Low molecular weight heparin (dalteparin) as adjuvant treatment of thrombolysis in acute myocardial infarction--a pilot study: biochemical markers in acute coronary syndromes (BIOMACS II).
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OBJECTIVES: This randomized, double blind, placebo-controlled pilot trial evaluated the effect of dalteparin as an adjuvant to thrombolysis in patients with acute myocardial infarction regarding early reperfusion, recurrent ischemia and patency at 24 h. BACKGROUND: Low-molecular-weight heparin, given subcutaneously twice daily without monitoring, might be an attractive alternative to conventional intravenous heparin in the treatment of acute myocardial infarction. METHODS: In 101 patients dalteparin/placebo 100 IU/kg was given just before streptokinase and a second injection 120 IU/kg after 12 h. Monitoring with continuous vector-ECG was done to obtain signs of early reperfusion and later ischemic episodes. Blood samples for myoglobin were obtained at start and after 90 min to evaluate signs of reperfusion. Coronary angiography was performed after 20-28 h to evaluate TIMI-flow in the infarct-related artery. RESULTS: Dalteparin added to streptokinase tended to provide a higher rate of TIMI grade 3 flow in infarct-related artery compared to placebo, 68% versus 51% (p = 0.10). Dalteparin had no effects on noninvasive signs of early reperfusion. In patients with signs of early reperfusion, there seemed to be a higher rate of TIMI grade 3 flow, 74% versus 46% (myoglobin) (p = 0.04) and 73% versus 52% (vector-ECG) (p = 0.11). Ischemic episodes 6-24 h. after start of treatment were fewer in the dalteparin group, 16% versus 38% (p = 0.04). CONCLUSIONS: When dalteparin was added as an adjuvant to streptokinase and aspirin, there were tendencies for less ECG monitoring evidence of recurrent ischemia and better patency at 24 h, warranting further study. (+info)
QT dispersion as an attribute of T-loop morphology.
(2/97)
BACKGROUND: The suggestion that increased QT dispersion (QTD) is due to increased differences in local action potential durations within the myocardium is wanting. An alternative explanation was sought by relating QTD to vectorcardiographic T-loop morphology. METHODS AND RESULTS: The T loop is characterized by its amplitude and width (defined as the spatial angle between the mean vectors of the first and second halves of the loop). We reasoned that small, wide ("pathological") T loops produce larger QTD than large, narrow ("normal") loops. To quantify the relationship between QTD and T-loop morphology, we used a program for automated analysis of ECGs and a database of 1220 standard simultaneous 12-lead ECGs. For each ECG, QT durations, QTD, and T-loop parameters were computed. T-loop amplitude and width were dichotomized, with 250 microV (small versus large amplitudes) and 30 degrees (narrow versus wide loops) taken as thresholds. Over all 1220 ECGs, QTDs were smallest for large, narrow T loops (54.2+/-27.1 ms) and largest for small, wide loops (69. 5+/-33.5 ms; P<0.001). CONCLUSIONS: QTD is an attribute of T-loop morphology, as expressed by T-loop amplitude and width. (+info)
Admission risk assessment by cardiac troponin T in unstable coronary artery disease: additional prognostic information from continuous ST segment monitoring. TRIM study group. Thrombin Inhibition in Myocardial Ischemia.
(3/97)
OBJECTIVES: We investigated whether the addition of 24 h of continuous vectorcardiography ST segment monitoring (cVST) for an early (within 24 h of the latest episode of angina) determination of cardiac troponin T (cTnT) could provide additional prognostic information in patients with unstable coronary artery disease (UCAD), i.e., unstable angina and non-Q wave myocardial infarction. BACKGROUND: Determination of cTnT at admission and cVST are individually reported to be valuable techniques for the risk assessment of patients with UCAD. METHODS: Two hundred and thirty-two patients suspected of UCAD were studied. Patients were followed for 30 days, and the occurrence of cardiac death or acute myocardial infarction (AMI) were registered. RESULTS: One ST segment episode or more (relative risk [RR] 7.43, p = 0.012), a cTnT level > or = 0.20 microg/liter (RR 3.85, p = 0.036) or prestudy medication with calcium antagonists (RR 3.31, p = 0.041) were found to carry independent prognostic information after multivariate analysis of potential risk variables. By combining a cTnT determination and subsequent cVST for 24 h, subgroups of patients at high (25.8%) (n = 31), intermediate (3.1%) (n = 65) and low risk (1.7%) (n = 117) of death or AMI could be identified. CONCLUSIONS: Twenty-four hours of cVST provides additional prognostic information to that of an early cTnT determination in patients suspected of having UCAD. The combination of biochemical and electrocardiographic methods provides powerful and accurate risk stratification in UCAD. (+info)
Prognostic value of maximum ST-vector magnitude during the first 24 h of vectorcardiographic monitoring in patients with unstable angina pectoris.
(4/97)
AIMS: To assess the prognostic importance of alternate ways of quantifying myocardial ischaemia by continuous ST analysis, the maximum ST vector magnitude and the area under the ST vector magnitude trend curve during the first 24 h of continuous ST monitoring. METHODS AND RESULTS: During a 22-month period from 1991 to 1993, 195 patients admitted to our CCU with suspected unstable angina pectoris, were included in the study. During the first 24 h the patients were monitored for ischaemic episodes with computerized vectorcardiography, using a MIDA 1000 system. Twenty seven (14%) of the 195 patients died or had a non-fatal myocardial infarction within 1 year and the maximum ST vector magnitude among those patients was, on average, 201 microV compared with 118 microV in patients who survived 1 year free of myocardial infarction (P<0.01). The area under the ST vector magnitude trend curve was, on average, 1598 microVmin compared with 164 microVmin (P<0.01). By multivariate analysis, the maximum ST vector magnitude emerged as a superior predictor of death or myocardial infarction, compared with the area under the ST vector magnitude trend curve and the number of ST vector magnitude and ST change vector magnitude episodes. The maximum ST vector magnitude and age were independent predictors of death or non-fatal myocardial infarction within 1 year. CONCLUSION: Maximum ST vector magnitude during the first 24 h of vectorcardiographic monitoring seems to be a strong predictor of subsequent death or non-fatal myocardial infarction. (+info)
Comparison of vectorcardiographic and 12-lead electrocardiographic detections of abnormalities in repolarization properties due to preexcitation in patients with Wolff-Parkinson-White syndrome: proposal of a novel concept of a "remodeling gradient".
