Biomedical subjects

S Holmberg

Publications and source records attributed to S Holmberg.

At least 181 records · Page 10Linked to original sources

PubMed1984

Effects of felodipine on systemic and coronary haemodynamics in patients with angina pectoris.

In order to study the systemic and coronary haemodynamic effects of felodipine, a new dihydropyridine derivative, 10 patients with coronary artery disease were studied during cardiac catheterization. Measurements were performed at rest and during pacing-induced angina pectoris. At rest, the heart rate rose from 70 +/- 20 to 78 +/- 20 (P less than 0.05), the systemic arterial pressure decreased by about 20% (P less than 0.01) and the cardiac index rose from 2.9 +/- 1.2 to 4.0 +/- 1.0 (P less than 0.05). The coronary sinus flow (CSF) increased about 50% (P less than 0.01). During pacing to the same heart rate as in the control measurements, felodipine induced similar changes in systemic haemodynamic values as in the resting position. Myocardial lactate extraction and ST segment depression were not significantly altered. After felodipine, the pacing rate could be further increased in 7 patients as compared with the control value. Both systemic and coronary effects were then very similar compared with those during the lower pacing rate. In conclusion, felodipine is a very potent systemic and coronary vasodilator with potential value in the treatment of hypertension and cardiac failure. The drug may also be of value in the treatment of ischaemic heart disease, but further studies with titration of optimal doses are needed in that respect.

Adult↗

PubMed1984

Effect of metoprolol on chest pain in acute myocardial infarction.

A total of 1395 patients aged 40 to 74 years were included in a double blind trial with the beta 1 selective blocker metoprolol in suspected acute myocardial infarction. Metoprolol was given intravenously (15 mg) as soon as possible after admission to hospital followed by 200 mg daily for three months. A placebo was given in the same manner. The severity of chest pain in the acute phase was calculated by recording the number of injections of analgesics given and the time from the start of blind treatment to the time when the last analgesic was given (duration of pain). The patients receiving metoprolol were given a lower mean number of injections of analgesics during the first four days and after randomisation than those receiving a placebo. The estimated duration of pain was shorter in the metoprolol group than in the placebo group. These effects were related to the initial heart rate, the initial systolic blood pressure, and the final site of the infarct as determined electrocardiographically. Thus metoprolol given in the acute phase of suspected or definite myocardial infarction appears to reduce the severity of chest pain.

Adult↗

PubMed1984

Development of congestive heart failure after treatment with metoprolol in acute myocardial infarction.

In a double blind study of metoprolol in the treatment of suspected acute myocardial infarction 698 patients (study group) received metoprolol and 697 a placebo (control group). Metoprolol was given in an intravenous dose of 15 mg as soon as possible after admission to hospital followed by 50 g by mouth four times a day for two days and thereafter 100 mg twice a day for three months. A placebo was similarly given. Congestive heart failure occurred in a similar percentage of patients in both the study (27%) and the control groups (30%). Its severity was estimated by calculating the total dose of frusemide given during the first four days in hospital. Less frusemide was given to patients treated with metoprolol compared with those given a placebo in the total series. An appreciably lower total dose of frusemide was given to patients included in the trial less than or equal to 12 hours after the onset of pain and treated with metoprolol compared with a placebo, while no difference was seen among patients treated later. The initial heart rate, systolic blood pressure, and infarct site affected the results.

Adult↗

PubMed1984

Pacemaker dependence in patients with bifascicular block during acute anterior myocardial infarction.

Eleven patients with bifascicular block complicating anteroseptal acute myocardial infarction were studied to determine the effect of prophylactic permanent pacing; eight of them also had transient high grade atrioventricular block during the acute phase of the infarction. One month after the infarction an electrophysiological study was performed and a bradycardia indicating pacemaker implanted. All the patients were followed for two years. Six had bradycardia detected, two of whom did not have high grade atrioventricular block during the index infarction. Seven patients died, four of them suddenly. There was no correlation between the electrophysiological findings and subsequent development of bradycardia. Thus pacemaker dependence seems to be common in patients with bifascicular block complicating acute myocardial infarction. Mortality is, however, also high in patients treated with pacemakers. Prospective studies to determine the predictive factors in those patients with an anterior acute myocardial infarction and who benefit from a combination of permanent pacemaker treatment and antiarrhythmic treatment are needed.

