Potassium and myoglobin release and ST and QRS vector changes during acute myocardial infarction.

Thirty-three consecutive patients aged 39 to 77 years with signs of myocardial infarction with a duration of symptoms of less than 4 h took part in the study. Serial blood sampling was done for the determination of myoglobin (MG), creatine-kinase (CK) and potassium (K). Continuous vectorcardiography was monitored. Peak rates of K and MG release occurred 7.0 +/- 3.7 and 6.5 +/- 3.9 hours, respectively, after the onset of symptoms not different from the end of ST vector change that occurred after 7.6 +/- 2.8 h. Following the end of ST vector change there was a 4-hour delay until the end of QRS vector change and another 8-hour delay to the end of MG release occurring about 20 h after the onset of symptoms. At the time for peak rate of MG release 48 +/- 17% of total MG release had occurred. In conclusion, the physiologically different indicators of myocardial damage showed signs of maximum release within the same time range, 6-8 h after the onset symptoms and 8-10 h before signs of completed infarction.

Quantitative and temporal relation between the release of myoglobin and creatine kinase and the evolution of vectorcardiographic changes during acute myocardial infarction in man.

The relation in time and magnitude between QRS vector changes (QRS-VD), ST vectors (ST-VM), and the cumulated release of myoglobin, total creatine kinase, and creatine kinase isoenzyme MB was studied. Seventy four patients with a first myocardial infarction and a history of symptoms of up to 5 h were included. Blood samples for enzyme analysis were taken every 4-6 h for 72 h and cumulated enzyme release was calculated from a monocompartmental first order model. QRS-VD and ST-VM were determined every 10 min for 24 h by computer analysis of Frank lead vectorcardiograms. Infarct sizes were visually determined from the different enzymatic and vectorcardiographic evolution curves. Eight patients were excluded from the analysis because they had a QRS width greater than or equal to 120 ms or ill defined plateaus of the release curves. The relation between infarct sizes estimated from QRS-VD and total creatine kinase was r = 0.62; QRS-VD and myoglobin release r = 0.57; total creatine kinase and myoglobin release r = 0.72, showing that these variables are good and complementary indices for estimating myocardial infarct size. Median infarct evolution curves were computed after the individual curves were normalised to 100%. ST-VM fell rapidly during the first 7 h to 40% of the initial values. QRS-VD and myoglobin release were closely associated and completed their development on average 15 h after the onset of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)

Fever after acute myocardial infarction in patients treated with intravenous timolol or placebo.

Body temperature was studied in 65 patients admitted to hospital within four hours of the onset of symptoms of acute myocardial infarction. Thirty three patients had been randomly assigned to intravenous timolol treatment and 32 to placebo treatment. Infarct evolution was assessed by continuous vectorcardiography and creatine kinase release. Maximum and mean temperatures during the first eight days were significantly lower in the timolol group, who were discharged from hospital one day earlier. Eight patients in the placebo group had temperatures of greater than 39 degrees compared with one in the timolol group. Both the mean temperature and the maximum temperature correlated significantly with indices of infarct size and ischaemic area as estimated by cumulative creatine kinase release, QRS vector difference, and ST vector magnitude. The results were consistent with the view that reduction of infarct size may partly explain the reduced pyrexial response after timolol treatment. Other mechanisms are probably also involved in larger infarcts. Because high fever has detrimental haemodynamic effects in acute myocardial infarction, reduction of this response may be beneficial. The results support the early use of beta adrenoceptor blockade in acute myocardial infarction.

Course of chest pain and its relation to CK release and ST/QRS vector changes in patients with acute myocardial infarction randomized to treatment with intravenous timolol or placebo.

Assessments of hourly pain scores (0 to 4) were made in 135 patients during the initial 24 hours after admission to the hospital. The duration of chest pain and the cumulative pain score obtained by adding the pain scores hour by hour were compared to ST and QRS vector changes and CK release. The cumulative pain score over a 24-hour period after admission correlated to the maximal QRS vector difference (r = 0.51) and the cumulative CK release (r = 0.58). The time until patients had complete relief of pain was closely related to the time during which QRS vector changes were seen to continue (r = 0.73). No corresponding correlation was found between pain duration and CK release time (r = 0.24). The ST decline time correlated to the duration of the first uninterrupted episode of chest pain in the placebo group only (r = 0.50). Pain duration showed no correlation to our indices of infarct size. There was a recurrence of pain in 41% of the patients, of whom 36% had a time-associated further increase of the ST vector magnitude. We conclude that chest pain is an important clinical symptom that signals ongoing necrosis. Furthermore, assessments of a "soft" parameter, such as the cumulative pain score, can add valuable information concerning the severity of myocardial damage.

Effect of timolol on changes in serum potassium concentration during acute myocardial infarction.

One hundred and six patients with acute myocardial infarction admitted to hospital within four hours after the onset of symptoms were randomised to treatment with intravenous timolol (54 patients) or placebo (52 patients). Serum potassium concentrations were estimated at frequent intervals during the first 24 hours of admission. Patients in both treatment groups, who did not receive subsequent diuretic treatment, had a transient rise in serum potassium concentration, which was maximal after four hours. This rise was abolished by diuretic treatment in the placebo group but not in the timolol group, in which there was a pronounced and prolonged rise in serum potassium concentration. The change in serum potassium concentration in the first four hours after admission correlated with cumulative creatine kinase release in the placebo group, but not in the timolol group. Hypokalaemia (serum potassium concentration less than or equal to 3.5 mmol/l) occurred in 15 (28.8%) patients in the placebo group and in seven (13%) in the timolol group and was independent of infarct size. The frequency of hyperkalaemia was not increased in the timolol group. By increasing the serum potassium concentration and preventing hypokalaemia, the use of intravenous timolol early in acute myocardial infarction may have important clinical effects in addition to reducing infarct size.

