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L E Strandberg

Publications and source records attributed to L E Strandberg.

14 recordsLinked to original sources

Comparison of adenosine and exercise stress test for quantitative perfusion imaging in patients on beta-blocker therapy.

UNLABELLED: Beta-blocker therapy is used to decrease myocardial ischemia during exercise but may cause suboptimal diagnostic performance in exercise stress testing. The aim of the present study was to compare results of quantitative technetium-99-sestamibi single photon emission tomography (SPECT), following exercise stress test or pharmacological stress test with adenosine. We chose adenosine as comparison, since betablockers may not interfere with adenosine induced vasodilatation and therefore possibly may not interfere with its diagnostic performance. Sixteen patients with angiographically documented coronary disease (5 single-vessel, 6 two-vessel and 5 three-vessel disease), who were chronically treated with beta-blockers, performed SPECT imaging at rest, following bicycle exercise and following adenosine infusion in random order. The SPECT data were analyzed visually and quantitatively, using dedicated computer software (CEqual). According to both visual and quantitative SPECT analysis, adenosine was superior to show reversibility. Higher reversibility extent (50 +/- 15 vs. 26 +/- 12 pixels, p < 0.01) and more intense reversibility severity (110 +/- 29 vs. 49 +/- 23 sum of SDs, p < 0.05) were observed during adenosine than exercise. CONCLUSIONS: Less myocardial perfusion abnormalities during exercise than during adenosine stress in patients treated with beta-blockers may indicate less ischemia but also an impaired diagnostic performance. Thus adenosine stress test should be preferred to optimize the diagnostic sensitivity in patients during beta-blocker treatment.

Adenosine↗

Diabetes mellitus is a strong negative prognostic factor in patients with myocardial infarction treated with thrombolytic therapy.

OBJECTIVES: To assess the long-term prognostic values of baseline demographic data, occurrence of vectorcardiographic signs of reperfusion, left ventricular function and coronary angiographic features. DESIGN: Longitudinal study of morbidity and mortality. SETTING: Coronary care unit at Danderyd Hospital, Stockholm, Sweden. SUBJECTS: A total of 222 patients (mean age 61 years) with a suspected acute myocardial infarction treated with thrombolysis were investigated and followed for 2-5 years (mean 1216 days). MAIN OUTCOME MEASURES: Death or a new myocardial infarction. RESULTS: Age above 55 years (P < 0.05), a previous diagnosis of diabetes mellitus (P < 0.005), hypertension (P < 0.05), heart failure (P < 0.001) and myocardial infarction (P < 0.05), a previous use of beta-blockers (P < 0.05) and an ejection fraction below 60% (P < 0.01) were predictors for death or a new myocardial infarction in univariate analysis. Sex, a previous history of smoking or angina pectoris, vectorcardiographic signs of reperfusion or degree of coronary artery disease had no prognostic values. In multivariate analysis including age above 55 years, a previous diagnosis of diabetes mellitus, hypertension and myocardial infarction, and an ejection fraction below 60%, only age (P < 0.05), diabetes mellitus (P < 0. 01) and ejection fraction (P < 0.05) were predictors for death or a new myocardial infarction. CONCLUSIONS: The results of the present study emphasize the importance of diabetes mellitus as a long-term prognostic risk factor in patients with myocardial infarction treated with thrombolysis. Further studies are needed to determine the mechanisms behind this increased risk.

Aged↗

Prognostic information from on-line vectorcardiography in acute myocardial infarction.

