[Treatment of pain in suspected acute myocardial infarction--current views on therapeutical alternatives].
Explore the source record for details and available documents.
Adrenergic beta-Antagonists↗
Biomedical subjects
A Hjalmarson
Publications and source records attributed to A Hjalmarson.
International beta-blocker review in acute and postmyocardial infarction.
The benefits of beta blockade in acute and postmyocardial infarction are well documented. More than 50 placebo-controlled trials have been performed, involving more than 40,000 patients with short- or long-term follow-up. In long-term follow-up studies in approximately 20,000 patients, mortality was reduced by 21% and reinfarction by 24%. When high-risk patients were assessed separately, the reduction in mortality after early intervention was significantly greater than in low-risk patients. The trial medication was withdrawn in approximately 24% and 28% of patients in the placebo and beta-blocker groups, respectively, in the major trials. In addition to reduction of mortality and reinfarction rates, benefits have clearly been demonstrated in prevention of arrhythmias and thromboatherosclerotic complications. Significantly more patients had hypotension and bradycardia with beta-blocker treatment than with placebo; no clear-cut difference between the placebo and beta-blocker groups was found for atrioventricular block or congestive heart failure when patients with these conditions were excluded. In the Stockholm Metoprolol Trial, 3 years of metoprolol treatment in about 300 patients after myocardial infarction prolonged both survival and time spent completely asymptomatic, in an optimal functional state, or both. Patients receiving metoprolol spent less time disabled after serious atherosclerotic complications, including bypass surgery. Long-term beta blockade after myocardial infarction reduces mortality and morbidity in 80% of patients by 21% and 24%, respectively, but causes adverse reactions in approximately 10%. With proper selection of patients and the type and dose of beta blocker, survival without atherosclerotic complications or adverse effects can be prolonged.
Adrenergic beta-Antagonists↗
Prediction of rupture in acute myocardial infarction.
In two patient series including 809 and 327 patients, respectively, with acute myocardial infarction we have compared those who died in myocardial rupture (verified at autopsy, Group A) with those who died without rupture (autopsied, Group B), and those who survived hospitalization (Group C) with regard to previous history and clinical course in hospital. Rupture among autopsied patients was observed in 45% and 40% of the cases in the respective studies. Previous infarction was observed in each study as 0% and 0% in Group A compared with 25% and 31% in Group B, and 20% and 34% in Group C. Previous angina pectoris was observed in 26% and 22% in Group A compared with 50% and 54% in Group B and 52% and 54% in Group C. Maximum serum enzyme activity in Group A did not differ from Group B, but was higher than in Group C (p less than 0.001). Group A patients tended to have a higher initial pain score and a higher requirement of analgesics compared with other groups, whereas initial heart rate or systolic blood pressure did not differ in these patients compared to others. We thus conclude that patients with myocardial rupture have a very low occurrence of previous myocardial infarction and angina pectoris, and that their pain course appears to be particularly severe in the acute phase.
Aged↗
Long-term morbidity in patients where the initial suspicion of myocardial infarction was not confirmed.
The morbidity and mortality during a 5-year follow-up in patients admitted to the coronary care unit with chest pain presenting an initial suspicion of acute infarction, but in whom the diagnosis could not be confirmed, is reported. They were divided into four groups: Possible myocardial infarction (29%), angina pectoris (24%), chest pain of uncertain origin (32%), and nonischemic cause of chest pain (15%). The overall 5-year mortality rate was 13.3% and did not differ substantially between the four groups. During the 5-year follow-up a confirmed myocardial infarction developed in 28% and 22% among patients with the diagnosis possible infarction and angina pectoris, respectively, and in about 10% of the remaining patients. Stroke developed in 4% of patients with possible infarction and in 2-3% in the remaining subgroups. In all, 59% of the patients were rehospitalized for a mean duration of 30 days in hospital. Among survivors at 5 years, 54% reported chest pain equivalent to angina pectoris and 25% had chest pain daily. A high prevalence of angina pectoris, a high frequency of rehospitalization due to chest pain, and a high consumption of cardiovascular drugs could be found in all four groups.
Adult↗
Morbidity during five years after myocardial infarction and its relation to infarct size.
In 809 patients with a recent myocardial infarction, morbidity during 5-year follow-up was assessed. The overall 5-year mortality rate was 33% (39% in patients with larger infarcts and 26% in patients with smaller infarcts) as judged from maximum serum enzyme activity (p less than .001). In terms of morbidity, no significant association with estimated infarct size was observed. Patients with smaller infarcts tended to have a higher reinfarction rate and were rehospitalized more often, whereas a similar proportion of patients with large and small infarcts developed stroke. Among survivors, chest pain tended to be more common in patients having smaller infarcts, whereas symptoms of dyspnea and claudicatio intermittens were similar in both groups, as were smoking habits, work capability, and varying forms of medication. We thus conclude that during a 5-year follow-up after acute myocardial infarction, mortality, but not morbidity, was related to the original infarct size.
