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      Catecholaminergic Activation in Acute Myocardial Infarction: Time Course and Relation to Left Ventricular Performance


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          Aim: The study was designed to assess (1) the time course of catecholaminergic activation in acute myocardial infarction (AMI) as estimated by adrenaline (ADR) and noradrenaline (NOR) concentrations, and (2) to relate activation of these hormones to predict the outcome of cardiac performance. Patients and Methods: Eighteen patients with first AMI were studied. Blood samples were drawn within the first 4–18 h, after 18–24 h, on day 2, day 3 and on day 6 as well as after 1 year. Radionuclide ventriculography was performed on the day of discharge and after 1 year to determine left-ventricular ejection fraction (LVEF). Results: In the study group as a whole, the concentrations of ADR decreased from (mean ± SEM) 0.80 ± 0.12 nmol/l on admission to 0.33 ± 0.03 nmol/l at discharge (p < 0.05). NOR decreased from 4.19 ± 0.78 to 2.44 ± 0.33 nmol/l (p < 0.05). Initial peak concentrations of both ADR and NOR on admission were correlated to LVEF at discharge (r = –0.56, p < 0.05 and r = –0.72, p < 0.05, respectively). If NOR was normal (<3 nmol/l) at admission, the LVEF was normal or almost normal (= 0.46) at discharge. The mean plasma level of ADR and NOR after 1 year follow-up was 0.34 ± 0.04 and 1.95 ± 0.25 nmol/l, respectively. The values after 1 year were unchanged compared to values at discharge, at day 6 (n.s.). Mean LVEF was 0.50 ± 0.03 (range: 0.23–0.69) at discharge and unchanged 0.46 ± 0.05 (range: 0.18–0.72) at 1 year follow-up (n.s.). During hospitalisation, the group with LVEF <0.50 had an 86% higher initial ADR and an 82% higher initial NOR concentration compared to values in patients with LVEF >0.50 (p < 0.05). Conclusion: (1) Catecholaminergic activation, as measured by plasma ADR and NOR in AMI, is acute and restricted to the first 5 days. Thereafter, the hormone levels are normal and stable. (2) The magnitude of the early catecholaminergic activation correlates with left ventricular systolic performance. (3) Normal NOR values at admittance predicts normal or almost normal LVEF at discharge.

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          Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial

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            Serial plasma catecholamine response early in the course of clinical acute myocardial infarction: relationship to infarct extent and mortality.

            Clinical and experimental evidence suggest that sympathoadrenal activation contributes to mortality in patients with ischemic heart disease. To determine the level of sympathoadrenal activation in the very early phase of acute myocardial infarction (AMI) and to determine if location of infarction (anterior versus inferior) was related to sympathoadrenal activation, we studied norepinephrine (NE) and epinephrine (E) within 4 hours after the onset of symptoms and prior to any rise in plasma creatine kinase (CK). Mean (+/- SE) initial (NE = 591 +/- 111 pg/ml and E = 73 +/- 19 pg/ml), peak (NE = 1356 +/- 178 and E +/- 1098 +/- 608) and average (NE = 815 +/- 142 and E = 252 +/- 68) plasma catecholamine concentrations were considerably above normal (NE = 228 +/- 10 and E = 34 +/- 2 pg/ml, n 60) and values were similar for inferior and anterior infarctions. During an 18-month follow-up, three patients died in whom the AMI mean NE and E and peak CK were higher than in the eight late survivors. Thus the three AMI patients with peak EP values greater than 1000 died, whereas the eight AMI patients with peak EP values less than 1000 survived (p less than 0.01). The magnitude of sympathoadrenal activation early in the course of clinical AMI appeared related to the extent of myocardial damage and late mortality.
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              Systemic and cardiac catecholamines during elective PTCA and during immediate PTCA for acute myocardial infarction.

              This study investigated arterial and coronary venous catecholamine concentrations in patients undergoing either elective coronary angioplasty (PTCA) or direct PTCA for acute myocardial infarction. We included 17 patients with stenoses of the left anterior descending coronary artery (LAD) and 10 patients with acute anterior myocardial infarction (AMI) undergoing PTCA. During the initial balloon dilatation arterial and coronary venous plasma concentrations of norepinephrine and epinephrine were determined. In elective PTCA, coronary occlusion (2 min) resulted in a transient increase of arterial concentrations of norepinephrine (2.04 +/- 0.30 vs. 1.26 +/- 0.13 nmol/L before dilatation) and epinephrine (0.52 +/- 0.08 vs. 0.34 +/- 0.04 nmol/L) in the first minute of reperfusion, whereas coronary venous concentrations of catecholamines were not changed after dilatation. Among the 10 patients with AMI, immediate reperfusion of the LAD (TIMI grade 3) was achieved in 6 patients. In these patients, baseline arterial concentrations for norepinephrine (3.91 +/- 1.16 nmol/L) and epinephrine (4.68 +/- 2.07 nmol/L) were elevated and no transcardiac gradient for catecholamines was found. In the first minute after successful reopening of the LAD we detected a distinct rise of the transcardiac norepinephrine gradient from -0.10 +/- 0.53 to 85.02 +/- 24.64 nmol/L, which declined in the fifth minute of reperfusion of 4.36 +/- 2.30 nmol/L. Conversely, venous epinephrine and arterial concentrations for both catecholamines remained unchanged within the observation period. In the four patients with incomplete (TIMI 0-2) reopening of the LAD, we found no cardiac washout of norepinephrine. In summary, a transient rise of systemic catecholamines, but no cardiac release of norepinephrine was observed in patients after brief coronary occlusion. Conversely, a massive washout of norepinephrine from the infarcted myocardium occurred during AMI.

                Author and article information

                S. Karger AG
                September 2003
                22 September 2003
                : 100
                : 1
                : 23-28
                aDepartment of Clinical Physiology and Nuclear Medicine, Glostrup Hospital, University of Copenhagen, bDepartment of Internal Medicine M, Glostrup Hospital, University of Copenhagen, cDepartment of Clinical Physiology and Nuclear Medicine, Frederiksberg Hospital H:S, University of Copenhagen, dDepartment of Pathology, Rigshospitalet H:S, University of Copenhagen, eDepartment of Clinical Physiology and Nuclear Medicine, Rigshospitalet H:S, University of Copenhagen, fDepartment of Medical Physiology, The Panum Institute, University of Copenhagen, Copenhagen, Denmark
                72388 Cardiology 2003;100:23–28
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 2, References: 24, Pages: 6
                Coronary Care


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