Inhibition of ADP-induced platelet adhesion to immobilised fibrinogen by nitric oxide: evidence for cGMP-independent mechanisms.

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Characteristics, treatment patterns, and residual cardiovascular risk of patients with a first acute myocardial infarction: A nationwide population-based cohort study in Norway

There are few nationwide descriptive studies of longitudinal drug use and residual cardiovascular risk in patients with myocardial infarction (MI) in contemporary clinical practice. The objectives of this work were to describe characteristics and longitudinal cardiovascular drug use of patients with a first acute MI in Norway, and to quantify residual risks of cardiovascular events and death. Using nationwide health registries in Norway, we identified 43 750 adults with a first MI (2010 to 2015) and ≥1 prescription for antiplatelet medication. We described cardiovascular medication post-MI and calculated residual cardiovascular risks. Between 3 months and 13–15 months post MI, medication use dropped from 93.3% to 75.1% for low-dose aspirin, 78.1% to 11.0% for dual antiplatelet therapy, 91.6% to 78.7% for antihypertensives, and 88.0% to 70.7% for lipid-lowering therapy. Incidence rate ratios (IRRs) for recurrent MI were similar between subpopulations at 12 months and notably different at 12–36 months. IRRs (95% CIs) at 12–36 months were 1.52 (1.26–1.82) for 65–74 years, 2.26 (1.88–2.71) for 75–84 years, and 3.97 (3.29–4.79) for ≥85 years (vs. 18–49 years), 2.42 (2.18–2.69) for those with ischaemic heart disease (IHD), 2.26 (1.97–2.59) for peripheral artery disease (PAD), 2.17 (1.98–2.36) for hypertension, and 1.82 (1.65–2.01) for diabetes. In conclusion, secondary prevention medication use 13–15 months following a first MI is suboptimal among patients in Norway. The elderly and those with IHD, PAD, diabetes, or hypertension are at high-risk for recurrent MI/stroke/death and should be managed closely beyond the first year

Characteristics, treatment patterns, and residual cardiovascular risk of patients with a first acute myocardial infarction: A nationwide population-based cohort study in Norway

There are few nationwide descriptive studies of longitudinal drug use and residual cardiovascular risk in patients with myocardial infarction (MI) in contemporary clinical practice. The objectives of this work were to describe characteristics and longitudinal cardiovascular drug use of patients with a first acute MI in Norway, and to quantify residual risks of cardiovascular events and death. Using nationwide health registries in Norway, we identified 43 750 adults with a first MI (2010 to 2015) and ≥1 prescription for antiplatelet medication. We described cardiovascular medication post-MI and calculated residual cardiovascular risks. Between 3 months and 13–15 months post MI, medication use dropped from 93.3% to 75.1% for low-dose aspirin, 78.1% to 11.0% for dual antiplatelet therapy, 91.6% to 78.7% for antihypertensives, and 88.0% to 70.7% for lipid-lowering therapy. Incidence rate ratios (IRRs) for recurrent MI were similar between subpopulations at 12 months and notably different at 12–36 months. IRRs (95% CIs) at 12–36 months were 1.52 (1.26–1.82) for 65–74 years, 2.26 (1.88–2.71) for 75–84 years, and 3.97 (3.29–4.79) for ≥85 years (vs. 18–49 years), 2.42 (2.18–2.69) for those with ischaemic heart disease (IHD), 2.26 (1.97–2.59) for peripheral artery disease (PAD), 2.17 (1.98–2.36) for hypertension, and 1.82 (1.65–2.01) for diabetes. In conclusion, secondary prevention medication use 13–15 months following a first MI is suboptimal among patients in Norway. The elderly and those with IHD, PAD, diabetes, or hypertension are at high-risk for recurrent MI/stroke/death and should be managed closely beyond the first year

cGMP-independent inhibition of integrin alphaIIbbeta3- mediated platelet adhesion and outside-in signalling by nitric oxide

NoWe examined the influence of S-nitrosoglutathione (GSNO) on alpha(IIb)beta(3) integrin-mediated platelet adhesion to immobilised fibrinogen. GSNO induced a time- and concentration-dependent inhibition of platelet adhesion. Inhibition was cGMP-independent and associated with both reduced platelet spreading and protein tyrosine phosphorylation. To investigate the cGMP-independent effects of NO we evaluated integrin beta(3) phosphorylation. Adhesion to fibrinogen induced rapid phosphorylation of beta(3) on tyrosines 773 and 785, which was reduced by GSNO in a cGMP independent manner. Similar results were observed in suspended platelets indicating that NO-induced effects were independent of spreading-induced signalling. This is the first demonstration that NO directly regulates integrin beta(3) phosphorylation