Electrocardiography↗
Occurrence of hypokalemia in suspected acute myocardial infarction and its relation to clinical history and clinical course.
In 1350 patients with suspected acute myocardial infarction, serum potassium levels during the first 3 days in hospital was correlated to clinical history and clinical course. A higher incidence of hypokalemia was observed in women, in patients with hypertension, and in those on chronic diuretic treatment. Patients with anterior infarction had a higher incidence of hypokalemia than those with inferior infarction, as did patients with large as compared with small infarcts. No clear difference was observed between patients whose infarction was confirmed and those in whom the diagnosis was not confirmed. Independent predictors for hypokalemia were treatment with diuretics before admission to hospital, infarct size, and female sex. Hypokalemia during the first 3 days of hospitalization was associated with the occurrence of severe ventricular arrhythmias during hospitalization, but not with survival during a 5-year follow-up.
Female↗
The relationship between infarct size and mortality and morbidity during short-term and long-term follow-up after acute myocardial infarction.
Explore the source record for details and available documents.
Arrhythmias, Cardiac↗
Body temperature in acute myocardial infarction and its relation to early intervention with metoprolol.
In a subsample of 223 patients participating in a double-blind trial with metoprolol in suspected acute myocardial infarction, body temperature during the first 5 days in hospital was recorded. Patients developing infarction had a mean temperature of 37.3 degrees C compared with 36.8 degrees C for those with no infarction (P less than 0.001). A positive association was observed between enzyme-estimated infarct size and body temperature (P less than 0.001). Patients given metoprolol had a mean temperature of 37.0 degrees C as compared with 37.2 degrees C in those given placebo (P = 0.03). The most marked difference between metoprolol and placebo was observed among those treated very early. We conclude that early treatment with metoprolol in suspected acute myocardial infarction appears to lower body temperature during the following days. This might reflect limitation of the infarct size.
Adult↗
The effect of diabetes on phosphatidylinositol turnover and calcium influx in myocardium.
Diabetes was induced in rats by administration of streptozotocin. Diabetes occurred within 24 h after treatment. Two forms of diabetes were studied, an acute form (4 days) and a chronic form (2 months). In a separate experiment the effect of insulin and an aldose reductase inhibitor on acute diabetes was studied. Phosphoinositide labelling was done in biopsies of heart with [3H] myo-inositol. It was shown that the incorporation of myo-inositol amounted to about 65% in acute diabetes and 80% in chronic diabetes compared to age-matched controls. The incorporation both in atria and ventricles was affected in a similar way. Muscarinic receptor-mediated phosphatidylinositol breakdown and release of myo-Ins-1 P (myo-inositol 1-phosphate) was unaffected in diabetic hearts in the chronic model. In hearts of diabetic ketotic animals uncoupling of the muscarinic receptor from the phosphoinositide metabolism was apparent. Calcium net influx was significantly reduced in both acute and chronic diabetes compared to age-matched controls. Insulin supplementation to acute diabetic animals significantly improved phosphoinositide labelling with [3H] myo-inositol. No improvement was seen in calcium transport. An aldose reductase inhibitor also facilitated phosphoinositide labelling without improving calcium transport. It is suggested that phosphoinositide metabolism and calcium entry through the slow inward current are independent of one another and the former is sensitive to insulin. It is suggested that insulin by regulating the pool of phosphoinositides and release of endogenous calcium may modulate cardiac function.
Animals↗
Effects on mortality during five years after early intervention with metoprolol in suspected acute myocardial infarction.
This study reports the mortality over a 5-year-period determined a double-blind trial, which evaluated the effect of early intervention with metoprolol in suspected acute myocardial infarction. In all, there were 1,395 randomized patients, 698 and 697 of whom were allocated to metoprolol 200 mg daily and placebo treatments, respectively, for the first 3 months. Thereafter, the two groups were treated in a similar fashion implying beta-blockade to a majority. Within the first 3 months, mortality in the metoprolol group was 5.7% versus 8.9% of the placebo group (p = 0.02). This difference persisted after 2 years (metoprolol 13.2%; placebo 17.2%; p = 0.04). Over a 5-year-period, 24.2% of the patients who originally were allocated to metoprolol had died as compared to 25.7% of those originally allocated to placebo (p greater than 0.2). Among patients in whom treatment started early (less than or equal to 8 hours after onset of pain = the median delay time), enzyme activities in the metoprolol group was lower (p = 0.03) than in the placebo group. Mortality during the first 2 years among these patients treated early was lower in the metoprolol (11.8%) than in the placebo group (17.3%; p = 0.04). Corresponding figures after 5 years were 22.0% and 25.3%, respectively (p greater than 0.2). Among patients in whom treatment started later than 8 hours onset of pain, there was neither any difference in enzyme activity nor in mortality after 2 and 5 years. It can be concluded that early treatment with metoprolol in suspected acute myocardial infarction reduced mortality during the first 3 months compared with placebo. The difference persisted after 2 years. However, 5 years after randomization, no significant difference in mortality was observed between the two treatment groups.
