Platelet serotonin transporter in stroke patients.

OBJECTIVES: Post-stroke depression can be treated with serotonin transport inhibitors suggesting a role for the serotonin system in these patients. The number of platelet serotonin transporters in stroke patients and in control subjects have been measured in this study. MATERIAL AND METHODS: Newly admitted stroke patients who did develop or who did not develop a post-stroke depression, non-acute patients who previously had had a stroke and control subjects were compared. The number of platelet serotonin transporters was analysed by ligand binding methodology. RESULTS: The number of platelet serotonin transporters was low shortly after a stroke compared with normal subjects; no difference was found between the stroke patients who developed a post-stroke depression and those who did not. CONCLUSION: A low number of platelet serotonin transporters may be a non-specific state marker for a condition as acute stroke.

Early reperfusion assessment and repeated thrombolysis in acute myocardial infarction estimated by repeated standard electrocardiography. A randomised, double-blind, placebo-controlled pilot study.

Thrombolytic therapy with streptokinase (SK) in acute myocardial infarction (AMI) does not result in early reperfusion in approximately 25% of patients. We hypothesized that early repeated thrombolysis with rt-PA in patients with early failed reperfusion would result in myocardial reperfusion. Fifty-nine AMI patients with a symptom delay of <6 h, treated with SK were included. ECG was taken on admission and after 90 and 180 min. An ST recovery of > or =25% at 90 min was interpreted as successful reperfusion. Sixteen patients had failed reperfusion at 90 min and were randomized to repeated thrombolysis with rt-PA or placebo. At 180 min from SK start, ST recovery was higher in the placebo group than in the rt-PA group (71 vs. 40%, p = 0.05). No serious bleeding complications were observed. Due to the limited sample size it was not possible to draw prominent conclusions.

[Clinical studies on glycoprotein IIb/IIIa receptor antagonist]. / Kliniske studier med glycoprotein IIb/IIIa-receptorantagonist.

Platelet activation plays a major role in the pathophysiology of acute coronary syndromes (ACS), and inhibition of platelet function is the basic pharmacological treatment of ACS. Platelet membrane glycoprotein IIb/IIIa inhibitors, a new class of potent antiplatelet agents, have been used in the treatment of ACS, as well as in the prevention of complications after percutaneous coronary interventions. The aim of this article is to describe the potential possibilities of platelet inhibition and to review the pharmacology of glycoprotein IIb/IIIa inhibitors, the results of the clinical trials with these agents, and their current use in the pharmacological treatment of ACS and in relation to percutaneous coronary intervention.

[Prognosis of acute myocardial infarction after introduction of thrombolytic therapy]. / Prognosen ved akut myokardieinfarkt efter introduktion af trombolysebehandling.

The present study describes the use of intravenous thrombolytic therapy, the in-hospital and the long-term mortality in a cohort of 1881 consecutive patients with confirmed myocardial infarction. Thirty-two percent received thrombolytic therapy. Common reasons for not administering thrombolytic therapy were contraindications, diagnostic problems and late hospital admission. The total in-hospital mortality was 14% among patients treated with, and 27% among those treated without thrombolytic therapy (p < 0.001). The mortality among all patients after 48 months of follow-up was 50%. Advanced age, previous myocardial infarction and a higher Killip class on admission were independent predictors of an adverse outcome. In conclusion, in an unselected population with confirmed myocardial infarction the long-term prognosis continues to be dubious, despite the advances in coronary care including intravenous thrombolytic therapy.

[Serum myoglobin as a non-invasive marker of coronary reperfusion after intravenous thrombolytic therapy in patients with acute myocardial infarction]. / Serummyoglobin som ikkeinvasiv markør for koronar reperfusion efter intravenøs trombolysebehandling hos patienter med akut myokardieinfarkt.

Non-invasive methods for evaluation of intravenous thrombolytic treatment in patients with acute myocardial infarction (AMI) are needed, since approximately 30% of the patients never obtain coronary reperfusion. These patients could be candidates for additional thrombolytic treatment or acute PTCA. This study included 63 AMI patients. Intravenous and/or intracoronary thrombolysis was given to 52 patients, and 11 patients received conservative treatment (placebo). Serum myoglobin was measured every 15 min. Acute coronary angiography showed a patent coronary artery in 49 patients ("Reperfusion" group), and 14 patients had no coronary reperfusion ("No-Reperfusion" group). Mean time to peak serum myoglobin was 149 (57-194) minutes in the "Reperfusion" group and 476 (330-660) minutes in the "No-Reperfusion" group, p < 0.0001. An observed peak serum myoglobin < 5 hrs. after initiation of intravenous thrombolysis would indicate coronary reperfusion with sensitivity = 0.94; specificity = 0.79; predictive values of positive and negative test: 0.94 and 0.79, respectively. It is concluded that an peak serum myoglobin < five hrs. after start of thrombolysis predicts reperfusion status with a high level of accuracy.

[The effect of thrombolytic therapy on the outcome of early exercise test in patients with acute myocardial infarction]. / Effekt af trombolytisk behandling på udfaldet af tidlig arbejdstest hos patienter med akut myokardieinfarkt.