Quantitative assessment of myocardial ischemia and necrosis by continuous vectorcardiography and measurement of creatine kinase release in patients.

The accuracy of the use of the maximal QRS vector difference to estimate myocardial infarct size irrespective of infarct location was compared with that of measurement of cumulative creatine kinase (CK) release. Sixty patients with acute myocardial infarction and a history of symptoms of less than 4 hr duration were followed for 24 to 72 hr with orthogonal vectorcardiography and CK release analysis. Spatial QRS vector differences were calculated between the first QRS complex recorded and subsequent QRS complexes at timed intervals. The QRS vector difference increased rapidly and reached a plateau at an average 12.1 hr after onset of symptoms, as compared with 34.0 hr for the cumulated CK release. In 42% of the patients a stepwise progression of infarct evolution was observed. Irrespective of infarct location the maximal spatial ST vector magnitude was related to the ultimate QRS vector difference (r = .80) and to the cumulative amount of CK released (r = .64). Furthermore, maximal QRS vector difference correlated well with the maximal cumulative CK release (r = .64) Ten patients had possible infarct expansion, as indicated by recurrent QRS changes without concomitant CK release. Fifteen patients had infarct extension that was indicated by secondary CK release and that in seven patients was associated with further QRS changes. Infarct extension caused an approximate 25% increase in infarct size. Spatial ST vector magnitude, QRS vector difference, and cumulative CK release are complementary measures in the quantification of evolving myocardial injury after acute coronary occlusion and in the determination of sequels to therapeutic interventions.

Relation between ST and QRS vector changes and myoglobin release in acute myocardial infarction.

We analysed serum time activity curves for myoglobin (MG) and changes in the ST and QRS vectors for 18 consecutive patients with acute myocardial infarction admitted within 4 h of the onset of pain. The MG release was completed 16 +/- 7 (7 to 36) h after onset of symptoms, and the QRS vector changes were completed after 14 +/- 5 (4 to 23) h. the ST vector decline ceased after 11 +/- 5 h. The temporal correlation between completion of: a) ST vectors and MG release was r = 0.78 (P less than 0.001); b) QRS vectors and MG release was r = 0.85 (P less than 0.001). Stepwise release of MG and changes in ST and QRS vectors were often related. Seventeen additional ST-peaks were followed by further MG-release in 13 instances and for 10 additional changes of the QRS vector eight were associated with further MG-release. We conclude that VCG changes and MG-release show a close temporal relationship. Additional events are often simultaneously reflected by these independent markers of myocardial ischaemia and necrosis.

Continuous vectorcardiography in acute myocardial infarction. Natural course of ST and QRS vectors.

We made continuous recordings of the X, Y and Z Frank leads in 43 patients with their first myocardial infarction admitted within 4 hours of the onset of pain. Sequential hourly analysis of the ST and QRS vector changes during the first 24 hours was performed. In short-term survivors (n = 38) mean serial changes of ST vectors showed an initial rapid decline until the 8th-10th hour, whereas QRS vector changes lasted longer and were completed within 13.5 +/- 3.6 hours (inferior infarction) and 10.2 +/- 2.4 hours (anterior infarction) respectively. The initial ST vector magnitude was significantly correlated to the subsequent cumulative QRS vector change (r = 0.82). The individual ST vector changes showed a rapid decline in 33 of 38 patients (87%), whereas in 5 patients the ST vector magnitude increased to reach its maximum after 4-6 hours. After the initial decline new increases of the ST vector magnitude was noted in 16 patients on 20 occasions. In 13 instances this was associated with recurrent pain. The spatial change of ST vector direction with reference to the initial direction was significantly greater when recurrent ST rises were accompanied by additional QRS vector changes, compared to those without associated QRS changes (P less than 0.025). The individual QRS vector slopes could be characterized as (1) monophasic (n = 21, 55%), (2) polyphasic (n = 11, 29%) and (3) irregular (n = 6, 16%). We conclude that continuous vectorcardiography is a suitable method for following ST and QRS vector changes that accompany acute myocardial infarction and that ST vector changes can be used to predict subsequent QRS vector changes.

Emergency room resuscitation of patients with cardiac arrest outside hospital. Outcome and immediate prognosis in 319 patients.

Resuscitation was attempted in 319 patients brought to hospital with cardiac arrest during a 5-year period. Primary successful results were achieved in 50 patients (15.7%). Twelve patients were long-term survivors (3.4%), 10 of whom had normal brain function, whereas 2 had mild cerebral dysfunction. To improve prognostication in patients with initially successful resuscitation, Bayes' theorem was applied using 4 clinical findings after 24 hours' treatment: reactions to painful stimuli, pupillary size, light reactions and BP, Bayes' theorem as well as coma depth after 24 hours gave valuable information regarding individual prognosis.