Aged↗

PubMed1984

Enzymatically and electrocardiographically estimated infarct size in relation to pain in acute myocardial infarction.

In 563 patients with acute myocardial infarction and no previous myocardial infarction, the estimated infarct size was related to the estimated duration of pain and the amount of analgesics given. The size of infarction estimated from analyses of heat-stable lactate dehydrogenase (EC 1.1.1.27) at 12-hour intervals for 48-108 h and from Q- and R-wave changes in the ECG correlated positively, although weakly with duration of the pain and the amount of analgesics given. These data support the hypothesis that larger infarcts, as a group, evolve over a longer time period than smaller infarcts and that the duration of pain in many patients might be an indicator of the infarct size. In the individual patient, however, one cannot predict the size of the infarction from the severity of pain.

Adult↗

PubMed1984

Preoperative 99mTc-MDP scintimetry of femoral neck fractures.

Preoperative 99mTc-MDP-scintimetry was performed in 117 patients with femoral neck fractures. Scintimetry was shown to be superior to visual evaluation. The ratio was calculated of the uptake in the femoral head of the fractured side over that in the unfractured side, with compensation for the increased trochanteric femoral activity found on the fractured side. A ratio above 0.90 correlated well with uneventful healing in both undisplaced and displaced fractures. Preoperative scintimetry is of great value in the choice of primary treatment of femoral neck fractures.

Adult↗

PubMed1983

Effect of metoprolol on indirect signs of the size and severity of acute myocardial infarction.

In a double-blind randomized trial, 1,395 patients with suspected acute myocardial infarction (MI) were investigated to evaluate the possibility of limiting indirect signs of the size and severity of acute MI with the beta 1-selective adrenoceptor antagonist metoprolol. Metoprolol (15 mg) was given intravenously and followed by oral administration for 3 months (200 mg daily). Placebo was given in the same way. The size of the MI was estimated by heat-stable lactate dehydrogenase (LD[EC 1.1.1.27]) analyses and precordial electrocardiographic mapping. Lower maximal enzyme activities compared with placebo were seen in the metoprolol group (11.1 +/- 0.5 mukat X liter-1) when the patient was treated within 12 hours of the onset of pain (13.3 +/- 0.6 mukat X liter-1; n = 936; p = 0.009). When treatment was started later than 12 hours, no difference was found between the 2 groups. Enzyme analyses were performed in all but 20 patients (n = 1,375). Precordial mapping with 24 chest electrodes was performed in patients with anterior wall MI. The final total R-wave amplitude was higher and the final total Q-wave amplitude lower in the metoprolol group than in the placebo group. Patients treated with metoprolol less than or equal to 12 hours also showed a decreased need for furosemide, a shortened hospital stay, and a significantly reduced 1-year mortality compared with the placebo group, whereas no difference was observed among patients treated later on. After 3 months, however, there was a similar reduction in mortality among patients in whom therapy was started less than or equal to 12 hours and greater than 12 hours after the onset of pain. The results support the hypothesis that intravenous metoprolol followed by oral treatment early in the course of suspected myocardial infarction can limit infarct size and improve long-term prognosis.

Aged↗

PubMed1983

A double-blind trial of metoprolol in acute myocardial infarction. Effects on ventricular tachyarrhythmias.

