Læknablaðið - 15.09.1986, Blaðsíða 19
LÆKNABLAÐIÐ
197
mestu. Endurtekin meðferð eykur hins vegar
líkurnar á þeim (36).
Aukaverkanir streptókínasameðferðar
verður að skoða í ljósi þess hve alvarlegan
sjúkdóm er verið að meðhöndla og hver
væntanlegur árangur meðferðar er. Fram-
angreind rannsókn bendir til að gagnsemi
streptókínasagjafar við bráða kransæða-
stíflu vegi mun þyngra en hugsanlegt tjón, sé
rétt að verki staðið.
SUMMARY
This article describes the first experience in Iceland with
a high dose intravenous streptokinase therapy in acute
myocardial infarction. Patients had to fulfill the follo-
wing criteria: 1. Less than four hours from onset of
symptoms to beginning of therapy. 2. ST-segment ele-
vation equal or more than 2 mm. 3. No response to
sublingual 0.25 mg nitrglycerine. 4. No contraindication
to thrombolytic therapy. Since November 1983 until end
of 1985 thirty three patients received treatment accor-
ding to this protocol. Two patients were given repeated
treatment. Average time from onset of symptoms to
therapy was 138 minutes. Clinical reperfusion was re-
cognised by: 1. Sudden relief of chest pain during
streptokinase infusion. 2. Lowering of ST segments
within two hours after thrombolytic therapy. 3. An
abrupt increase in CK and CK-MB activity with nadir
within thirteen hours from cessation of streptokinase
infusion. 4. Typical reperfusion arrhythmias and dis-
appearance of conduction defects. According to these
criteria the reperfusion rate was 68%. Coronary angio-
graphy and ventriculography was done in 27 patients on
average 79 days after therapy. The infarct related artery
was patent in 65% of patients with clinical signs of
reperfusion but four (20%) patients in this group had a
reinfarction before angiography. Patients with reperfu-
sion had an average ejection fraction of 60% as com-
pared to 46% in the group without reperfusion
(p<0.05). The systolic motion of the infarct-site myo-
cardium was better in the reperfusion group (p < 0.01),
their vocational ability seemed to be higher (p >0.05) and
there was a tendency for them to be less dependent on
heart failure therapy (p>0.05). Reinfarction occurred
in 8 patients (24%). In five of them this occurred during
the first fourteen days after thrombolytic therapy. Seven
patients (20%) had minor adverse effects from strepto-
kinase therapy and one had various hemorrhages and
died from myocardial rupture.
Although this is not a controlled study and includes
rather few patients the authors conclude that a high dose
intravenous streptokinase therapy is useful in acute
myocardial infarction given due precaution.
ÞAKKARORÐ
Höfundar vilja þakka starfsfólki hjartadeilda Land-
spítalans og Borgarspítalans og lyfjadeildar
Fjórðungssjúkrahússins á Akureyri fyrir framlag þeirra
til rannsóknarinnar. Sérstaklega er Þorkeli Guðbrands
syni yfirlækni þakkað, en hann hafði umsjón með þeim
sjúklingum, sem fengu meðferð á
Fjórðungssjúkrahúsinu á Akureyri. Ottó J. Björnsson
tölfræðingur veitti ráðgjöf varðandi töflur III og IV.
HEIMILDIR
1. Fletcher AP, Sherry S, Alkjaersig N, Smyrniotis
FE, Jick S. The maintenance of a sustained throm-
bolytic state in man. II. Clinical observations on
patients with myocardial infarction and other
thrombotic disorders. J Clin Invest 1959; 38:
1111-9.
2. European Cooperative Study Group for Strepto-
kinase Treatment in Acute Myocardial Infarction.
Streptokinase in acute myocardial infarction. N
Engl J Med 1979; 301: 797-802.
3. Aber CP, Bass NM, Berry CL et al. Streptokinase
in acute myocardial infarction: a controlled multi-
centre study in the United Kingdom. Br Med J 1976;
2: 1100-4.
4. Berry CL. Thrombolytic therapy and myocardial
infarction. J Clin Path 1975; 28: 352-6.
5. Kao KJ, Hackel DB, Kong Y. Hemorrhagic myo-
cardial infarction after streptokinase treatment for
acute coronary thrombosis. Arch Pathol Lab Med
1984; 108: 121-4.
6. DeWood MA, Spores J, Notske MD, et al. Pre-
valence of total coronary occlusion during the early
hours of transmural myocardial infarcton. N Engl
J Med 1980; 303: 897-902.
7. Kennedy JW, Gensini GG, Timmis GC, Maynard
C. Acute myocardial infarction treated with intra-
coronary streptokinase: A Report of the Society for
Cardiac Angiography. Am J Cardiol 1985; 55:
871-7.
8. Kennedy JW, Ritchie JL, Davis KB, Fritz JK.
Western Washington Randomized Trial of Intra-
coronary Streptokinase in Acute Myocardial In-
farction. N Engl J Med 1983; 309: 1477-82.
9. Kennedy JW, Ritchie JL, Davis KB, Stadius ML,
Maynard C, Fritz JK. Western Washington rando-
mized trial of intracoronary streptokinase in acute
myocardial infarction. A 12-Month Follow-up Re-
port. N Engl J Med 1985; 312: 1073-8.
10. Nielsen JD. Fibrinolytic intervention in acute myo-
cardial infarction. Ugeskr Læger 1984; 146: 259-65.
11. Kahlé LH, Henny CP, Barwegen MGM, Cate JW.
Plasminogen and Antiplasmin; relevant para-
meters for monitoring fibrinolytic therapy. In:
Trubestein G and Etzel F eds. Fibrinolytic Therapy.
International Symposium on Fibrinolytic Therapy
Bonn, April 28-30, 1982. Stuttgart: F. K. Schat-
tauer Verlag, 1983: 43-50.
12. Schröder R, Biamino G, Leitner ER, et al. Intra-
venous short-term infusion of streptokinase in
acute myocardia! infarction. Circulation 1983; 67:
536-48.
13. Neuhaus KL, Tebbe U, Sauer G, Kreuzer H,
Köstering H. High dose intravenous streptokinase
in acute myocardial infarction. Clin Cardiol 1983;
6: 426-34.
14. Spann JF, Sherry S, Carabello BA, et al. Coronary
thrombolysis by intravenous streptokinase in acute
myocardial infarction: Acute and Follow-Up Stu-
dies. Am J Cardiol 1984; 53: 655-61.
15. Ganz W, Geft I, Shah PK, et al. Intravenous
streptokinase in evolving acute myocardial infarc-
tion. Am J Cardiol 1984; 53: 1209-16.
16. Gruppo Italiano Per Lo Studio Della Streptochinasi
Nell’Infarto Miocardico. Effectiveness of intra-