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Background: The role of different endothelium-derived vasoactive substances in the regulation of coronary circulation during tachycardia is not well defined. In order to elucidate the contribution of prostacyclin to the adaptation of coronary blood flow to tachycardia, the effect of meclofenamate, a cyclooxygenase inhibitor on the coronary blood flow response to rapid atrial pacing was analyzed in a porcine model., Methods: A group of seventeen pigs were instrumented for coronary blood flow, aortic pressure and atrial pacing. Heart rate was increased by 20 beats every 5 minutes. Coronary blood flow and aortic pressure were measured, and coronary resistance calculated, basally and at each pacing interval, before and after saline serum (n = 6), meclofenamate 5 mg/kg, i.v. (n = 7) or meclofenamate 35 mg/kg, i.v. (n = 4)., Results: Neither saline nor meclofenamate modified the normal increase of coronary blood flow provoked by rapid atrial pacing (163 +/- 28% increase before versus 172 +/- 29% after saline; 159 +/- 21% increase before versus 161 +/- 22% after meclofenamate low doses and 201 +/- 39% before vs 172 +/- 36 after meclofenamate high doses). There were no differences in the response of coronary vascular resistance to tachycardia before and after meclofenamate (44% reduction vs 40% respectively)., Conclusion: Cyclooxygenase blockade does not modify the response of coronary circulation to rapid atrial pacing, suggesting that prostacyclin does not play a limiting role in the regulation of coronary blood flow during tachycardia in this model.

Background: Diagnostic of chest pain in the emergency services supposes a serious problem. This study wants objective if the new non enzymatic markers of myocardial necrosis (T troponin and I troponin) may be an aid for the diagnostic and prognostic stratification of patients with myocardial ischemia., Patients and Methods: 82 successive patients who went to the emergency room for chest pain were studied. Electrocardiogram and blood samples were obtained at 0,4, and 12 house of admission. A clinic-evolutive study was performed at discharge, and they were classified in 3 categories: a) myocardial infarction, b) unstable angina (Braunwald classification) and no coronary pains., Results: In the 27 patients with myocardial infarction the markers of troponin group were more sensitive than creatinine kinase to determine myocardial necrosis at 4 hours of admission. Of 41 patients with unstable angina, 34% were of Braunwald III-B class. Troponin group markers discriminate a group of high risk patients, 70% of the patients that need an emergency coronarography for bad clinical evolution were troponin group marker positive., Conclusions: The use in the emergency room of troponin necrosis markers (T and I troponin) allows to optimize the sanitary resources, detecting quickly the patients with acute myocardial infarction and discriminate a group of high risk of patients with angina.

Background: The role of endogenous nitric oxide as mediator of flow-dependent dilation is well established. However, its role in the adaptation of coronary blood flow to tachycardia is less well defined. This study was designed to determine whether nitric oxide is a mediator in pacing-induced hyperaemia., Methods: Twenty pigs were instrumented for coronary blood flow, aortic pressure and atrial pacing measurements. Their heart rate was increased by 20 beats every 5 min. Coronary blood flow was measured basally and at each pacing interval before and after each of the following interventions: intracoronary saline infusion (n = 6), N omega-nitro-L-arginine methyl ester infusion (L-NAME, 20 micrograms/kg per min intracoronarily, n = 9) and infusion of L-NAME plus L-arginine (0.3 mg/kg per min intracoronarily, n = 5)., Results: The coronary peak flow increased with atrial pacing. The maximum increase in coronary blood flow with pacing was significantly reduced after infusion of L-NAME (159 +/- 33 versus 143 +/- 30%), whereas no change was observed in the saline group (163 +/- 28 versus 172 +/- 29%). However, it increased significantly in the group receiving L-NAME plus L-arginine (147 +/- 29 versus 182 +/- 40%)., Conclusions: In the pig, the increase in coronary blood flow and therefore the vasodilation of the microvasculature that accompanies tachycardia depend, partly, on the release of endogenous nitric oxide.