[Intravenous amiodarone in life-threatening ventricular arrhythmias].
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Biomedical subjects
Publications and source records attributed to L Mogensen.
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In a prospective controlled study the frequency of arrhythmias during the early phase of acute myocardial infarction (AMI) was evaluated in 73 consecutive patients randomly assigned to either high or low dose furosemide prophylaxis. The high dose group (HDG) received 120 mg and the low dose group (LDG) 20 mg furosemide i.v. during the initial 24 hours in hospital. Increased diuresis, haemoconcentration and augmented heart rates were found in the HDG. No electrolyte disorders separated the groups. Hypokalemia was seen in two HDG patients and in one LDG patient on admission, and in two and three patients respectively after 24 hours. Continuous ECG recordings at a paper speed of 10 mm s-1 were obtained from all patients. Two patients in the HDG had ventricular fibrillation, none in the LDG. The number of patients with various arrhythmias was not significantly different in the two groups. Supraventricular tachyarrhythmias were more common in the HDG, whereas ventricular tachycardia and ventricular extrasystoles were seen more often in the LDG. We conclude that heart rate and recurrence of tachyarrhythmias in AMI may be influenced by furosemide therapy, seemingly through mechanisms other than electrolyte imbalance.
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Transthoracic electrical impedance (TEI) is related to thoracic fluid content. In order to analyze this relation, we studied the acute effects of changes in body posture and of intravenous administration of furosemide on TEI in patients with different diuretic regimens. The TEI was measured using a tetrapolar electrode system, and a 100 microA constant current at 100 kHz. The measurements were performed repeatedly during the first two days in 15 consecutive patients with acute myocardial infarction (AMI) and without overt left heart failure, as evaluated from clinical data and bedside catheterization. It was concluded that TEI appears to be a sensitive, noninvasive means of evaluating changes in thoracic fluid content in AMI.
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Following myocardial damage as in acute myocardial infarction (AMI) or open heart surgery, the tissue damage might result in a release of mitochondrial CK (CK-MIT). The presence of this CK isoenzyme in serum may be detected after chromatographic separation of CK-activity on Sephacryl S-200. By combining chromatographic separation of CK-MB with immunologic inhibition of CK-M, both CK-MB and CK-MIT can be estimated in serum. Using this procedure changes in enzyme activities were studied in ten patients with AMI and twelve patients subjected to open heart surgery using cardioplegia. Following AMI CK-MB peaked about 24 h after onset of ischaemic symptoms. CK-MIT increased similarly and reached a plateau after 24 h where it remained during an additional 24-36 h. At peak CK-MB concentration, the corresponding CK-MIT activity was about 22% of the CK-MB activity. Following cardiac surgery there was a rapid release of CK-MB with a peak about 5 h after release of aortic cross-clamping, and with a simultaneous CK-MIT activity amounting to 19% of the CK-MB activity. In conclusion, CK-MIT is released into serum following myocardial ischaemia. Its appearance has time characteristics similar to that of other mitochondrial enzymes. The CK-B method does not specifically determine CK-B, but non-CK-M, which in cardiac ischaemia at peak serum CK-MB concentrations includes about 20% CK-MIT.
In an effort to standardize terminology and criteria for clinical electrocardiography, and as a follow-up of its work on definitions of terms related to cardiac rhythm, an Ad Hoc Working Group established by the World Health Organization and the International Society and Federation of Cardiology reviewed criteria for the diagnosis of conduction disturbances and pre-excitation. Recommendations resulting from these discussions are summarized for the diagnosis of complete and incomplete right and left bundle branch block, left anterior and left posterior fascicular block, nonspecific intraventricular block, Wolff-Parkinson-White syndrome and related pre-excitation patterns. Criteria for intraatrial conduction disturbances are also briefly reviewed. The criteria are described in clinical terms. A concise description of the criteria using formal Boolean logic is given in the Appendix. For the incorporation into computer electrocardiographic analysis programs, the limits of some interval measurements may need to be adjusted.
