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Biomedical subjects

L Erhardt

Publications and source records attributed to L Erhardt.

At least 91 records · Page 5Linked to original sources
PubMed1988

Trends in coronary care. A retrospective study of patients with myocardial infarction treated in coronary care units.

Data on the 2,008 patients in the Swedish Co-operative Study from 1969 were compared with 773 consecutive cases with definite myocardial infarction (MI) admitted to the coronary care unit (CCU) of Danderyd Hospital in Stockholm 1984-85. We found a significant decrease in hospital mortality from 26.6% to 12.9% despite the admission of older patients to our CCU. Mean age for men was 63.8 vs. 65.6 years and for women, 69.8 vs. 72.3. The incidence of previous hypertension and diabetes was higher and the incidence of heart failure and angina lower in 1984-85. No differences were noted as regards the incidence of ventricular fibrillation, atrial fibrillation and AV-block III in the acute phase despite a much more frequent use of antiarrhythmics in 1969 (33% vs. 4%). A decreased use of cardiac glucosides was also noted (34% vs. 16%). Asystole, however, was noted in 10% of the patients in 1969 compared with 3% in our patients. beta-Adrenergic blockers were not used in 1969 but commonly given in 1984-85 (67%), also in those with heart failure (54%). Delay between onset of symptoms and admission was longer in 1969, 47% being admitted within 6 hours compared with 75% in 1984-85. In conclusion, our study shows a marked change in the use of various cardiac drugs in the treatment of MI. Differences between the populations as regards mortality and different clinical findings are more difficult to evaluate and may also be explained by change in the selection of patients treated in the CCU.

Age Factors↗
PubMed1987

Metoprolol in acute myocardial infarction reduces ventricular arrhythmias both in the early stage and after the acute event.

Fifty three of the 5778 patients included in the MIAMI (Metoprolol in Acute Myocardial Infarction) trial were investigated with long-term ECG recordings in order to evaluate the effect of acute beta-blockade on premature ventricular complexes in and after acute myocardial infarction. Twenty five patients were given placebo and 28 metoprolol in a double-blind randomized fashion for 15 days. After this period the patients were put on open beta-blockade without breaking individual study codes. The mean number of premature ventricular complexes during the inclusion day (day 0) was the same in the two groups. The median numbers were also similar in the two groups: 190 and 154 in the placebo and metoprolol groups, respectively. Metoprolol significantly reduced the median number of premature ventricular complexes in the randomized period. The median numbers on days 1, 2 and 15 were 146, 101, 84 in the placebo group and 73, 59 and 10 in the metoprolol group, respectively (P less than 0.05). Also during the further follow-up, when investigated 1, 3 and 6 months after the infarction, the median number of premature ventricular complexes was lower in the metoprolol group (74, 257, 142 in the placebo group and 7, 5 and 11 in the metoprolol group, P less than 0.05). This indicates that metoprolol treatment in the acute phase of myocardial infarction reduces ventricular arrhythmias both in the early stage and also after the acute event.

Arrhythmias, Cardiac↗
PubMed1987

Haemodynamic aspects of nitrate tolerance.

Development of tolerance to the haemodynamic effects of nitrates is influenced by the degree of left ventricular dysfunction and a number of other factors related to the circulatory system. Patients with angina pectoris and normal cardiac function at rest differ in response compared with patients with chronic congestive heart failure. Several studies have shown that haemodynamic tolerance to nitrates will develop in patients with angina pectoris. Slow-release oral nitrates and transdermal nitrates, as well as higher dosages, are more likely to induce tolerance. Patients with congestive heart failure will usually not develop tolerance after oral nitrate therapy. With transdermal therapy, however, tolerance frequently develops even in these patients. The individual response of patients to the effects of nitrates and the development of tolerance is variable, regardless of clinical status. Future studies on the development of tolerance must consider the complexity of the effects of nitrates and the various factors that may affect the haemodynamic changes.

Cardiovascular System↗
PubMed1986

Repeated exercise and redistribution thallium-201 scintigrams in patients with myocardial infarction treated with timolol or placebo.

Repeat exercise thallium-201 scintigrams were performed 2 weeks, 3 months, and 6 months in 27 patients following their first myocardial infarction. All patients were treated with timolol or matching placebo, administered intravenously starting within 5 hours of onset of chest pain. The extent of transient perfusion defects in 15 timolol-treated patients increased significantly between 2 weeks and 3 months compared to a decrease in 12 placebo-treated patients (p less than 0.05). Between 3 and 6 months the extent of transient defects did not change in the two groups, and there was no difference between the groups. The extent of permanent defects was not significantly different between the timolol- and placebo-treated patients on any occasion. However, patients in the timolol group had a decrease in permanent defects with time in contrast to patients in the placebo group (p less than 0.05). Thus, early intervention with timolol in the acute phase of myocardial infarction may have consequences for the postinfarction phase, as reflected in repeat thallium-201 scintigrams.

Adult↗
PubMed1986

Short-term haemodynamic effects of dopexamine in patients with chronic congestive heart failure.

Dopexamine (FPL 60278) is a new dopamine analogue which possesses a combination of dopamine receptor and beta-2-adrenoreceptor agonist properties. The aim of our study was to evaluate the short-term haemodynamic effects of dopexamine administered by intravenous infusion at different dosage rates. Eight patients with chronic congestive heart failure were studied. A dose of 1 microgram kg-1 min-1 produced a 27% decrease in systemic vascular resistance index (32.6 to 23.9 res. units m2, P less than 0.001 and a significant increase in cardiac index (2.7 to 3.6 l min-1 m-2, P less than 0.001). Stroke volume index and heart rate increased significantly by 22% and 7%, respectively. An increase in left ventricular stroke work index was also seen at the dose level inducing the maximum cardiac output. Left ventricular filling pressures and arterial blood pressures were not affected. We conclude that administration of dopexamine to patients with congestive heart failure augments cardiac performance at rest.

