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Biomedical subjects

L Mogensen

Publications and source records attributed to L Mogensen.

At least 19 recordsLinked to original sources
PubMed1991

Diffuse embolization following percutaneous transluminal coronary angioplasty of occluded vein grafts: the blush phenomenon.

Percutaneous transluminal coronary angioplasty (PTCA) was performed on 146 saphenous vein grafts in 116 patients. In 29 patients, 31 grafts were totally occluded. Myocardial staining lasting over 5 minutes--"the blush phenomenon"--followed the opening of the occluded grafts in 9 of these patients. In 5 of these 9, enzyme release suggested infarction. A sixth patient died within a few hours of PTCA, with suspected infarction. Autopsy demonstrated diffuse and extensive distal coronary arterial embolization of grumous material, including cholesterol crystals, platelets, and fibrin. The blush phenomenon was not seen following PTCA in the remaining 20 patients with total occlusions, nor in any of the 87 patients with stenosed grafts. We have not observed the blush phenomenon following PTCA of more than 3300 coronary arteries. Of the 9 patients demonstrating the blush phenomenon, 6 had a recent history of myocardial infarction or unstable angina pectoris, compared with 4 of the remaining 20 patients with occluded grafts. We now approach occluded grafts with injection of intragraft thrombolytic agents or with atherectomy prior to PTCA. Future approaches may include atherectomy or laser angioplasty.

Adult↗
PubMed1988

Exercise capacity prior to myocardial infarction relates inversely to enzyme activity during infarction.

Epidemiological studies suggest that myocardial infarction occurs less commonly in physically fit individuals, indicating an inverse relationship between fitness and coronary arterial disease. In this study, the exercise capacity measured prior to infarction, was related to enzyme activity during subsequent infarction. Out of 512 consecutive male patients with acute infarction 35 were found who had previously performed an eligible exercise test. The exercise capacity was inversely related to enzymic activity during the infarction.

Adult↗
PubMed1988

Provocation of chest pain in patients with coronary insufficiency using the vasodilator adenosine.

Chest pain provoked by intravenous injection of adenosine was compared with natural angina pectoris in five patients with ischaemic heart disease. In seven healthy subjects a possible myocardial site for provocation of the chest pain was evaluated by analysis of time delays from injection to symptoms. The healthy volunteers were given the maximum tolerable dose of adenosine intravenously, together with 99Technetium-diethylentriaminpentaacetate (99Tcm-DTPA). Chest pain started after 4.1 +/- 2.4 s and reached its maximum 8.4 +/- 4.1 s after maximum left ventricular radioactivity. The patients with a history of typical angina pectoris were given similar doses of intravenous adenosine and the provoked chest pain did not differ in quality from the patients' habitual angina pectoris. The patients did not develop electrocardiographic signs suggesting myocardial ischaemia. Heart rate and blood pressure did not indicate increased myocardial work. In conclusion, the results concur with the hypothesis that adenosine elicits angina pectoris by stimulation of intracardiac adenosine receptors.

Adenosine↗
PubMed1987

Depressed melatonin secretion in patients with nightmares due to beta-adrenoceptor blocking drugs.

Nocturnal urinary melatonin excretion was evaluated in six patients with nightmares and hallucinations during treatment with beta-adrenoceptor blocking agents, and compared to six control patients with similar diagnoses and treatment but without such symptoms from the central nervous system (CNS). Nightly melatonin excretion was lower in all cases with nightly CNS-symptoms than in the control patients. The results also suggest drug differences and dose dependency. It is concluded that in predisposed patients CNS side-effects induced by beta-adrenoceptor antagonists are related to depressed nightly melatonin secretion.

Adrenergic beta-Antagonists↗
PubMed1987

Transthoracic electrical impedance at 1 and 100 kHz--a means for separating thoracic fluid compartments?

The electrical impedance of biological tissues varies with their water and electrolyte contents. Alternating current above 5-10 kHz passes both intra- and extracellular fluid, and lower frequency current preferentially extracellular fluid. In an attempt to evaluate thoracic fluid in different compartments, transthoracic electrical impedance (TEI) was measured at 1 and 100 kHz in 15 consecutive patients, without overt left heart failure and under haemodynamic surveillance, during the first two days of myocardial infarction. To achieve different states of hydration the patients were given i.v. furosemide, either 40 mg t.i.d. (high dose group--HDG) or 20 mg once daily (low dose group--LDG). Effects of altered body position and the respective furosemide injections, were evaluated on both days. Mean 24-h-diuresis was 3.9 l in the HDG and 2.5 l in the LDG. After 24 h mean pulmonary arterial diastolic pressure had decreased by 30% in the HDG but remained almost unchanged in the LDG. By then mean basal TEI was increased only in the HDG, by 17% at 1 kHz and 13% at 100 kHz. On Day 1, within one hour after furosemide, TEI increased temporarily by 3-5%, at both frequencies and in both groups. On Day 2, this short-term increase was similar in the LDG at both frequencies and in the HDG at 100 kHz, but not at 1 kHz, consistent with a major extracellular fluid loss in the HDG. TEI at 1 and 100 kHz may thus reflect extracellular and total thoracic fluid, respectively.

Acute Disease↗
PubMed1986

Influence of prophylactic furosemide on arrhythmias in acute myocardial infarction--a controlled study.

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.

Aged↗
PubMed1986

Influence of furosemide and body posture on transthoracic electrical impedance in AMI.

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.

Body Water↗
PubMed1985

Release patterns of CK-MB and mitochondrial CK following myocardial ischaemia.

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.

Adult↗
PubMed1985

Criteria for intraventricular conduction disturbances and pre-excitation. World Health Organizational/International Society and Federation for Cardiology Task Force Ad Hoc.

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.

Bundle-Branch Block↗