Fifty-seven consecutive patients with acute myocardial infarction (AMI), admitted to a coronary care unit (CCU) within 6 h from onset of symptoms were included in the study and randomly allocated to nifedipine treatment or placebo. The 23 patients in the treatment group received 10 mg nifedipine orally at the onset of the study, after 30 min, and then every 6 h. Placebo was given to the 34 patients in the control group. The study was double blind. Serum time-activity curves for creatine-kinase-MB (CK-MB) and myoglobin (MG) were established from frequent determinations. The two patient groups did not differ significantly regarding average cumulative MG and CK-MB release. In both groups the range was wide, with the largest maximal individual release about 30 times larger than the smallest. In most patients the enzyme release occurred stepwise, resulting in two or more separate peaks. In the treatment group significantly fewer patients had multiple peaks of MG (P less than 0.05) and CK-MB (P less than 0.025) release. The initial peaks had a longer duration in the treatment group and total release tended to stop earlier. In the control group a highly significant correlation between cumulative MG and CK-MB release was obtained, while in the treatment group no such correlation was observed. In conclusion, oral administration of nifedipine during acute myocardial infarction appears to influence the pattern of enzyme release, although no effect on the total cumulative release could be demonstrated.
A case of fatal thromboembolic occlusion of the left coronary artery at selective coronary arteriography is described. The course of events and the findings at autopsy suggest that thrombotic material was deposited on one intravascular catheter and transferred to a second catheter inserted over the same guide wire. Contrast injection through the second catheter into the left coronary ostium resulted in immediate and fatal occlusion of the two major branches of the left coronary artery.
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In prospectively collected consecutive patient data from two coronary care units (CCU), 32 patients with acute myocardial infarction (AMI) developed primary or complicating ventricular fibrillation (VF). A 12-lead ECG on the day of admission was available in 30 patients, and was compared to similar ECGs from a control group of 90 consecutive AMI patients without VF. Left anterior hemiblock (LAH) occurred in 33% of the VF patients and in 11% of the controls; the difference is statistically significant. In 20 of the 32 patients the VF occurred during continuous ECG registration. The QRS complex initiating the VF was as frequently of left as it was of right bundle branch block configuration. When compared with a second control group of 77 consecutive AMI patients under continuous ECG recording who did not develop VF, the heart rate in the VF patients was significantly higher just prior to the development of this arrhythmia. The VF initiating coupling interval was shorter than the upper normal limit of the QT interval in 40% of the VFs. In primary VF and in patients not treated with antiarrhythmic drugs the coupling intervals were close to the upper normal limit of the QT interval. In complicating VF and particularly when antiarrhythmic therapy was used the coupling intervals showed a wider variation.
Fifty consecutive patients with acute myocardial infarction admitted to a coronary care unit within 6 hours from onset of symptoms were randomly assigned either to a treatment group (n=27) receiving glucose-insulin-potassium-albumin (GIKA) or to a control group (n=23), comparable regarding clinical data, receiving 5.5% glucose. Both infusions were given intravenously at a rate of 1.2 ml/kg b.wt./hour during 48 hours. The GIKA solution contained 40 mEq K+, 10 ml 20% albumin and 16 IU regular crystalline insulin per 1000 ml 10% glucose. Before the infusion, the treatment group received an i.v. loading dose of 50 ml 50% glucose. Serum time activity curves for creatine kinase (CK) and myoglobin (MG) were established from frequent blood level determinations. A 15-minute single-lead ECG was recorded every fourth hour and subsequently analysed for ventricular arrhythmias. The two patient groups did not differ regarding cumulative MG and CK release. The GIKA group had significantly more patients with high MG/CK ratios (p less than 0.02). No clinically significant difference was found between the two patient groups regarding ventricular arrhythmias, even if ventricular extrasystoles tended to occur less frequently in the GIKA group.
Fifty-five patients with acute myocardial infarction were examined with thallium-201 scintigraphy before discharge from hospital. Fifty-one showed significant scintigraphic defects. The number of abnormal Q waves in a 12-lead ECG but not the maximal ASAT value for each patient were correlated to the total estimated image defect. Mortality during the follow-up period of 14-28 months was not related to the estimated total image defect, but the two early deaths occurred among patients with the most dilated left ventricles.
Serum creatine kinase (CK) isoenzyme MB and total CK activity concentrations in 11 patients with acute myocardial infarction (AMI) were compared with the corresponding enzyme activities in 25 patients after coronary bypass surgery, not complicated clinically by AMI. Peak CK-MB occurred 2 +/- 0 (mean +/- SEM) hours after the end of surgery (mean duration of operation 6 hours), but 17 +/- 1 hours from the onset of symptoms in AMI. The plasma half"life for CK-MB was 11 +/- 1 hours under both conditions. Peak total CK was found after about 20 hours in both series of patients. Total CK half-life was 17 +/- 2 hours in AMI, but 30 +/- 3 hours following surgery. CK kinetics were thus different in these two situations, indicating different mechanisms for the elevations of serum CK-MB activity. In conclusion, the time course for the transient CK-MB elevation following bypass surgery should be considered in the diagnosis of peri operative infarction.
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