Shortening of Electromechanical Systole as a Manifestation of Excessive Adrenergic Stimulation in Acute Myocardial Infarction
Author(s) -
Richard P. Lewis,
Harisios Boudoulas,
Wilbur F. Forester,
Arnold M. Weissler
Publication year - 1972
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.46.5.856
Subject(s) - medicine , myocardial infarction , cardiology , infarction , adrenergic , catecholamine , excretion , chest pain , stimulation , propranolol , coronary care unit , receptor
The relationship between shortened electromechanical systole (QS2I) and 24-hour urinary catecholamine excretion (E+NE) was studied in 51 patients admitted to the coronary care unit with suspected acute myocardial infarction. Among these patients, 24 had a documented acute myocardial infarction while 27 had chest pain without evidence of recent myocardial infarction. Patients receiving cardioactive drugs or with impaired renal function were excluded. Initial elevation of catecholamine excretion was found in 22 of 24 subjects with myocardial infarction and 14 patients without documented myocardial infarction. A close linear correlation (r = -0.82, P < 0.001) was noted between shortening of the QS2I and catecholamine excretion among all patients irrespective of the presence of documented infarction. Patients with serious arrhythmias had significantly higher levels of catecholamine excretion. In 13 patients with a short QS2I, 2.5 mg of propranolol given intravenously produced a significant lengthening of the QS2I while no change in the QS2I occurred in normal controls. This test provided useful corroborative evidence that the short QS2I was related to excessive adrenergic stimulation. In view of the current availability of effective beta-adrenergic blocking agents, these results may improve the selection of patients for antiarrhythmic therapy with these drugs.
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