduce vascular smooth muscle contractility, leading to a
reduction in systemic vascular resistance and BP.2,3 This
property of naproxcinod should provide an effective countermechanism
to the antiprostacyclin effects typically seen
with the traditional NSAIDs.
A major focus of clinical research associated with the
traditional NSAIDs and cyclooxygenase-2-selective inhibitors
has been the potential destabilization of BP in patients
with hypertension who are receiving antihypertensive drugs, in
particular the angiotensin-converting enzyme inhibitors or angiotensin
receptor blockers, # blockers, and diuretics.9 In
patients taking renin-angiotensin blocking agents, some of
the NSAIDs and cyclooxygenase-2 inhibitors have been
shown to destabilize systolic BP control by 3 to 8 mm
Hg.10–14 In a large trial using clinic systolic BP as the
primary end point,5 rofecoxib 25 mg/day induced significant
increases in systolic BP in patients who were taking angiotensin-
converting enzyme inhibitors and # blockers but not
in those who were taking calcium antagonists. Similarly, in
the present study, destabilization of systolic BP was more
frequent in patients randomized to naproxen compared to
those randomized to naproxcinod when they were treated
with a blocker of the RAS (Figure 1, Table 3). These results
support the notion that RAS-blocking drugs depend on
vascular prostacyclin and/or NO as part of their mechanism
of action.6,11–13 Additionally, calcium antagonists and other
non–RAS blockers may not be affected by increases in total
body sodium associated with the antinatriuretic effects of
NSAIDs, as are the RAS-blocking drugs.
Meta-analyses of traditional NSAIDs from the early
1990s suggested that NSAIDs could increase mean arterial
pressure by an average of 5 to 6 mm Hg in patients with
hypertension.15,16 The impact of these relatively small differences
(i.e., #5 mm Hg) in systolic BP in patient populations
with hypertension and vascular diseases has been
demonstrated in epidemiologic and large prospective clinical
trials.17–19 Differences of 3 to 4 mm Hg in systolic BP
control in an older population of patients with hypertension
with vascular diseases randomly assigned to 2 antihypertensive
treatment groups (amlodipine vs valsartan) resulted in a
significant relative increase in cardiac events of #40% in the
less well controlled group (valsartan recipients) during the first
6 months of the trial.19 The present study demonstrated that
naproxcinod was less likely to destabilize the control of
systolic BP compared to naproxen (Figure 3) and behaved
in a similar fashion to placebo in the entire study group as
well as in patients treated with antihypertensive therapies
involving blockade of the RAS. This has important implications,
because most patients with hypertension are treated
with #1 of these agents in modern-day clinical practice.20
In conclusion, we would infer that the hypertensive burden
induced by traditional NSAIDs in patients with osteoarthritis
and hypertension could be reduced by an NO-donating
agent such as naproxcinod."
je rajouterai mème que c'est dans l'interet èconomique pour les responsables puisque je cite
"Selon William J. Elliott, professeur de médecine interne et de Rhumatologie à Rush University à Chicago, si une méthode pour traiter l'arthrose qui ne faisait pas augmenter la PAS de 3.1 mmHg était disponible en 2009, cela permettrait de sauver 128 000 morts liées à des accidents cardiovasculaires et 3.2 milliards de dollars aux Etats-Unis."
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"RESULTS: As expected the cost savings and QALY benefits associated with
avoided cardiovascular events increased with the level of RRR and
10-year absolute CV risk. Potential cost savings ranged from GBP 181 to GBP 1,591, whereas the QALY benefits ranged from 0.05 to 0.44.
CONCLUSIONS: An NSAID with an improved BP profile has the potential to provide significant health economic benefits, especially in patientswith elevated CV risk." p pfister holmstrom