title: Arterial stiffness and pharmacological interventions--the TRanscend arterial stiffNess Substudy (TRANS study).
abstract: The degree of arterial stiffness is correlated with the risk of cardiovascular diseases and it is a powerful predictor for morbidity and mortality. Studies have shown that arterial stiffness reduction is associated with an improvement in survival. Reduction of arterial stiffness by pharmacological drugs varies according to the drugs and doses used and duration of treatment. This effect on the arteries differs among the various classes of drugs and among individual drugs in the same class. Quantification of the stiffness and other properties of the arterial wall can be used to monitor the responses to therapy in individuals with hypertension and other cardiovascular diseases. These measures can then be used as surrogate markers for the risk of clinical events. Inhibition of the renin-angiotensin system (RAS) is associated with an important decrease in cardiovascular risk. Findings from clinical trials support the hypothesis that the protective effects of RAS inhibition are partly independent from blood pressure reduction and related to several mechanisms including vascular protective effects. The aim of the TRanscend Arterial stiffNess Substudy (TRANS) is to assess the effect of an angiotensin II receptor blocker (ARB), telmisartan, on the arterial stiffness in a subgroup of patients from the Telmisartan Randomized Assessment Study in aCE iNtolerant subjects with cardiovascular Disease (TRANSCEND) trial. The TRANSCEND trial is an international, multicenter, randomized double blind placebo controlled trial oftelmisartan that enrolled patients at high risk for cardiovascular events. Some clinical baseline data of the TRANS substudy are reported. When completed, the results of the TRANS substudy will show whether the beneficial effects of treatment with telmisartan on cardiovascular outcome may be related to an improvement in arterial stiffness.
authors.affiliation: The CardioVascular Institute, Paris, France.
authors.forename: Jirar
authors.initials: J
authors.lastname: Topouchian
authors.forename: Ramzi
authors.initials: R
authors.lastname: El Feghali
authors.forename: Bruno
authors.initials: B
authors.lastname: Pannier
authors.forename: Shuyu
authors.initials: S
authors.lastname: Wang
authors.forename: Feng
authors.initials: F
authors.lastname: Zhao
authors.forename: Karel
authors.initials: K
authors.lastname: Smetana
authors.forename: Koon
authors.initials: K
authors.lastname: Teo
authors.forename: Roland
authors.initials: R
authors.lastname: Asmar
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects* / Q000503:physiopathology; D001562:Benzimidazoles / Q000627:therapeutic use*; D001565:Benzoates / Q000627:therapeutic use*; D001783:Blood Flow Velocity / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects; D002318:Cardiovascular Diseases / Q000503:physiopathology / Q000517:prevention & control*; D019963:Clinical Chemistry Tests; D004311:Double-Blind Method; D004548:Elasticity; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D000077333:Telmisartan; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D001562:Benzimidazoles; D001565:Benzoates; D000077333:Telmisartan