Why the study?
Does urinary catecholamine excretion correlate with the degree of cardiac damage and functional impairment in patients with myocardial infarction or ischaemia?
Does urinary catecholamine excretion correlate with the degree of cardiac damage and functional impairment in patients with myocardial infarction or ischaemia?
Urinary catecholamine excretion is elevated following myocardial infarction and correlates with the extent of myocardial damage, hemodynamic disturbance, and incidence of arrhythmias.
Elevated catecholamine excretion was associated with MI severity and complications; leaves open its added value for risk stratification.
Summary Serial daily estimations were made of the urinary catecholamine excretion in 64 patients during the first two weeks after the onset of myocardial infarction and in 27 patients after the onset of chest pain subsequently diagnosed as myocardial ischaemia. In most patients with myocardial infarction, the total excretion rate of catecholamines was elevated, mainly due to elevation of the noradrenaline excretion rate. The level of catecholamine excretion correlated well with the peak levels of S.G.O.T., LD.H. and w.e.e. Higher levels of all these variables were found in patients with cardiac failure, hypotension and ventricular arrhythmias. On the other hand, catecholamine excretion, enzyme levels and wee were only slightly elevated in the patients with sinus or nodal bradycardia, and catecholamine excretion was barely elevated in patients who suffered chest pain without infarction. Thus, catecholamine excretion after myocardial infarction correlates with the degree of cardiac damage, functional impairment and the incidence of some arrhythmias. It is concluded that the increased catecholamine excretion originates from the sympathetic nerve endings as a reflex result of the haemodynamic disturbance, with some possible contribution from the sympathetic endings in the damaged heart muscle.
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Rosenbaum et al. (1970) studied this question.
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