[Actilyse (a recombinant tissue-type plasminogen activator] in the treatment of acute myocardial infarct. Comparison of the effects of Actilyse and streptokinase]. / Preparát Actilyse (rekombinacní tkánový typ aktivátoru plazminogenu) v lécbe akutního infarktu myokardu. Srovnání úcinku Actilysy a Streptokinázy.

The preparation Actilyse--a tissue plasminogen activator prepared by recombination--is an effective fibrinolytic drug. The authors recorded in a group of 33 patients reperfusion in 91%, evaluated on the basis of indirect criteria. In a group of 18 patients treated with streptokinase reperfusion was achieved in 74%. Based on changes of CK and CK-MB values--an earlier rise of values following Actilyse administration and conversely their more marked increase during subsequent sampling after streptokinase administration--it may be assumed that earlier dissolution of the thrombus in the coronary artery occurs after Actilyse administration, as compared with streptokinase. It may be thus assumed that there is also a smaller necrotic focus after Actilyse treatment, as compared with streptokinase. Early re-occlusion--according to indirect indicators--occurred in 8.6% in the Actilyse treated groups, as compared with 5.9% in the streptokinase treated group. The fibrinogen values decline in the Actilyse group to 40% and in the streptokinase group to 28%. Later enhanced new formation of fibrinogen occurs and the fibrinogen values rise to 160% in the Actilyse treated group and to 250% of the initial value in the streptokinase treated group. The elevated fibrinogen value, as compared with the baseline value, persists for the 12 days of the follow-up. No severe spontaneous haemorrhage was recorded, haemorrhagic manifestations were associated with blood sampling and i.v. administration of drugs only. The necessity to administer blood was due to a complication during puncture of the subclavian vein in one patient.(ABSTRACT TRUNCATED AT 250 WORDS)

[Late ventricular potentials in patients without ventricular tachycardia 3 years after myocardial infarct]. / Pozdní komorové potenciály u nemocných bez komorové tachykardie 3 roky po infarktu myokardu.

In 57 patients who in the course of 29-48 months (mean 36 months) after myocardial infarction did not develop sustained ventricular tachycardia, late ventricular potentials were investigated. Positive findings were revealed in 13 (22.8%) patients using a 25-250 Hz filter and in 14 patients resp. (24.6%) using a 40-250 Hz filter. Late ventricular potentials were significantly more frequent in patients after myocardial infarction of the lower rather than the anterior wall (p less than 0.05). No differences were revealed between groups with positive and negative late ventricular potentials as regards the occurrence of repeated infarction, left-side cardiac failure, ectopic ventricular contractions, diabetes mellitus, arterial hypertension and cardiothoracic index. The assembled data are comparable with data in the literature pertaining to the incidence of late ventricular potentials in patients after myocardial infarction without sustained ventricular tachycardia.

[Severe antihistamine poisoning complicated by ventricular tachycardia]. / Závazná intoxikace antihistaminiky komplikovaná komorovou tachykardií.

A 26-year-old female clerk without previous heart disease ingested with suicidal intensions antihistaminic drugs--H1 blockers, astemizole (a total of 700 mg) and terfenadine (a total of 900-1200 mg). The main sign of intoxication was repeated polymorphous ventricular tachycardia type torsade de pointes, which at the onset of hospitalization changed into ventricular fibrillation. Therapeutically the impaired rhythm was controlled by electric cardioversion and atrial stimulation with a frequency of 120/min. On the third day it was possible to discontinue atrial stimulation and later the patient was discharged without any permanent sequelae.

[Cardiac tamponade as a complication of acute myocardial infarct. (Clinical and pathologico-anatomic analysis of patients with acute myocardial infarct and cardiac tamponade)]. / Srdecní tamponáda jako komplikace akutního srdecního infarktu. (Klinický a patologicko-anatomický rozbor nemocných s akutním srdecním infarktem a srdecni tamponádou.)

Cardiac tamponade is a frequent cause of death in acute myocardial infarction--in as many 23%. It is encountered in particular in the 7th and 8th decade, in patients with a first infarction which is frequently situated in the anterior wall of the left ventricle. 93% of the patients have obvious ECG manifestations of Q infarction. The diagnosis of cardiac tamponade is easy when during an acute terminal attack slow activity on the ECG tracing is found without a haemodynamic response and the pulse on the great arteries is not palpable even after external cardiac massage. In 80% the onset of cardiac tamponade is very sudden. The presence of shock or cardiac failure makes the diagnosis of cardiac tamponade more difficult. As to investigated indicators, in the development of cardiac tamponade the systemic pressure--systolic as well as diastolic--on admission or during hospitalization, may play a part. The patients have a less marked coronary sclerosis, fibrosis of the cardiac muscle is less frequently present. Previous necroses of the heart muscle may have probably a certain protective effect on the development of cardiac tamponade. Anticoagulants obviously do not influence the development of cardiac tamponade.