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THE CATECHOLAMINE RESPONSE TO ACUTE MYOCARDIAL INFARCTION: EFFECT OF EARLY ADMINISTRATION OF SOTALOL
Author(s) -
McGRATH B.,
ARNOLDA L.,
SALTUPS A.
Publication year - 1986
Publication title -
australian and new zealand journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.596
H-Index - 70
eISSN - 1445-5994
pISSN - 0004-8291
DOI - 10.1111/j.1445-5994.1986.tb00007.x
Subject(s) - sotalol , medicine , myocardial infarction , placebo , heart rate , catecholamine , anesthesia , tachycardia , cardiology , blood pressure , alternative medicine , pathology , atrial fibrillation
Thirty‐five patients with suspected acute myocardial infarction were studied in a randomised controlled trial to determine whether the catecholamine response to myocardial infarction was altered by administration of the beta blocker, sotalol, given within six hours of the onset of chest pain. Myocardial infarction evolved in 30 patients (15 placebo‐treated, 15 sotalol‐treated) and was associated with markedly increased plasma and urine noradrenaline and adrenaline levels. Intravenously administered sotalol was well tolerated and produced significant acute falls in blood pressure and heart rate. The reduction in heart rate was maintained in the sotalol group with once‐daily therapy. Plasma levels of both catecholamines showed slow but very similar falls in the two groups, the decline being evident earlier for adrenaline than for noradrenaline. This was also reflected in the pattern of catecholamine excretion: significant falls in adrenaline but not noradrenaline excretion were seen on day 2 in both groups. Although mean plasma and urinary catecholamine levels tended to be higher in the sotalol group throughout the study, the differences between the sotalol and placebo groups for the changes in plasma or urinary catecholamines with time were not statistically significant. Episodes of ventricular tachycardia occurred in 68% of the patients on day 1 and 27% of patients on day 2. More patients in the sotalol group experienced episodes of ventricular tachycardia (sotalol 89% placebo 54%) but this difference was not statistically significant. Infarct size as assessed by cumulated release of creatine kinase was similar in sotalol (184±21 IU/I) and placebo (199±24 IU/I) groups and correlated with day 1 adrenaline excretion (r = 0.40, n = 30, p 0.05). Early administration of sotalol did not appear to confer any significant benefits in the acute phase of myocardial infarction.