PubMed Health⌕ Search

Biomedical subjects

E Hoberg

Publications and source records attributed to E Hoberg.

35 records · Page 2Linked to original sources

[Perioperative myocardial ischemia in patients with peripheral arterial occlusive diseases].

Patients with peripheral vascular disease (PVD) often have coronary artery disease (CAD) which means an increased risk during anesthesia. The prevalence of CAD is nearly 50% among such patients. Owing to claudication, diagnostic stress tests can rarely be performed in PVD patients. In order to evaluate the frequency of transient perioperative myocardial ischemia, Holter monitoring was performed in 30 consecutive PVD patients with ASA II-III and AVK scale (Fontaine) II-IV who were undergoing femoropopliteal bypass surgery. Patients who had left bundle branch block and left ventricular hypertrophy or were taking digitalis medication were excluded from Holter monitoring. The ST-segment analysis of the frequency modulated recordings (n = 19) revealed episodes of myocardial ischemia in 26% of the patients. Most (75%) of the episodes occurred preoperatively, and 25%, during or after the anesthesia or during preparation for it. Risk factors for CAD were more often found in patients with ST segment alterations than in patients without ST segment deviations, even though the preoperative antianginal medication administered was comparable in the two subgroups. It is concluded that in a considerable subset of PVD patients silent myocardial ischemia occurs, which can be related to the different perioperative intervals by means of ST segment analyses of Holter recordings. The ST segment may allow a better insight into the cardiac state of PVD patients. Further studies are necessary in larger populations to test our suspicion.

Aged↗

Circulating cardiac myosin light chains in patients with angina at rest: identification of a high risk subgroup.

To detect myocardial cell damage, serum samples of 42 consecutive patients with angina at rest were screened for cardiac myosin light chains, which were detected in 22 patients (52%). In 17 of these patients there was a persistent release of myosin light chains lasting until the 4th hospital day, whereas in 7 patients myosin light chains were only detectable during the initial 24 h after admission. The presence of myosin light chains correlated with signs of ischemia in the electrocardiogram (ECG) (p less than 0.05) and with the extent of coronary artery narrowing (p less than 0.05). Cardiac myosin light chains were elevated in serum only if there was a greater than or equal to 75% diameter narrowing in at least one major vessel. In all five patients who developed transmural myocardial infarction during the course of their hospital stay, myosin light chains were detectable greater than or equal to 28 h before the diagnosis of myocardial infarction could be established by ECG criteria and conventional serum enzymes. Thus the detection of circulating cardiac myosin light chains enables one to identify a subgroup of patients with angina at rest having more severe coronary artery disease with a worse outcome.

Adult↗

Monoclonal antibodies specific for human cardiac myosin: selection, characterization and experimental myocardial infarct imaging.

Radiolabelled anti-myosin antibodies (AM Ab) specifically accumulate in necrotizing myocytes and, therefore, allow the scintigraphic detection of myocardial infarction. In order to provide a constant supply of myosin-specific antibodies, the somatic cell fusion technique was used for the selection and propagation of AM Ab. Out of 126 antibody producing cell lines, nine were selected for further subcloning, due to their high affinity for purified myosin. For the in vivo imaging, two IgG-antibody molecules appeared particularly useful based on their antigenic specificity as assessed by immunoblotting and indirect immunofluorescence technique. After radiolabelling with iodine-123, undigested antibody molecules or their Fab fragments were injected into 10 dogs with experimental myocardial infarction. The accumulation of radioactivity in myocardial infarction was assessed by in vivo imaging and in vitro scintigraphy of ventricular slices stained by tetrazolium. The use of undigested AM Ab resulted in a high uptake ratio of radioactivity in the infarcted as compared to normal myocardium (20:1). In vivo infarct imaging, however, was not possible due to sustained labelling of the blood pool. The uptake ratio of iodine-123 labelled Fab fragments was only 9:1, but due to a faster plasma clearance of the Fab fragments, uptake in the heart could be visualized 5 h after intravenous injection. Clear differentiation between infarcted and noninfarcted myocardium, however, was limited by accumulation of radioactivity in the thoracotomy wound, in the liver, and in the stomach.

Animals↗

[Balloon dilatation in unstable angina pectoris and acute myocardial infarct].

Early results after percutaneous transluminal coronary angioplasty (PTCA) in patients with unstable angina or acute myocardial infarction were compared with those in patients with stable angina. The primary success rate in 115 patients with unstable angina was 72%, in 73 with acute myocardial infarction 78%, and in 213 with stable angina 79%, i.e. there was no difference between the three groups. In patients with acute myocardial infarction and primary successful PTCA control angiography was performed one month after PTCA, in patients with unstable and stable angina 6 months after PTCA. Angiographic findings were identical in the three groups. But the results after successful balloon dilatation were dependent on the extent of primary success: in all three groups, patients in whom the post-dilatation control angiography revealed recurrence of stenosis the primary results were worse than in those without. There was no difference between those patients with lasting success and those with recurrence as regards cholesterol level, arterial hypertension, diabetes, and smoking habits. It is concluded that in every patient with acute symptoms of coronary heart disease the indication for PTCA should be considered.