During a double-blind trial in which patients with suspected myocardial infarction received metoprolol or placebo, we analyzed the occurrence of ventricular tachyarrhythmias. Metoprolol (15 mg intravenously) was given as soon as possible after admission, and thereafter 200 mg was given daily for three months. Antiarrhythmic drugs were given only for ventricular fibrillation and sustained ventricular tachycardia (greater than 60 beats per second). Definite acute myocardial infarction developed in 809 of the 1395 participants, and probable infarction in 162. Metoprolol did not influence the occurrence of premature ventricular contractions or short bursts of ventricular tachycardia. However, there were 17 cases of ventricular fibrillation in the placebo group (697 patients) and only 6 in the metoprolol group (698 patients, P less than 0.05). During the hospital stay significantly fewer patients receiving metoprolol (16) than placebo (38) (P less than 0.01) required lidocaine. In a separate analysis of 145 patients, metoprolol did not influence the occurrence of premature ventricular contractions or short bursts of ventricular tachycardia during the first 24 hours of treatment. Despite a lack of effect on less serious ventricular tachyarrhythmias, metoprolol had a prophylactic effect against ventricular fibrillation in acute myocardial infarction.

Double-Blind Method↗

PubMed1983

Cell culture of renal epithelium derived from rabbit microdissected cortical collecting tubules.

Cortical collecting tubules were dissected from rabbit kidney and cultured in a hormonally defined serum-free medium. Morphologic studies of the cultured cells derived from the collecting tubule indicated that the cells maintained their epithelial nature. These studies also revealed the presence of two distinct cell types that closely resemble the principal and intercalated cell types of the cortical collecting tubule. Several biochemical characteristics of the cultured cells were found to be similar to previously reported values for the cortical collecting tubule. The cells retain hormonal responsiveness to antidiuretic hormone (ADH), as demonstrated by a 12-fold increase in cAMP in response to ADH. Cultured cortical collecting tubule cells produce prostaglandins, with prostaglandin E2 as the predominant cyclooxygenase product. This study presents the first morphologic and biochemical characterization of cortical collecting tubule epithelial cells grown in culture.

Animals↗

PubMed1983

Electrophysiological effects of lidocaine in acute myocardial infarction with bifascicular block or complete A-V block.

Electrophysiological effects of lidocaine were studied in 27 patients with acute myocardial infarction complicated by bifascicular block (group I: 20), and complete A-V block (group II: 7). Lidocaine was administered intravenously in bolus doses of 100 mg each at intervals of 10 min. In group I, there was no significant change in the heart rate (Before (B) = 84.85 +/- 24.19, After (A) = 87.25 +/- 20.26 beats/min) intra-atrial (PA) conduction time (B = 25 +/- 6.18, A = 27.22 +/- 6.69 ms), A-V nodal (AH) conduction (B = 111.5 +/- 56.12, A = 111.5 +/- 56.5 ms) or His bundle to ventricular (HV) activation time (B = 59.5 +/- 19.32, A = 61.25 +/- 18.62 ms) after lidocaine administration. In group II, 2 patients reverted to sinus rhythm, one with 1:1 conduction and the other with type II Wenckebach's block, with being prepared for the study, but both had complete A-V block within 1 h of the His bundle electrogram recordings. Of the remaining 5 patients, 4 had supra and 1 infra His A-V block. After lidocaine, 2 patients developed asystole. In the remaining 4 patients, there was no change in the escape rate or various conduction intervals.

Aged↗

PubMed1983

Mechanisms of angina relief after nifedipine: a hemodynamic and myocardial metabolic study.