The present study assesses the prognostic information from continuous on-line vectorcardiography in patients with acute myocardial infarction (AMI). A series of 203 patients with AMI were studied. Vectorcardiographic (VCG) recordings were obtained continuously for 24 hours. Analysis was performed on-line with the commercial system MIDA CoroNet. QRS vector difference (QRS-VD), ST change vector magnitude (STC-VM), and ST vector magnitude (ST-VM) were monitored. Patients were followed for 538 +/- 220 days. During follow-up, 36 patients died from cardiac causes and 38 patients had reinfarction. A significantly higher occurrence of transient VCG changes (QRS-VD, STC-VM, and ST-VM; p < 0.001) was seen in patients who died from cardiac causes or experienced either cardiac death or reinfarction at follow-up. The end value for QRS-VD was higher in patients who died from cardiac causes and correlated with the maximal value for creatine kinase when all patients were considered (r = 0.66; p < 0.001). Significantly lower mortality was seen in patients with VCG trend curves suggestive of coronary reperfusion (p < 0.01). In multivariate analysis, occurrence of transient changes in STC-VM, high QRS-VD end value, and VCG trend curves not suggestive of reperfusion gave additional prognostic information beyond that of age, gender, maximal creatine kinase value, heart size on chest x-ray, occurrence of ventricular fibrillation during hospitalization, and the inability to perform exercise tests. VCG monitoring during the first 24 hours of hospitalization for an AMI is a promising method for early detection of patients with increased risk for subsequent cardiac death or reinfarction.

Aged↗

Continuous ST- and QRS-vector changes and myoglobin release during streptokinase-treated acute myocardial infarction.

Twenty-two consecutive patients with a first myocardial infarction treated with streptokinase (SK) were compared to a group of 33 consecutive patients who did not receive SK. Age, infarct localization, duration of symptoms and infarct size, as estimated by cumulative creatine kinase (CK) release, did not differ between the two groups. Myoglobin (MG) release stopped after 5.5 +/- 3.3 h in SK-treated patients, which was 11 h earlier than in the controls (P less than 0.0001). CK release ceased after 15 +/- 7.8 h, about 13 h earlier than in the controls (P less than 0.0001). ST and QRS vector changes, registered by continuous vectorcardiography, were completed after 2.9 +/- 2.0 and 4.4 +/- 2.5 h respectively, about 2 and 4 earlier than in the controls (P less than 0.005 and P less than 0.0001 respectively). With SK, the termination of ST and QRS vector changes occurred more uniformly than corresponding vector changes in the controls, in whom a longer time interval between the termination of ST and the end of QRS vector changes was observed. With SK, the difference between the end of ST and QRS vectors decreased by about 3 h to 1.6 +/- 1.5 h (P less than 0.0001). Temporal relations between MG release and ST and QRS vector changes were similar but more uniform than in those of the reference group. In conclusion, we found that SK resulted in an accelerated and more uniform development of the infarct process, ending about 10 h after onset of therapy, compared with 20-30 h in the reference group.

Aged↗

Continuous vectorcardiography in patients with chest pain indicative of acute ischemic heart disease.

To assess the clinical usefulness of continuous on-line vectorcardiography (VCG), we studied 61 patients admitted to the coronary care unit (CCU) with chest pain, supposedly ischemic. Continuous VCG was performed for 24 h, monitoring QRS vector difference (QRS-VD), ST-change vector magnitude (STC-VM) and ST vector magnitude (ST-VM) measured 20 and 60 ms after the termination of the QRS complex. The patients were divided into four groups based on the final diagnosis; group A, 15 patients with normal exercise tests and extracardiac causes of chest pain; group B, 15 patients with unstable angina; group C, 15 patients with non-Q-wave myocardial infarction (MI); group D, 16 patients with Q-wave MI. Treatment was given according to a normal routine. Of 31 patients with MI, 16 received treatment with streptokinase. Groups A and B showed no significant permanent changes in QRS-VD, STC-VM or ST-VM. However, group B showed a higher occurrence of transient episodes (duration: 2 min-6 h) of a significant change of QRS-VD by > 15 microVs and of STC-VM, ST-VM 20 and ST-VM 60 by > 0.1 mV. Groups C and D showed both permanent changes and transient episodes for the studied vector parameters. Transient episodes were significantly fewer in group D than in group B. In patients with MI, the permanent change of vector parameters evolved more rapidly and reached a plateau earlier in those treated with streptokinase (QRS-VD: 178 +/- 82 vs. 293 +/- 100 min, p < 0.001; ST-VM 20: 142 +/- 75 vs. 293 +/- 89 min, p < 0.005). The magnitude of the end value for QRS-VD correlated with infarct size estimated by the maximal value of creatine kinase (r = 0.89; p < 0.001). We conclude that in patients admitted to the CCU with chest pain, continuous VCG monitoring early differentiates patients suffering from ischemic heart disease (IHD) from patients without IHD. It also differentiates patients with unstable angina from patients with MI.

