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Biomedical subjects

L Erhardt

Publications and source records attributed to L Erhardt.

At least 73 records · Page 4Linked to original sources
PubMed1992

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↗
PubMed1992

Does diffuse coronary atherosclerosis affect the relation between coronary stenoses and uptake of thallium-201 after exercise?

It has been proposed that diffuse coronary atherosclerosis influences the myocardial perfusion. We performed a study of 94 young men with previous myocardial infarction in order to find out whether the presence and extent of diffuse coronary atherosclerosis affected the relation between maximal stenosis and myocardial perfusion in areas remote from the infarction. The patients were examined by planar-imaging thallium-201 scintigraphy, following exercise, and coronary angiography within 6 months after myocardial infarction. The maximal distinct stenosis and diffuse coronary atherosclerosis, comprising both plaque size and extent, were semiquantitatively assessed. The correlation coefficients between maximal stenosis within the LAD, RCA, and LCX vascular territories and the corresponding initial uptake of thallium were 0.52 (P = 0.0001), 0.30 (P = 0.04), and 0.46 (P = 0.02), respectively. No change of the correlations was found, except for a slight increase of the r-value from 0.30 to 0.37 in regions corresponding to RCA, after controlling for the diffuse atherosclerosis score in a multiple stepwise regression analysis. These findings indicate no impact of diffuse coronary atherosclerosis on regional myocardial perfusion in areas remote from the infarction.

Angiography↗
PubMed1992

Myocardial reperfusion in thrombolysis A 99Tcm-Sestamibi SPECT study in patients with acute myocardial infarction.

This study presents the outcome of myocardial scintigraphy performed before and after thrombolytic treatment in 16 patients with acute myocardial infarction using 99Tcm-Sestamibi (Cardiolite, Du Pont Scandinavia AB, Kista, Sweden). The patients were given 99Tcm-Sestamibi intravenously as soon as possible after the decision to give thrombolytic treatment. When the patients were in a clinically stable state after the thrombolytic treatment, myocardial perfusion was analysed with the gamma camera using single photon emission computerized tomography (SPECT). A second 99Tcm-Sestamibi tomography was carried out on the second to fourth day after the myocardial infarction. Data reconstruction was done with the 'Bull's eye technique'. Nine patients received thrombolysis < 3 h from the onset of pain. In this group six patients (66%) improved their myocardial perfusion by > 10% after treatment, while all seven patients who received treatment > or = 3 h after the onset of pain improved their myocardial perfusion by < 10%. This study emphasises the importance of early diagnosis and treatment of patients with acute myocardial infarction in order to salvage myocardium.

Aged↗
PubMed1992

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↗
PubMed1991

Beta receptor antagonists in the treatment of heart failure.

The use of beta-receptor antagonists in the treatment of heart failure is controversial. Available data do not allow general recommendations regarding their use. In dilated cardiomyopathy, several studies suggest that long-term treatment in individual patients reduces symptoms and increases exercise capacity. Short-term treatment is usually not beneficial, except in patients with ischemically induced left ventricular dysfunction. In heart failure, post myocardial infarction and in chronic ischemic heart disease, no proper long-term study has been performed to evaluate its effects. However, patients with acute myocardial infarction tolerate beta blockers, despite the presence of left ventricular dysfunction and long-term prognosis is improved. Newer agents, some with ancillary properties, such as intrinsic activity and vasodilatation, may have advantages. In the future we need a better description of the cardiac status in our patients in order to be able to select those that will respond favorably to beta-receptor antagonists. The mechanisms by which some patients improve are still obscure. Protection against receptor downregulation, restoration of receptor density, protection against cardiotoxicity of catecholamines, and improvement in ischemic systolic and diastolic left ventricular function are all possible. The fear that beta-receptor antagonists are dangerous in heart failure is in most instances not warranted, but an initial deterioration may have to be accepted in order to gain long-term beneficial effects. Ongoing studies in both idiopathic cardiomyopathy and in postinfarction failure will hopefully help us to define the use of beta-adrenoceptor antagonists in the future.

Adrenergic beta-Antagonists↗
PubMed1990

Two-year survival after myocardial infarction.

We have studied 773 consecutive cases (706 individuals) with definite myocardial infarction treated in the Coronary Care Unit at Danderyd Hospital in Stockholm during the period 1984-85. Hospital mortality was 12.9% in all patients and 8.9% in patients under 70 years of age. Six hundred and six patients were discharged from the hospital and followed up for 2 years. The 2-year mortality in ischaemic heart disease was 14.4% in all patients and 9.5% in patients under 70 years of age and, including all causes of death, 20.3% and 14.6%, respectively. Our policy for medical treatment included frequent use of beta-adrenergic blocking agents, even in heart failure, and restricted use of antiarrhythmic drugs and digitalis. A short delay of admission may have been beneficial for the result of different kinds of anti-ischaemic intervention. Furthermore, a routinely performed exercise ECG before discharge and after 6 weeks, as part of a structured follow-up, has improved our ability to detect complications at an early stage and to optimize medical treatment.

Aged↗
PubMed1988

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↗