To elucidate the mechanisms of action of nifedipine in angina pectoris, 14 patients were studied before and after sublingual administration of 10 mg nifedipine. Systemic and coronary hemodynamic and myocardial metabolic measurements were taken at rest and during pacing. At the pacing rate that induced pain in the control situation, no patient experienced angina after nifedipine administration. Lactate production during control turned into extraction after nifedipine administration (p less than .05), and the double product was reduced (p less than .001). Systemic and coronary vascular resistance were reduced by 26% (p less than .001) and 19% (p less than .005), respectively. Systolic blood pressure fell from 160 +/- 29 to 127 +/- 25 mm Hg (p less than .001) and diastolic from 100 +/- 14 to 79 +/- 11 mm Hg (p less than .001). Pulmonary artery diastolic blood pressure fell from 14 +/- 4 to 10 +/- 3 mm Hg (p less than .01). When the pacing rate was further increased after nifedipine administration until pain developed, the double product and the degree of lactate production were the same as during pain before nifedipine was administered. The pacing rate was 131 +/- 12 compared with 119 +/- 13 during control (p less than .001). Both the systolic and diastolic blood pressures were still significantly reduced compared with control pacing values, 131 +/- 26 mm Hg (p less than .01) and 84 +/- 13 mm Hg (p less than .01), respectively. Our data demonstrate that the antianginal efficiency can be partly explained by afterload reduction, which decreases myocardial oxygen consumption. The data also suggest additional mechanisms, possibly an increase in collateral flow, direct dilatation of stenotic parts of epicardial arteries, or a decrease in myocardial back pressure secondary to reduced left ventricular filling pressure.

Adult↗

PubMed1983

The Göteborg metoprolol trial. Effects on mortality and morbidity in acute myocardial infarction.

In the Göteborg Metoprolol Trial, 1395 patients with suspected acute myocardial infarction were, on admission, randomly allocated to double-blind treatment, 697 to placebo and 698 to metoprolol (15 mg i.v. + 200 mg/day) for 90 days. During this period, there were 62 deaths in the placebo group (8.9%) and 40 in the metoprolol group (5.7%), a mortality reduction of 36% (p less than 0.03). This effect persisted regardless of age, previous infarction or previous chronic beta blockade. All deaths were classified as cardiovascular. After 3 months, all patients were recommended open treatment with metoprolol, and the difference in mortality between the two groups was maintained after 1 year. Early institution of metoprolol (within 12 hours) influenced infarct development during the first 3 days (infarct diagnosis and indirect measures of infarct size). Metoprolol also reduced the incidence on fatal and nonfatal infarction during the next 4-90 days by 35%. Furthermore, fewer episodes of ventricular fibrillation were recorded in the metoprolol than in the placebo group (six vs 17 patients). The tolerance was judged to be very good. The same percentage of patients (19%) was withdrawn from the blind treatment in the two groups. Fewer patients in the metoprolol group used lidocaine, furosemide and analgesics. We conclude that metoprolol therapy instituted on admission in patients with suspected acute myocardial infarction reduced 3-month mortality and exerted beneficial clinical effects.

Adult↗

PubMed1983

Hepatic artery occlusion for liver cancer.

The survival of patients with tumour growth in the liver is very restricted. Interruption of the arterial blood supply to the liver is one method used to control tumour growth. This method is based on the findings that liver tumours are mainly nourished by the hepatic artery. Different methods are used in order to interrupt the arterial blood supply to the liver. Hepatic artery ligation (HAL) has been found in animal experiments to be the most reproducible method to temporary retard tumour growth. Survival has been shown to be prolonged in animals with liver tumours subjected to HAL compared with untreated controls. In humans no effect on the survival time has been observed, but the quality of life of these patients has been claimed to be improved especially those with the carcinoid syndrome. Although interruption of the hepatic arterial blood supply has been used clinically for more than 15 years the method is still an experimental procedure. Further clinical research in this field requires properly designed randomized studies.

Adenocarcinoma↗

PubMed1983

Effects of iohexol and metrizoate on myocardial blood flow and metabolism.

In 10 patients coronary sinus blood flow (CSBF) was measured during and after injection of iohexol and meglumine-Na-Ca metrizoate in the left coronary artery. Oxygen saturation, lactate concentration and hematocrit were determined in the aorta and coronary sinus before and after a second injection of the two contrast media. The increase in CSBF was significantly more marked and sustained after injection of metrizoate than after iohexol and myocardial arterio-venous oxygen difference was significantly lower. Myocardial oxygen consumption and lactate metabolism were not adversely affected by any of the contrast media. The fall in hematocrit in coronary sinus blood was significantly greater after metrizoate.

Contrast Media↗

PubMed1982