UNLABELLED: Exercise test variables, such as an impaired heart rate response, are known to be related to left ventricular function and patient prognosis following acute myocardial infarction. The present study was performed to compare exercise test variables in acute myocardial infarct patients following either intravenous thrombolysis or placebo. Symptom-limited bicycle ergometer tests, carried out one to two weeks from the infarction, were performed in 85 patients randomized to intravenous streptokinase (n = 41) or placebo (n = 44) given within 12 hours from onset of symptoms. Resting heart rate, systolic blood pressure and rate-pressure product were similar in the two groups. At maximum workload the streptokinase treated patients had a significantly higher median maximal heart rate than controls (136 vs. 126 min-1; p < 0.01) but only a trend towards higher systolic blood pressure was seen (175 vs. 163 mmHg; p = 0.09). Rate-pressure product at maximal exercise was 23.620 vs. 20.100 mmHg x min-1; p < 0.01). A significantly smaller number of patients in the streptokinase group had exercise capacity below 50 W (0% vs. 15.9%; p < 0.01). IN CONCLUSION: patients treated with intravenous streptokinase for acute myocardial infarction reach both higher heart rates and rate-pressure products at maximum workload than their controls thus indicating that the beneficial effects of thrombolysis after acute myocardial infarction are reflected in an improved heart rate response during exercise.

[Diagnosis of long QT syndrome with the help of atropine provoked ventricular tachycardia]. / Diagnostik af langt QT-syndrom med ventrikulaer takykardi ved hjaelp af atropininjektion.

A 49-year-old woman was admitted because of several syncopes during sports activity. She was appeared well, and the physical examination revealed no pathological findings, particularly no heart murmurs. The electrocardiogram had a normal PQ, QRS and the corrected QT (QTc)interval was 0.44 s. During the exercise test no arrhythmias were seen and the QTc was unchanged of 0.44 s, but 0.6 mg atropine injected intravenously provoked prolonged QTc = 0.49 s followed by nonsustained ventricular tachycardia. Electrophysiological examination and coronary arteriography showed no inducible arrhythmias and no presence of coronary artery disease. Beta-blocker treatment was started. During one year of observation she presented no syncope, and was still active in sports. It is concluded that patients presenting with syncope and an ECG with borderline QT prolongation should undergo several provocation trials, if simple stress test is initially negative, because undiagnosed patients without prophylactic treatment have a high mortality.

[Serum creatine kinase isoenzyme MB and myoglobin in patients with acute myocardial infarction and coronary reperfusion]. / Serum-kreatinkinase isoenzym-MB og -myoglobin hos patienter med akut myokardieinfarkt og koronar reperfusion.

Thrombolytic therapy in patients with acute myocardial infarction (AMI) changes the time-concentration curve of serum creatine kinase isoenzyme MB (CK-MB) and serum myoglobin. In this study, 60 AMI patients received thrombolytic therapy and acute coronary arteriography, or conservative treatment. Group one (n = 32) demonstrated a patent infarct-related artery after intravenous thrombolytic therapy; group two (n = 17) had an initially occluded coronary artery which became patent during catheterisation; group three (n = 11) did not receive thrombolytic therapy. Frequent serum CK-MB and myoglobin measurements showed that patients with acute coronary reperfusion had a rapid increase, an earlier peak value and less total release of both CK-MB and myoglobin to blood compared to AMI patients treated conservatively. The changes in serum myoglobin compared to CK-MB demonstrated an even more rapid, more uniform, and relatively greater increase. Measurements of serum myoglobin may be a useful non-invasive method for evaluation of thrombolytic therapy in AMI patients.

Precordial ST segment depression predicts a worse prognosis in inferior infarction despite reperfusion therapy. The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group.

The impact of associated precordial ST segment depression in inferior myocardial infarction on angiographic and clinical outcomes after thrombolytic therapy and selective coronary angioplasty was studied in 583 patients with acute myocardial infarction. Anterior infarction (Group I), inferior infarction with precordial ST segment depression (Group II) and inferior infarction without precordial ST segment depression (Group III) were present in 289, 135 and 159 patients, respectively. Precordial ST segment depression was more frequent in circumflex than right coronary infarct-related arteries (44 [71%] of 62 versus 91 [40%] of 230; p = 0.000). Although acute patency rates were not statistically different, there was a trend toward different patency rates at day 7 (Group I 88%, Group II 84%, Group III 80%; p = 0.089) partly because of insignificantly higher reocclusion rates in inferior infarction without precordial ST segment depression (Group I 11%, Group II 10%, Group III 18%, p = 0.104). Infarct zone regional wall motion (standard deviations/chord) in inferior infarction was lower with precordial ST segment depression, both acutely (Group I -2.8 +/- 0.9, Group II -2.5 +/- 1.2, Group III 2.0 +/- 1.1; p = 0.000) and at day 7 (Group I -2.2 +/- 1.1, Group II -2.3 +/- 1.1, Group III -1.9 +/- 1.3; p = 0.011). Precordial ST segment depression was associated with a lower ejection fraction in inferior infarction both acutely (Group I 47 +/- 11%, Group II 53 +/- 11%, Group III 58 +/- 9%; p = 0.000) and at day 7 (Group I 49 +/- 12%, Group II 53 +/- 10%, Group III 58 +/- 8%; p = 0.000). Complication rates tended to be higher in inferior infarction when precordial ST segment depression was present. Mortality rates for Groups I, II and III were 8%, 6% and 5%, respectively. These results suggest that precordial ST segment depression in inferior infarction predicts a worse ventriculographic and clinical outcome despite reperfusion therapy.