Læknablaðið - 15.01.1994, Blaðsíða 50

40
LÆKNABLAÐIÐ 1994; 80: 40-41
NÝR DOKTOR í LÆKNISFRÆÐI
AXEL SIGURÐSSON
Þann 15. október síðastliðinn varði Axel
Sigurðsson doktorsritgerð við háskólann í
Gautaborg. Ritgerðin nefnist: Neurohormonal
activation in patients with acute myocardial
infarction or chronic congestive heart
failure. With special reference to treatment
witli angiotensin converting enzyme
inhibitors. Fer ágrip hér á eftir.
Neurohormonal activation may provide
a pathophysiological link between acute
myocardial infarction and chronic congestive
heart failure and modulation of neurohormonal
activity may be an important therapeutic target
in these conditions.
Plasma neurohormones were studied in 55
patients with acute myocardial infarction.
Angiotensin II, noradrenaline and ANP were
elevated in the early phase but tended to
normalise during the first week in patients
without signs of heart failure. In patients with
heart failure angiotensin II and noradrenaline
remained elevated for 1 month and ANP for
4-6 months. During head-up tilt, angiotensin II
and noradrenaline increased most in patients
with heart failure. In patients with a first
myocardial infarction, there was a positive
coiTelation between sustained neurohorntonal
activation and infarct size.
Almost complete suppression of plasma ACE
activity was achieved within 30 minutes in 48
patients treated with intravenous enalaprilat,
initiated within 24 hours from the onset of
infarction. The drug was tolerated in dosages
of 1.0-1.2 mg given over 1-2 hours. Patients
with systolic blood pressure between 100-
110 mmHg had more risk of hypotension
than those with higher blood pressure.
Tolerance was not worse among patients
Key words: Neurohormonal activation, renin-angiotensin
sysiem, noradrenaline, acute myocardial infarction,
congestive heart failure, head-up tilt, exercise, ACE
inhibition.
treated with intravenous diuretics, metoprolol
or nitroglycerin.
A total of 98 patients were randomized
to treatment with enalapril or placebo,
initiated within 24 hours from the onset of
infarction and continued for 4-6 months.
No significant differences were found in
plasma levels of angiotensin II, aldosterone,
ANP or catecholamines between groups.
Echocardiographic recordings were done in
28 patients. In patients on placebo, there was
a positive correlation between plasma levels
of noradrenaline at day 5-7 and the increase
in left ventricular voluntes during the study
period, and an inverse correlation between
plasma aldosterone at day 5-7 and the increase
in left ventricular ejection fraction during
the study. No such correlation was found on