Angina Pectoris↗

Holter monitoring before, during and after percutaneous transluminal coronary angioplasty for evaluation of high-resolution trend recordings of leads CM5 and CC5 for ST-segment analysis.

Frequency-modulated Holter monitoring of leads CM5 and CC5 was performed before, during and after percutaneous transluminal coronary angioplasty (PTCA) in 16 patients with stenosis of the left anterior descending coronary artery, in 5 patients with stenosis of the left circumflex coronary artery, and in 5 patients with stenosis of the right coronary artery. All patients presented with 1-vessel coronary artery disease and stable or unstable angina pectoris. ST-segment analysis was based on high-resolution trend recordings. During balloon inflations all patients had significant (at least 0.1 mV) ST-segment changes in lead CM5. In lead CC5, associated ST-segment deviations were found in 22 of 26 patients. During 29.2 +/- 13.6 hours before PTCA, 90 spontaneous episodes with significant ST-segment deviations were detected in 10 patients. Of these episodes, 17% were characterized by ST-segment deviations in lead CC5 only, 57% by ST-segment deviations in lead CM5 only, and 27% by simultaneous ST-segment deviations in both leads. Asymptomatic episodes occurred twice as frequently as symptomatic episodes (66 vs 34%). Symptomatic episodes were more often characterized by ST-segment deviations of at least 0.15 mV (48 vs 9%, p less than 0.001) and by ST-segment deviations observed in both leads simultaneously (48 vs 15%, p less than 0.001). During 34.8 +/- 10.6 hours after successful PTCA, 5 spontaneous asymptomatic episodes with significant ST-segment deviations were detected in 2 patients.

Adult↗

[Silent ischemia in stable angina pectoris. Characteristics in frequency-modulated long-term ECG].

Frequency-modulated (FM) long-term ECGs, leads CM5 and CC5, were analysed to define the features which characterize silent ischemia in stable angina. Of 40 consecutively examined out-patients with angiographically proven coronary heart disease 22 had more than three ischemia-type episodes, of which at least one each was symptomatic or asymptomatic. Compared with the asymptomatic ones, the symptomatic episodes had significantly more ST deviations of greater than or equal to 0.15 mV (45.5% vs 17.3%; P less than 0.001) or greater than or equal to 0.2 mV (24.2% vs 5.8%; P less than 0.001). Simultaneous ST deviations in both leads were registered more frequently during symptomatic than silent episodes (43.9% vs 22.4%; P less than 0.01). The incidence of prolonged (greater than or equal to 10 min) ST-deviations was not significantly different during symptomatic and asymptomatic episodes (47.0% vs 40.4%; P greater than 0.05). While only 29.7% of all identified episodes were accompanied by symptoms, interindividual comparison indicated that in 63.6% of patients the ischemic episode with maximal ST deviation was symptomatic. It is concluded from these results that in stable angina the occurrence of anginal symptoms is influenced by the intensity and extent of the myocardial ischemia.

Ambulatory Care↗

Myoglobin, creatine kinase-B isoenzyme, and myosin light chain release in patients with unstable angina pectoris.

In 27 patients presenting with angina pectoris at rest and normal serum creatine kinase (CK) activity, cardiac myosin light chains (CM-LC), myoglobin (MG), and CK-B isoenzyme were determined in 7 serial blood samples by radioimmunoassays. Measurable amounts of CM-LC were found in at least one serum sample in 13 patients. MG was found to be elevated in 9, and CK-B in 8 of these patients. In the 189 serum samples determined, CM-LC were found more frequently elevated (21.7%) than MG (13.2%, P less than 0.05) or CK-B (12.2%, P less than 0.05). Coronary angiograms were obtained in 21 of the 27 patients. Elevated marker protein concentrations were found only in patients with coronary artery stenosis greater than or equal to 70% of at least one coronary artery. The incidence of elevated serum concentrations of any of the 3 marker proteins determined was higher in patients with 3 vessel disease than in those with 1 or 2 vessel disease (33.9% vs 15.6%, P less than 0.05), and it was higher in patients with a history of previous myocardial infarction than in those without (34.5% vs 11.4%, P less than 0.001). The findings suggest that in a subgroup of patients with angina pectoris at rest but without evidence of acute myocardial infarction, ischaemic damage of small myocardial areas can be detected by serological assays of high sensitivity. Among the marker proteins studied, CM-LC were found the most sensitive.

Adult↗

[Long-term frequency-modulated ECG recordings after PTCA in a patient with unstable angina pectoris. A case report].