Adult↗
Mortality and morbidity during a five-year follow-up of diabetics with myocardial infarction.
In 787 patients with acute myocardial infarction originally participating in the Göteborg Metoprolol Trial, mortality and morbidity during 5 years' follow-up were assessed and related to whether patients had diabetes mellitus. Diabetes occurred in 78 patients (10%). Patients with diabetes had a different risk factor pattern, including higher age, higher occurrence of angina pectoris and hypertension, whereas smoking habits did not differ. In the early phase (hospitalization), patients with diabetes had a higher mortality (12% versus 8%), required more treatment for heart failure and stayed longer in hospital. Other morbidity aspects, such as severity of pain, occurrence of severe supraventricular and ventricular arrhythmias, high-degree AV-block and infarct size did not differ. During 5 years' follow-up mortality rate in patients with diabetes mellitus was 55% as compared with 30% among patients with no diabetes (p less than 0.001). Reinfarction rate during 5 years was 42% in diabetics versus 25% in non-diabetics (p less than 0.001). In a multivariate analysis, taking into account the differences in risk factor pattern, diabetes turned out to be an independent determinant for long-term mortality and reinfarction (p less than 0.001). We conclude that patients with diabetes mellitus, developing acute myocardial infarction, is a group with particularly high risk of death and reinfarction. Interventions aiming at its reduction have priority.
Aged↗
Studies on calcium exchange in platelets in human diabetes.
Calcium has a key role in platelet aggregation. In order to assess the role of calcium metabolism in the platelet in diabetes mellitus, calcium exchange into and out of the cytosol was investigated in platelets from eight patients with insulin-treated diabetes with a mean duration of 10 years without any clinical complications. Their mean HbAIc (glycosylated haemoglobin) was 9% (normal range 3.4-5.4%). Influx rate of 45Ca2+ was significantly increased by 35% in diabetic platelets compared with controls. The efflux rate was significantly reduced during the first 15 min but total efflux measured over 2 h was equal in diabetic and control platelets. Access to sequestered non-mitochondrial calcium in the dense tubular system was gained by permeabilization of the cells with saponin. Into cells loaded with 45Ca2+, Inositol 1, 4, 5 triphosphate (IP3) was introduced and release of the sequestered ion would be determined. In control platelets calcium release was prompt and amounted to 43%. In diabetic platelets the response to IP3 was blunted and was only 17%. The nutritional and hormonal status influenced the response to IP3 in diabetes and, to a lesser extent, in controls. In the fasting state and without insulin the release was reduced but in the fed state and after insulin the release of calcium from diabetic platelets was equal to those of controls. It is concluded that abnormalities exist in platelet calcium handling in diabetes that can be influenced by insulin and the nutritional status.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Infarct size limitation after early intervention with metoprolol in the MIAMI Trial.
One of the secondary objectives of the MIAMI Trial which evaluated the role of the beta-1-selective blocker metoprolol in suspected acute myocardial infarction was to further assess whether early intervention with beta-blockade can limit infarct size. A total of 5,778 patients from 104 worldwide centres were randomized into the trial. Various enzymes such as aspartate aminotransferase (ASAT), creatine kinase (CK), CK MB, CK B, lactate dehydrogenase (LD) and LD isoenzyme I were analysed. All enzymes were used according to the clinical routine of the respective hospital, except ASAT which was analysed once daily for 3 days in the majority of cases and LD I which was analysed every 12 h for 72 h in a subsample. A consistent observation was the lower serum enzyme activity among patients receiving metoprolol and randomized early after onset of symptoms, whereas no difference between metoprolol and placebo was observed in patients treated later in the course. The results of the MIAMI Trial support previous observations that early institution of metoprolol therapy limits infarct size, as indicated by the maximum serum enzyme activity.
Adolescent↗
5-year mortality rate in patients with suspected acute myocardial infarction in relation to early diagnosis.