Adrenergic Agonists↗
PubMed1986

Nitrate tolerance. State of the art--chairman's summary.

The development of tolerance to the effects of nitrates is well documented in the literature. It can be induced and rapidly reversed with all types of nitrates and it is more pronounced in the arterial as compared to the venous circulation. Cross-tolerance between different nitrates exists. Furthermore, tolerance seems more related to high and continuous plasma concentrations and may possibly be avoided by intermittent dosing. The importance of such factors as patient selection, type of nitrate preparation, duration of therapy, the significance of target organs, methods of evaluating the development of nitrate tolerance as well as a summary of the discussions during the workshop is presented.

Drug Tolerance↗
PubMed1985

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.

Adult↗
PubMed1985

Long-term treatment with metoprolol after myocardial infarction: effect on 3 year mortality and morbidity.

The effects of metoprolol treatment in patients surviving acute myocardial infarction have been investigated in a double-blind randomized study. The patients were stratified according to age, infarct size and type of ventricular arrhythmias before administration of metoprolol, 100 mg twice daily (n = 154), or placebo (n = 147). All patients were followed up for 36 months. There were 31 (29 cardiac) and 25 (20 cardiac) deaths in the placebo and metoprolol groups, respectively. Subgroup analyses showed a significant reduction of cardiac death in patients with a large infarct (32.1% with placebo versus 12.5% with metoprolol, p less than 0.05) as a result of active treatment. Sudden death rates were 14.7% in the placebo versus 5.8% in the metoprolol group (p less than 0.05). The incidence of nonfatal reinfarction was 21.1% in the placebo versus 11.7% in the metoprolol group (p less than 0.05). The reduction in nonfatal reinfarction was similar in all pretreatment risk strata. The difference between the two groups in cumulative number of cardiac deaths and patients experiencing nonfatal reinfarction increased throughout the study. Furthermore, cerebrovascular events (p less than 0.05) and coronary bypass surgery (p = 0.058) were more frequent in the placebo group. In conclusion, after 36 months of metoprolol treatment after myocardial infarction, there was a significant reduction of nonfatal reinfarction and sudden death in all patients and a reduction of cardiac death in those with a large infarct.

Aged↗
PubMed1983

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.

Adult↗
PubMed1983

Comparative study of tocainide and lidocaine in patients admitted for suspected acute myocardial infarction.

The antiarrhythmic effects of tocainide, administered as a bolus injection of 750 mg followed by oral therapy, and conventional lidocaine therapy were evaluated in 40 patients admitted for suspected acute myocardial infarction (AMI) and showing high-grade premature ventricular complexes (PVCs). The mean hourly PVC rate before therapy was 928 and its reduction was equally significant in the tocainide group, 73%, and in the lidocaine group, 68%. The number of 5-minute periods with multiform, paired and R/T PVCs or ventricular tachycardia was also significantly reduced, by 78% in the tocainide group and by 71% in the lidocaine group. Ten patients in the tocainide group reported moderate side-effects, compared to 13 in the lidocaine group, where the infusion had to be discontinued in 5 patients and the rate had to be reduced in 4. Tocainide, an amine analogue of lidocaine, is considered just as effective as lidocaine in patients with high-grade PVCs and suspected AMI.

Adult↗
PubMed1983

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.

Adult↗
PubMed1980

Effect of metoprolol on QTc intervals after acute myocardial infarction.

The effect of metoprolol on corrected QT interval (QTc) was studied retrospectively in 111 survivors of AMI below 70 years of age. Prior to discharge the patients were stratified by age, infarction size and ventricular arrhythmias and randomized. Metoprolol, 100 mg b.i.d., or placebo were given double-blindly to 59 and 52 patients, respectively. QTc intervals were measured four times prior to randomization and three times during the follow-up year. The highest QTc mean was registered on the second day in the CCU. QTc intervals subsequently decreased significantly in both groups between discharge and the three-month control (p < 0.001). Patients on metoprolol had significantly shorter QTc intervals during the follow-up year than those on placebo (0.394 +/- 0.028 vs. 0.406 +/- 0.034 sec, p < 0.001). The QTc-shortening effect of beta-receptor blockade was most marked in patients with prolonged QTc intervals at discharge. Patients who died suddenly had prolonged QTc intervals prior to discharge. In this group the proposed beneficial effect of beta-receptor blockade on QTc interval cannot be evaluated as most of these patients had died before the first control.

Adult↗
PubMed1980

Relation between ventricular arrhythmias and psychological profile.

The association between psychological characteristics and ventricular arrhythmias was investigated in 150 men (50 with manifest IHD, 50 with risk indicators of IHD and 50 healthy men). Arrhythmias were recorded with 24-hour Holter monitoring. Psychological characteristics were assessed by the Emotions Profile Index and the Structured Interview for pattern A behaviour. A depressive emotional state was associated with prognostically severe ventricular arrhythmia in healthy men, but not in men with overt IHD or risk indicators of IHD. When clinical characteristics and age were taken into account, depressiveness was-among healthy men-the second most important factor after high age. The results suggest that-in absence of IHD or other cardiovascular disease-a depressive emotional state may participate in the formation of ventricular arrhythmia.

Adult↗