A patient presenting with unstable angina due to severe stenosis of the left anterior descending coronary artery encountered 6 episodes with ST segment depressions greater than or equal to 0.1 mV during frequency-modulated Holter monitoring. Four episodes were associated with anginal pain, 2 were asymptomatic. Percutaneous transluminal coronary angioplasty (PTCA) was performed. During balloon inflations horizontal ST segment depressions occurred. After successful PTCA, the patient remained asymptomatic and no significant ST segment changes were detected by Holter monitoring. Thus, by frequency-modulated Holter monitoring before, during, and after PTCA, the ischaemic cause of episodes with ST segment depressions greater than or equal to 0.1 mV could be demonstrated.

Angina Pectoris↗

[Sudden cardiac death in long-term electrocardiography].

An analysis has been made of long-term ECG recordings in 11 patients, 9 men and 2 women, mean age 69 +/- 7 years, who were carrying ECG recording equipment at the time of sudden death. Nine patients had coronary heart disease, one patient a dilatative cardiomyopathy and another one a combined aortic valve defect. Seven patients had a history of syncope. All patients had signs of cardiac insufficiency (NYHA index 3.0 +/- 0.6, heart-thorax quotient 0.55 +/- 0.05). Sudden death occurred predominantly whilst resting. In one patient it was due to bradyarrhythmia, in 10 to tachyarrhythmia, mostly ventricular tachycardia (initial heart rate 198 +/- 43/min; n = 8) which degenerated into ventricular fibrillation. Atrial fibrillation was present in 8 patients at the time of sudden death. Premonitory warning arrhythmias were not consistently detectable: comparison of arrhythmias in the first and last hour showed significant increases only in single ventricular extrasystoles (135 vs. 278 VES/h, P less than 0.05), not however in repetitive arrhythmias. An R-on-T phenomenon, as trigger mechanism of ventricular tachycardia, occurred in 5 cases. A synopsis of the published reports on approximately 110 patients with sudden death during long-term electrocardiographic monitoring confirmed that acute death is caused by bradyarrhythmias in approximately 15% (17 patients), and by tachyarrhythmias in 85% (94 patients). An increase in ventricular arrhythmias in the hour prior to death was observed in about 50% of patients and the R-on-T phenomenon, as the initiating mechanism for ventricular tachycardia, in 42%.

Aged↗

[R-wave amplitude during left ventricular volume changes in healthy hearts].

The relationship between R-wave amplitude and left ventricular volume was studied in four tests, each including six normal adults. The means of 10 heart cycles of the R-wave amplitude in surface ECG lead V5 (RV5) and the echocardiographically determined left ventricular enddiastolic dimension (LVEDD) were compared before and during different interventions. After inhalation of 0.3 ml isoamylnitrit, LVEDD was reduced to 7.7%, RV5 to 15.0% below control. During a maneuver of Valsalva, LVEDD decreased to 8.6%, RV5 to 12.9% below control. In both tests heart rates increased markedly. After oral application of propranolol (0.7 to 1.0 mg/kg) LVEDD did not change, whereas RV5 decreased to 8.2% below control. During rapid intravenous infusion of 1 l NaCl 0.9% in 10 to 15 minutes, LVEDD increased to 15.7% above control. R-wave amplitude remained constant. Thus the results of these last two tests let us doubt whether the Brody-effect can be translated without limitation on the in-vivo situation in man.

Adult↗

[ST-segment depression and R-amplitude changes during bicycle stress test in patients with coronary artery disease (author's transl)].

56 patients were examined with bicycle stress tests. Sensitivity and specificity of ST-segment depression were compared with R-wave amplitude changes. All patients had a coronary angiography because of suspected coronary artery disease (CAD). The specificity of ST-segment depression was 71%, for R-wave amplitude changes 50%. The sensitivity for ST-segment depression was 76% and for R-wave amplitude changes 50%. In addition in 7 patients with angiographically demonstrated CAD repeated stress tests were done. The ST-segment changes were nearly constant in all examinations, whereas the R-wave amplitude in V5 in 5 out of 7 patients changed considerably between decrease and increase. Considering these intraindividual changes, it seems doubtful whether the evaluation of the R-wave amplitude proves to be an improvement of the non-invasive diagnostic procedures of CAD.

Coronary Disease↗

Influence of endogenous S-adenosylmethionine on the determination of catechol O-methyltransferase activity in red blood cells.

A double isotope method for the simultaneous determination of S-adenosylmethionine (SAM) and catechol O-methyltransferase (COMT) activity in red blood cells was developed. Healthy persons contained 7.9 +/- 1.9 nmol SAM per ml red blood cells and 1.9 to 3.8 nmol per ml plasma. Epinephrine increases the SAM biosynthesis rate in red blood cells. The possible influence of endogenous SAM on previous methods to determine COMT activity in red blood cells is discussed. The statement of Briggs and Briggs (Briggs, M.H. and Briggs, M. (1973) Experientia 29, 278--281) that COMT activity in red blood cells is lower during the last 3 months of pregnancy could not be verified by us.

Catechol O-Methyltransferase↗