Adolescent↗

[Reocclusion following thrombolytic treatment in acute myocardial infarct].

Currently there are five thrombolytic substances undergoing evaluation: streptokinase, tissue plasminogen activator, acylated plasminogen streptokinase activator complex, urokinase and single chain urokinase plasminogen activator. Equal results for mortality reduction (25 per cent) and reocclusion (6-24 per cent) has been reported in the literature for the five substances. Reocclusion can be divided into an early (greater than 24 hours) and a late phase. The early phase is most likely due to an imbalance between thrombolysis and the formation of a thrombus. During late reocclusion there is formation of a thrombus on the underlying coronary plaque or residual thrombotic mass, following thrombolytic therapy. The residual stenosis following thrombolysis seems to be the most important prognostic factor for reocclusion. A residual stenosis of over 75 per cent is unfavourable. Early reocclusion is prevented through simultaneous antithrombotic and thrombolytic therapy. Patients with a residual stenosis of over 75 per cent should be considered for some sort of active intervention to prevent late reocclusion.

Acute Disease↗

Haemodynamic response to dopexamine hydrochloride in postinfarction heart failure: lack of tolerance after continuous infusion.

Dopexamine is a new vasodilator with a combination of dopamine receptor and beta 2 adrenoreceptor agonist properties. Its haemodynamic effects were assessed after dose titration and during infusion for up to 24 hours in 15 patients with heart failure after acute myocardial infarction. At the initial titration a dose of 1 micrograms/kg/min produced a 25% decrease in the systemic vascular resistance index and a 32% increase in cardiac index. Stroke volume index and heart rate increased by 23% and 9% respectively. Left ventricular filling pressures and mean blood pressures were not affected. The short term effects were well sustained during the long term infusion and tolerance did not develop. Administration of dopexamine to patients with heart failure after acute myocardial infarction augments cardiac performance at rest.

Aged↗

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↗

Anticoagulant effects of low-molecular-weight heparin following thrombolytic therapy in acute myocardial infarction: a dose-finding study.

The aim of the present study was to gain clinical experience with different dose levels of dalteparin, a low-molecular-weight heparin, following thrombolytic therapy in acute myocardial infarction. Compared to heparin, dalteparin has a longer half-life and a greater and highly predictable bioavailability, which would suggest dalteparin to be a convenient alternative. Twenty patients with ECG signs of acute transmural myocardial ischemia received streptokinase (1.5 million IU for 60 min) and were allocated to a control group or to open treatment with 50, 75 or 100 IU of dalteparin/kg b.w. s.c. b.i.d., starting 4 h later, for 6 days. Each group consisted of 5 patients. Except for the control group, aspirin was withheld during dalteparin treatment. Anti-factor-Xa (anti-FXa) values increased dose-dependently during the first 24 h and were maintained throughout the study period. On day 6, anti-FXa levels after 100 IU/kg b.w. were 0.79 (0.59-1.00) IU/ml (median, min.-max.) 4 h after administration of dalteparin, and 0.51 (0.34-0.82) IU/ml before the subsequent dose of dalteparin. In conclusion, our results indicate that a dalteparin dose slightly higher than 100 IU/kg b.w. is required in order to obtain the presumed therapeutic range of anti-FXa (0.6-1.0 IU/ml).

Adult↗