Clinical studyFree noradrenaline and adrenaline excretion in relation to clinical syndromes following myocardial infarction
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Cited by (138)
Association of Circulating Ketone Bodies With Functional Outcomes After ST-Segment Elevation Myocardial Infarction
2021, Journal of the American College of CardiologyCitation Excerpt :We hypothesize that the large increase in circulating KBs at admission was a direct consequence of the stress response to MI, which resulted in a systemic catecholamine surge and free fatty acid release, which predominantly occurred during the first hours after the onset of symptoms (14,17). After presentation with STEMI, catecholamines only gradually decline (18,19), explaining the persistent elevation of KB concentrations at 24 hours after admission, although these concentrations were lower compared with admission. Similar increases in KB concentrations at presentation were detected in experimental models of cerebral ischemia (261-924 μmol/L) (20,21).
Early expressed circulating long noncoding RNA CHAST is associated with cardiac contractile function in patients with acute myocardial infarction
2020, International Journal of CardiologyGlucose-insulin-potassium therapy for acute myocardial infarction: What goes around comes around
2004, American Heart JournalCitation Excerpt :Under normal conditions, the myocardium depends on aerobic metabolism oxidizing free fatty acids (FFAs) as the primary energy substrate.11 However, under conditions of myocardial ischemia, a number of important metabolic changes occur,12 including increased secretion of catecholamines,13 increased concentration of circulating FFAs,9 and impaired glucose metabolism.14 These are insulin-dependent metabolic adjustments that occur with or without underlying diabetes, but are most pronounced among patients with diabetes due to relative or absolute insulin deficiency.
Metabolic causes and prevention of ventricular fibrillation during acute coronary syndromes
2002, American Journal of MedicineCitation Excerpt :Indeed, modification of the catecholamine response or minimization of some of its other effects may prevent primary ventricular fibrillation. As myocardial ischemia and infarction develop, plasma norepinephrine concentrations increase within minutes (9), particularly in patients with complications (10), and remain elevated for up to 20 hours depending on the severity of the stress response. Norepinephrine, which is released from postganglionic sympathetic nerves, binds to adrenergic receptors in myocardial cells and the media of coronary arterioles.
Esmolol and cardiopulmonary bypass during reperfusion reduce myocardial infarct size in dogs
2001, Annals of Thoracic SurgeryCitation Excerpt :Increased plasma levels of free fatty acids have been shown to trigger ventricular arrhythmias and to impair activity of Ca2+ pumps in sarcoplasmic reticulum [12, 13]. As the increased release of free fatty acids during myocardial infarction is a predominantly norepinephrine-mediated response, this reaction may be attenuated by β-blockade [14]. Myocardial reperfusion injury is associated with substantial intracellular and interstitial edema formation.
Admission serum potassium in patients with acute myocardial infarction: Its correlates and value as a determinant of in-hospital outcome
2000, ChestCitation Excerpt :However, since 9 of the 10 patients with VFand LK had this arrhythmia at pre-emergency department or emergencydepartment settings, and only 3 of them were taking diuretics, LK mayreflect a postresuscitation epiphenomenon and/or may be related to anearly presentation in the emergency department, rather than be thecause of VF. In our study, the association of LK after resuscitation from VFwith early presentation to the emergency department, large MIs, and nolink to diuretic therapy suggests a “stress”-induced intracellularserum potassium shift as the explanation for LK.484950 Itsmechanism has been traced to a β2-adrenergicstimulation in normal volunteers and borderline hypertensivepatients.51525354
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British Council Scholar. Present address: Universita de Perugia, Instituto di Patologia Speciale Medica e Metodologia Clinica, Policlinico Monteluce, Perugia, Italy. Dr. Valori gratefully acknowledges financial assistance from the British Council and the Wellcome Association.