Impact of telmisartan in modifying vascular risk

Telmisartan, a selective angiotensin II type 1 receptor blocker (ARB), has been investigated in many trials, in particular, in order to assess its antihypertensive effect in various situations and its ability to protect organs susceptible to hypertension. In addition to its antihypertensive properties, it has positive metabolic and vascular effects (partly because of its sustained action). Several large-scale trials have focused on the effect of telmisartan on cardiovascular morbidity and mortality, including comparisons of that with an angiotensin-converting enzyme inhibitor in subjects at high vascular risk. Telmisartan was used in the largest ARB research programme (the Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial [ONTARGET] and Telmisartan Randomized Assessment Study in ACE Intolerant Subjects with Cardiovascular Disease [TRANSCEND] trial)

Influence des facteurs génétiques et du stress oxydatif sur les variations du baroréflexe chez les sujets sains et les patients hypertendus

NANCY1-SCD Medecine (545472101) / SudocSudocFranceF

Engagement des patients sous traitement anticoagulant oral dans le suivi des recommandations médicales

International audienc

Platelet hyperactivity during exercise leading to iterative coronary stent thrombosis: clinical implications.

International audienceExercise may induce platelet activation in spite of using antiplatelet treatment. We present a case where the initial acute coronary syndrome and the iterative stent thrombosis always occurred after intense and prolonged physical effort. For this patient the at rest response to platelet inhibition with antiplatelet treatments was assessed as adequate, but after exercise the patient developed platelet activation which could be the trigger of his stent thrombosis

Resistance to platelet antiaggregants: an important cause of very late thrombosis of drug eluting stents? Observations from five cases.

International audienceBACKGROUND: Very late thrombosis of drug eluting stents is a rare complication that might be triggered by resistance to platelet antiaggregants (PAAs). AIM: Following an initial case where clinical data strongly suggested resistance to PAAs, we carried out a prospective systematic analysis of platelet aggregation in four subsequent cases of late thrombosis. METHODS: Resistance to aspirin was investigated with the PFA-100 test employing a collagen-epinephrine cartridge (Platelet Function Analyzer; Dade Behring). Resistance to clopidogrel was determined by flow cytometry of intraplatelet vasodilator-stimulated phosphoprotein (VASP) phosphorylation. RESULTS: All four cases showed resistance to either aspirin or clopidogrel, and two cases showed dual resistance to both of these PAAs. CONCLUSION: Analysis of platelet function in a patient with late stent thrombosis is useful and may allow adaptation of subsequent patient management. The value of monitoring platelet function after implantation of a drug eluting stent should be evaluated in prospective studies

A single intravenous sTNFR-Fc administration at the time of reperfusion limits infarct size--implications in reperfusion strategies in man.

International audienceBACKGROUND: Reperfusion of the ischemic myocardium is associated with increased inflammatory processes that can exert deleterious effects and therefore contribute to cardiac dysfunction. The aim of the present study was to verify whether the administration of sTNFR-Fc, a scavenger of the pro-inflammatory cytokine TNF-alpha, at the time of reperfusion would protect against myocardial infarction and reduce the severity of early mechanical dysfunction. METHODS: Male Wistar rats were subjected to 60 min coronary occlusion followed by reperfusion. A bolus of sTNFR-Fc (10 microg/kg, i.v.) (MI + sTNFR-Fc group) or a placebo (MI group) was injected prior to reperfusion. Cardiac geometry was assessed by echocardiography 1, 3 and 7 days after reperfusion. Eight days after reperfusion, left ventricular (LV) function was evaluated under basal conditions and during an experimental challenge of volume overload. Finally, infarct size was measured after euthanasia. RESULTS: sTNFR-Fc administration markedly reduced infarct size (P < 0.01) and decreased LV dilation as assessed by the echocardiographic measurement of the LV end diastolic area, 7 days post-MI (P < 0.01). Moreover, LV end-diastolic pressure was significantly preserved by sTNFR-Fc 1 week after myocardial infarction, under basal conditions (P < 0.05) as well as during cardiac overload (P < 0.05). CONCLUSION: A single administration of sTNFR-Fc at the time of reperfusion after myocardial infarction is able to limit infarct size and to reduce early LV diastolic dysfunction in rats. These findings suggest that intravenous neutralization of TNF-alpha during surgical cardiac reperfusion might improve the outcome of myocardial infarction in humans