20 research outputs found
Effects of Aspirin on Endothelial Function and Hypertension
PURPOSE OF REVIEW: Endothelial dysfunction is intimately related to the development of various cardiovascular diseases, including hypertension, and is often used as a target for pharmacological treatment. The scope of this review is to assess effects of aspirin on endothelial function and their clinical implication in arterial hypertension. RECENT FINDINGS: Emerging data indicate the role of platelets in the development of vascular inflammation due to the release of proinflammatory mediators, for example, triggered largely by thromboxane. Vascular inflammation further promotes oxidative stress, diminished synthesis of vasodilators, proaggregatory and procoagulant state. These changes translate into vasoconstriction, impaired circulation and thrombotic complications. Aspirin inhibits thromboxane synthesis, abolishes platelets activation and acetylates enzymes switching them to the synthesis of anti-inflammatory substances. SUMMARY: Aspirin pleiotropic effects have not been fully elucidated yet. In secondary prevention studies, the decrease in cardiovascular events with aspirin outweighs bleeding risks, but this is not the case in primary prevention settings. Ongoing trials will provide more evidence on whether to expand the use of aspirin or stay within current recommendations
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The effect of sentence accent on non-native speech perception in noise
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162038.pdf (publisher's version ) (Open Access)INTERSPEECH, 08 september 201
Daytime pulmonary hypertension in patients with obstructive sleep apnea - The effect of continuous positive airway pressure on pulmonary hemodynamics
Background. Limited information exists regarding the development of
pulmonary hypertension in patients with obstructive sleep apnea (OSA) in
the absence of lung and heart comorbidity. Objectives: The aims of this
study were to investigate whether OSA patients without any other cardiac
or lung disease develop pulmonary hypertension, and to assess the effect
of continuous positive airway pressure (CPAP) treatment on pulmonary
artery pressure (P-PA). Methods: Twenty-nine patients aged 51 +/- 10
years with OSA and 12 control subjects were studied with pulsed-wave
Doppler echocardiography for estimation Of P-PA before and after 6-month
effective treatment with CPAP. Results: A significantly higher mean P-PA
was found in OSA patients as compared to control subjects (17.2 +/- 5.2
vs. 12.1 +/- 1.9 mm Hg, p < 0.001). Six out of the 29 OSA patients had
mild pulmonary hypertension (P-PA greater than or equal to 20 mm Hg).
Significant differences were observed between pulmonary hypertensive and
normotensive OSA patients with respect to age (62 +/- 4 vs. 48 +/- 15
years, respectively, p < 0.05), body mass index (41 +/- 7 vs. 32 +/- 4
kg/m(2), p < 0.02) and daytime PaO2 (81 +/- 9 vs. 92 +/- 9 mm Hg, p <
0.05). CPAP treatment was effective in reducing mean PPA in both groups
of pulmonary hypertensive and normotensive OSA patients (decreases in
P-PA from 25.6 +/- 4.0 to 19.5 +/- 1.5 mm Hg, p < 0.001; from 14.9 +/-
2.2 to 11.5 +/- 2.0 mm Hg, respectively, p < 0.001). Conclusions: A
proportion (20.7%) of OSA patients without any other lung or heart
disease and characterized by older age, greater obesity and lower
daytime oxygenation develop mild pulmonary hypertension which has been
partially or completely reversed after 6-month CPAP treatment. In
conclusion, OSA alone constitutes an independent risk factor for the
development of pulmonary hypertension. Copyright(C)2001 S. KargerAG,
Basel