In 1,395 patients admitted to hospital between 1976 and 1981 due to suspected acute myocardial infarction, the 5-year mortality rate was related to whether they developed infarction or not during the first 3 days. In all, patients with definite myocardial infarction had a 5-year mortality rate of 33.4% as compared with 13.3% in patients not fulfilling the criteria for this diagnosis (p less than 0.001). When separately analyzing patients with no previous myocardial infarction before admission and discharged from hospital, the corresponding mortality rate was 24.1% for myocardial infarction patients versus 8.1% in nonmyocardial infarction patients (p less than 0.001). Among all patients with nonconfirmed myocardial infarction, those who partly fulfilled the criteria (possible myocardial infarction) had a 5-year mortality rate of 16.7% as compared with 12.0% in those in whom myocardial infarction was completely ruled out (p = 0.18). Independent risk factors for death among patients not developing early infarction were high age and a clinical history of previous myocardial infarction and smoking. We conclude that in this study the long-term prognosis among patients admitted to hospital due to suspected acute myocardial infarction was clearly related to whether they developed an infarction or not during the first 3 days in hospital.
Double-Blind Method↗
Morbidity and quality of life 5 years after early intervention with metoprolol in suspected acute myocardial infarction.
In 1,395 patients in the age range 40-74 years participating in a double-blind trial with metoprolol in suspected acute myocardial infarction morbidity and quality of life were assessed during the first 5 years after randomization. During the first 3 months patients were given 200 mg metoprolol daily or placebo. Thereafter the two groups were treated similarly. Mortality during 5 years was 24.2% in patients originally randomized to metoprolol versus 25.7% in patients originally randomized to placebo (p greater than 0.2). No difference was observed regarding reinfarction rate, stroke or occurrence of bypass surgery during the 5-year follow-up. During the first 3 months 10% of patients in the metoprolol group were rehospitalized for various reasons versus 13% in the placebo group. The corresponding figures for 5 years were 59 and 60%, respectively. Among patients surviving 5 years 84% in both groups were on some medication of which beta-blockade was the dominating one. Symptoms of chest pain, dyspnea, claudicatio, smoking habits and working capacity did not differ and neither did quality of life according to the Nottingham Health Profile. We thus conclude that morbidity and quality of life were not significantly affected 5 years after early intervention with metoprolol in patients with suspected acute myocardial infarction.
Adult↗
Age and sex differences in cardiovascular reactivity to adrenergic agonists, mental stress and isometric exercise in normal subjects.
Dose-response curves for intravenous bolus injections of isoprenaline were carried out in 40 normal subjects, in four groups of 10 comprising young and middle-aged males and females. The isoprenaline dose required to raise the heart rate by 50 beats/min, the CD50 (chronotropic dose 50 beats/min), was calculated individually and taken as a measure of the beta-adrenergic responsiveness. Females had significantly higher sensitivity to isoprenaline than males, i.e. lower CD50 values (95% confidence interval 0.07-0.11 versus 0.12-0.17 micrograms/kg body weight, p less than 0.001), and young subjects had higher sensitivity than middle-aged subjects (95% confidence interval for CD50 0.07-0.10 versus 0.12-0.18 microgram/kg body weight, p less than 0.001). Dose-response curves were also carried out for intravenous prenalterol, a partial beta 1-adrenergic agonist. The maximal heart-rate response to prenalterol (delta HRP) showed a significant inverse linear relationship with the CD50 (delta HRP = 44.8-0.11 x CD50, r = -0.53, rs = -0.69, p less than 0.001). A mental stress programme and isometric exercise gave significant increases in heart rate and blood pressure for all groups, but there was no significant relationship between the CD50 and the heart-rate response. By applying a theoretical model, developed by Kenakin and Beek [13], to the isoprenaline-prenalterol data, it is suggested that the observed age and sex differences in beta-adrenergic responsiveness are caused by a tissue-related difference in the stimulus-response mechanism.
Adrenergic beta-Agonists↗
Methanol in dark clouds.
We report observations, for the first time, of the 2(0) - 1(0)A+ and E, 2(-1) - 1(-1) E, and 1(0) - 0(0)A+ lines of methanol (CH3OH) in three dark cold clouds, TMC1, L134N, and B335. The CH3OH emission is extended in these clouds and shows a complex velocity structure. Clear indications of non LTE excitation are observed in TMC 1. Estimated column densities are a few 10(13) cm-2. Although less abundant than formaldehyde (H2CO), methanol is almost an order of magnitude more abundant than acetaldehyde (CH3CHO), in these clouds. Dimethyl ether was searched for in L134N, to an upper limit of 4 10(12) cm-2 (3 sigma). Implications for dark cloud excitation and chemistry are discussed. A new, more accurate, rest frequency 96741.39(0.01) MHz is determined for the 2(0) - 1(0) A+ E line of methanol.
Acetaldehyde↗
Calcium exchange in platelets in human diabetes.
Explore the source record for details and available documents.
Adult↗