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Repolarization abnormalities after radiofrequency ablation in patients with manifest Wolff-Parkinson-White syndrome (WPW) have been attributed to cardiac memory of pre-existing changes in repolarization properties. We compared spatial ventricular gradient (VG) from vectorcardiograms with QRST values of 12-lead ECG in 41 patients with WPW (group A, manifest WPW due to left-sided accessory pathway (n = 20); group B, manifest WPW due to right-sided accessory pathway (n = 12); group C, concealed WPW (n = 9)) before and after ablation. Group N (n = 607) served as control. In groups A and B, the abnormalities of spatial VG and QRST values of 12-lead ECG that existed before and 1 day after ablation significantly decreased 1 week after ablation. In group C, spatial VG and QRST values of 12-lead ECG showed no significant changes. The diagnostic ability of spatial VG is almost equivalent to that of the QRST value of ECG in detecting repolarization abnormalities in patients with WPW before and after ablation. We propose a new concept of a "remodeling gradient" directing from the preexcited area to the opposite side of the ventricle as a result of preexcitation-induced electrical remodeling. (+info)
Classification of ventricular pre-excitation. Vectorcardiographic study.
(6/97)
In a study of 45 cases of ventricular pre-excitation, 19 were classified as type A and 20 as type B according to Rosenbaum's criteria, which depend on the polarity of the major deflections in the right praecordial leads and not, as is commonly thought, on the direction of the delta vector. Six cases that could not be classified as type A or type B were termed intermediate. Vectorcardiograms were recorded from 29, and these showed a wide but continuous range of values for both the delta and the main QRS vectors in all three planes. Any classification based on these features must, therefore, depend on arbitrary quantitative data. Three patients in this series had associated right bundle-branch block. A review of the published reports on the association of pre-excitation and bundle-branch block failed to provide a rational basis for the classification of pre-excitation. It is emphasized that Rosenbaum's classification is empirical and its validity is questioned. (+info)
Localization of heart vectors produced by epicardial burns and ectopic stimuli; validation of a dipole ranging method.
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Location of the equivalent cardiac dipole has been estimated but not fully verified in several laboratories. To test the accuracy of such a procedure, injury vectors were produced in 14 isolated, perfused rabbit hearts by epicardial searing. Strongly dipolar excitation fronts were produced in 6 additional hearts by left ventricular pacing. Twenty computer-processed signals, derived from surface electrodes on a spherical electrolyte-filled tank containing the test preparation, were optimally fitted with a locatable cardiac dipole that accounted for over 99% of the root-mean-square surface potential. For the 14 burns (mean radius 5.0 mm), the S-T injury dipole was located 3.4 plus or minus 0.7 (SD) mm from the burn center. For the 6 paced hearts, the dipole early in the ectopic beat was located 3.7 mm (range 2.6 to 4.6 mm) from the stimulating electrode. Phase inhomogeneities within the chamber appeared to have a small but predictable effect on dipole site determination. The study demonstrates that equivalent dipole location can be determined with acceptable accuracy from potential measurements of the external cardiac field. (+info)
Deterioration in peak systolic velocity is closely related to ischaemia during angioplasty: a vectorcardiographic and tissue Doppler imaging study.
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We tested the hypothesis that the extent of signs of ischaemia detected by vectorcardiography (VCG) during elective coronary angioplasty (percutaneous transluminal coronary angioplasty; PTCA) is related to systolic and diastolic myocardial velocities, as determined by tissue Doppler echocardiography. A total of 15 patients undergoing PTCA (12 men/three women; age 61+/-9 years), without prior myocardial infarction and with an ejection fraction of >50%, were included. The balloon inflation was repeated three times, with minimum intervals of 2 min between inflations. Tissue Doppler echocardiography was performed, in an apical two- or four-chamber view, before and at the end of each inflation. Peak systolic velocity, time-to-peak systolic velocity (TTP), peak early (E(m)) and late (A(m)) diastolic velocities, the E(m)/A(m) ratio and isovolumic relaxation time were measured in the basal segments of the left ventricle. VCG recordings were carried out during the whole procedure. ST vector magnitude (ST-VM) and ST change vector magnitude (STC-VM) were monitored. The total duration and area of each VCG change during inflation were calculated for each patient. Isovolumic relaxation time, peak E(m) and A(m) values and the E(m)/A(m) ratio did not change significantly during inflation. Peak systolic velocity decreased (6.7+/-2.0 to 5.3+/-1.9 cm/s; P<0.001) and TTP increased (157+/-60 to 192+/-60 ms; P<0.01) during inflation. Both STC-VM time (r=-0.68, P<0.01) and STC-VM area (r=-0.68, P<0.01) were related to peak systolic velocity during inflation. STC-VM time was also related (r=0.55, P<0.05) to the difference in peak systolic velocity during compared with before inflation. ST-VM was less closely related to peak systolic velocity. Thus the duration and degree of ischaemia, as measured by VCG, are related to peak systolic velocity in the basal segments of the left ventricle. (+info)