The HEART score provides the clinician with a quick and reliable predictor of outcome, without computer-required calculating. Low HEART scores (0-3), exclude short-term MACE with >98% certainty. In these patients one might consider reserved policies. In patients with high HEART scores (7-10) the high risk of MACE may indicate more aggressive policies.

No abstract

The HEART score helps in making accurate diagnostic and therapeutic decisions without the use of radiation or invasive procedures. The HEART score is an easy, quick, and reliable predictor of outcome in chest pain patients and can be used for triage.

1 We evaluated the role of SH-groups in improvement of endothelial dysfunction with ACEinhibitors in experimental heart failure. To this end, we compared the vasoprotective e ect of chronic treatment with zofenopril (plus SH-group) versus lisinopril (no SH-group), or Nacetylcysteine (only SH-group) in myocardial infarcted (MI) heart failure rats. 2 After 11 weeks of treatment, aortas were obtained and studied as ring preparations for endothelium-dependent and -independent dilatation in continuous presence of indomethacin to avoid interference of vasoactive prostanoids, and the selective presence of the NOS-inhibitor L-NMMA to determine NO-contribution. 3 Total dilatation after receptor-dependent stimulation with acetylcholine (ACh) was attenuated (749%, P50.05) in untreated MI (n=11), compared to control rats with no-MI (n=8). This was in part due to impaired NO-contribution in MI (750%, P50.05 versus no-MI). At the same time the capacity for generation of biologically active NO after receptor-independent stimulation with A23187 remained intact. 4 Chronic treatment with n-acetylcysteine (n=8) selectively restored NO-contribution in total dilatation to ACh. In contrast, both ACE-inhibitors fully normalized total dilatation to ACh, including the part mediated by NO (no signi®cant di erences between zofenopril (n=10) and lisinopril (n=8)). 5 Zofenopril, but not lisinopril, additionally potentiated the e ect of endogenous NO after A23187-induced release from the endothelium (+100%) as well as that of exogenous NO provided by nitroglycerin (+22%) and sodium nitrite (+36%) (for all P50.05 versus no-MI). 6 We conclude that ACE-inhibition with a SH-group has a potential advantage in improvement of endothelial dysfunction through increased activity of NO after release from the endothelium into the vessel wall. Furthermore, this is the ®rst study demonstrating the selective normalizing e ect of Nactylcysteine on NO-contribution to ACh-induced dilatation in experimental heart failure.

Cardiac ACE is activated in the early stage after induction of heart failure and is related to the amount of dysfunction. ACE in the kidney is activated only in the chronic stage. The cardiac renin-angiotensin system therefore already appears to be an important neurohumoral adjustment in the early stage of heart failure and is thereby a suitable target for early intervention by ACE inhibitors.