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upcl.univ-lyon1.fr

Cardiovascular risk reduction in diabetic patients is a multidimensional task. Long-term decrease of glycaemia by the use of insulin or sulfonylureas had disappointing effects on cardiovascular events, whereas metformin effects are ambiguous. On the contrary, controlling risk factors like hypertension or hypercholesterolaemia decrease the incidence of cardiovascular events in diabetic as in non-diabetic patients. Similarly, clinical trials have shown the efficacy of treatments that decrease cardiovascular risk whatever the cause, such as antiplatelet drugs in secondary prevention and high-dose ramipril in secondary prevention or in hypertensive patients. The absolute benefit conferred by efficient therapies is higher in diabetic patients because they are at an increased risk of events compared with their non-diabetic counterparts.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11795124&dopt=Abstract




Arch Cardiol Mex. 2001 Oct-Dec;71(4):278-85.
[Significance of angiotensin converting enzyme (ACE) in coronary circulation]

[Article in Spanish]

Mauer Diaz K, Exaire Murad JE, Escalante Acosta BA.

Departamento de Biomedicina Molecular del Centro de Investigacion y de Estudios Avanzados del Instituto Politecnico Nacional, Mexico D.F.

It has been suggested that angiotensin II can be synthesized by other enzymatic pathways besides angiotensin converting enzyme. We evaluated the importance of angiotensin converting enzyme in the coronary circulation during the development of hypertension. Hearts obtained from normotensive (n = 4) and hypertensive rats (n = 4) as well as from hypertensive rats treated with ramipril (n = 4) were stimulated with either angiotensin II or angiotensin I. In a Langendorff perfusion system, angiotensin II induced a greater dose-dependent coronary vasoconstriction in the hearts of hypertensive rats than in normotensive rats (p < 0.05). Furthermore, angiotensin I also induced coronary vasoconstriction, which was greater in the hearts of hypertensive rats than in normotensive rats (p < 0.05). Acute angiotensin converting enzyme inhibition reduced angiotensin I-induced vasoconstriction by 78% in the hearts of normotensive rats and by 82% in the hypertensive rats (p < 0.05), whereas in vivo angiotensin converting enzyme inhibition potentiated angiotensin I-induced vasoconstriction in the hearts of normotensive and hipertensive rats (p < 0.05). Bradykinin receptor's blockade decreased ramiprilat's inhibitory effect on angiotensin I-induced vasoconstriction (p < 0.05). Thus, the present study suggests that, in coronary circulation, angiotensin II synthesis is mainly angiotensin converting enzyme dependent. However, chronic in vivo inhibition could favor induction of other enzymes involved in angiotensin II synthesis. Evenmore, it is possible that the effect of angiotensin converting enzyme inhibition in coronary circulation depends on bradykinin activity.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11806030&dopt=Abstract

medforsk.mas.lu.se

OBJECTIVE: To assess the effects of a 6-month angiotensin-converting enzyme (ACE) inhibitor intervention on myocardial ischaemia. METHOD: We randomized 389 patients with stable coronary artery disease to double-blind treatment with ramipril 5 mg/day (n = 133), ramipril 1.25 mg/day (n = 133), or placebo (n = 123). Forty-eight-hour ambulatory electrocardiography was performed at baseline, and after 1 and 6 months. RESULTS: Relevant baseline variables were similar in all groups. Changes over 6 months in duration of >/= 1 mm ST-segment depression (STD), total ischaemic burden and maximum STD did not differ significantly between the treatment groups. There was no difference in the frequency of adverse events between the groups. CONCLUSION: ACE inhibitor treatment has little impact on incidence and severity of myocardial ischaemia in patients with stable ischaemic heart disease.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11806779&dopt=Abstract [PubMed - as supplied by publisher]













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